Internal medicine #1

Developed this algorithm, not based on my theoretically correct imagination, but based on
having read the newest guidelines.1 In terms of how this might be spun on the USMLE,
however, read below.
TB diagnosis2

PPD skin test is performed first diagnostically. If history of BCG vaccine, do

interferon-gamma release assay (IGRA) instead. Do not do IGRA in addition to
PPD.

If PPD is negative, repeat after one week. If negative again, no further studies
indicated. Repeats performed within 1 week may cause a false (+) secondary to a
“booster reaction.”2

If IGRA is negative, no further studies indicated.

If PPD or IGRA is positive, do CXR. Do not repeat positive PPD tests.

If CXR is negative, treat for latent TB / give TB prophylaxis. On the USMLE,

“treatment for latent TB” and “administer TB prophylaxis” mean the same thing.

If CXR is positive, treat for active TB.

Positive PPD test3

Measure induration only. Erythema does not count.4

5+ mm

• Recent contact with people with active TB

• HIV + status
• Organ transplant recipients
• Chronic prednisone use (>15mg/day for >1 month); anti-TNF-α agent use
• Findings consistent with TB on CXR

10+ mm

• Immigrant status (Western countries not included)

• IV drug users
• Healthcare workers; prison workers; homeless shelter personnel
• TB laboratory personnel
• Children under 4 years of age

15+ mm

• Everyone

Tx of latent TB5

• 9 months INH + pyridoxine (vitamin B6) – The USMLE Steps 1 and

2CK assess this as the answer.
• 4 months rifampin
• 3 months INH + rifapentine + pyridoxine
• Vitamin B6 must be given with INH to prevent vitamin B6 deficiency.6

Tx of active TB7

• Rifampin, INH, pyrazinamide, ethambutol (RIPE) for 2 months,

followed by RI alone for 4 more months (6 months total)
• And of course add pyridoxine (annoying that it sounds similar to
pyrazinamide)

HY lecture notes:

Empiric Tx for community acquired pneumonia is usually azithromycin. Covers

atypicals like Mycoplasma and also Strep pneumo.

Occasionally can use a fluoroquinoline instead of azithromycin, but 1) apparently

hospitals are apprehensive about its use due to the fear of resistance, and 2) it’s
only the answer if someone has been on other antibiotics the past three months.
Even patients with COPD will usually just get azithro first-line.
Most common cause of pneumonia in HIV / immunocompromised is Strep
pneumoniae, not Pneumocystis jirovecii (PJPneumonia).

It’s one of those tricky questions where questions where, for instance, they could
give you someone with history of asbestos exposure, but the answer is still
bronchogenic carcinoma, not mesothelioma, as the most likely lung cancer he or
she will develop.

The USMLE won’t ask you, “What’s the most common cause of x?” That type of
Q is more Qbank style.

For the exam, let’s say in an HIV patient with pneumonia, they expect you to
know that Strep pneumo is lobar, whereas PJP is bilateral and ground-glass on
CXR.

HIV patient + pneumonia:

Lobar –> Strep pneumo, not PJP

Bilateral ground-glass –> PJP

Mycoplasma is also bilateral, but the USMLE won’t make you guess PJP vs
Mycoplasma based on merely having bilateral presentation. In this type of
situation (i.e., when you have a bilateral pneumonia), do bronchoalveolar lavage
(BAL) to diagnose. It’s basically injecting sterile fluid down into the lungs and then
sucking it back up for analysis. Do silver staining of the fluid to look for yeast –>
PJP.

Atypical pneumonia is also known as interstitial pneumonia. The word “interstitial”

is really important. 9 out of 10 questions on atypical pneumonia will give you a
bilateral pneumonia with interstitial infiltrates. I’ve seen one question where they
said something along the lines of, “right lower lobe consolidation with interstitial
markings,” and the answer was Mycoplasma. In other words, “interstitial” wins
over “lobar” for pneumonia. Let me elaborate:

Pneumonia:

Right lower lobe consolidation with dullness to percussion –> Strep pneumo.
Treat empirically with azithro.

Bilateral interstitial infiltrates in immunocompetent patient –> Mycoplasma. Give

azithro.

Bilateral interstitial infiltrates in immunocompromised patient –> Mycoplasma or

PJP. But the USMLE wants PJP. Do BAL to Dx, then Tx with TMP-SMX. If pt is
already on PJP prophylaxis (also TMP-SMX), you know it can’t be PJP, so the
assumption would be Mycoplasma –> give azithro.

Right lower lobe consolidation with interstitial markings –> “Interstitial” wins over
the lobar picture –> Answer is Mycoplasma, not S. pneumo (1 out of 10 Qs –>
HARD).

Normal Ca+ level is 8.4-10.2 mg/dL

Give normal saline first to treat hypercalcemia. If giving a med after, give a
bisphosphonate (e.g, pamidronate).

For Step 3: Ca 10.2-12: fluids only; 12-14: add bisphosphonate only if

symptomatic; 14+: add bisphosphonate regardless

Hypercalcemia can cause nephrogenic diabetes insipidus (weird but assessed).

Renal failure with high BUN (uremia) –> causes uremic platelet dysfunction –>
NORMAL platelet count but increased bleeding time (normal range 2-7 minutes).
Qualitative, not a quantitative platelet problem. They’ll give you epistaxis in
someone with high BUN, normal platelet count, and low Hb –> answer is uremic
platelet dysfunction (or “acquired platelet dysfunction”). Hb is low simply bc the pt
has epistaxis.

High BUN can also cause neutrophil dysfunction, etc., but platelet dysfunction is
highest yield.

Friction rub in the setting of high BUN –> uremic pericarditis (fibrinous). Answer
on USMLE is immediate hemodialysis.

For pulmonary embolism, do heparin, THEN spiral CT.

If pregnant, do V/Q scan (ventilation/perfusion scan), NOT CT.

If the V/Q scan in pregnancy shows segmental defects (positive scan), and they
ask you for the next best step in diagnosis, the answer is CT. You might say “wtf?
I thought we don’t do CT in pregnant women.” It’s true. We don’t. But if they ask
you for the next best step in Dx after V/Q scan, the answer is still CT.

You need to know the acid-base disturance in PE is respiratory alkalosis –> low
O2, low CO2, high pH, normal bicarb. Bicarb is normal bc it doesn’t change so
acutely – takes 12-14 hours to really move. High respiratory rate gets rid of CO2
despite lung pathology bc CO2 diffuses really fast, whereas O2 diffuses more
slowly and requires healthy lung, so O2 is low.
Most common thing you see on an ECG in PE is sinus tachycardia. Don’t select
S1Q3T3. It’s apparently a highly specific finding for PE, but not commonly seen.

So they might say: “Shortness of breath. HR 92. ECG shows no abnormalities.”

But a HR of 92 + ECG that’s normal = sinus tachy right? Makes sense.

BPH is treated with alpha-1 blocker, e.g, terazosin, tamsulosin. 5-alpha-

reductase inhibitors are also first-line (finasteride). Combination therapy is
acceptable first-line over monotherapy and is superior / more effective.

For prostatic adenocarcinoma, give flutamide + leuprolide together. Flutamide

blocks androgen receptors. Leuprolide agonizes GnRH receptors, but
continuous administration desensitizes receptor, causing a decrease in LH and
FSH after a couple days. In practice, both are administered at the same
time. But if the USMLE forces you into a sequence, choose flutamide THEN
leuprolide (i.e., block androgen receptors first). This is bc leuprolide will cause
transient increase in LH and FSH, leading to higher T and DHT levels, before the
desensitization.

Leflunomide is for rheumatoid arthritis. Don’t confuse that with leuprolide.

Leflunomide is a dihydroorotate dehydrogenase inhibitor.

For RA, NSAIDs are used first-line for Sx relief in RA. Corticosteroids can be
used for Sx only when starting a DMARD or when transitioning between different
DMARDs. NSAIDs and steroids do not alter/slow disease trajectory.

DMARDs slow disease trajectory. Methotrexate is first-line.

Early RA: Methotrexate first. If insufficient, add leflunomide or sulfasalazine. OR,

stop methotrexate and give anti-TNF-alpha drug monotherapy (i.e., infliximab,
etanercept, adalimumab, golimumab, certolizumab).

Established RA: Methotrexate first. If insufficient, add anti-TNF-alpha agent.

USMLE won’t assess the high degree of specificity as per above, but you do
need to know the info about NSAIDS and steroids being only for Sx, as well as
that methotrexate is first, and that TNF-alpha the usual step-up after
methotrexate.

Methotrexate causes pulmonary fibrosis. So does RA interestingly (rheumatoid

lung). Both restrictive lung disease – might be hard to differentiate between
whether the cause is RA or the methotrexate (probably both in most patients).

Methotrexate also causes hepatoxicity and mouth ulcers.

 USMLE loves agranulocytosis (neutropenia) as a huge cause of mouth ulcers.
Not sure why this happens mechanistically but is super HY and common.

Ganciclovir, ticlopidine, methimazole, propylthiouracil, clozapine also HY causes

of neutropenia.

Carbamazepine and chloramphenicol can cause aplastic anemia (RBCs and

platelets also down in addition to neutrophils).

Low neutrophils or mouth ulcers + fever = febrile neutropenia / neutropenic fever

–> give immediate IV broad-spectrum antibiotics, such as pipericillin-tazobactam,
or cefepime + vancomycin.

HY lecture notes:

Normal pressure hydrocephalus (NPH) = wet, wacky, wobbly – urinary incontinence,

CNS dysfunction, gait instability

NPH also often has Parkinsonism. This is really HY on 2CK.

So NPH = wet, wacky, wobbly +Parkinsonism

Mechanism for incontinence = “failure to inhibit the voiding reflex” or “impingement

on corona radiata.”

Mid-shaft fracture of humerus fracture = radial nerve –> wrist drop in a pronated arm;
also Saturday night palsy (e.g., with crutches or falling asleep on a chair.).

Supracondylar fracture of humerus injury = median nerve; lateral hand/forearm

function

Surgical neck of humerus = axillary nerve = flattened deltoid or loss of sensation

over deltoid

Medial epicondylar = ulnar nerve = medial hand/forearm

Musculocutaneous nerve palsy = loss of sensation lateral forearm; decreased biceps

function

Erb-Duchenne = upper brachial plexus injury = C5/6 dysfunction = “Waiter tip”

positioning

Klumpke palsy = lowre brachial plexus injury = C8/T1 = claw hand

Ulnar nerve entrapment syndromes on the USMLE are super HY and under-
emphasized in resources.

Cubital tunnel syndrome = ulnar nerve entrapment at the elbow; paresthesias of

medial forearm and hand; do splint as treatment; always start with conservative Tx
on the USMLE for these MSK presentations.

Guyon canal syndrome = ulnar nerve entrapment at the wrist –> hook of hamate
fracture, or ongoing compression due to handle bars (i.e., in avid cyclists).

Polycythemia vera is a primary bone marrow overproduction problem due to JAK2

mutation. Causes high Hb, splenomegaly. Basophils are often elevated, causing
pruritis after showers. Can get flushing and signs of hyperviscosity syndrome –> pain
in fingertips / Raynauds, blurry vision, headache. EPO is down because it’s
suppressed.

In contrast, EPO is elevated in in secondary polycythemia due to low oxygen

tension, e.g., COPD, cystic fibrosis. In this case, only RBCs would be elevated, and
you’d expect O2 saturation certainly under 90%. These patients would presumably
be chronic CO2 retainers as well, with elevated bicarb to reflect chronic respiratory
acidosis. Can also be seen in obesity hyperventilation syndrome.

Interstitial nephropathy is the renal answer when pt takes beta-lactam or

cephalosporin and gets a rash + eosinophils in the urine. Rash need not be present
all of the time, but makes the Q super easy.

NSAIDs can also cause interstitial nephropathy, but eosinophils won’t be seen in
urine.

Acute tubular necrosis causes classically muddy brown granular casts, but “granular
casts” as a general term can also be seen in other things, e.g., pyelonephritis.

For example, 82 yr old granny with costovertebral angle tenderness, fever, and
“granular casts” (not muddy brown) on lab report. ATN and pyelo are both answers.
Answer = pyelo, not ATN.

ATN also is due to ischemia, e.g., from blood loss during surgery. Super HY. PCT
has high concentration of ATPase pumps that require a lot of O2, so ischemia
causes sloughing of PCT.

ATN also due to myoglobinuria (nephrotoxic) secondary to rhabdomyolysis, e.g.,

from electrical burns, alcoholism, McAardle syndrome, drugs like fibrates+statin
combo

Gentamicin (aminoglycoside) is highest yield cause of ATN on the USMLE probably.

Don’t confuse this with NSAIDs/cephalosporins, which, as we said, cause interstitial
nephropathy (aka interstitial nephritis; tubulointerstitial nephritis) instead. Drugs like
gold salts or sulfa drugs can cause regular membranous glomerulonephritis.

Low blood flow to kidney can cause ATN (intra-renal failure) or pre-renal azotemia.
So you need to look at BUN/Cr ratio. If >20 –> pre-renal; if <20, intra-renal (ATN).

If they just tell you episode of low BP during surgery and blood was given, and they
give you no other information whatsoever, choose ATN over hypovolemia as the
cause of renal failure.

Pre-renal is usually due to congestive heart failure or chronic NSAIDs. BUN/Cr >20;
FeNa <1%; high urine osmolality. This is because the PCT is trying to absorb more
water to compensate for what is perceived as low blood volume. In order to reabsorb
water, cations are reabsorbed, namely Na, and then water follow sodium. So there’s
lower sodium in the urine in prerenal –> indicates PCT is trying to retain water.

One can even go on to say that this causes low Na flow distally at the macula densa
(DCT), which is a trigger for renin release from JGC. That is, if the macula densa
senses low sodium, it means the PCT is trying to reabsorb it, so our volume must be
low (or the kidney just isn’t getting blood flow, e.g., renal artery stenosis or
fibromuscular dysplasia), so RAAS is upregulated.

In intra-renal, BUN/Cr is <20. FA for Step 1 had said <15 for intra-renal, 15-20 for
post-renal, and >20 for pre-renal, but I can tell you that there are various questions
on 2CK NBMEs where you’ll get ratios of, e.g., 17, where the answer is ATN, clearly
intra-renal.

So I just go with >20 = pre-renal; <20 = not pre-renal.

Post-renal could be due to BPH or urethral stricture, etc. Hydronephrosis can occur.
USMLE likes “increased Bowman capsule hydrostatic pressure” as an answer in
post-renal failure. Iow, since the latter is increased, there’s decreased ability to filter
through the glomerulus. Renal failure by definition is decreased GFR. So that’s the
mechanism.

Answer for BPH and urinary retention / post-renal insufficiency always = insert a
catheter as the next best step, even if he’s got a fever of 100F and 1+ bacteria in the
urine. Insert the catheter before giving Abx.

HY lecture notes: 4

Do colonoscopy starting age 50 and do every ten years. If first degree relative
(parent or sibling) has Hx of colon cancer, start at age 40 or 10 yrs before that family
member was diagnoses, whichever is earlier, then do every 5, not 10 years.
In patients diagnosed with IBD (Crohn or UC), do colonoscopy 8 years after Dx is
made, followed by every 1-2 years thereafter. Sounds outrageously often, but it’s
what the literature says.

In patients with Peutz-Jeghers syndrome, although the hamartomatous polyps are

non-cancerous, there is still increased risk of multi-system malignancy in PJS,
including CRC. Do colonoscopy at age 8. If positive for polyps, continue every three
years. If negative at age 8, repeat at age 18, then do every 3 years.

For BPH, always insert a catheter first, even if he has bacteriuria.

So for instance, if 72-year-old male with suprapubic mass (bladder), fever 100F, and
1+ bacteria in the urine, insert catheter before giving antibiotics.

Calcified pleural / supra-diaphragmatic plaques = asbestosis.

Causes restrictive lung disease. Normal or increased FEV1/FVC.

FEV1 and FVC are both, as independent variables, decreased. But the ratio is
normal or increased.

There’s a Q on a newer NBME for Step 1 that forces you into a corner to choose
normal FEV1 as an independent variable, but it was the only answer that made
sense. So just be aware it’s never hard-and-fast rule for the variables.

Radial traction in restrictive lung disease = “stickiness” of fibrosis on the outside of

the airways, decreasing their ability to close –> FEV1 is greater than expected –>
FEV1/FVC is greater than expected. In contrast, obstructive lung disease the ratio is
decreased because radial traction isn’t involved.

Systemic inflammatory response syndrome = at least 2 out of 4 of the following:

• Temp <36 or >38

• RR >20
• HR >90
• WBCs <4,000 or >16,000 cells per mm3

Sepsis = SIRS + source of infection.

Septic shock = sepsis + low BP.

Treat community acquired sepsis with third-generation cephalosporin. Ceftriaxone is

most frequently used.

In pediatrics, cefotaxime is often chosen. There’s a Q on one of the IM forms that

says there’s an 11-month-old with sickle cell who missed a dose of penicillin
prophylaxis (for Strep pneumo) and now has septic shock. How do you treat? Wrong
answer was penicillin. Correct answer was cefotaxime. Ceftriaxone was not listed.

Cefotaxime apparently causes less displacement of bilirubin from albumin, so there’s

less chance of jaundice in peds.

But then there was a different question on NBME8 where it was a slightly older child
who had sepsis, and the answer was ceftriaxone. Cefotaxime wasn’t listed. So the
bottom line is, be aware that cefotaxime is frequently chosen in peds, and if you’re
given it as an answer choice next to ceftriaxone, choose cefotaxime. But if either
drug is the only third-gen ceph listed, just go with whichever they list.

Empiric Tx for meningitis = vancomycin + ceftriaxone (+/- steroids).

Do lumbar puncture BEFORE antibiotics, the same way all blood cultures are done
before giving antibiotics.

Indications for doing a head CT before an LP in suspected meningitis:

• Seizure
• Focal neurologic signs (e.g., motor or sensory dysfunction)
• Papilledema or if the optic fundi cannot be visualized
• Confusion that interferes with the neurologic exam / decreased Glasgow
score

If confirmed Neisseria meningitidis meningitis, give rifampin to close contacts –>

decreases nasopharyngeal colonization.

Rifampin upregulates P-450. If on hormonal contraception, give ciprofloxacin instead

(inhibits P-450).

N. meningitidis classically causes non-blanching rash; that’s how you know it’s the
causal organism in the vignette, versus, e.g., S. pneumo, which doesn’t cause non-
blanching rash.

Low blood pressure in someone with meningococcal septicemia = Waterhouse-

Friderichsen syndrome = hemorrhagic necrosis of the adrenal glands.

Give normal saline (0.9% NaCl) first. But if that’s insufficient,

give hydrocortisone. The adrenal necrosis means decreased cortisol, so you need
to replace glucocorticoid.

Cortisol normally maintains BP by upregulating alpha-1 expression on vascular

endothelium so that NE and E can bind and constrict. It is permissive of the effects of
catecholamines, meaning without its presence, NE and E cannot do their job. So
even though NE is classically given in septic shock as a pressor agent, in the setting
of WFS, give hydrocortisone.
Fludrocortisone is the treatment for Addison disease (primary adrenal insufficiency,
where aldosterone and cortisol are both low).

All glucocorticoids have varying degree of mineralocorticoid effect, meaning they can
very marginally act similar to aldosterone in the kidney.

Glucocorticoids like prednisone, hydrocortisone, and dexamethasone have very little

mineralocorticoid effect. That is, they are very similar to cortisol and dissimilar to
aldosterone.

Fludrocortisone has very high mineralocorticoid effect, meaning it can function like
cortisol AND aldosterone, and is therefore appropriate in Addison.

Cushing syndrome can sometimes cause an isolated decrease in potassium

because chronically elevated cortisol levels can lead to enough mineralocorticoid
effect at the kidney to cause potassium wasting. But it requires very high, and
chronic, glucocorticoid / cortisol levels to achieve this. But that’s a heads up,
because you might get a patient with Cushing syndrome who has a K of 3.0, and
that’s why.

HY lecture notes:5 IM

Tx for Pneumocystis jirovecii pneumonia (PJP) = TMP-SMX. However, add steroids

when A-a gradient is >35, or pO2 <70 mm Hg.

New literature (2019) has suggested mortality rates improve when adding steroids in
patients with pO2 <60 mm Hg.

The bottom line is that if a patient is in severe respiratory distress in the vignette and
has PJP, AND they give you TMP-SMX + steroids as an option alongside standard
TMP-SMX, the former is correct.

Zenker diverticulum (false diverticular outpouching of posterior esophageal wall) will

present classically with halitosis (bad breath), regurgitating undigested food, and/or
gurgling sound when drinking fluids.

Sometimes what they’ll do is give you an equivocal vignette and then show you a
barium (or a gastrografin water soluble contrast) swallow where there’s an
outpouching, and the answer is: “Cricopharyngeal muscle spasm.”

Increased oropharyngeal pressure is also a big risk factor for Zenker, as this is
conducive for the herniation to occur. This can be seen in patients who
have dysphagia, as this can lead to increased strain/force required by the patient to
achieve swallowing. Tx is surgical.
Achalasia classically presents as dysphagia to both solids and liquids. Neurogenic
causes present with dual dysphagia. Esophageal manometry (pressure studies) is
best test to diagnose, but barium (or gastrografin) swallow is best next step.

If they give you both barium swallow and esophageal manometry as answers in
someone with a vignette that might sound like achalasia, choose barium, not
manometry, as the next best step.

Manometry will be the answer if they show you a radiographic image of a contrast
swallow exhibiting the “bird’s beak” appearance:

Achalasia is often idiopathic but may also be due to Chagas disease (Typanosoma
cruzi).

Treatment for achalasia is either medical therapy with nitrates or calcium channel
blockers, or surgical with pneumatic dilatation or myotomy. The latter is more
effective than balloon dilatation.

Dysphagia to solids that PROGRESSES to dysphagia to solids and liquids =

esophageal cancer. This is especially the case in someone with big Hx of GERD
(adenocarcinoma) or heavy smoking/drinking (squamous cell carcinoma).

It’s generally the answer on the USMLE to do an endoscopy in a patient who has
history of GERD and new-onset dysphagia. We talked above about how contrast
swallows are done first for suspected Zenker and achalasia, but if the patient has Hx
of GERD, that changes everything and he or she needs an endoscopy. Equivocal
vignettes that give you, e.g., a presentation that sounds similar to Zenker or
achalasia, in a patient who is clearly a heavy smoker/drinker, the USMLE wants
endoscopy for that too.
CREST syndrome is also known as limited systemic sclerosis. Systemic sclerosis
can be either diffuse or limited.

Limited systemic sclerosis = CREST = scleroderma = anti-centromere Abs = less

propensity for systemic phenomena such as renal involvement.

Diffuse = anti-topoisomerase (anti-scl70 Abs) = renal involvement.

Both can cause pulmonary fibrosis with restrictive lung disease –> normal or
increased FEV1/FVC.

Pulmonary hypertension can result from the fibrosis, so if you get a vignette of
CREST and they say what is this patient at increased risk for, the answer is
pulmonary hypertension.

Pulmonary hypertension can cause cor pulmonale –> right-sided heart failure due to
a pulmonary origin. That is, the cause cannot be left heart failure. Pulmonary
capillary wedge pressure (PCWP) is normal in cor pulmonale because the left heart
is fine. If PCWP is high, the Dx is not cor pulmonale.

PCWP is elevated in cardiogenic shock.

For CREST syndrome (calcinosis, Raynaud phenomenon, esophageal dysmotility,

sclerodactyly, telangiectasias), you need to know LES tone and esophageal
peristalsis are both decreased (both down arrows); this was on one of the retired
Step 1 NBMEs.

CREST can also involve the intestines in a smaller fraction of patients. There’s a
question on one of the surgery forms where they said a patient with CREST had a
12-cm cecum, and the answer was laparotomy because the Dx was toxic
megacolon.

Tx Raynaud phenomenon with calcium channel blockers.

Most common cause of nephrotic syndrome in sickle cell is focal segmental

glomerulosclerosis (FSGS). So protein in the urine + no blood = FSGS in sickle cell.

If this patient has ascites as a result of the nephrotic syndrome, this can lead to
spontaneous bacterial peritonitis (SBP). Must diagnose with paracentesis (aspiration
of peritoneal fluid). Don’t confuse with pericardiocentesis.

Do a gram stain of the peritoneal fluid. Also check for >250 white cells per high-
power field.

SBP will be seen in three different vignettes: hepatic cirrhosis with ascites; someone
who’s just undergone peritoneal dialysis; or someone with nephrotic syndrome. On
one of the newer peds forms, a vignette gives an 8-year-old with nephrotic syndrome
who has a diffusely tender abdomen + fluid wave + fever; answer = paracentesis. Tx
SBP with ceftriaxone.

HY lecture notes:6 im

CML –> splenic enlargement; bloods show increased metamyelocytes +

myelocytes. Seeing these two cell types in a question is essentially synonymous with
CML. Let’s just say 19 times out of 20. Only time it won’t be CML is if they literally
explicitly say “hey, the alkaline phosphatase activity is high” –> then you know it’s
“leukemoid reaction,” not CML; LR is just a response to infection. In CML, LAP is low,
not high.

AML –> myelocytes, myeloblasts, promyelocytes on CBC.

CML –> myelocytes, metamyelocytes, neutrophils on CBC.

Treatment for CML is imatinib –> bcr-abl tyrosine kinase inhibitor. Imatinib causes
fluid retention (edema).

Student asks about which other drugs I’ve mentioned that cause fluid retention –>
Dihydropyridine calcium channel blockers such as nifedipine are exceedingly HY for
causing edema.

CLL –> smudge cells + warm autoimmune hemolytic anemia (IgG antibodies against
RBCs)

AML –> Auer rods

ALL –> kids; Down syndrome

Before starting isotretinoin (high-dose vitamin A for acne), must do pregnancy test
(beta-hCG). There is also a USMLE question floating around where they say they start
a girl on OCPs due to starting isotretinoin, and they ask what else you should do, and
the answer is “recommend barrier contraception.” Students will get this wrong
because they say, “Wait, I don’t get it, why two methods?” We can debate it all we
want, but it’s still on the NBME. This may have been on NBME 7 or 8 for 2CK.

Acne management:

1. Topical retinoids first (i.e., topical tretinoin; NOT oral isotretinoin) ; cause
photosensitivity (rash); also used for photoaging; mechanism is decreasing
sebum production.
2. Benzoyl peroxide used second; often coadministered with topic retinoids;
mechanism is the killing of bacteria.
 3. Topical clindamycin
4. Oral tetracycline; causes photosensitivity (blistering)
5. Oral isotretinoin; must do beta-hCG in women; recommend barrier
contraception even if on OCP; can cause elevations in LFTs; can cause
dyslipidemia; main complaint is dry skin + peeling; takes several weeks to
really start working but ultra-effective according to most patients; can be
commenced earlier in patients with severe nodulocystic acne; works by
diffusely shutting of sebum production

Student may ask, “USMLE is actually that pedantic about acne management?” My
answer: 2CK will assume you know #1+2 are used first and that #5 is last resort for
most patients, and that #1 and #4 cause photosensitivity; Step 1 wants you to know
mechanisms of the drugs in terms of how they actually treat the acne (which I’ve
written above).

African-American female in 20s-30s with dry cough:

Chest x-ray (CXR) normal: answer = asthma = “activation of mast cells.”

CXR: multiple nodular densities = bihilar lymphadenopathy = sarcoidosis = “non-

caseating granulomas.”

About one-third of patients with asthma present with just a dry cough. This is really
HY for the USMLE. This is known as cough-variant asthma.

For instance, person has dry cough in winter, allergies in spring, a bit of itchiness of
antecubital fossae in summer –> atopy –> dry cough is actually asthma; doesn’t need
they need Tx; but it’s the diagnosis. And the 2CK expects you to know that.

Wegener granulomatosis is now known as granulomatosis with polyangiitis (GWP).

It’s not also known as; it’s formerly known as Wegener. Learn the new name. I had a
student get an easy Wegener Q on the exam, and she said the answer was
“polyangiitis.”

GWP causes hematuria + hemoptysis + “head-itis” (inflammation/pathology involving

the head, such as mastoiditis, otitis, sinusitis, nasal septal perforation).

GWP is anti-PR3 (anti-proteinase 3; aka c-ANCA.

Churg-Strauss, now known as eosinophilic granulomatosis with polyangiitis (EGWP),

is anti-MPO (anti-myeloperoxidase; aka p-ANCA). Microscopic polyangiitis (MP) is
same antibodies as EGWP.

EGWP is asthma + eosinophilia + p-ANCA.

MP is hematuria + p-ANCA.

GWP is hematuria + hemoptysis + head finding + c-ANCA.

Goodpasture syndrome is hematuria + hemoptysis + anti-GBM antibodies (glomerular

basement membrane).

Goodpasture is antibodies against the alpha-3 chains of type IV collagen. Causes

linear immunofluorescence on renal biopsy.

Alport syndrome is mutations in type IV collagen, not antibodies. X-linked recessive

(some sources say XD, but NBME 19 for Step 1 had XR as the answer). Presents as
eye + ear problem in boy or man with red urine.

HY lecture notes:7

On the USMLE, new onset murmur + fever = endocarditis until proven otherwise.

Empiric treatment means that which is given before the culture results are known. It
is based on educated guessing. The word empiric comes from the Greek
word empeiria, which in direct translation means experience.

Empiric treatment for endocarditis

• Vancomycin or ampicillin/sulbactam, PLUS an aminoglycoside (e.g.,

gentamicin)
• Add rifampin in patients with prosthetic valves

This means in most patients treatment is vancomycin + gentamicin, OR

Ampicillin/sulbactam + gentamicin. In patients with prosthetic valves, rifampin must
be added.

Treatment for tinea capitis = oral griseofulvin for patient only (one of the IM forms
asks for patient only vs also give to close contacts; answer was patient only);
Trichophyton tonsurans is fungal cause. Black under Woods lamp. Griseofulvin
inhibits microtubules (Step 1).

Tinea corporis (ring worm) Tx is topical clotrimazole or miconazole.

Tinea pedis = topical terbinafine; but have also seen a Q where it was topical -azoles.
In this latter Q, it was the only antifungal listed, but topical terbinafine should be
known as the main way to Tx.
Onychomycosis = fungal infection of nails. First-line Tx is oral terbinafine (6 weeks
for fingernails; 12 weeks for toenails; USMLE won’t ask duration, but I write that hear
as interesting side-context). Second-line is griseofulvin.

Tinea versicolor (Malassezia furfur) = Tx with topical selenium.

Tx of scabies = topical permethrin.

Tx of lice (pediculosis) = also is topical permethrin.

Supraventricular tachycardia (SVT) Tx with carotid massage (vagal maneuvers),

followed by adenosine. SVT is NARROW complex QRS complexes (needle-shape).
80-120 normal.

VT use anti-arrhythmics, e.g., amiodarone. VT is wide-complex. Rarely SVT with BBB

can be wide-complex, but you won’t see that on the USMLE. You need to know wide
is VT, full-stop.

If pt has tachy arrhythmia and is unconscious, do direct cardioversion as Tx.

A random wide complex beat on an ECG strip = premature ventricular complex (PVC)
= ventricular ectopic beat. No Tx necessary if asymptomatic. HY.

Pacemaker for third-degree heart block and Mobitz type II.

Third degree is super slow HR (e.g., 30-40) + no relation between p-waves and QRS
complexes.

Mobitz II is when you have a random drop of the QRS complex, where the PR-
interval does not gradually increase before the dropped complex. Can become a
third-degree HB, which is why pacemaker is used for this.

Mobitz I (Wenckebach) is gradually prolonging PR-interval followed by dropped QRS.

Don’t need pacemaker.\

Vaccines:

At birth: Hep B (+ vitamin K)

2, 4, 6 months: Pneumococcal PCV13, rotavirus (live oral), H. influenzae type B, TdP,

Polio Salk (killed, IM), Hep B.

New guidelines might not require Hep B at 4 months.

Give MMR first dose at 12-15 months; second dose 4-6 years.

Varicella give 12-18 months.

HPV give age 9-45 years.

Influenza give starting at 6 months (killed IM); can give to pregnant women; give
every year in fall/winter; can give live nasal spray vaccine to non-pregnant, non-
immunocompromised persons age 2-49.

Alpha-1-antitrypsin deficiency –> codominant inheritance –> enzyme normally

produced in liver but goes to the lungs; disease causes hepatic cirrhosis + emphysema
young-ish non-smoker; family Hx of someone who’s had emphysema or liver disease.
One question says dad died of alcoholic liver disease at age 55 –> probably implying
increased susceptibility to severe liver disease bc of the alpha1aT deficiency. Alpha-1
antitrypsin normally breaks down elastase, so increased elastase can cause pan-
acinar emphysema; smoking causes centri-acinar. Bullous changes or increased
lucency on CXR means emphysema.

More anemia of chronic disease (in hematology #5 lecture):

Renal failure –> increased Cr, Hb low, Hct low, MCV normal, ferritin normal, iron low,
transferrin saturation normal –> anemia of chronic disease (AoCD)

Can be due any type of chronic disease, e.g., RA, SLE, IBD; can also be due to chronic
infections like HepC.

Can treat with EPO is renal failure is etiology; if not renal failure, CANNOT give EPO
and you treat underlying condition.

AoCD is usually normal MCV (80-100), but some 2CK Qs are presenting with low
MCV; but if this is the case, you’d easily be able to eliminate the other answer choices
in the Q.

For instance, if Q is presentation with a kid who has obvious JRA (Still disease) –
salmon rash (about half the time), high ESR, recurrent joint pain – and MCV is, e.g.,
72, answer is still AoCD if anemia is present.

Transferrin saturation = Fe / TIBC (total iron binding capacity)

Anemia of chronic disease: iron is low; ferritin is normal or even elevated; transferrin
low; transferrin saturation low or normal (bc TIBC is low, bc transferrin low)

Iron deficiency: iron low; ferritin low; transferrin high; transferrin saturation super low
(bc TIBC very high, since transferrin high)
HY lecture notes:8

Congenital hip dysplasia –> Dx with “clicking/clunking” of hip (Ortolani + Barlow

maneuvers) –> if (+), do ortho referral next. Sounds incredibly wrong, since referral is
supposed to notoriously be a wrong answer, but it’s what the USMLE wants (this is
even assessed a couple times in UWorld for Step 3).

If ortho referral is not listed, go straight to imaging. Do ultrasound if under 6 months;

do x-ray if over 6 months. The 4-6 month-range is borderline, but don’t worry about
it. Essentially if ultrasound is negative or equivocal between 4-6 months of age, x-ray
may have some utility if done subsequently, but the USMLE highly likely won’t go
there. Just choose ultrasound if under 6 months and x-ray of hip if over 6 months.

Tx = Pavlik harness, but on the USMLE, they’ll say “abduction harness.” It’s a frog-leg-
looking harness.

Slipped capital femoral epiphysis (SCFE) –> 11-13-year-old (preadolescent)

overweight boy with a painful limp. X-ray will show slippage of the epiphyseal plate
of the hip. Tx with surgical pinning.

Idiopathic avascular necrosis of the hip (Legg-Calve-Perthes) will be a kid 5-8 years
old who has a painful hip. It’s the fact that it’s idiopathic that makes the Dx LCP
disease. If there’s a known cause, e.g., sickle cell or chronic / high-dose corticosteroid
use, the Dx isn’t LCP, and is instead just “avascular necrosis.”

So, e.g., random kid with avascular necrosis of hip –> Dx = LCP disease

Kid with sickle cell has avascular necrosis of hip –> Dx = avascular necrosis.

The femoral head will classically be “contracted” on x-ray. This is really really HY. This
word overrides pretty much any other descriptor you can get in a question stem. For
example, there’s a Q on one of the NBME forms where they say it’s a kid who’s 8
years old with a painful limp, and they tell you the x-ray shows a “contracted femoral
epiphysis.” So immediately you’re like, “Oh that sounds like SCFE bc of the ‘femoral
epiphysis’ part.” But the Dx is Legg-Calve-Perthes because the word “contracted”
wins.

X-ray can be negative in the first few weeks of the avascular necrosis, but it’s the
next best step in diagnosis regardless. If they tell you the x-ray is negative, do a bone
scan or MRI to diagnose. There’s a Q on one of the newer peds forms where they say
a bone scan (bone scintigraphy) was performed on a young kid with hip pain –>
what’s the Dx? –> answer was LCP disease. So if you only thought x-ray was used,
you’d be wildly confused.
For non-atrial fibrillation patients with TIA / stroke / retinal artery occlusion, if they
blindly ask you which lifestyle change will best decrease risk of recurrence, the
answer is hypertension control, not smoking cessation. Hypertension control is more
important than smoking cessation for decreasing risk of embolic phenomenon from
the carotid arteries. If the patient has atrial fibrillation as the etiology, that’s entirely
different.

So guy who’s middle age has elevated blood pressure and is heavy smoker; he has a
TIA –> how to best decrease recurrence? –> answer = lisinopril, not smoking
cessation.

Hypertension causes endothelial damage notably at the carotids bc of the systolic

impulse pounding on the endothelial cells there due to their proximity to the heart.
Current guidelines want carotid endarterectomy as the Tx if carotid occlusion on
duplex ultrasound being > 70% when symptomatic (sympomatic = TIA, stoke, or
retinal artery occlusion), or >80% when asymptomatic. A bruit isn’t a symptom; it’s a
sign.

If under those thresholds, do medical therapy with statin + clopidogrel, OR statin +

dypridamole + aspirin.

USMLE also wants you to know rhabdomyolysis –> false (+) blood on urine dipstick.
So you’ll see 2+ blood on dipstick but 0-4 RBCs/HPF on light microscopy.

Rhabdo is seen in alcoholics, electrical burns, McArdle, drugs such as statins + fibrates
combo.

Rhabdo is nephrotoxic –> can cause acute tubular necrosis + hyperkalemia.

Tx for acute gout = indomethacin, steroids, or colchicine. All are equally acceptable
according to current literature, but USMLE favors indomethacin first as standard Tx.

If indomethacin + steroids are not listed, colchicine will be the answer.

Steroids are the answer in patients with renal insufficiency or Hx of renal transplant.

Chronic gout Tx with allopurinol or febuxostat (xanthine oxidase inhibitors). Never

give these in acute gout as they can make it worse.

Uricosurics such as probenecid are not first-line for chronic gout and should not be
used in those with uric acid overproduction because of risk of precipitating renal
stones. Probenecid can also be used to maintain beta-lactam levels in the blood.

Two biggest risk factors for pseudogout (Calcium pyrophosphate deposition disease;
CPPD) are hemochromatosis and primary hyperparathyroidism.
Will present as monoarthritis of a large joint, such as the knee, or as an osteoarthritis-
like presentation in someone with hemochromatosis or primary
hyperparathyroidism. Tx acutely same as gout. For chronic, Tx underlying cause,
since xanthine oxidase inhibitors clearly are unrelated.

Tx of osteoarthritis (OA) = weight loss (if overweight) + acetaminophen. NSAIDs can

also be used first-line for Sx, but acetaminophen is superior bc it won’t affect the
kidney. USMLE wants acetaminophen as the answer; this on on the family medicine
forms.

They might tell you in a vignette that an older woman is taking high doses of
naproxen (an NSAID) to Tx her OA (clearly not what someone should be doing, but
then they go on to explain that she has renal pathology because of it). They say she
has peripheral edema. –> Why does she have edema –> answer = decreased renal
excretion of sodium / increased renal retention of sodium.

Basically NSAIDs knock out prostaglandin synthesis –> decreased afferent arteriolar
dilatation –> decreased renal blood flow –> pre-renal insufficiency ensues –> kidney
tries to increase fluid retention because it thinks blood volume is low –> upregulation
of RAAS –> AT II causes increased PCT reabsorption of sodium –> increased sodium
retention through PCT –> water follows sodium –> edema.

This also explains why fractional excretion of sodium (FeNa) is low in pre-renal
etiologies of renal failure –> kidney tries to reabsorb sodium as the mechanism for
increasing fluid retention.

HY lecture notes:

Strongest indication for anticoagulation on the USMLE = having a prosthetic valve.

This is asked straight-up on one of the NBME forms.

Tx of asthma outpatient:

1. Short-acting beta 2 agonist (albuterol) SABA

2. Add low-dose inhaled corticosteroid (ICS)- Fluticasone
3. Maximize dose of ICS
4. Add long-acting beta 2 agonist (salmeterol) LABA

This above order is universal. Then I say “dot dot dot dot dot……..give oral
corticosteroids” because oral steroids are last resort, and the drugs that are given in
between the LABA and the corticosteroids are subjective and variable as to the order,
i.e., mast cell stabilizers (e.g., nedocromil, cromolyn sodium), lipoxygenase inhibitor
(zileuton), leukotriene receptor blockers (montelukast, zafirlukast).

For instance:
12-year-old currently uses an albuterol inhaler but still gets weekly episodes. What’s
the next best step? –> Add low-dose ICS.

12-year-old currently uses an albuterol inhaler but still gets weekly episodes. What’s
the most effective way to decrease recurrence? –> Answer = oral corticosteroids.

Now this is where students go, “Wait wtf do you mean. I thought oral steroids are last
resort.” You’re right, they are. But they’re still most effective.

And this isn’t me writing statements for entertainment purposes. Those questions are
on the IM and FM forms (there’s a lot of overlap).

Inhaled corticosteroids have zero role in acute asthma management. In acute asthma
attack, use the albuterol inhaler. In emergency situations, nebulized albuterol with
oxygen is given. Then IV steroids are administered (i.e., not ICS or oral).

Acute asthma attack:

Bicarb NORMAL (too acute to change); CO2 is LOW, NOT HIGH because respiratory
rate is high (CO2 diffuses quickly, so even if your lungs are loaded with secretions
and there’s bronchoconstriction, it can still get out easily in the setting of high RR). pH
is therefore high, not low.

Therefore: acute asthma attack, hyperventilates = respiratory alkalosis = normal

bicarb, low CO2, high pH, low O2.

The same is true for pulmonary embolism. One is breathing quickly so the CO2 is low,
not high. Bicarb won’t change for at least 12-24 hours, so it’s normal acutely. pH will
be high.

So acute asthma attack + PE both are respiratory alkalosis.

The combination of CO2 and O2 both being low = type I respiratory failure. As the
patient gets tired, CO2 and pH will begin to normalize because the patient is getting
tired:

Patient getting tired, hypoventilates–> bicarb still normal, CO2 normal, pH normal,
O2 low –> the patient is now in transition to a type II respiratory failure (O2 and CO2
will become opposite directions).

That means if you see bicarb still normal, CO2 normal, pH normal, O2 low in the
setting of acute asthma attack –> answer = intubate.
Aspirin toxicity causes a respiratory alkalosis acutely (only if <20 minutes; I explain
timing more below). So if <20 minutes, you’ll see normal O2, low CO2, high pH,
normal bicarb (won’t change so acutely).

After 20 minutes, pathology becomes mixed metabolic acidosis-respiratory

alkalosis. In this case, bicarb is low (NOT A COMPENSATORY RESPONSE TO THE
RESPIRATORY ALKALOSIS; IT LOOKS LIKE COMPENSATION BUT IT’S NOT; it
can’t be compensation because of how acute it is; this is due to the aspirin itself being
an acid). So after 20 minutes –> bicarb low (metabolic acidosis), CO2 low (respiratory
alkalosis), pH low or normal, O2 normal (not a lung pathology). I’ve seen Qs where pH
is super-low; I’ve also seen it lower end of normal; but the metabolic acidosis part will
always win over the respiratory alkalosis. This is a high-anion gap metabolic acidosis
(salicylate toxicity).

Now with respect to the timing: On one of the 2CK pediatrics forms (or it might be
NBME 6 I can’t remember), they say a girl consumed a bottle of aspirin 20 minutes
ago, and now she’s lethargic and has high RR. What’s the acid-base disturbance? And
they list all of the different possibilities. Answer is mixed metabolic acidosis-
respiratory alkalosis, not isolated respiratory alkalosis. It’s what the USMLE wants. I
don’t know what to say. I’ve tended to notice that “lethargy” somewhat non-
specifically implies metabolic acidosis in acid-base Qs; I’ve seen lethargy in Qs for
patients with lactic acidosis.

Tx for aspirin toxicity = sodium bicarb –> increased excretion through urinary
alkalinization –> deprotonates aspirin from -OH –> O–. Ionic oxalate isn’t absorbed
through the renal tubules as readily.

In renal failure, bicarb is low, calcium is low, phosphate is high, potassium high,
sodium variable.

USMLE wants mechanism for low calcium in chronic renal failure as “decreased
intestinal absorption.” Which means the decreased vitamin D activation to 1,25-OH2-
D3 is the reason for it.

Phosphate and potassium are high in RF because kidney can’t excrete them. Sodium
is variable (I’ve seen it all over the place in questions).

In chronic renal failure, patient will have vitamin D deficiency, BUT YET PHOSPHATE
IS STILL HIGH.

Iow, it’s pretty standard to know that vitamin D deficiency = low calcium AND low
phosphate, but in the setting of renal failure, the effect of the renal failure wins, so
phosphate is still high. That is, despite decreased intestinal absorption of phosphate,
the inability to excrete it causes it to be high.
In acute renal failure, if calcium declines, the answer would be impaired reabsorption
(too acute to be anything vitamin D-related).

HY lecture notes:

Tx cystitis with nitrofurantoin; notably the answer in pregnant women; but there’s
also a Q on one of the 2CK NBMEs where it’s the answer in a non-pregnant patient.

Osteoporosis –> Ca, PO4, PTH, and ALP are all normal.

In renal failure, secondary hyperparathyroidism –> low Ca, high PO4.

Primary hyperparathyroidism is due to adenoma –> high Ca, low PO4. Diffuse
hyperplasia can be seen in MEN1 or MEN2A, but may also be adenoma.

Urinary cAMP is increased if PTH is high.

Urinary calcium is increased, not decreased, in primary PTH, despite the renal
reabsorption of Ca. Why? Because blood calcium is high, so urine calcium is already
high.

Evaluation of thyroid:

Palpate the thyroid gland first. (Sounds obvious and weird, but it’s an answer on the
FM forms, even though, yes, this is an IM lecture).

If nodule palpated, do TSH (in real life you’d also order T3 and T4, but the USMLE
assesses management in terms of TSH).

Cancer is cold, meaning it doesn’t secrete thryoid hormone.

So if TSH is normal or elevated, the patient is not hyperthyroid, so the nodule you
palpated is clearly not hyper-secreting and could be cancer –> you do fine-needle
aspiration (FNA) as next best step. It’s technically an ultrasound-guided FNA, but on
the exam, if they ask you FNA vs USS, choose FNA.

If the TSH is low, then the patient is hyperthyroid (secondary hypothyroidism is due
to decreased TSH, but the USMLE won’t go there with this type of Q because they’re
genuinely looking to see if you can manage thyroid nodule without the gymnastics).

Because the patient is hyperthyroid, you do uptake scan next. You want to see if the
nodule is a toxic adenoma (isolated nodule uptake) or if the nodule is part of toxic
multinodular goiter (elderly; multiple nodules) or Graves (diffuse uptake).
So palpate thyroid gland –> nodule present.

Do TSH.

If TSH normal or high –> FNA.

If TSH low –> radioiodine uptake scan.

Criteria for pathologic jaundice in peds IM:

1. Any jaundice on the first day of life period, regardless as to the supposed
cause.
2. Any jaundice present after one week if term, or after two weeks if pre-
term.
3. Total bilirubin >15 mg/dL.
4. Direct/conjugated bilirubin >10% of total, even if total is <15.
5. Rate of change of increase of total bilirubin >0.5 mg/dL/hour.

If pathologic, do phototherapy first to Tx. If insufficient and neonate getting worse –>
exchange transfusion is the answer. Despite being pedantic about criteria for
pathologic jaundice, the USMLE does not care about the exact guidelines for
commencing phototherapy (that might be Qbank). They will merely give you a case of
pathologic jaundice and then want you to choose phototherapy as the correct Tx
modality, followed by exchange transfusion.

Breastfeeding jaundice –> pathologic jaundice due to increased enterohepatic

circulation in the absence of adequate feeding. –> Assist with neonate’s ability to
attach to breast.

Breastmilk jaundice –> pathologic jaundice due to increased enterohepatic circulation

due to hormonal effects of breastmilk.

HY lecture notes:11

Bone age = chronologic age = true short stature.

Bone age less than chronologic age = constitutional short stature (right-shifted
growth curve) –> parents normal height, and kid will become average, but he’s just
slow to start.

If USMLE doesn’t mention bone age, they might say a 14 year-old boy is still Tanner
stage 2, which is akin to saying his growth curve is shifted to the right and he’ll catch
up.
I’ve seen a vignette that mentions a short girl who’s Tanner stage 1 or 2 with shield
chest and webbed neck, etc., and they say bone age = chronologic age. Constitutional
short stature is a wrong answer to this Q. Dx clearly = Turner syndrome.

Adrenal insufficiency can cause eosinophilia. Weird detail if you’ve never heard of it
before, but it means don’t go off chasing stool ova and parasites. If they tell you a guy
has high K, low Na, low-ish BP, fatigue, and eosinophils of 8-15%, go with Addison,
not helminth infection / stool ova and parasites.

Viral- or chemotherapy-induced aplastic anemia (usually Parvo B19, but new Q on

one of the NBME forms has hepatitis A as the cause [weird]) –> all cell lines are down
(low RBCs, WBC, and platelets) –> Dx with bone marrow aspiration. Sounds overkill
but it’s the answer they want.

In contrast, SLE can cause pancytopenia due to anti-hematologic cell-line antibodies

(i.e., antibodies against RBCs, WBCs, and platelets). SLE is frequently associated
with thrombocytopenia, but if you get a vignette where all cell lines are down, the
WRONG answer is “defective bone marrow production.” The correct answer is
“increased peripheral destruction” (due to antibodies).

Pityriasis rosea = self-limiting viral exanthem caused by HHV6/7. Starts as Herald

patch (pink ellipse) that then becomes eruption that spreads up the back and onto the
shoulder blades (Christmas tree rash). This is classic, but the Herald patch and rash
can start elsewhere (e.g., on the neck, etc.). Lasts 1-8 weeks, with average duration 5
weeks; itchy in 25%; most common in adults in their 20s. Can use calamine lotion to
control itch.

Pediatric shingles “is a thing.” In other words, the first time people hear of this they’re
100% of the time like wtf? It can occur in peds following VZV vaccine or after true
chickenpox infection. Kids with inherent NK cell problems are more susceptible.

Tx plaque psoriasis with topical vitamin D and topical high-dose steroids. Oral vitamin
A, called acitretin, can also be used. Systemic psoriasis (i.e., psoriatic arthritis) can be
treated with methotrexate, similar to rheumatoid arthritis. Psoriasis part of HLA-B27
phenomena –> PAIR –> Psoriasis, Ankylosing spondylitis, IBD, Reactive arthritis.

Tinea corporis (ring worm) –> Tx with topical -azole –> clotrimazole or miconazole.

Tinea capitis (cradle cap) –> Oral griseofulvin for patient only (not close contacts; this
was in a family med Q where you needed to know it was patient only).

Tinea pedis –> topical terbinafine; can also use topical -azoles. But the former is
better. USMLE won’t give you both to choose between; the answer on the exam will
be the only antifungal listed. But I’ve seen the latter as an answer as well.
Onychomycosis (fungal nail infection) –> oral terbinafine (6 weeks for finger nails; 12
weeks for toe nails).

Candidal esophagitis (odynophagia in immunocompromised patient) –> oral

fluconazole

Oropharyngeal candidiasis –> nystatin mouthwash

Biggest risk factor for candida is diabetes, NOT obesity.

Diabetes I and II are both >> risk factors than obesity.

However USMLE likes to give this Q as an morbidly obese patient with a BMI of, e.g.,
67, who has a large, moist, red plaque under a breast (cutaneous candida), and then
they’ll ask for the biggest risk factor –> answer = insulin resistance, not obesity. But
once again, of course this could occur in a type I DM patient as well, but the answer
would be something like hyperglycemia or dysglycemia, rather than insulin resistance,
in a patient who is presumably of more normal BMI. Treat cutaneous candidal
infections with oral fluconazole.

HY Lecture notes:12

Travelers diarrhea –> dude goes traveling and gets self-limiting watery diarrhea;
sometimes green; but the point is it’s not liters and liters of rice-water stool, which is
instead cholera. Mexico is an obvious location, but Middle East is on one of the newer
2CK IM assessments. Cause is ETEC HL and HS toxins.

Treat C. difficile with oral vancomycin. Used to be oral metro, but this is now a
WRONG answer. As of February 2018, guidelines were updated for oral vancomycin
first-line.

Vanc has terrible oral bioavailability and is usually given IV, but in the case of C.
difficile, it makes sense that it should stay confined to the bowel.

Diagnose C. difficile with stool AB toxin test, NOT stool culture. If colonoscopy is
performed, shows pseudomembranes.

Mechanism of colonocyte necrosis is cytoskeletal disruption (Step 1).

Toxic megacolon diagnose with abdominal x-ray. Do laparotomy.

C. jejuni you get from poultry (chicken), not beef. Most common cause of bacterial
gastroenteritis in adults in the US. Bloody stool. Gram (-) rod with 1-3-day incubation
period. Can cause Guillain-Barre syndrome.
Entamoeba histolytica causes bloody stool. Treat with metronidazole + iodoquinol.
Can also use paromomycin.

Vaccines (also discussed a bit in internal medicine #7 lecture, sorry about occasional
repeat info. But let that reinforce for you that certain things are really HY).

At birth: Hep B (+ vitamin K)

2, 4, 6 months: Pneumococcal PCV13, rotavirus (live oral), H. influenzae type B, TdP,

Polio Salk (killed, IM), Hep B.

New guidelines might not require Hep B at 4 months.

Give MMR first dose at 12-15 months; second dose 4-6 years.

Varicella give 12-18 months.

HPV give age 9-45 years.

Influenza give starting at 6 months (killed IM); can give to pregnant women; give
every year in fall/winter; can give live nasal spray vaccine to non-pregnant, non-
immunocompromised persons age 2-49.

Yersinia enterocolitica causes bloody diarrhea with appendicitis-like pain

(pseudoappendicitis). Can cause arthritis in adults.

Dude gets shortness of breath walking up stairs –> needs a stress test; classically
ECG-excercise stress test. But if patient has abnormal baseline ECG (such as BBB),
must do echo-exercise stress test.

USMLE loves pulmonary capillary wedge pressure (PCWP). Increased in cardiogenic

shock, or any cause of left heart path, e.g., MI, LVH, mitral regurg, etc.

Pericarditis –> diffuse ST elevations on ECG; pain worse supine, better when leaning
forward; treatment = NSAIDs, steroids, colchicine; can be caused by autoimmune
disease like RA (serous); can also be caused by MI soon after (post-MI fibrinous
pericarditis) or 2-6 weeks after MI (Dresser syndrome; also a fibrinous pericarditis but
is antibody-mediated).

Pericardial effusion + tamponade = electrical alternans on ECG.

Tamponade is a pericardial effusion, but there’s also hemodynamic decompensation

(low BP).
This is because the heart can’t fill bc of the pressure of the fluid compressing the
heart.

Tamponade presents with Beck Triad (hypotension, JVD, muffled heart sounds). Also
has pulsus paradoxus (drop in systolic BP >10 mm Hg with inspiration; reflects
inability of heart to fill).

Acuteness of fluid accumulation is >>> more important than volume, i.e., stab wound
or post-MI LV free-wall rupture with fast-accumulating low-volume effusion can
cause tamponade, but higher volume effusion that accumulates slowly might not
cause tamponade, e.g., lymphoma.

For tamponade, do echo before pericardiocentesis. Echo must be done first to

confirm the tamponade, then the pericardiocentesis is done to treat. This is on the
NBME.

Pericardial window can also be an answer instead of pericardiocentesis. There’s a

question on one of the newer NBMEs for 2CK where there’s a woman with breast
cancer leading to tamponade, and the answer is pericardial window
(pericardiocentesis wasn’t listed as an answer).

HY lecture notes:13

Contact dermatitis –> type IV hypersensitivity –> linear vesicles / streak for poison
ivy/sumac –> T cell-mediated

Cor pulmonale = right heart failure secondary to a lung pathology; PCWP must be
normal to establish that the left heart is not the cause of the pulmonary hypertension
(I talk more about PCWP in the Cardiology #3 lecture).

USMLE wants you to know straight up that cor pulmonale is caused by pulmonary
hypertension. If you have any lung disease with chronic hypoxemia (e.g., COPD, CF,
obesity hypoventilation syndrome) –> hypoxic vasoconstriction –> pulmonary
hypertension –> RVH –> right heart failure secondary to a lung cause.

So in cor pulmonale, you’ll get a patient with, e.g., 80-pack-year smoking Hx who has
a loud S2 + JVD + peripheral edema +/- hepatomegaly –> this says right heart failure
secondary to COPD.

The loud S2 (P2 component) means the pulmonic valve is slamming shut because the
pressure distal to it (in the pulmonary arteries) is high. The pulmonic valve will close
when pressure in the RV falls below pressure in the pulmonary artery at the end of
systole. In the case of pulmonary hypertension, this will be easier to achieve since the
pulmonary artery pressure is greater.
After the RV hypertrophies, this process will begin to reverse as 1) the gradient
becomes less pronounced, and 2) it actually takes longer for the pulmonic valve to
shut because RV pressure increases –> wide splitting of S2 (P2 occurs much later
than A2, rather than slightly after).

Bottom line is, if you see loud P2 in a question, just think that there’s definitely
pulmonary hypertension in the setting of a right ventricle that hasn’t compensated
sufficiently (right heart failure), regardless as to its absolute degree of hypertrophy.

The JVD + peripheral edema = right heart failure (right heart can’t handle the preload
of the venous return).

I say +/- hepatomegaly because that’s a late finding for right heart failure (nutmeg
liver). And by all means there can be splenomegaly too.

In prerenal failure –> BUN/Cr is >20, FeNa is <1%, urine osmolality is high –> some
causes are heart failure (decreased perfusion to kidney), dehydration, and renal artery
stenosis / fibromuscular dysplasia –> kidney increases PCT reabsorption of water to
compensate for perceived (or real) low volume status –> it accomplishes this by
reabsorbing Na in the PCT –> water follows sodium –> FeNa under 1% + high urinary
osmolality (concentrated urine).

Intrarenal failure –> acute tubular necrosis is most common cause –> BUN/Cr is <20,
FeNa >1%, urinary osmolality is low –> if you get a question where they say acute
blood loss (e.g., in patient who needed resuscitation + packed RBCs) or acute
ischemia (e.g., in episode of VF where the patient required defibrillation), and the
patient goes on to get oliguria –> answer = acute tubular necrosis.

Postrenal failure –> BPH classically –> USMLE likes “increased Bowman capsule
hydrostatic pressure” as the answer in an old man who has high BUN and Cr –> the
BUN/Cr is <20, FeNa >1%, urinary osmolality low, same as intrarenal.

First Aid for Step 1 had made a distinction between intra- and postrenal as far as
intrarenal being BUN/Cr <15, and postrenal 15-20, but I’ve seen several questions on
2CK-level NBMEs where these ranges were violated, most notably for ATN
presenting with sometimes 16 or 17. So I always just teach the ranges as: prerenal
>20, and the others <20.

Allergic bronchopulmonary Asperillosis (ABPA) –> asthma + eosinophilia –>

hypersensitivity to Aspergillus antigen. Tx = combination of corticosteroid +
fluconazole. The CXR for this lecture is ABPA.
HY lecture notes 14 (double-posting this lecture as Surgery #5 because it’s
exceedingly HY for both shelf exams; this is the only double-posted lecture):

Stress testing may be done prior to surgery in those who are at moderate-high risk of
ischemia –> the body’s cortisol-mediated stress response to surgery puts some
patients at risk of perioperative MI.

This external article talks about the importance of stress testing in mitral
regurgitation.

USMLE is obsessed with differentiating stroke/TIA/retinal artery occlusion caused by

atrial fibrillation vs carotid plaques + management.

Carotid plaques are caused by hypertension. The strong systolic impulse from the
heart pounds the carotids –> endothelial damage –> atherosclerosis.

So if you get a vignette of a guy who’s, e.g., 55, with BP of 150/90, who experiences
a TIA, the first thing you want to think about is, “Does this guy have a carotid plaque
that has resulted in a clot embolizing to his brain.” –> do a carotid duplex ultrasound.

In contrast, if you get a guy who’s, e.g., 80, who has good blood pressure (e.g.,
110/70), and he gets a stroke or TIA, you want to think, “Does he have atrial
fibrillation with a LA mural thrombus that’s now embolized to the brain.” –> do an
ECG. Now in this scenario, there are two points to note:

1. 8% of people over age 80 have atrial fibrillation, which is why age is a huge risk
factor here. In other words, if the vignette says the guy is 58, AF is probably less
likely just based on shear probability, regardless of hypertensive status.” And
2. AF is often paroxysmal, meaning the USMLE might give you a scenario, e.g., with
the above 80M, where they already tell you an ECG shows sinus rhythm with no
abnormalities.

So regarding the second point, you’re probably like, “Wtf? So it’s not AF?” No, it is
likely AF, but in order to pick up the paroxysmal aspect of it, the next best step is a
Holter monitor (24-hour wearable ECG). This means that later in the day when he sits
down to have dinner and then pops into AF, the Holter monitor will pick it up.

So in summary, if stroke/TIA/retinal artery occlusion:

Age 50s-60s + high BP –> answer = carotid duplex ultrasound to look for carotid
plaques

Age >75 + good BP –> answer = ECG to look for AF –> if normal, do Holter monitor
to pick up paroxysmal AF.
The exception to this scenario could be, e.g., a 55M + good BP + carotid bruit heard
on auscultation –> answer = carotid duplex ultrasound to look for carotid plaques. –>
In this case, if they are obvious and explicit about the suspected etiology of the
stroke, TIA, or retinal artery occlusion, then you can just do the carotid duplex
ultrasound here.

When we consider management for carotid plaques, we have to ask whether the
patient is symptomatic or asymptomatic. A bruit does not count as symptoms (that’s a
sign). Symptomatic means stroke, TIA, or retinal artery occlusion.

Carotid occlusion >70% if symptomatic, or >80% if asymptomatic –> answer = do

carotid endarterectomy.

Below these thresholds –> answer = statin, PLUS clopidogrel OR dipyridamole +

aspirin.

The USMLE will actually not be hyper-pedantic about the occlusion %s. They’ll make
it obvious for you which answer they want. They’ll say either 90% –> answer =
carotid endarterectomy, or they’ll say 50% –> answer = statin + anti-platelet therapy.

I had seen one question where they said a guy had 10 and 30% occlusion in the left
vs right carotids, respectively, and he was already on anti-platelet therapy + a statin,
and the answer was “maintain current regimen.”

For AF management:

We have to consider both arms of management: blood thinning + treating the actual
AF.

For blood thinning, CHADS2 score is standard in terms of evaluating risk (there are
variants, but the USMLE won’t ever be borderline with how this plays into a question;
they’ll either give you a full-blown obvious high-risk patient where all are positive, or
they’ll make it clear that the patient is low-risk and merely just has AF alone).

• CHADS2 = CHF, HTN, Age 75+, Diabetes, Stroke/TIA (latter is 2 points; the rest
are 1 point)
• If 0 or 1 points, give aspirin (anti-platelet therapy).
• If 2+ points, give warfarin (anti-coagulation therapy).
• If valvular AF (i.e., AF in someone with a mitral or aortic valve lesion),
we must give warfarin.
• If non-valvular AF, can give other agents (e.g., dabigatran, apixaban).

For the actual Tx of the AF, we do rate control before rhythm control (the
management is actually heavily involved, but for the USMLE know the following):

• Rate control:
 • Beta-blocker first-line (metoprolol)
• If beta-blocker contraindicated (i.e., depression, sexual dysfunction,
COPD, Hx of asthma requiring oxygen or hospitalization, 2nd/3rd-
degree heart block), verapamil is the next choice.
• If rate control fails, go to rhythm control.
• Rhythm control:
• Flecainide (type-Ic Na channel blocker) first-line in those without any
structural (i.e., LVH or valvular problems) or coronary artery disease
(any symptomatology of CVD or PVD means patient has coronary
artery disease).
• In those who cannot receive flecainide, other anti-arrhythmics like
amiodarone, dronedarone, and dofetilide may be used.

HY lecture notes 15
Impetigo (“school sores”), which is divided into bullous and non-bullous types.1 When
“impetigo” is stated alone, the implication is non-bullous.

Impetigo is largely pediatric and presents as erythematous plaques with a yellow crust
caused by Staph and/or Strep. The lesions may be itchy or painful and are highly
contagious.1

Staph aureus now exceeds Strep pyogenes (Group A Strep) as the most likely
causal organism of non-bullous impetigo.

Regarding non-bullous (i.e., “normal” impetigo)

Staph aureus has always been the most implicated causal organism in
bullous impetigo.

Treatment8

• Topical
• Mupirocin, retapamulin, and fusidic acid.
• For the USMLE, they are obsessed with topical mupirocin as a
treatment for impetigo.
• Oral
• Dicloxacillin
• Cephalexin
• Amoxicillin/clavulanate
• You must know that you these oral agents cover S. aureus.
• If you give penicillin or amoxicillin alone, they will NOT cover Staph
due to its beta-lactamase production.

HY lecture notes:16

• Difference between Cushing syndrome and Cushing disease? –> syndrome = what
you look like + can be any cause of Cushingoid appearance; Cushing disease only
= anterior pituitary ACTH-secreting tumor; in other words, Cushing disease is a
cause of Cushing syndrome.

• Most common cause of Cushing syndrome –> exogenous glucocorticoids (e.g.,

prednisone).

• 34F + SLE + point tenderness over vertebra; Dx? –> Cushing due to exogenous
steroids leading to osteoporotic compression fracture. HY.

• Pt not on exogenous steroids + Cushingoid; most common cause? –> Cushing

disease most common cause of endogenous Cushing syndrome.
• Main causes of Cushing syndrome? –> exogenous steroids (most common overall),
Cushing disease (most common endogenous), small cell bronchogenic carcinoma
(ectopic ACTH), cortisol-secreting tumor (or diffuse hyperplasia) of zona fasculata
of adrenal cortex; CRH tumor rare as fuck.

• Patient with chronic disease (i.e., IBD, SLE, RA) + Cushingoid; what are the ACTH
+ cortisol levels –> need to know this means patient is taking prednisone –> low
ACTH + low cortisol (prednisone is NOT the same thing as cortisol) –> prednisone
suppresses CRH and ACTH secretion at hypothalamus and anterior pituitary –>
decreased endogenous cortisol production.

• Patient with Cushing disease; ACTH + cortisol levels? –> high ACTH + high
cortisol.

• Smoker + Cushingoid –> small cell bronchogenic carcinoma.

• Smoker + Cushingoid; ACTH + cortisol levels? –> high ACTH (ectopic) + high
cortisol.

• When to do dexamethasone suppression test –> Cushingoid patient not on

exogenous glucocorticoids and has high serum cortisol.

• Low-dose dexamethasone suppression test –> tells us yes or no, patient has
pathologic cause of Cushing syndrome (i.e., Cushing disease, or SCC of lung, or
cortisol-secreting tumor), but we can’t establish the causation from this; if cortisol
doesn’t suppress –> yes, patient has true Cushing syndrome (proceed to high-
dose test); if cortisol suppresses à no, patient does not have Cushing syndrome
(do not proceed to high-dose test).

• High-dose dex –> only cause of Cushing syndrome that will suppress in response
is Cushing disease.

• Pt has no suppression to low-dose dex + suppresses to high-dose –> Dx =

Cushing disease (ACTH secreting tumor of anterior pituitary).

• Pt has no suppression to low- or high-dose dex –> ACTH high? –> Yes, answer =
SCC of lung; No, answer = cortisol-secreting tumor (or diffuse hyperplasia) of
adrenal cortex.

• Cushingoid + low ACTH + low cortisol –> exogenous steroids.

• Cushingoid + low ACTH + high cortisol –> cortisol-secreting tumor (or diffuse
hyperplasia) of adrenal cortex.

• Cushingoid + high ACTH + high cortisol –> Cushing disease.

• Most accurate test for Dx Cushing syndrome –> 24-hour urine cortisol.

• Why dex test not most accurate? –> false-positives in e.g., depression, alcoholism.

• Acanthosis nigricans + low K + hyperpigmentation –> Cushing syndrome.

• Why acanthosis nigricans –> caused by insulin resistance (unrelated: also can be
caused by visceral malignancies).

• Why low K in Cushing syndrome –> chronic elevation of glucocorticoid effect at

kidney can push out potassium similar to aldosterone.

• Why hyperpigmentation –> high ACTH secretion means POMC is high –> high
alpha-MSH as well.

• Purple striae in obese patient –> Cushing syndrome –> cortisol weakens
connective tissue and causes microbleeds.

• Why purple striae? –> glucocorticoids weaken collagen –> once again, this causes
microbleeding into skin.

• Why hypertension in Cushing syndrome –> cortisol upregulates alpha-1 receptors

on arterioles, thereby allowing NE and E to do their job.

• Graph shows you two scenarios: 1) NE given alone, then BP increases a little; 2)
NE + cortisol given together, then BP increases a lot; why the difference? –>
cortisol is permissive of the effects of catecholamines (don’t choose synergistic or
additive); once again, cortisol merely allows NE and E to do their job; cortisol isn’t
directly increasing BP.

• Why normally ratio of E to NE in the blood is 80/20? –> NE draining venously out
of the adrenal medulla passes through the adrenal cortex –> cortisol upregulates
PNMT (converts NE to E).

What does low cortisol cause? –> chronic fatigue syndrome (super important).

Difficulty to get up from chair-proximal muscle weakness- glucocorticoid myopathy

HY lecture notes: 17

If USMLE asks you how to decrease risk of type II diabetes mellitus the most – low-
carbohydrate diet or low-calorie diet – what’s the answer? –> Low-calorie diet is
correct. High BMI is the risk factor is why.
Diabetes insipidus –> low urine osmolality + high serum sodium.

Central –> decreased ADH (can be due to head trauma); Tx with desmopressin.

Nephrogenic –> decreased sensitivity of the kidney to ADH (ADH levels are high in
the blood); can be due to lithium, demeclocycline, hypercalcemia; Tx with NSAID +
thiazide diuretic. The NSAID will decrease renal blood flow by inhibiting
prostaglandin synthesis (decreased opportunity for filtration by the kidney, so less
chance for fluid loss); for the thiazide, the distal Na loss will cause the PCT to
compensate by increasing Na reabsorption, and water follows sodium — less fluid loss
overall compared to not being on the diuretic; in someone who doesn’t have DI, the
thiazide will of course cause net fluid loss, not retention.

In states of severe dehydration and shock, lactic acidosis can be seen –> decreased
oxygen delivery –> increased anaerobic respiration at tissues –> increased lactic acid
–> decreased serum bicarb. Not just limited to DI, but any type of shock on the
USMLE (hypovolemic, septic, cardiogenic, etc.), you can get low bicarb, and the
reason is frequently lactic acidosis for this reason. This is really HY on 2CK in
particular.

SIADH –> high urine osmolality + low serum sodium.

Classically caused by small cell lung cancer ectopic ADH secretion; can also be caused
by head trauma (similar to central DI).

Cannot do surgery for small cell lung cancer; chemotherapy (treating underlying
condition) may help; otherwise ADH receptor antagonists such as conivaptan and
tolvaptan can be used.

Psychogenic polydipsia –> low urine osmolality + low serum sodium

Person is drinking too much.

For SIADH, DI, and PP, fluid restriction is done as the first step in diagnosis – i.e., see
how their urine + serum change when you withhold fluid.

In DI, fluid restriction won’t cause a decrease in urinary output; the patient will still be
polyuric + serum sodium will stay elevated.

In SIADH, fluid restriction won’t cause serum sodium to go – i.e., ADH remains
elevated, so excess free water reabsorption persists.

In PP, the patient is physiologically normal, so fluid restriction will both decrease
urinary output as well as increase serum sodium.
Addison disease = primary hypoadrenalism –> adrenal cortex is unable to adequately
make aldosterone AND cortisol (both are low).

High ACTH + hyperpigmentation (low cortisol –> decreased negative feedback at

hypothalamus + anterior pituitary –> increased POMC, which is the precursor to both
ACTH and alpha-MSH –> the latter causes hyperpigmentation) + high potassium +
low sodium + low bicarb + low pH.

Therefore Addison = high potassium + low sodium + low bicarb + low pH in a patient
with high ACTH and hyperpigmentation.

Aldosterone normally reabsorbs sodium in the cortical collecting duct and secretes
potassium and protons; so low aldosterone –> high potassium + low sodium + low
bicarb + low pH.

Low cortisol causes chronic fatigue syndrome.

The combination of low cortisol + low aldosterone –> low blood pressure in fatigued
patient.

Diagnose Addison with ACTH stimulation test –> patient will already have been
measured to have high ACTH; if we give more ACTH (exogenous ACTH) and cortisol
fails to rise appreciably, a Dx of Addison is made.

Treat with fludrocortisone (very similar to aldosterone structurally, but also takes care
of low cortisol).

Waterhouse friderichsen syndrome may be a cause of Addison –> meningococcal

septicemia followed by bilateral hemorrhagic infarction of the adrenal cortices. After
giving normal saline for the low BP, must give hydrocortisone to compensate for the
low cortisol.

Cortisol normally helps maintain blood pressure by upregulating alpha-1 receptor

expression on arterioles –> permits norepinephrine + epinephrine to bind and
constrict the vasculature –> if low cortisol, then NE + E simply can’t do their job and
BP is low.

Secondary hypoadrenalism –> caused by low ACTH –> only cortisol is low;
aldosterone is normal or elevated.

Because ACTH is low, there’s no hyperpigmentation (POMC is also low because the
anterior pituitary lacks synthesis capacity).

In secondary hypoadrenalism, the adrenal gland itself is functioning fine (i.e., there’s
nothing wrong with the actual adrenal parenchyma; the problem is merely ACTH isn’t
there to stimulate it), aldosterone will be normal or slightly elevated because RAAS is
still intact.

This means potassium is not elevated like it is in Addison. And if aldosterone is

elevated, it’s not at the level where potassium secretion is in excess; there’s merely an
increased basal secretion (i.e., you won’t get full-blown hypersecretion causing
hypokalemia; the emphasis is merely that one’s baseline aldosterone would be slightly
increased).

I make this point because there’s an NBME Q for Step 1 where, in Sheehan
syndrome, the arrows they wanted were ↓ prolactin, ↓ TSH, ↓ ACTH, and ↑
aldosterone. Sheehan syndrome is ischemic infarction of the anterior pituitary
following postpartum hemorrhage, where there is pan-hyposecretion by the anterior
pituitary.

So for secondary, potassium is normal, sodium is normal, bicarb is normal, pH is

normal in a patient with low ACTH and no hyperpigmentation.

Tx with hydrocortisone. Fludrocortisone isn’t needed because aldosterone is intact.

In patients with adrenal insufficiency, they cannot mount a stress response (i.e., they
cannot secrete cortisol in response to trauma, surgery, illness, etc.) and can
experience hypotensive episodes. After giving fluids, give hydrocortisone (same as
we talked about above for WFS).

USMLE also wants you to be aware that “autoimmune diseases go together.”

Meaning, if the vignette is hinting at a presentation like Addison disease, they might
also throw in that the patient has a history of autoimmune thyroiditis, or has a sibling
who has rheumatoid arthritis, etc.

HY lecture notes:

Super HY inheritance patterns in no particular order

Autosomal recessive

G6Pase (von Gierke)

CF

Friedreich ataxia (GAA TNR)

Hemochromatosis
Wilson disease

Sickle cell

All glycogen storage diseases

Lysosomal storage diseases (minus Fabry and Hunter, which are XR)

Familial hyperchylomicronemia

Autosomal dominant

Achondroplasia (if inherited, but most patients’ mutations are de novo)

vWD

Phakomatoses (NF1, NF2, TSC, VHL)

Marfan syndrome

MEN syndromes

Hereditary spherocytosis

Huntington disease (CAG TNR)

Myotonic dystrophy (CTG TNR)

Porphyrias

Familial hypercholesterolemia

Familial hypertriglyceridemia

X-linked recessive

G6PD

Hemophilia A + B

Wilson disease

Hemochromatosis
Duchenne + Becker muscular dystrophies

Alport syndrome

Lesch-Nyhan syndrome

Fragile X (CGG TNR)

Fabry disease

Hunter syndrome

X-linked dominant

Kallmann syndrome

Hypophosphatemic rickets

Codominant

Alpha-1-anti-trypsin deficiency

AB blood types

HY lecture notes:19

Most common cause of carotid plaques? –> HTN –> the strong systolic impulse from
the heart pounds the carotids –> endothelial damage –> atherosclerosis.

55M + BP 150/90 + TIA; next best step in Mx? –> carotid duplex USS à the first thing
you want to think about is, “Does this guy have a carotid plaque that has resulted in a
clot embolizing to his brain.”

80M + good blood pressure (e.g., 110/70) + stroke or TIA; next best step in Mx? –>
ECG à you want to think, “Does he have atrial fibrillation with a LA mural thrombus
that’s now embolized to the brain.”

80M + good blood pressure (e.g., 110/70) + stroke or TIA + ECG shows sinus rhythm
with no abnormalities; next best step in Mx? –> Holter monitor –> when you first see
this scenario you’re probably like, “Wait, the ECG is normal, so it’s not AF?” –> No, it
is likely AF, but AF is often paroxysmal, so in order to detect it in this scenario, the
next best step is a Holter monitor (24-hour wearable ECG). This means that later in
the day when he sits down to have dinner and then pops into AF, the Holter monitor
will pick it up.

What % of people over age 80 have AF? –> 8% of people over age 80 have AF, which
is why age is a huge risk factor. In other words, if the vignette says the guy is 58, AF is
probably less likely just based on shear probability, regardless of hypertensive status.”
And, once again, knowing that AF is often paroxysmal is really important.

Age 50s-60s + high BP + TIA/stroke/retinal artery occlusion; next best step in Dx? –>
answer = carotid duplex ultrasound to look for carotid plaques.

Age >75 + good BP + TIA/stroke/retinal artery occlusion; answer = ECG to look for
AF –> if normal, do Holter monitor to pick up paroxysmal AF.

55M + good BP + carotid bruit heard on auscultation; next best step in Mx? –>
answer = carotid duplex ultrasound to look for carotid plaques –> in this case, if they
are obvious and explicit about the suspected etiology of the stroke, TIA, or retinal
artery occlusion, then you can just do the carotid duplex ultrasound.

How to Mx carotid plaques? –> first we have to ask whether the patient is
symptomatic or asymptomatic. A bruit does not count as symptoms (that’s a sign).
Symptomatic means stroke, TIA, or retinal artery occlusion. According to recent
guidelines: carotid occlusion >70% if symptomatic, or >80% if asymptomatic –>
answer = do carotid endarterectomy.

Below these thresholds –> answer = medical management = statin, PLUS clopidogrel
OR dipyridamole + aspirin.

The USMLE will actually not be hyper-pedantic about the occlusion %s (that’s Qbank).
They’ll make it obvious for you which answer they want. They’ll say either 90% à
answer certainly = carotid endarterectomy, or they’ll say 50% –> answer = medical
management only. There’s one NBME Q where they say a guy has a bruit but is
asymptomatic, and has 10 and 30% occlusion in the left vs right carotids, respectively,
and he’s already on aspirin + statin, and the answer is “maintain current regimen” –> if
he were symptomatic, even with low occlusion, he’d certainly need statin, PLUS
clopidogrel OR dipyridamole + aspirin.

68F + diabetic + diffuse, dull abdo pain 1-2 hours after meals; Dx? –> chronic
mesenteric ischemia due to atherosclerosis of SMA or IMA, not duodenal ulcer (if
they want the latter, they’ll say 29M from Indonesia) –> essentially stable angina of
the bowel.

68F + Hx of intermittent claudication + CABG + abdo pain 1-2 hours after eating
meals; Dx? –> chronic mesenteric ischemia.
78M + Hx of AF + acute-onset severe abdo pain “out of proportion to physical exam”;
Dx? –> acute mesenteric ischemia due to embolus.

16F + Hx of severe anorexia + BMI of 14 + has episode of ventricular fibrillation due

to hypokalemia + now has severe abdo pain; Dx? –> acute mesenteric ischemia due
to episode of decreased blood flow (should be noted that hypokalemia causing
arrhythmia is most common cause of death in anorexia).

68F + diabetic + Hx of diffuse, dull abdo pain 1-2 hours after meals + now has 2-day
Hx of severe abdo pain out of proportion to physical exam; Dx? –> acute on chronic
mesenteric ischemia due to ruptured atherosclerotic plaque (akin to an “MI” of the
bowel).

Dx of acute + chronic mesenteric ischemia? –> USMLE answer = mesenteric

angiography.

Tx of acute mesenteric ischemia? –> endarterectomy might be able to restore blood

flow if caught in time, but on the USMLE, they will say “IV antibiotics are
administered; what’s the next best step in Mx?” and the answer is just “laparotomy.”

Tx of chronic mesenteric ischemia –> endarterectomy to clear vessel.

Tx for acute limb ischemia –> endarterectomy; but if medicinal –> heparin + oxygen +
morhphine.

Question on one of the surgery or IM NBME forms where they say patient has an
ischemic posterior cerebral stroke + a false lumen is visualized in one of the vertebral
arteries; next best step in Mx? –> heparin –> apparently stasis can occur within
arterial false lumina and heparin has utility in the Tx.

HY lecture notes: 20 IM

16F + painless lateral neck mass + mediastinal mass; Dx? –> Hodgkin lymphoma

16F + painless lateral neck mass + hepatomegaly; Dx? –> Hodgkin lymphoma

Above two presentations are HY. Not hard, but if you haven’t heard them clearly
stated, you might be like hmm wtf is the diagnosis here.

The mediastinal mass is not a thymic lesion; it’s mediastinal lymphadenopathy.

Hodgkin will be B cell origin.

Reed-Sternberg cells (“Owl-eye” on histo; [unrelated, but CMV-infected cells also
carry this description]). RS cells have CD15 + CD30 positivity.

Different types of Hodgkin:

Nodular sclerosing = type most frequently seen in women.

Lymphocyte-rich = high ratio of lymphocytes to RS cells (i.e., fewer RS cells).

Lymphocyte-deplete = low ratio of lymphocytes to RS cells (i.e., more RS cells).

More RS cells = worse prognosis. So lymphocyte-deplete = worse prognosis.

Many regimens to Tx. But “ABVD” is classic and HY = Adriamycin (doxorubicin);

Bleomycin, Vinblastine, Dacarbazine.

Adriamycin causes dilated cardiomyopathy –> enlarged cardiac silhouette +

pulmonary edema (diffuse infiltrates or “bat wings” on CXR)

Bleomycin causes pulmonary fibrosis –> reticulonodular / reticular pattern (honey-

combing) on CXR.

Don’t confuse vinblastine (bone marrow toxic –> neutropenia –> mouth ulcers +
fever) with vincristine (neurotoxic).

Dacarbazine is an alkylating agent (you won’t get asked on it).

Hodgkin can lead to minimal change disease. This one’s always a weird one for
students:

40M + Hodgkin + renal issue + no blood in the urine; renal Dx? –> answer = minimal
change disease. Student says “wtf? That’s peds though.” Yeah, but it’s also
Hodgkin. Due to a cytokine effect at the glomerulus. You learn something new every
day.

32-year-old African-American woman + dry cough + nodular densities on CXR (bihilar

lymphadenopathy); answer = sarcoidosis = “non-caseating granulomas.”

32-year-old African-American woman + dry cough + no changes on CXR; answer =

asthma = “activation of mast cells.”
Nephrology #1

HY lecture notes:1

Gold salts + sulfa drugs –> membranous glomerulonephritis –> nephrotic syndrome.

Aminoglycosides (e.g., gentamicin) –> acute tubular necrosis –> oliguria + dark urine
with muddy brown granular casts.

Beta-lactams (e.g., nafcillin) + cephalosporins –> acute interstitial nephropathy

(tubulointerstitial nephritis; interstitial nephritis) –> WBCs in the urine (eosinophils)
+/- WBC casts –> the renal manifestation of an allergic reaction, and in turn, often
associated with rash (but not mandatory in Qs).

Intersititial nephritis just means inflammation of the interstitium of the kidney, and
whilst frequently due to allergic reaction from the above agents, can occur in the
absence of allergy as well (NSAIDs). NSAIDs –> analgesic nephropathy –> due to
ischemic damage from decreased renal blood flow.

Analgesic nephropathy is an umbella term which just means damage to the kidneys
due to analgesics, but the type of damage may be interstitial nephropathy or renal
papillary necrosis (ischemic damage; dark urine).

Patient is on beta-lactam or cephalosporin for several weeks –> WBCs in the urine –>
answer = intersititial nephropathy.

Patient is on high-dose analgesics (NSAIDs, phenacetin) for several weeks, or lower

dose analgesics for months to years –> peripheral edema –> answer = interstitial
nephropathy (and because the etiology is analgesics, we can label it “analgesic
nephropathy,” but the Dx is still interstitial nephritis). The edema is due to decreased
renal blood flow –> kidney perceives fluid status as low –> compensatory increase in
Na reabsorption through the PCT –> water follow sodium –> edema, FeNa <1%, and
BUN/Cr >20.

Hepatitis B can also cause membranous glomerulonephritis.

Hepatitis C can cause membranoproliferative glomerulonephritis.

Child has edema, eyelid swelling, and/or ascites –> no blood in the urine –> minimal
change disease (MCD; lipoid nephrosis). Usually caused by viral infection, but the
vignette doesn’t have to mention that. MCD can also be caused by adults with
Hodgkin lymphoma (cytokine effect).

Thrombotic thrombocytopenic purpura –> antibodies against ADAMTS13 –> pentad

of thrombocytopenia + schistocytosis (hemolytic anemia) + hematuria + fever +
neurologic signs. ADAMTS13 is normally responsible for cleaving vWF multimers –>
in TTP, can’t cleave these multimers, so platelet clumps build up and can cause the
shearing of RBCs (schistocytes).

Hemolytic uremic syndrome (HUS) –> due to EHEC shiga-like toxin (verotoxin) or
shigella’s shiga toxin. Triad of thrombocytopenia + schistocytosis (hemolytic anemia)
+ hematuria. Toxin binds to GB3 receptors in the kidney (more receptors in kids than
in adults). This causes leukocytes to bind to the endothelial cells –> endothelial
damage –> platelets come in to heal damage –> platelets get consumed
(thrombocytopenia). Toxin inactivates ADAMTS13, so the platelet clumps can’t get
cleaved –> shear RBCs flying past in the renal microvasculature (same as TTP) –>
schistocytosis.

Kid with sore throat. Red urine 1-3 DAYS later –> answer = IgA nephropathy

Kid with sore throat. Red urine 1-2 WEEKS later –> answer = post-streptococcal
glomerulonephritis (PSGN).

Kid with yellow crusties (school sores) on the skin. Red urine 7 days later –> answer =
PSGN (from impetigo). Can also occur from erysipelas and cellulitis caused by Group
A Strep

HY lecture notes:2

Sulfa drug or gold salts + kidney issue + no blood in urine; Dx? –> membranous
glomerulonephropathy (MG).

Biopsy finding in MG? –> subepithelial deposits; “spike and dome” appearance is
prevalent in resources / Qbank but buzzy and not on the NBMEs.

HepB or C + nephrotic syndrome; Dx? –> MG –> usually due to HepB.

Autoantibodies in membranous glomerulonephropathy? –> sometimes patients are

positive for anti-phospholipase A2 receptor antibodies.

HepC + nephritic syndrome; Dx? –> MPGN.

Multiple myeloma + renal diagnosis? –> renal amyloidosis –> immunoglobulin light
chains in high levels moving through the kidney (Bence Jones proteinuria) leads to
deposition in the renal parenchyma. You should memorize the sentence: “Multiple
myeloma is the most common cause of renal amyloidosis.”

First change in the kidney with diabetes? –> hyperfiltration –> increased filtered
glucose pulls water with it.

First histologic change in the kidney with diabetes? –> thickening of the glomerular
basement membrane –> due to non-enzymatic glycosylation of basement membrane.
If the question asks you for the first renal change seen overall in diabetes, select
hyperfiltration.

USMLE Q mentions guy with diabetes + polyuria; asks why he has increased urinary
output –> answer = “increased glomerular filtration rate.”

Amount of glucose reabsorbed in PCT? –> 100% physiologically; glycosuria not seen
until serum levels exceed around 180 mg/dL.

Late finding seen histologically in diabetic nephropathy? –> Kimmelstiel-Wilson

nodules.

What are KW nodules composed of? –> hyaline à HY on Step 1 for some reason;
don’t confuse this fibrin, which is the answer for the crescents in RPGN.

Example of type II diabetes drug that acts in the kidney? –> Dapagliflozin (SGLT2
inhibitor in PCT; prevents reabsorption of glucose).

What is hyaline arteriolosclerosis? –> hyaline deposition in the arterioles of the

kidney usually seen in diabetes –> non-enzymatic glycosylation of vascular
endothelium leads to leakage of plasma proteins into vessel walls.

First drug given to diabetics with HTN or proteinuria? –> ACEi (e.g., enalapril) or ARB
(e.g., valsartan).

Most common cause of chronic renal failure? –> diabetes mellitus.

BUN/Cr ratio in pre-, intra-, vs post-renal failure? –> >20 in pre-; <20 if not pre- –>
FA for Step 1 had stratified this out as <15 for intra- and 15-20 for post-, but I’ve
seen at least three 2CK NBME/CMS Qs where the diagnosis was acute tubular
necrosis and the BUN/Cr was in the 16s or 17s. So I’ve learned to just tell students:
>20 = pre-; if >20, you simply know it’s not pre-.

Fractional excretion of sodium (FeNa) in pre-/intra-/post-renal failure? –> need to

know it’s <1% in pre-renal; >1% in intra-/post-renal –> the low FeNa in pre-renal is
due to the PCT’s attempt to reabsorb Na (water follows sodium) in low-volume state
(or in FMD, RAS).

Urine osmolality in pre-/intra-/post-renal failure? –> concentrated (high; >500

mOsm) in pre-; dilute (low; <350 mOsm) in intra-/-post.

When is pre-renal failure the answer apart from the BUN/Cr >20? –> CHF classically
(decreased renal perfusion); can also be hypovolemia generally not in the acute
setting; it’s to my observation that if the NBME/CMS Q mentions acute hypovolemia
+ no other information (i.e., does not mention BUN or Cr), the answer is acute tubular
necrosis (intra-renal), not pre-renal. Pre-renal can also be the answer for contrast-
nephropathy; regarding this point, contrast agents can cause either pre-renal (due to
afferent arteriolar spasm) or intra-renal (direct nephrotoxicity); always give fluids to
prevent (HY). The USMLE Q will sometimes give a presentation of pre-renal + ask the
etiology, and the answer is “decreased glomerular filtration” (NBME).

Guy has MI + has low BP; NBME Q asks what is most likely to be seen (ask a bunch of
reabsorption / secretion answers); answer = “increased potassium secretion” –> low-
volume status leads to RAAS upregulation and distal renal K wasting.

When is intra-renal failure the answer? –> classically acute tubular necrosis (ATN)
secondary to episodes of hypoxia at the kidney, usually due to blood loss (i.e, intra-
operative requiring lots of blood, or traumatic exsanguination), or arrhythmia (i.e.,
patient had episode of VF and was resuscitated) –> vignette will mention one of the
above scenarios and then tell you patient has acute oliguria +/- dark urine. They do
not have to mention BUN, Cr, or muddy brown granular casts for ATN.

Other causes of intra-renal failure? –> drugs (i.e., gentamicin); rhabdomyolysis

(myoglobin is nephrotoxic); contrast nephropathy.

Why does acute hypoxia cause acute tubular necrosis? –> proximal convoluted
tubules have high concentrations of transporters (namely Na/K-ATPases) with high
oxygen demand; also explains why diffuse cortical necrosis is classically associated
with obstetric catastrophes.

Lab animal is given 100% nitrogen in dumb experiment; most likely part of the kidney
to experience anoxic injury (they list everything) –> answer = “proximal tubule.”

Classic finding in urine with ATN? –> muddy brown granular casts; it should be noted
that general “granular casts” are not specific to ATN. There’s an IM CMS Q with an
elderly woman who has CVA tenderness + granular casts on U/A; answer is pyelo not
ATN.

USMLE Q gives guy who has MI requiring resuscitation + subsequent oliguria; then
they ask what you see on microscopic examination of the kidney; answer =
“degenerating epithelial cells and dirty brown granular casts” or “necrosis of epithelial
cells in proximal convoluted tubules.”

Electrolyte disturbance in ATN? –> first week is oliguric phase (hyperkalemia due to
decreased filtration); weeks 2-3 are polyuric phase (hypokalemia due to increased
kaliuresis from PCT cells not being able to reabsorb K yet) –> btw, kaliuresis means
urination of K (great word if you want to feel sophisticated).

When is post-renal the answer? –> classically BPH or distal obstruction secondary to
strictures or malignancy.

How does USMLE like to assess post-renal? –> classically will give you BPH + show
you a pic of hydronephrosis (massively dilated kidney), then they’ll ask the most likely
cause of this patient’s condition; answer = “increased Bowman capsule hydrostatic
pressure,” or “increased tubular hydrostatic pressure.” This answer is on several
NBMEs.

BPH Tx? –> alpha-1 blocker (e.g., tamsulosin, terazosin) and/or 5-alpha-reductase
inhibitor (i.e., finasteride); patients may receive mono- or dual therapy.

Tx for prostatic adenocarcinoma? –> flutamide + leuprolide administered together (if

the USMLE forces you to choose a sequence, pick flutamide then leuprolide, but in
practice their administered together) à flutamide blocks androgen receptors;
leuprolide is a GnRH receptor agonist (given continuously it shuts off LH/FSH
secretion).

When is renal papillary necrosis the answer? –> classically in sickle cell; can also from
drugs like NSAIDs; urine will be dark –> renal papillae in the medulla receive less
blood flow, so small changes in the microvascular supply can lead to sloughing +
necrosis of the medulla. You’ll be able to contrast this disorder from diffuse cortical
necrosis and acute tubular necrosis because the latter two conditions, in the context
of ischemia, are associated with massive, acute events.

HY lecture notes:3

“Small blue cells” on prostate or renal biopsy specimens, especially in a patient who
has fever, should scream infection. These are leukocytes.

68M + urinary hesitancy + interrupted stream + 100F + tender prostate; Dx? –>
prostatitis

72M + urinary hesitancy + interrupted stream + biopsy of prostate shows small blue
cells; Dx? –> prostatitis –> most older men will have BPH, but if they give you the
blue cells, choose prostatitis.
Exquisitely tender prostate on digital rectal exam; Dx? –> prostatitis.

Prostatitis Tx? –> ciprofloxacin, OR ampicillin + gentamicin.

82M + treated for prostatitis + sore ankle when he goes out metal detecting; Dx? –>
Achilles tendonitis from ciprofloxacin.

Costovertebral angle tenderness + fever; Dx? –> pyelonephritis.

Costovertebral angle tenderness + granular casts –> pyelonephritis –> correct, super-
weird; NOT acute tubular necrosis; this is on 2CK NBME; apparently “granular casts”
can be seen in a variety of conditions; it’s the muddy/dirty brown granular casts that
indicate ATN.

Is chronic pyelonephritis ever an answer? –> usually young patient, i.e., 3-4-year-old,
who has recurrent bouts of acute pyelo –> need to know recurrent acute pyelo is
what causes chronic pyelo. For Step 1 level, they will show an image of a small,
scarred kidney and give you the aforementioned description, then the answer is
simply “vesicoureteral reflux” as the mechanism. They might also ask what you see on
biopsy; answer = “tubular atrophy.” Ultrasound shows “broad scars with blunted
calyces.” The phrase “thyroidization of the kidney” is buzzy and more Qbank, not
NBME. You need to walk away knowing that chronic pyelo will produce scarred renal
calyces in someone who’s had recurrent acute pyelo.

Innervation of external urethral sphincter –> pudendal nerve (somatic; voluntary).

Innervation of internal urethral sphincter –> hypogastric nerves (sympathetic).

Innervation of detrusor muscle –> pelvic splanchnic nerves (parasympathetic; S2-4).

What is Brenner tumor? –> ovarian tumor with bladder (transitional cell) epithelium.

Tx for simple UTI –> nitrofurantoin is classic answer (need not be cystitis in pregnant
women; this is listed as the correct answer in many 2CK-level NBME/CMS Qs);
TMP/SMX is also classic combo.

Q asks best initial Mx to prevent UTIs –> answer = postcoital voiding. If unsuccessful,
NBME wants “postcoital nitrofurantoin prophylaxis” next; if not listed, choose “daily
TMP/SMX prophylaxis.” The latter sounds incredibly wrong, and I agree, sounds
outrageous, but it’s correct on one of the obgyn CMS forms and everyone gets it
wrong.

22F + Sx of dysuria for 6 months + anterior vaginal wall pain + U/A completely
normal + afebrile; Dx? –> chronic interstitial cystitis –> answer on one of the obgyn
forms. Must have at least 6 weeks of UTI-like Sx without any identifiable pathology.
Tx for asymptomatic bacteriuria –> if pregnant, must Tx. If not pregnant, do not Tx.
Exceedingly HY for 2CK.

Why must Tx asymptomatic bacteriuria in pregnancy? –> progesterone slows ureteric

peristalsis, increasing the risk of pyelo.

Neurology #1

HY lecture notes:

Slightly move quantitative version of the above chart (but qualitative suffices for the
USMLEs):
Herpes causes temporal lobe hemorrhage, which is why there’s blood in the CSF. CT
can often be negative, but one thing I have seen in Qs is “slowing pattern” or
“temporal complexes” on EEG, essentially implying HSV encephalitis.

Meningitis = nuchal rigidity (stiff neck), headache, and photophobia. Can also present
with ophthalmoplegia.

Encephalitis (encephalopathy more generically) = confusion.

Meningoencephalitis = combination of the two.

Chiari malformation = downward displacement of the cerebellar tonsils through the

foramen magnum. There are many types.

Type I is less severe than type II. Type II is aka Arnold-Chiari malformation.

Type I presents with syringomyelia of the cervical spinal cord, which is a syrinx (fluid
filled cyst within the spinal cord) affecting the anterior white commissure –> causes
bilateral loss of pain and temperature sensation below the level of the lesion. Type I
vignettes will generally be in a young adult.

Type II presents with a more severe inferior displacement of the tonsills + vermis than
type I. It is accompanied by a lumbar or lumbosacral myelomeningocele. Only type II
is referred to as the Arnold-Chiari malformation.

Immunodeficiency + autoimmune disease increase risk for non-Hodgkin lymphoma,

namely primary CNS lymphoma. If they show you a large-ish, irregular primary lesion
with tiny adjacent lesions, the latter are merely satellite lesions. I point this out
because metastases are classically multiple lesions, but the pattern is not that of a
large lesion with adjacent tiny satellite lesions. USMLE likes SLE causing CNS
lymphoma (they will show you an irregular ring-enhancing lesion + tell you explicitly
that it’s a ring enhancing lesion + patient has SLE –> answer = CNS lymphoma, not
Toxo).

HY lecture notes:2, neuro

Important locations

Broca area: left inferolateral posterior frontal lobe.

Wernicke area: left posterior temporal lobe (superior temporal gyrus).

Broca aphasia
 • Expressive, non-fluent aphasia –> sometimes described as “telegraphic
speech” because the patient exhibits forceful effort to produce language
(spoken or written) with a propensity to leave out non-essential
grammatical words, like prepositions and articles.
• Comprehension remains intact.
• Caused by stroke of superior branch of left middle cerebral artery.
• Repetition usually impaired. –> if vignette sounds like Broca but they
explicitly tell you repetition is intact, choose “transcortical motor aphasia,”
not Broca.

Wernicke aphasia

• Receptive, fluent aphasia –> patient has difficulty comprehending written

or spoken language –> reciprocally, patient also produces language that
lacks content or meaning (“word salad”).
• Fluency remains intact in the sense that the patient can produce language
effortlessly; but as stated, it just simply lacks content and meaning.
• Caused by stroke of inferior branch of left middle cerebral artery.
• Repetition usually impaired. –> if vignette sounds like Wernicke but they
explicitly tell you repetition is intact, choose “transcortical sensory aphasia,”
not Wernicke.

Conduction aphasia

• Lesion of arcuate fasciculus.

• Repetition alone is impaired.

Global aphasia

• Lesion of Broca, Wernicke, and arcuate fasciculus.

• Vignette will sound like both Broca + Wernicke together, AND repetition is
impaired.
• If repetition, not impaired, choose “mixed transcortical aphasia” instead.

USMLE also loves showing you a gross brain specimen and then asking you where a
stroke lesion is (and its blood supply) based on the patient’s signs:
Before you freak out, the starting point is identifying the central sulcus, which is the
line running transversely across the brain between points D and E, and then again
between C and F.

Anterior to the central sulcus = primary motor cortex. (C and D)

Posterior to the central sulcus = primary sensory cortex. (E and F)

The next step is saying, “Ok, are we medial or lateral on the hemisphere?” As you can
see, D and E are clearly medial; C and F are lateral.

If the contralateral legs are affected due to a stroke, that’s medial brain (D and E)
supplied by the anterior cerebral artery (ACA).

If the contralateral face and arms are affected, that’s lateral brain (C and F) supplied
by the middle cerebral artery (MCA).

So if vignette says, e.g., an 82M with AF has sudden numbness and paresthesias of
the right leg and they asked you to choose the letter, what would you say?

Well, we say we’re clearly looking at the left side of the brain, so that makes sense.
Second, since it’s the leg, we know we’re dealing with D and E. Finally, because it’s
sensory, not motor, we know we’re dealing with posterior to the central sulcus, so we
know it’s E as the answer. And if they had asked you for the blood vessel affected by
an embolus instead, it would be ACA because it’s medial brain.

Likewise, if they told you a guy with hypertension and a carotid bruit now has right-
sided arm weakness + facial droop, which letter would you say corresponds?

Well, we say we’re clearly looking at the left side of the brain, so that makes sense.
Second, since it’s the arm + face, we know we’re dealing with C + F. Finally, because
it’s motor, not sensory, we know we’re dealing with anterior to the central sulcus, so
we know it’s C as the answer. And if they had asked you for the blood vessel affected
by an embolus instead, it would be MCA because it’s lateral brain.
HY lecture notes:

Diabetic retinopathy

Leading cause of blindness ages 20-64.

Caused by non-enzymatic glycosylation of retinal microvessels –> vascular damage

with degeneration of capillaries –> reduced retinal blood flow + ischemia + damage to
neurons of inner retina.

Initially it is non-proliferative, meaning there is no neovascularization of the retina,

and many patients won’t notice any visual changes.

As retinal ischemia progresses, neovascularization occurs; this is called proliferative

diabetic retinopathy. The tiny new blood vessels are fragile and can easy rupture,
causing blindness. In addition, they can also grow into the vitreous humor, eventually
leading to vitreous hemorrhage.

Cotton wool spots may be seen on fundoscopy, which are axonoplasmic aggregates
from neuronal degeneration. HTN is the other common cause of cotton wool spots.

Treatment for diabetic retinopathy is with injections of VEGF inhibitors or laser

photocoagulation.

Optic neuritis

Optic neuritis literally means inflammation of the optic nerve –> classically seen in
multiple sclerosis –> can present with a wide array of visual changes, e.g., blurry
vision, loss of color vision, and central scotoma. Essentially in the vignette they’ll say a
woman 20s to 30s who has an episode of blurry vision + urge incontinence + other
sensory or motor dysfunction –> answer = MS with optic neuritis.

Optic neuritis causes a Marcus Gunn pupil, which is also known as a relative afferent
pupillary defect (RAPD).

In RAPD, shining a light in the eyes and moving it side to side will make it appear as
though the affected eye’s pupil dilates, rather than constricts, in response to light. In
reality, it doesn’t dilate; it just doesn’t constrict as much as the unaffected side.

In order to understand this, you must first know that optic nerve (CN II) afferent input
from either eye will cause a bilateral efferent response via the oculomotor nerve (CN
III), causing both eyes to constrict.
When you shine a light into one eye, the resultant constriction of that eye’s pupil is
called a direct response. The constriction of the contralateral pupil is called
the consensual response.

When CN II from one eye receives a light stimulus, that is transmitted in the form of
an afferent signal to the Edinger-Wesphal nucleus of the midbrain, which will then
relay an efferent signal back to both eyes via CN III, yielding both a direct and
consensual response.

If CN II of the left eye is affected by optic neuritis, the left CN II is essentially

communicating, “we don’t need to constrict either pupil that much because there’s
not much light here; let’s constrict both pupils just a little.” So the result is, the direct
and consensual constrictive response is weak. However, the right eye is normal, so if
you shine the same light into it, the afferent signal will be much stronger, so the
degree of constriction, as received via the efferent response, will also be stronger
bilaterally.

Therefore, when you go back to the affected side with the light, the lesser degree of
direct response will make it appear as though the pupil is dilating, when in reality it’s
just constricting less relative to the robust level of constriction from the previous
consensual response.

For instance, if we have a Marcus Gunn pupil in the right eye (left side of following
diagram), this is what we’d see:
You’re probably like, “Oh wow fuck yeah. That diagram is actually crazy helpful. I
don’t even think I totally understood MG pupil until now truthfully.” Yeah, I know.
You like that.

Internuclear ophthalmoplegia

In MS, although optic neuritis is common, it is non-specific, and can be caused by

other pathologies (e.g., sarcoidosis) and drugs (e.g., ethambutol). In contrast,
internuclear ophthalmoplegia (INO), aka medial longitudinal fasciculus syndrome
(MLF syndrome) is pathognomonic of MS (i.e., you only see it in MS).
In INO, when one eye abducts via abducens nerve (CN VI), the contralateral eye
cannot adduct via CN III because of inflammation of the MLF.

The side that cannot adduct is the side whose MLF is affected. The normal side’s eye
will demonstrate nystagmus.

It must also be stated that although the affected side cannot adduct, there is no CN
III lesion, as evidenced by the patient being able to converge the eyes normally.

So if the left MLF is affected:

Right eye abducts (CN VI) –> left eye tries to adduct (CN III) but cannot, so there is
nystagmus in the right to attempt to bring the eyes together in the midline. However
patient can converge normally (CN III therefore intact on left, so Dx = INO).

Weber syndrome –> midbrain infarct characterized by ipsilateral CN III defect +

contralateral hemiparesis/hemiplegia.

Lateral pontine syndrome –> (in FACIAL spelled backward –> AICA) –> AICA infarct
+ ipsilateral Bell palsy (facial); ipsilateral hearing loss (central deafness) + loss of
pain/temperature sensation to ipsilateral face (facial hemianesthesia) + contralateral
body.

Lateral medullary syndrome (Wallenberg syndrome) –> PICAchew (Pikachu) –> PICA
infarct + dysphagia +/- ipsilateral Horner syndrome + ipsilateral facial sensory deficit.
Horner syndrome is classically caused by pancoast tumor of the lung, but knowing it
is caused by lateral medullary syndrome is really HY in terms of being able to
differentiate these stroke syndromes!

Medial medullary syndrome –> infarct of paramedian branch of anterior spinal

artery –> ipsilateral tongue deviation (CN XII) + contralateral
hemiparesis/hemiplegia.

CN III palsy –> down and out –> can classically occur due to impingement from a
posterior communicating artery (PCom) aneurysm.

CN IV palsy –> slightly elevated pupil in the midline –> worsens when head is tilted
toward ipsilateral shoulder –> due to weakness of superior oblique (moves pupil
inferomedially).

CN VI palsy –> medially-directed pupil.

Central pontine myelinolysis (CPM) –> causes locked-in syndrome –> caused by
corrected hyponatremia (<135 mEq/L) too quickly with hypertonic (3%) saline. Na
should be corrected no more than 6 to 12 mEq/L in the first 24 hours, and no more
than 18 mEq/L in the first 48 hours. If hyponatremia is severe, a 100-150-mL bolus of
hypertonic (3%) saline is acceptable. In contrast, if hypernatremia is corrected too
quickly with hypotonic saline, cerebral edema will ensue.

The header image for this lesson is CPM.

Cardiopulmonary #1

HY lecture notes:1

Atrial septal defect (ASD) you’d hear wide, fixed splitting of S2. Usually due to patent
foramen ovale.

S2 denotes the closure of the semilunar valves (aortic + pulmonic) and the onset of
diastole. A2 normally closes before P2.

When we talk about changes in splitting of the S2 heart sound (i.e., wide splitting,
paradoxical splitting, etc.), if pressure in a ventricle is greater, the sound will occur
later / is protracted.

So if RV pressure becomes greater for whatever reason –> P2 occurs later –> wider
splitting. So pulmonary artery hypertension = wide-splitting.

If LV pressure becomes greater –> A2 occurs later, and can even occur after P2 –>
paradoxical splitting. So LVH = paradoxical splitting.

When R or L ventricular pressure exceeds the pulmonic arterial and aortic pressure,
respectively, the valves open. Then the ventricle will lose pressure as blood ejects,
followed by isovolumetric relaxation marking the onset of diastole, and the pressure
within the ventricle falls below the pressure distal to the valve –> valve shuts.

Normally splitting oscillates with the respiratory cycle.

Inhalation causes P2 to occur later –> decrease in intrathoracic pressure –> increased
venous return to right atrium –> more blood in right ventricle = more preload = more
pressure –> time it takes for RV pressure to fall below pulmonic arterial pressure is
greater –> P2 will occur slightly later with inhalation.

With exhalation it’s the opposite. P2 occurs slightly sooner because increased
intrathoracic pressure will attenuate venous return –> less preload in RV –> less
pressure in RV –> time it takes for RV pressure to fall below pulmonic arterial
pressure is less –> pulmonic valve closes slightly sooner –> distance between A2 and
P2 is less.
When you’ve got an ASD, blood is constantly moving L –> R from LA –> RA (pressure
is always greater on the left side). So the effects of inhalation/exhalation are
minimized in terms of the A2-P2 split bc you’ll always have more right-sided preload.
This causes a wide, fixed-splitting.

Bottom line is “fixed splitting of S2” is exceedingly HY for ASD. If you memorize it as
“wide, fixed splitting,” that’s okay too, but for the USMLE only the fixed part matters.

Bicuspid aortic valve is autosomal dominant and is the most important cause of aortic
stenosis (AS) in the population. Valve should normally have three leaflets. Will calcify
in middle age as opposed to elderly age, leading to stenosis. But can also easily cause
AS in young patients.

Bc it’s AD and runs in families, do transthoracic echo (TTE) to diagnose. If present,

monitor with yearly TTE. If cross-sectional area falls below 1.0cm2, do aortic valve
replacement. One of the NBME surgery questions had 0.8 as the cross-sectional area,
and the answer was aortic valve replacement, so this isn’t just some pedantic detail
I’m romanticizing.

AS and hypertrophic obstructive cardiomyopathy (HOCM) are both crescendo-

decrescendo systolic (aka mid-systolic) murmurs auscultated best over the second
intercostal space, right sternal border. USMLE wants you to know how to
differentiate.

HOCM and MVP (mitral valve prolapse) are the two murmurs that get worse with
LESS volume in the heart; all other murmurs get worse with more volume in the
heart.

So if you do a clinical maneuver that decreases volume (Valsalva, going from supine
to sitting/standing, nitrate administration), HOCM should get worse, and AS better or
no change.

If you do a clinical maneuver that increases volume (lying down, squatting, leg raise
while supine, hand grip), HOCM should get better / no change, and AS worse. (Hand
grip actually increases afterload, which then prevents ejection of blood, which in turn
actually keeps more blood in the heart; but using the word “preload” to describe hand
grip’s effect on keeping volume in the heart would be misleading and inaccurate.)

The USMLE will slam you on this. They’re going to say young athlete (“oh em gee,
sudden death in young athlete = HOCM!”), who has a 2/6 mid-systolic murmur, and
then they’ll tell you that there’s no change with Valsalva maneuver.

If there’s no change with Valsalva, then that’s AS, not HOCM. The answer would
simply be “bicuspid aortic valve,” as they expect you to know that’s synonymous with
AS. And once again, you don’t need to be older with a calcific valve for it to cause AS.
Myxomatous degeneration of mitral valve = mitral valve prolapse on the USMLE. It’s
a type of connective tissue degeneration, seen classically in Marfan and Ehlers-
Danlos syndromes.

Don’t confuse myxomatous degeneration with atrial myxoma, which is usually an

adult-onset heart tumor that will cause a “ball-in-valve” murmur effect. That is, they’ll
say there’s a diastolic rumble that disappears when the patient is positioned in an
unusual way, e.g., lying down on his or her right side. Kids with tuberous sclerosis get
cardiac rhabdomyoma, not myxoma.

Carney complex can cause myxoma in kids = perioral melanosis (hyperpigmentation

around the lips), endocrine hypersecretion (usually granular, bilateral zona fasciculata
hyperplasia leading to Cushing syndrome, but can be hyperthyroidism or acromegaly),
and cardiac myxoma (not rhabdomyoma). I promise this is on the USMLE as low-yield
as that sounds. No USMLE resource mentions it. But I’m mentioning it.

Remember, MVP gets WORSE with less volume in the heart (same as HOCM). MVP =
mid-systolic click.

You can also get an “ejection click” sometimes with aortic stenosis. Or they’ll say a
“late-peaking” systolic murmur. But most of the time, you’ll see just mid-systolic
murmur for AS.

MVP is most common murmur in the population overall and is usually just a benign,
incidental finding in otherwise healthy people.

Mitral valve prolapse syndrome = “fleeting” and sharp left-sided chest pain that will
occur in people teens to 30s, and they’ll have many episodes (i.e., at least 30) in their
history. You don’t treat it generally, even when symptomatic. This was a question on
one of the 2CK NBMEs somewhere, where you’d think you’d give propranolol to slow
heart rate and increase diastolic filling, but the answer was no Tx necessary.

Rheumatic heart disease (rheumatic fever, RF) causes mitral regurg (MR) acutely but
mitral stenosis (MS) later in life.

Almost all mitral stenoses are due to previous rheumatic heart disease. But when the
infection with S. pyogenes (Group A Strep) actually occurs, it’s MR, not MS.

MR = holosystolic murmur at the 4th intercostal space, left-midclavicular line, with

radiation to the axilla; but USMLE can just as easily say left sternal border, or not
even mention radiation.

MS = opening snap with a mid-late diastolic descrescendo rumble; same location as

MR without the radiation.
Rheumatic heart disease = JONES = joints (polyarthritis), O (supposed to look like the
heart; carditis); nodules (subcutaneous); erythema marginatum (not multiforme, which
is instead caused by drugs or infection); Sydenham chorea (abnormal movements).

Caused by S. pyogenes M-protein. Immune system makes antibodies against it, which
cross-react with mitral valve (molecular mimicry; type II hypersensitivity).

12-year-old, sore throat, salmon maculopapular body rash + strawberry tongue =

Scarlet fever = give penicillin to prevent RF.

If this 12-year-old gets a murmur, answer = MR, not MS.

But ten years later, answer is MS, not MR.

MS often shows up in pregnancy. Increased preload by second trimester (plasma

volume expands >50%) hits threshold by which MS becomes symptomatic and
dyspnea occurs. In contrast, dyspnea usually later in pregnancy, circa parturition, is
peripartum cardiomyopathy, which is antibody mediated. But just making a point that
MS both in real life and on the USMLE will often surface in pregnancy in second
trimester.

MS can rarely be seen in situations like Libman-Sack endocarditis in SLE causing anti-
phospholipid syndrome secondary to lupus anticoagulant. But once again, almost all
MS is due to previous RF.

RF will never occur following skin infection (e.g., impetigo, cellulitis, erysipelas), but
instead will occur following Strep pharyngitis. Post-streptococcal glomerulonephritis
(type III hypersensitivity) frequently occurs following Strep skin infections however.
Treat skin with oral dicloxacillin or oral cephalexin for cellulitis and erysipelas. Use
topical mupirocin for impetigo. Orals can be used for impetigo, but topical is first-line.

HY lecture notes:

Pericardial effusion + cardiac tamponade on ECG –> “electrical alternans” or

“alternating amplitudes of QRS complexes.”

Cardiac tamponade is merely a pericardial effusion that has hemodynamic

decompensation (low BP).

Cardiac tamponade always presents with Beck triad in questions –> JVD,
hypotension, muffled heart sounds.

The acuteness of fluid accumulation is what determines whether a fluid collection

around the heart is a tamponade or not. For instance, a stab wound or LV free-wall
rupture (post-MI) can cause a low-volume accumulation of blood around the heart
that is super-fast and hence can cause decompensation (tamponade), whereas, e.g.,
malignancy (lymphoma or breast cancer) could cause a slow-accumulating chylous or
serosanguinous effusion that could be large volume but doesn’t cause tamponade.

Tx for effusions/tamponade = do echo first, then pericardiocentesis or pericardial

window –> student says “wtf? No way that’s right. Pericardiocentesis or pericardial
window is definitely the first answer.” It’s not. This is on one of the 2CK NBME forms
(I think surgery), where they had pericardiocentesis or echo, and echo was next best
step for tamponade. Apparently you have to view the fluid around the heart
first, then do the intervention.

USMLE won’t put both pericardiocentesis and pericardial window as two separate
answers for the intervention; it will be one or the other. On NBME 8 for 2CK
pericardial window was an answer, but pretty much any other Q I’ve seen has been
pericardiocentesis.

Acid-base disturbance in PE –> respiratory alkalosis –> low O2, low CO2, high pH,
normal bicarb –> O2 diffuses slowly; CO2 diffuses quickly; so you require healthy
lungs to get O2 in, whereas CO2 can adequately get out despite decreased perfusion
(PE) or increased secretions/bronchoconstriction (asthma; acid-base disturbance is
the same acutely). High RR means CO2 is low. Bicarb is normal because it’s too acute
to change (requires minimum 12-24 hours to go down).

For any type of shock, USMLE wants you to know you can get lactic acidosis causing
low bicarb. Super HY. Once again, can be any type of shock. If you see low
bicarb/pH, that’s why –> decreased perfusion to vital organs –> increased ischemia –
> increased anaerobic respiration –> lactic acid production.

Also, don’t pigeon-hole findings in vignettes. For instance, there’s a Q on one of the
NBMEs where they give obvious septic shock (old guy has catheter in + fever + high
leukocytes + low BP), but they say his extremities are cold and clammy. Answer was
septic shock, not hypovolemic shock. Student says, “Wait, why the fuck is he cold and
clammy then?” Yeah, weird. But this is my point about not pigeon-holing things.

After ABCs (airway, breathing, circulation), first answer is generally just giving simple
fluids (normal saline; 0.9% NaCl or Ringer lactate).

But shock-specific drugs:

Anaphylactic –> IM epinephrine

Septic –> Norepinpehrine

Cardiogenic –> Dobutamine (beta-1 agonist) or Dopamine

Cardiogenic shock –> most important parameter is high PCWP (pulmonary capillary
wedge pressure). If all else fails, don’t forget that for shock for the USMLE.

Cardiogenic shock: low VR, low CO, high TPR, high PCWP –> HR can be high or low
–> bottom line is your heart can’t pump –> cardiogenic shock is the answer after an
MI. It can sometimes occur after sepsis –> the way to differentiate is they’ll say “hazy
lung fields and dilated heart” in the setting of sepsis, and the answer is dobutamine or
dopamine.

Hypovolemic shock: low VR, low CO, high TPR, low PCWP

Anaphylactic and septic shock: high VR, high CO, low TPR, normal PCWP

Neurogenic shock: low VR, low CO, low TPR, normal PCWP

HY lecture notes:3

Pulmonary capillary wedge pressure (PCWP) is exceedingly HY on the USMLE and

remains a concept students struggle with.

PCWP = left atrial pressure.

If you stick a catheter tip through the venous system all the way up to the right
atrium, then right ventricle, then pulmonary arteries, until it can’t go any farther
within a pulmonary capillary, any pressure waves it senses at the distal tip of the
pulmonary capillary must be coming from the left atrium, since the LA is just distal to
the pulmonary circulation. So if LA pressure is up for whatever reason, so is PCWP.

High PCWP occurs if there is any left heart pathology. Not just in cardiogenic shock,
but also in mitral stenosis (increased afterload on LA –> so more pressure in LA –>
higher PCWP) or mitral regurg (higher preload in LA –> higher pressure –> higher
PCWP), as well as any cause of left ventricular hypertrophy (if the LV is experiencing
a pressure or volume overload, that effect will back up to the LA).

In aortic stenosis –> higher afterload on LV (concentric hypertrophy) –> therefore

higher afterload on LA –> higher PCWP.

In aortic regurg –> higher preload on LV (eccentric hypertrophy) –> therefore higher
preload on LA –> higher PCWP.

It should also be noted that it is very rarely stated that the left atrium
“hypertrophies”; the LV will hypertrophy; the LA will dilate. So any pathology at the
level of the mitral valve or later (LV, aortic valve, or aorta) will cause left atrial
dilatation and increased PCWP.
Most pleural effusions are due to either congestive heart failure (CHF) or malignancy.

CHF = left heart failure + right heart failure.

The most common cause of right heart failure is left heart failure.

Therefore in CHF, PCWP is high –> this increased pulmonary pressure leads to
pulmonary hypertension (where there is actual hypertrophy of the tunica media of
the pulmonary arteries) –> backs up to the RV –> right heart failure.

So let’s say you’ve got fluid in the lungs, but they say PCWP is normal –> that means
the fluid in the lungs can’t be due to left-heart origin because, if it were, PCWP would
have to be high.

ARDS (acute respiratory distress syndrome) presents with normal PCWP. ARDS is
when proteinaceous fluid leaks out into the alveoli bilaterally and is frequently due to
sepsis, trauma, or pancreatitis. So USMLE Qs like to say, e.g., 44M alcoholic with
abdominal pain gets dyspnea with bilateral infiltrates + his PCWP is normal –> Dx =
ARDS.

In ARDS, pO2/FiO2 must be less than 300. It is treated with low-tidal-volume

mechanical ventilation (prevents barotrauma) + permissive hypercapnia (we allow
CO2 to be slightly elevated [>44 mmHg] to prevent barotrauma).

Hypovolemic shock: low VR, low CO, high TPR, low PCWP

Distributive shock (anaphylactic, septic, neurogenic): high VR, high CO, low TPR,
normal PCWP

Cardiogenic shock: low VR, low CO, high TPR, high PCWP

After giving fluids, give:

Anaphylactic –> IM epinephrine

Septic –> Norepinpehrine

Cardiogenic –> Dobutamine (beta-1 agonist) or Dopamine

HY lecture notes:4

Atrial fibrillation –> absent p-waves + irregularly irregular intervals between QRS
complexes.
For Step 1, you literally just need to know the ECG strip. For 2CK, you need to know
how to Tx.

There are two arms of management: 1) blood-thinning, and 2) actual Tx of the AF.

Regarding blood thinning, we use the CHADS2 / CHA2DS2-VASc score.

Congestive heart failure, HTN, Age 75 or older, Diabetes, Hx of Stroke/TIA (the latter
is 2 points).

If a patient has AF and has 0 or 1 points, give aspirin.

If a patient with AF has 2 or more points, give anticoagulation:

• If valvular AF (meaning pt has MR/MS or prosthetic valve), give warfarin.

• If non-valvular AF (meaning pt doesn’t have any valve issues), give a
NOAC (New Oral AntiCoagulants). NOACs refer to the direct thrombin
inhibitor dabigatran and the direct Xa inhibitors rivaroxaban, apixaban, and
edoxaban.

Because there are variants to this score, the USMLE will never be borderline or
ambiguous with what kind of answer they want: you’re either going to get a vignette
where he or she has AF but no other CHADS risk factors, or you’ll get a vignette
where the patient literally has all of the risk factors, where you don’t even need to
calculate the score because qualitatively the result is obvious for needing to give
anticoagulation.

Then to address the actual AF, do rate control before rhythm control. Management is
complex and pedantic, but for the USMLE what you need to know is:

Rate: First drug we give is metoprolol. If cannot receive, give verapamil. These drugs
both intercept the AF rhythm at the AV node.

Contraindications to beta-blockers are depression (beta-blockers cause depression),

sexual dysfunction, COPD, asthma (if Hx of hospitalization or oxygen use), and 2nd or
3rd-degree heart block. Although metoprolol is beta-1 selective, there’s still
considered to be marginal degree of beta-2 overlap such that we simply avoid the
drug if the patient has any of the aforementioned contraindications.

If patient fails rate control, we go to rhythm control.

If the patient has no structural (e.g., LVH) or coronary artery disease, the first drug we
use is flecainide, which is a type Ic sodium channel blocker.
If the patient has structural or coronary artery disease, use one of the other
antiarrhythmics such as amiodarone, dronedarone, or dofetilide.

HY lecture notes:5

Pulmonary embolism –> most common thing you see on an ECG = sinus tachycardia
(really HY) –> they might say patient has HR of 92 and that ECG shows no
abnormality (same thing; that’s sinus tachy) –> first Tx is heparin, then do spiral CT
scan of chest.

In pregnant women, do V/Q scan (ventilation/perfusion scan), not spiral CT, because
of the radiation.

Now this is where it gets weird: if they tell you a pregnant woman has a V/Q scan
that shows segmental defects (positive for PE), and then they ask you for the next
best step in diagnosis, the answer is spiral CT. This is where you say, “Wtf? You just
said we don’t do spiral CT in pregnant women cuz of the radiation.” Correct, we don’t.
We definitely do V/Q scan instead. But if the question asks you what the next best
step in diagnosis is after a V/Q scan has already been performed, the answer is still
spiral CT. Weird, I know. But this is actually in UWorld for 2CK, and everyone gets it
wrong for obvious reasons.

Dead space vs shunt

Dead space = ventilation without perfusion, PE

Shut = perfusion without ventilation, peanut

Physiologic (total) dead space = anatomic dead space + alveolar dead space.

Anatomic dead space = ventilation within the conducting zone of the airways that is
unable to participate in gas exchange because there is simoply an anatomical lack of
respiratory epithelium; this includes the trachea, bronchus, bronchioles, and terminal
bronchioles; in contrast, the respiratory bronchioles and alveoli participate in gas
exchange.

Alveolar dead space is ventilation within underperfused alveoli (usually negligible in

healthy patients).

USMLE wants you to know that pulmonary embolism = dead space because this
presents a scenario of ventilation without perfusion.

A shunt refers to pretty much any other cause of lung pathology, where ventilation is
reduced for whatever reason.
Shunt = foreign body aspiration; obstructive conditions, e.g., asthma, atelectasis,
bronchitis; certain restrictive lung conditions, e.g., pulmonary edema, fibrosis. These
conditions can all result in areas of lung that receive less ventilation.

Aspiration of a foreign object is an easy example –> area of lung gets closed off and
becomes underventilated –> this means we can say there’s “zero” for this part of the
lung –> so even if we were to give a patient oxygen and all of the areas of healthy
lung are maximally saturated with O2, the zero still averages in, making the sum of
the oxygenation for the entire lungs to be less than it should be –> result is patient
still has low arterial oxygen.

This process is called a shunt because the mixing of deoxygenated blood with
oxygenated blood is considered to be a “right to left” process. This is distinct from a
cardiac R –> L shunt (i.e., Eisenmenger syndrome with VSD, where deoxygenated
blood from the RV enters the LV, causing the systemic arterial oxygen to be low); a
pulmonary shunt means the R –> L mixing of an underventilated, deoxygenated lung
segment with other oxygenated ones, with the net result being the patient’s arterial
O2 is still low.

HY lecture notes:6

Phakomatoses is that obscure term that pretty much causes every convo with a
student to go like this:

“Wait, what… what did you just say.”

“Phakomatoses.”

“Phakomatoses? What the fuck does that mean.”

Phakomatoses are neurocutaneous disorders and refer to:

• NF1, NF2, TSC, VHL, and Sturge-Weber.

Neurofibromatosis type I (NF1)

• Chromosome 17
• Autosomal dominant
• Neurofibromas (benign cutaneous nerve tumors presenting as small, soft
bumps on the skin)
• Axillary and groin freckling
• Lisch nodules (iris hamartomas)
• Cafe au lait spots (hyperpigmented macules)
• Pheochromocytoma
• Optic nerve glioma
 • Glioblastoma multiforme
• Demonstrates variable expressivity

Neurofibromatotis type II (NF2)

• Chromosome 22
• Autosomal dominant
• Bilateral acoustic schwannomas
• Congenital cataracts
• Meningioma, ependymoma, oligodendroglioma, medulloblastoma

Tuberous sclerosis (TSC)

• TSC1 gene on chromosome 9 coding for hamartin protein, and

chromosome 15 coding for tuberin protein.
• Autosomal dominant
• Periventricular nodules seen on CT or MRI (tubers)
• Presents as seizure in young child (Qs like writhing movements in a kid’s
sleep)
• Adenoma sebaceum (angiofibromas; skin-colored papules in a butterfly
distribution on the face and in the nasolabial folds)
• Subungual fibromas (nailbed tumors)
• Cardiac rhabdomyoma
• Renal angiomyolipoma
• Pulmonary lymphangioleiomyomatosis (abnormal smooth muscle
proliferation of airways; can also affect pregnant women who do not have
TSC)

von Hippel–Lindau (VHL)

• Chromosome 3
• Autosomal dominant
• Cerebellar and retinal hemangioblastomas
• Bilateral renal cell carcinoma
• Constitutive activation of hypoxia-inducible factor (HIF), leading to vascular
proliferation

Sturge-Weber syndrome

• Not hereditary; caused by mosaic, somatic mutation in GNAQ gene

• Unilateral facial Port-wine stain birthmark (but may also present as
cutaneous violaceous papules in an ophthalmic-trigeminal nerve
distribution)
• Seizure
• Ipsilateral leptomeningeal angioma (arachnoid or pia mater vascular tumor)
/ arteriovenous malformation (AVM)
• Glaucoma
Arteriovenous malformation (AVM) can also cause SIADH.

In addition, pulmonary AVMs are seen in hereditary hemorrhagic

telangiectasia (Osler-Weber-Rendu syndrome).

Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome).

• Autosomal dominant
• Cutaneous telangiectasias.
• Epistaxis (nosebleeding) is super common from an early age.
• Can also cause GI bleeding leading to iron deficiency anemia.
• USMLE will always show you a picture of a tongue or fingernail with a red
dot, which is the telangiectasia.
• Pulmonary AVMs can be seen. USMLE will show you the tongue and then
say 44M has dysnpea and high-output cardiac failure; why? Answer is
pulmonary AVM.

AVMs can cause bounding pulses (wide pulse pressure; big difference between
systolic and diastolic pressure, e.g., 160/60, or 120/40) similar to aortic regurgitation
(and sometimes patent ductus arteriosus) because blood quickly leaves the arterial
circulation for the venous circulation.

HY lecture notes:7

What is PCWP? –> equal to left atrial pressure; if you stick a catheter through the
venous circulation all the way back to the right heart, and then into the pulmonary
circulation, and then into a distal pulmonary capillary such that it can’t go any farther,
the pressure reverberations are said to best reflect those of the left atrium. The
USMLE is obsessed with PCWP. You need to know it is increased not just in
cardiogenic shock, but also in left heart pathology of any kind (e.g., mitral regurg, MI,
LVH, etc.).

Need to know low bicarb in patient with dehydration (or any type of shock) –>
answer = lactic acidosis –> decreased perfusion to vital organs –> decreased oxygen
delivery –> increased anaerobic respiration –> increased lactic acid.

Hypovolemic shock arrows: CO down, VR down, TPR up, PCWP down (or normal).

Cardiogenic shock arrows: CO down, VR down, TPR up, PCWP up.

Septic + anaphylactic shock arrows: CO up, VR up, TPR down, PCWP normal.

Neurogenic shock + adrenal crisis arrows: CO down, VR down, TPR down, PCWP
normal.
First answer for Tx of shock on USMLE? –> manage ABCs, but fluids is what they
want –> normal saline (0.9% NaCl, or Ringer lactate).

After fluids:

Tx of anaphylactic shock? –> IM epinephrine.

Tx of septic shock? –> norepinephrine.

Tx of cardiogenic shock? –> dopamine or dobutamine.

Difference between epinephrine and norepinephrine binding? –> Epi binds alpha 1,
alpha 2, beta 1, and beta 2; NE does not bind beta 2.

What does that matter? –> beta 2 agonism opens the lungs so is ideal in anaphylaxis.
In addition, beta 2 dilates peripheral arterioles, and this is not preferred in septic
shock because we need strong peripheral vasoconstriction to maintain BP. Alpha 1’s
main effect is to constrict vessels peripherally, so for septic shock, NE is used because
we get strong alpha 1 without beta 2 – i.e., just strong vasoconstriction.

HY lecture notes:8

Which murmurs are holodiastolic (pandiastolic)? –> aortic regurgitation (aortic

insufficiency; AR) + pulmonic regurgitation (pulmonic insufficiency; PR).

Which murmur is pandiastolic and loudest in early-diastole? –> classically AR

(decrescendo holodiastolic murmur).

Important initial principle regarding heart murmurs –> all will get worse / more
prominent with more volume in the heart, however MVP and HOCM are the odd
ones out; they’ll get worse with less volume in the heart.

8F + sickle cell + fever + HR of 120 + normal BP + 2/6 mid-systolic murmur at upper

right sternal border; Dx? –> transient, functional high-flow murmur secondary to
tachycardia à murmur will subside once HR returns to baseline.

13F + Hb of 7 g/dL + HR of 120 + normal BP + 2/6 mid-systolic murmur at upper

right sternal border; Dx? –> once again, transient, functional flow murmur –> I point
this out because students often erroneously think there’s some heart abnormality
when they see this type of murmur.
Aortic stenosis (AS) – what will you auscultate? –> mid-systolic (crescendo-
decrescendo systolic) murmur classically at 2nd intercostal space, right sternal border,
with radiation to the carotids; however will also show up as “late-peaking systolic
murmur with an ejection click.” –> don’t confuse the latter with “mid-systolic click,”
which is mitral valve prolapse (MVP).

Who gets AS? –> classically bicuspid aortic valve –> can be familial autosomal
dominant; also seen in Turner syndrome (45XO) –> leads to early calcification of
valve in the 40s onward; however a young patient without significant calcification can
easily have AS.

What about if the patient doesn’t have bicuspid valve? –> AS can still occur in the
general population with normal senile calcification seen typically age 70s-80s onward
(i.e., incidental 1/6 or 2/6 mid-systolic murmur in otherwise healthy elderly patient).

If patient is diagnosed with bicuspid aortic valve, next best step in Mx? –> annual
transthoracic echos –> if valve cross-sectional area falls below 1.0 cm2 then do aortic
valve replacement; there’s a surgery NBME Q where they say cross-sectional area is
0.8 cm2 and the answer is straight-up “aortic valve replacement.”

How does AS classically present Sx-wise? –> SAD à Syncope, Angina, Dyspnea.

AS causes what kind of LVH? –> concentric hypertrophy due to pressure overload –
> can also cause hypertrophic cardiomyopathy with an S4 heart sound (stiff LV). This
is in contrast to aortic regurgitation (aortic insufficiency), which causes eccentric
hypertrophy due to volume overload.

What kind of pulse is seen in AS? –> slow-rising pulse (“pulsus parvus et tardus”).
Don’t confuse this with AR, which causes bounding pulses with head-bobbing (Q will
often say for AR: “pulse has brisk upstroke with precipitous downstroke.”).

Any weird factoid about AS? –> Heyde syndrome is the combo of AS +
angiodysplasia (painless rectal bleeding in elderly due to superficial tortuous vessels
on the bowel wall) –> shows up on NBME.

What does HOCM sound like? –> same as AS (mid-systolic murmur, aka crescendo-
decrescendo systolic murmur).

What causes HOCM? –> autosomal dominant mutation in beta-myosin heavy-chain

gene.

What’s the structural change in the heart with HOCM? –> asymmetric septal
hypertrophy that causes the anterior mitral valve leaflet to block off the LV outflow
tract under states of lesser preload –> student says, “if the LV outflow tract is
blocked off (i.e., where the aortic valve is), why is it the mitral valve leaflet that blocks
it off then?” Yeah, I know, it’s weird. But the asymmetric septal hypertrophy causes
this to happen.

What’s the cause of death in HOCM? –> ventricular fibrillation (really HY!!) –> the
“sudden death in young athlete” is not due to an MI –> i.e., the patient
has clean coronary arteries –> do not select coronary artery occlusion as the answer.

What about if the vignette is sudden death in middle-aged patient with heart disease?
–> answer = ischemic heart disease (MI), not HOCM.

18M athlete + 2/6 mid-systolic murmur at right sternal border 2nd intercostal space +
there is paradoxical splitting of S2 + there is no change in the murmur with Valsalva;
Dx? –> ”bicuspid aortic valve” (AS), not HOCM –> students say “oh em gee young
athlete! HOCM!” –> the USMLE will slam you on this and wants you to know that the
key way to distinguish between AS and HOCM murmurs is that HOCM gets worse
with lower volume in the heart; AS will soften or there will be no change. Don’t just
automatically jump on HOCM because it’s a young athlete.

How to Tx HOCM –> can give propranolol to keep HR from getting too fast (the
slower the HR, the more time the heart spends in diastole –> more diastolic filling –>
greater preload –> less occlusion of LV outflow tract) –> should be noted tangentially
that although beta-blockers increase preload, they decrease chronotropy + inotropy
so the net effect is still decreased myocardial oxygen demand.

Can you explain “splitting of S2”? What does that even mean? –> the aortic valve
normally shuts (A2) just before the pulmonic valve (P2), so A2 will occur slightly
before P2 –> when we talk about changes in splitting of the S2 heart sound (i.e., wide
splitting, paradoxical splitting, etc.), if pressure in a ventricle is greater, the sound will
occur later / is protracted. So if RV pressure becomes greater for whatever reason –>
P2 occurs later –> wider splitting. So pulmonary artery hypertension = wide-splitting.
If LV pressure becomes greater –> A2 occurs later, and can even occur after P2 –>
paradoxical splitting. So LVH = paradoxical splitting. When R or L ventricular pressure
exceeds the pulmonic arterial and aortic pressure, respectively, the valves open. Then
the ventricle will lose pressure as blood ejects, followed by isovolumetric relaxation
marking the onset of diastole, and the pressure within the ventricle falls below the
pressure distal to the valve –> valve shuts. Normally splitting oscillates with the
respiratory cycle. Inhalation causes P2 to occur later –> decrease in intrathoracic
pressure –> increased venous return to right atrium –> more blood in right ventricle –
> more preload à more pressure –> time it takes for RV pressure to fall below
pulmonic arterial pressure is greater –> P2 will occur slightly later with inhalation.
With exhalation it’s the opposite. P2 occurs slightly sooner because increased
intrathoracic pressure will attenuate venous return –> less preload in RV à less
pressure in RV –> time it takes for RV pressure to fall below pulmonic arterial
pressure is less –> pulmonic valve closes slightly sooner –> distance between A2 and
P2 is less.
What is fixed splitting of S2? –> Super HY for atrial septal defect (ASD) –> sometimes
can be written as “wide, fixed splitting of S2” –> it’s not the “wide” that matters; you
need to remember fixed splitting.

What does “splitting of S1 mean”? –> highly unlikely to show up on the USMLE, don’t
worry, but for the sake of some people who’d ask, it’s usually seen in right bundle
branch block (BBB), which causes delayed closure of the tricuspid valve.

Maneuvers that decrease blood in the heart –> Valsalva; standing up from seated
position; sitting up from supine position; administration of nitrates –> any of these
will cause MVP + HOCM to get worse; all other murmurs will soften or not change.

Maneuvers that increase blood in the heart –> Lying down; leg raise while supine;
squatting; hand-grip.

How does Valsalva decrease blood in the heart? –> attempted exhalation against a
closed glottis –> robust increase in intrathoracic pressure –> decreased venous return
–> decreased cardiac preload.

How do nitrates decrease blood in the heart? –> if administered venously –>
increased venodilatation + venous pooling –> decreased venous return to the heart –
> decreased cardiac preload. If administered arterially –> decreased afterload –>
easier for the LV to eject blood –> decreased blood in the LV; it should be noted that
it would be incorrect to say arterial nitrates decrease preload; this is an indirect effect
in this case.

How does hand-grip increase blood in the heart? –> hand-grip increases afterload –>
LV cannot eject blood as readily –> greater volume of blood left in the LV; it should
be pointed out, however, that it would be incorrect to say hand-grip increases
preload, as this effect is indirect.

How does respiration relate to left- vs right-sided murmurs –> inspiration makes
right-sided murmurs worse; exhalation makes left-sided murmurs worse.

Why does inspiration make right-sided murmurs worse? –> inspiration –> decreased
intrathoracic pressure –> easier for blood to return to the RA –> increased venous
return –> more preload in right heart –> worsening of TR, TS, PR, PS.

Why does inspiration soften left-sided murmurs? –> decreased intrathoracic pressure
–> increased pulmonary vascular compliance –> transient decrease in pulmonary
venous return to the LA –> decreased LA preload; it should be noted that although
RA preload increases, this effect does not carry over to the LA because of pulmonary
vascular pooling.
Why does expiration soften right-sided murmurs? –> expiration –> increased
intrathoracic pressure –> harder for blood to return to the RA –> decreased venous
return –> less preload in right heart –> softening of TR, TS, PR, PS.

Why does expiration intensify left-sided murmurs? –> expiration –> increased
intrathoracic pressure –> decreased pulmonary vascular compliance –> transient
increase in pulmonary venous return to the LA –> increased LA preload; it should be
noted that although RA preload decreases, this effect does not carry over to the LA
because of pulmonary vascular compression.

HY lecture notes:9 cardio

What is a parasternal heave? –> a parasternal heave means the heartbeat can be felt
(or sometimes seen) along the left sternal border, usually due to RVH (since the RV is
most anterior) –> RVH can be seen in ventricular septal defect (VSD), so parasternal
heave can be seen in VSD.

What is a palpable thrill? –> a palpable thrill is merely a palpable murmur; it carries no
additional diagnostic significance; a thrill is seen in grades 4-6 of the heart sounds.

What are the 6 grades of heart sounds? (not asked on USMLE, but just for your own
knowledge with respect to this document) –>

1. Very faint; not heard in all positions (“cardiologist only”);

2. Faint; heard in all positions;
3. Loud, with no thrill;
4. Loud with palpable thrill;
5. Loud with palpable thrill + can be heard with stethoscope partially off
chest;
6. Loud with palpable thrill + can be heard with the stethoscope completely
off the chest.

Which murmurs are holosystolic (aka pansystolic)? –> mitral regurgitation (mitral
insufficiency; MR) + tricuspid regurgitation (tricuspid insufficiency; TR); ventricular
septal defect (VSD).

Which murmurs are mid-systolic (crescendo-decrescendo systolic) –> aortic stenosis

(AS) + hypertrophic obstructive cardiomyopathy (HOCM) + pulmonic stenosis (PS).

Which murmur has a diastolic opening snap? –> mitral stenosis (MS) à has diastolic
opening snap, followed by a mid-late decrescendo diastolic murmur.

Which murmur has a mid-systolic click? –> mitral valve prolapse (MVP).
Which murmur can also be described as a late-peaking systolic murmur with an
ejection click? –> aortic stenosis.

Which murmur is continuous machinery-like? –> patent ductus arteriosus (PDA).

Which murmur is pansystolic-pandiastolic? –> PDA (same as continuous machinery-

like).

Which murmur is to-and-fro? –> PDA; outrageous, but it’s on NBME 6 for 2CK and
relies on you knowing this description to get it right; every student gets this Q wrong
and then says “wtf is to-and-fro.” (my students of course will say, “got that one right
because of you”).

Which murmur is fixed splitting of S2? –> atrial septal defect (ASD).

Which murmurs are holodiastolic (pandiastolic)? –> aortic regurgitation (aortic

insufficiency; AR) + pulmonic regurgitation (pulmonic insufficiency; PR).

Which murmur is pandiastolic and loudest in early-diastole? –> classically AR

(decrescendo holodiastolic murmur).

Young child + hypocalcemia + harsh systolic murmur at left sternal border; Dx? –>
DiGeorge syndrome associated with tetralogy of Fallot –> on the USMLE, you should
essentially think of ToF and DiGeorge syndrome as interchangeable –> you can by all
means get other heart defects in DiGeorge, e.g., truncus arteriosus, but I can’t
emphasize enough that ToF is almost always seen in DiGeorge on USMLE.

Important initial principle regarding heart murmurs –> all will get worse / more
prominent with more volume in the heart, however MVP and HOCM are the odd
ones out; they’ll get worse with less volume in the heart.

What does VSD sound like? –> USMLE will describe it two ways: 1) holosystolic
murmur (aka pansystolic) at the left sternal border (or lower left sternal border) with a
parasternal heave or thrill; 2) holosystolic murmur at the left sternal border with a
diastolic rumble (weird, but in NBME Qs and possibly an effect from movement
across the valve even during the diastolic filling stage).

Most common congenital heart defect? –> VSD.

If you patch/repair a VSD, what will happen to pressure in the LV, RV, and LA? (up or
down arrows) à repairing a VSD will cause up LV, down RV, down LA à the down
always confuses people –> repair of VSD means less blood entering RV –> less blood
going back through the lungs to the LA.
Who gets AVSD (atrioventricular septal defect)? –> Down syndrome (aka endocardial
cushion defect).

What does ASD sound like and why? –> as discussed earlier, fixed splitting of S2 –>
when you’ve got an ASD, blood is constantly moving L –> R from LA –> RA (pressure
is always greater on the left side). So the effects of inhalation/exhalation are
minimized in terms of the A2-P2 split bc you’ll always have relatively constant LA –>
RA flow (and resultant steady RA preload) irrespective of inspiration. The sound can
also be described as “wide, fixed splitting” bc of increased RV preload à delayed
closure of P2 relative to A2 –> slight widening, but it’s still fixed for the reasons
explained above.

HY lecture notes:10 cardio

Who gets pulmonic stenosis and what does it sound like? –> sounds like aortic
stenosis (midsystolic murmur) but increases in intensity with inspiration because it’s
right-sided; classically seen as part of tetralogy of Fallot in DiGeorge syndrome; also
seen classically in Noonan syndrome (USMLE will not ask you about Noonan
syndrome).

Who gets pulmonic regurg and what does it sound like? –> sounds like aortic regurg
(holodiastolic) but increases with inspiration; rare, but can be seen in endocarditis in
IV drug users.

Who gets tricuspid regurg and what does it sound like? –> same as mitral regurg
(holosystolic murmur) but gets louder with inspiration; seen in IV drug user
endocarditis; also seen in carcinoid syndrome (small bowel, appendiceal, or bronchial
neuroendocrine tumor that secretes serotonin, leading to diaphoresis, tachycardia,
diarrhea, and tricuspid regurg; Dx with urinary 5-hydroxyindole acetic acid [5-HIAA]);
2CK NBMEs love pulmonary hypertension causing TR (i.e., you’ll have cor pulmonale
with TR and be like “huh? Why is there TR? What am I missing here?” But once again
it can be seen in PH).

Who gets tricuspid stenosis and what does it sound like? –> sounds like mitral
stenosis presumably (diastolic rumbling murmur, with or without opening snap); very
rare; I’ve never seen this in any USMLE question.

28M IV drug user + 2/6 holosystolic murmur at left sternal border + fever; most likely
characteristic of valvular lesion? –> “large, friable, floppy vegetation” –> bacterial
endocarditis (probably tricuspid regurg in this case bc IV drug user).

How to Tx AF? –> we have to consider both arms of management: blood thinning +
treating the actual AF. For blood thinning, CHADS2 score is standard in terms of
evaluating risk (there are variants, but the USMLE won’t ever be borderline with how
this plays into a question; they’ll either give you a full-blown obvious high-risk patient
where all are positive, or they’ll make it clear that the patient is low-risk and merely
just has AF alone).

• CHADS2 = CHF, HTN, Age 75+, Diabetes, Stroke/TIA (latter is 2 points;

the rest are 1 point).
• If 0 or 1 points, give aspirin (anti-platelet therapy).
• If 2+ points, give warfarin (anti-coagulation therapy).
• If valvular AF (i.e., AF in someone with a mitral or aortic valve lesion),
answer = warfarin.
• If non-valvular AF, can give other agents (e.g., dabigatran, apixaban).

For the actual Tx of the AF, we do rate control before rhythm control (the
management is actually heavily involved, but for the USMLE know the following):

•
•
• Rate control: beta-blocker first-line (metoprolol). If
beta-blocker avoided (i.e., severe or psychotic
depression, sexual dysfunction, COPD, Hx of asthma
requiring oxygen or hospitalization, 2nd/3rd-degree
heart block), verapamil is the next choice. If rate
control fails, go to rhythm control.
• Rhythm control: Flecainide (type-Ic Na channel
blocker) first-line in those without any structural (i.e.,
LVH or valvular problems) or coronary artery disease
(any symptomatology of CVD or PVD means patient
has coronary artery disease). In those who cannot
receive flecainide, other anti-arrhythmics like
amiodarone, dronedarone, and dofetilide may be used

Hematology #1

HY lecture notes:

Pale RBCs –> think iron deficiency. In elderly, especially think per rectum blood loss.

Most common cause is diverticular bleed, but red flag is obviously colorectal cancer.
Angiodysplasia is another important cause (tortuous superficial intraluminal colonic
vessels).

Do colonoscopy to rule out CRC in elderly patient with fatigue, especially if fecal
occult blood is positive.
DDx like ulcerative colitis are of course also possible, but diverticular bleed, CRC, and
angiodysplasia are HY for elderly.- painless bleeding

Angiodysplasia [increase blood loss] + aortic stenosis [fight with wife] = Heyde
syndrome.

Thalassemia has target cells classically. More likely in children (major) or younger
adults (if minor).

Think demographics. For instance, USMLE Q likely won’t give you thalassemia in
elderly patient, the same way they won’t give you diverticulitis in younger patient.

Red cell distribution width (RDW) is decreased in thalassemia and increased in iron
deficiency. The USMLE likes that. The RBCs are uniformly small in thalassemia due to
Hb production problem, whereas in iron deficiency you have a larger range of RBC
size due to non-uniformity of how iron deficiency can affect bone marrow
production.

Thalassemia Qs will classically give decreased serum iron (same as iron deficiency),
but ferritin is normal in thalassemia. Both have microcytic anemia.

So microcytic anemia with low serum iron:

Ferritin normal + RDW low –> thalassemia

Ferritin low + RDW high –> iron deficiency

Thalassemia (notably alpha thalassemia trait; 1 out of 4 mutations) classically presents

as a microcytic hypochromic anemia that doesn’t respond to iron supplementation.
This is exceedingly HY, particularly for obgyn Qs. That is, pregnant woman has low
iron scrutinized at first appointment; she’s started on standard pregnancy vitamins
(include iron), then a few weeks later her ferritin is normal but iron is still low –>
answer = do hemoglobin electrophoresis to diagnose thalassemia.

Increased HbA2 = alpha2, delta2 –> increased in thalassemia.

Same way in sarcoidosis Qs, you might get a large, rambling paragraph, with the last
line saying, “oh and btw, there’s bihilar lymphadenopathy,” for thalassemia Qs, you
might get a big vignette, with the last line saying “oh and btw, HbA2 is 6%” –> beta
thalassemia.

CML is caused by t(9;22) translocation (Philadelphia chromosome; bcr-abl); treatment

= imatinib, a tyrosine kinase inhibitor; imatinib causes fluid retention (peripheral
edema).
Trastuzumab (Herceptin) used for ER/PR+ breast cancer. It’s cardiotoxic.

Tacrolimus (FK506 binder; decreases intracellular calcineurin) is an

immunosuppressant; causes diabetes + nephropathy (increased BUN and Cr).

Ticlopidine (ADP2Y12 blocker); anti-platelet agent known to cause agranulocytosis

(low neutrophils).

Ticagrelor also an ADP2Y12 blocker.

For aplastic anemia (can be caused by viral infection, eg Parvo B19) = defective bone
marrow production = do bone marrow aspiration (sounds overly invasive but it’s the
next best step USMLE wants).

Chemo-induced pancytopenia, if they want next best step to diagnose, answer also =
do bone marrow aspiration.

SLE causes antibodies against hematologic cell lines. Classically thrombocytopenia.

But can also cause antibodies against RBCs and WBCs. So for instance, if you have
SLE vignette with all cell lines down, the answer is NOT aplastic anemia (i.e., bone
marrow production problem is WRONG answer); the correct answer is “increased
peripheral destruction” due to antibodies. Hard Q there.

Fanconi anemia is AR aplastic anemia seen in Ashkenazi Jewish population; causes

aplastic/hypoplastic thumbs or radii (weird detail at first but pathognomonic).

Diamond-Blackfan anemia is pure-RBC aplasia that causes triphalyngeal thumbs. I can

recall this Q from UWorld for Step 3 actually.

Lecture notes:2 heme

Hereditary hemochromatosis is AR, chromosome 6, HFE gene. Most common

mutations are C282Y and H63D missense.

Heavy metal disorders are AR. So Wilson disease is also AR.

Causes increased duodenal iron absorption. Body has very limited mechanisms to
naturally dispose of iron. May do so via shedding of skin, or in women, menstruation.

Can cause dilated or restrictive cardiomyopathy.

If restrictive, you’ll get JVD, peripheral edema, HSM, etc.

If dilated, S3, big heart, crackles in the lungs.

Hereditary hemochromatosis and primary hyperparathyroidism are key causes of
pseudogout, which will present as either a monoarthritis of a large joint such as the
knee, or as an osteoarthritis-like presentation of the hands. The latter is how it shows
up in hemochromatosis. So if you get DIP involvement in someone with
hemochromatosis, answer is pseudogout, not OA.

Can also acquire secondary hemochromatosis (i.e., non-hereditary) from chronic

blood transfusions. This is called transfusional siderosis.

Treat hereditary hemochromatosis with serial phlebotomy. Treat secondary with

chelation therapy (i.e., deferoxamine).

Lecture notes:3 heme

Renal failure –> increased Cr, Hb low, Hct low, MCV normal, ferritin normal, iron low,
transferrin saturation normal –> anemia of chronic disease (AoCD)

Can be due any type of chronic disease, e.g., RA, SLE, IBD; can also be due to chronic
infections like HepC.

Can treat with EPO is renal failure is etiology; if not renal failure, CANNOT give EPO
and you treat underlying condition.

AoCD is usually normal MCV (80-100), but some 2CK Qs are presenting with low
MCV; but if this is the case, you’d easily be able to eliminate the other answer choices
in the Q.

For instance, if Q is presentation with a kid who has obvious JRA (Still disease) –
salmon rash (about half the time), high ESR, recurrent joint pain – and MCV is, e.g.,
72, answer is still AoCD if anemia is present.

Transferrin saturation = Fe / TIBC (total iron binding capacity)

Anemia of chronic disease: iron is low; ferritin is normal or even elevated; transferrin
low; transferrin saturation low or normal (bc TIBC is low, bc transferrin low)

Iron deficiency: iron low; ferritin low; transferrin high; transferrin saturation super low
(bc TIBC very high, since transferrin high)

HY Lecture notes:

Hemophilia A and B are XR. If you get a difficult vignette where you’re not sure of the
Dx, just remember you’ll never see these in girls.
Skewed X-inactivation is called lyonization. But don’t read between the lines: unless
the vignette specifically makes the Q about skewed X-inactivation, any XR disorder
will always be only in a boy.

vWD is AD. So you’ll often get a vignette with a girl. USMLE will “reward” you
sometimes with difficult vignettes. That is, if it’s a girl, you can instantaneously
eliminate hemophilia.

vWD is always a mix of a platelet and a clotting factor problem.

Platelet problem = epistaxis, petechiae, bruising; usually cutaneous

Clotting factor problem = excessive bleeding after tooth extraction; menorrhagia

(heavy periods)

So vWD vignette you will get, e.g., epistaxis + heavy periods; or petechiae + lots of
bleeding after tooth extraction; always a combo of the two

Platelet problem = increased bleeding time (BT); bleeding time has zero relation to
clotting factors / clotting

PT / aPTT = reflects clotting factors

In vWD, bleeding time 100% of the time is elevated.

vWF bridges Gp1b on platelets to underlying collagen / vascular endothelium;

necessary for platelet adhesion; does not affect aggregation (GpIIb/IIIa). That’s the
main function of vWF, which is why BT is always increased (normal is 2-7 MINUTES).

But vWF also has ancillary/secondary function of stabilizing factor VIII in plasma,
meaning sometimes aPTT is elevated (normal is 25-40 SECONDS).

Two points:

1. Because it’s an ancillary function of vWF, aPTT is only elevated about half
the time in questions; it’s not all the time, unlike BT.
2. If aPTT is increased, it’s not absurdly increased. Iow, normal aPTT might be
42 seconds. And if it is normal, it might be upper end of normal, like 38
seconds, which can still suggest to you it’s vWD.

PT is always normal in vWD.

Normal BT = 2-7 minutes

Normal PT = 10-15 seconds

Normal aPTT = 25-40 seconds

In hemophilia, because the issue is literally a deficiency of factor VIII in A, or IX in B –

and in severe cases, antibodies against these factors – the aPTT WILL be absurdly
elevated, like 90 seconds.

Hemarthrosis is a clotting factor issue, however it’s classic for hemophilia vignettes,
NOT vWD. Implication being that it takes major clotting factor defect to precipitate
full-blown hemarthrosis, whereas perhaps in vWD the effect isn’t salient enough to
lead to the bleed in the joint.

Hemophilia will be school boy with hemarthrosis, or if neonate, will be excessive

bleeding with circumcision.

Question on the 2CK Free-120 had given a vWD question where they said girl had
cut on her finger that took longer to stop than expected (they didn’t tell you bleeding
time explicitly, but expected you to easily infer that); then they said in the labs, PT
normal, aPTT normal. So remember, aPTT isn’t always elevated. They also say
“platelet aggregation studies: normal.” Which makes sense because vWF is necessary
for adhesion, not aggregation, as we said above.

Immune thrombocytopenia purpura (ITP) = viral infection in school-age kids causing

low platelets, about 80% of the time. 20% of the time the vignette will be a woman
30s-40s, without mention of viral infection, who just has random bruising = ITP.
Latter is harder but especially HY on USMLE 2CK.

ITP is caused by autoantibodies against GpIIb/IIIa (type II hypersensitivity); molecular

mimicry most likely due to viral infection.

Treatment of ITP = steroids first, then IVIG, then splenectomy.

Steroids = next best step in management. Splenectomy = most effective at decreasing

recurrence. Be careful as to what they ask for.

Viral-induced neutropenia is similar to ITP, but instead of autoantibodies against

platelets, they’re simply against neutrophils.

Low neutrophils + fever = neutropenic fever / febrile neutropenia = infection without

a way to control it via innate immunity = must give immediate broad-spectrum IV
antibiotics; generally third- or fourth-gen ceph + vancomycin; or pipericillin-
tazobactam.
Thrombotic thrombocytopenic purpura (TPP) is due to antibodies against ADAMTS13
protein, which is normally responsible for cleaving vWF multimers, leading to
decreased platelet-clumb breakdown. The clumps will shear RBCs flying past leading
to schistocytosis. Combination of thrombocytopenia + schistocytosis =
microangiopathic hemolytic anemia (MAHA).

TTP you see a pentad of 1) thrombocytopenia, 2) hemolytic anemia with

schistocytosis, 3) renal insufficiency with red urine; 4) fever + 5) neurologic signs

Hemolytic uremic syndrome (HUS) is just the triad of of #1-3 above; fever and
neurologic signs not typically seen in HUS.

HUS due to EHEC O157:H7 shiga-like toxin (aka verotoxin), or Shigella’s shiga toxin.
Toxin causes endothelial damage that leads to platelet consumption and “jagged
edges” in the vessels that shear RBCs. Schistocytes are seen.

Schistocytes = HUS, TTP, DIC, HELPP syndrome, prosthetic values (mechanical

hemolysis).

Vitamin K deficiency = increased PT and aPTT; bleeding time is normal

BT is normal because platelets aren’t involved whatsoever. Issue is decreased gamma-

carboxylation + activation of clotting factors II, VII, IX, X (and anti-clotting proteins C
and S).

Vitamin K deficiency can be seen in neonates with sterile bowels. Although fat-
soluble vitamin deficiencies can occur in small bowel malabsorptive disorders, i.e.,
with conditions like cystic fibrosis, Crohn disease, Celiac, chronic Giardiasis, etc., K
deficiency is rare because of functional large bowel with normal flora in non-
neonates; A, D, and E would be deficient. E.g., cystic fibrosis kid with rickets (D
deficiency).

USMLE wants you to know vitamin K deficiency can occur in patients who are on
chronic broad-spectrum antibiotics. They’ll say patient on Abx is requiring a lower
dose of warfarin to achieve same INR target range – why? → decrease in colonic
normal flora.

Lecture notes:5

Hairy cell leukemia – cytoplasmic projections; acid phosphatase +

ALL – kids; CD10, TdT positive; Down syndrome –> can cause ALL and AML, but ALL
more, especially in kids
Leukemias are usually B cell. If the USMLE wants T cell, you’ll get a positive
Pemberton sign with an SVC-like syndrome (superior vena cava-like syndrome),
where there’s flushing of the face with arms above the head. This is due to thymic
lesion with compression of SVC seen in T cell variant.

6-mercaptopurine used in Tx of ALL. Pure synthesis inhibitor. When used in the

treatment of leukemia, can cause tumor lysis syndrome (high K+, high phosphate, low
Ca, low bicarb, high uric acid). However, don’t give a xanthine oxidase inhibitor such
as allopurinol or febuxostat to prevent tumor lysis syndrome in the specific case of a
patient receiving 6-MP (or azathioprine, which is metabolized into 6-MP) bc 6-MP
requires xanthine oxidase for breakdown. 6-MP is activated by HGPRT ( same
enzyme deficient in Lesch-Nyhan syndrome; XR).

If ALL, lymphocyte count will be super high. Normal is 4-11k. But you’ll see like 30k+.

Pertussis (whooping cough) has super high lymphocyte count for whatever reason
(instead of neutrophils). Can resemble ALL based on bloods. But of course you’d have
presentation of whooping cough instead.

AML you get Auer rods on smear, which are myeloperoxidase +; APL (type M3 AML)
is t(15;17) translocation; can treat with all-trans retinoic acid.

CLL causes smudge cells on smear; can also cause warm autoimmune hemolytic
anemia; CD5 and CD23 positive

CML they like myelocytes and metamyelocytes elevated; these are almost buzzwordy
they’re so HY.

Don’t forget imatinib is Tx for CML; causes fluid retention (peripheral edema). Drug
targets bcr-abl tyrosine kinase.

Family medicine #1

HY lecture notes:1

Septic arthritis is becoming increasingly HY on Step 1, and is exceedingly HY on FM,

IM, surgery, and peds NBME forms – essentially just on the 2CK in general.

On the USMLE, for septic arthritis questions, there are three main points you need to
know:
 1. The answer always = “aspiration of the knee joint” or “arthrocentesis”
before antibiotics. We’re looking for elevated leukocytes + will do a culture
of the joint aspirate.
2. You do NOT need to have fever. There is an FM NBME Q where the temp
is 99F. In this Q, however, the rest of the presentation is hardcore obvious,
with the afebrile state being the odd factor out. Pretty much every time a
student sees this Q they always say, “but how can this be septic joint when
they don’t have a fever?” And I have to say, yeah I know, it’s weird.
Apparently you don’t have to have a fever, but as you can see, the rest of
the vignette is obvious for septic joint.
3. Biggest risk factor for septic arthritis = abnormal joint architecture.

The USMLE will give vignettes of septic arthritis in all of following patient groups:

• Prosthetic joints –> you can’t be more abnormal than having a prosthetic
joint, so these patients have the greatest risk.
• Rheumatoid arthritis (RA), osteoarthritis (OA), and juvenile rheumatoid
arthritis (JRA; Still disease).
• Recent intense exercise in otherwise young, healthy patients (the
implication being microtrauma causing the abnormal architecture –> e.g.,
16F had a kickboxing workout yesterday, or she went hiking for 8 hours
yesterday; a 17M had a soccer tournament last weekend.
• Recent joint trauma –> e.g., 16F who injured her knee in a car accident.

USMLE likes to give you a vignette of RA, where they’ll say 32F has sore
wrists/hands + ulnar deviation + hot, red, painful knee, where your initial thought
might be, “well she clearly has RA, so couldn’t her knee presentation just be part of an
RA flare?” It could be, yes, but we still have to rule out septic arthritis with an
arthrocentesis. Patients with RA absolutely are at increased risk of septic arthritis.

For osteoarthritis, they’ll say 55M + BMI of 40 + red, hot, painful knee –> answer =
“arthrocentesis.” Fairly simple. You just say, “okay, well the patient is overweight,
which is the biggest risk factor for osteoarthritis, and he has a red, hot, painful knee,
so it’s definitely septic arthritis they’re getting at.”

I’ve also seen a question on either an FM or IM form where they said a young-ish
woman who’s 6’2″ (correct, 6’2″) with a BMI of ~30 had a red, hot, painful knee.
Same deal –> OA –> “joint aspiration.” The trickier part being here, “well, she’s
actually on the younger side, which is less common for OA patients, as most OA
patients are >50, but she’s tall” –> patients who are “big and tall” are at increased risk
at a younger age –> e.g., a guy who’s 250 lbs and 6’4″ with “bad knees.”

I bolded the intense exercise and recent joint trauma points above because not only
are these presentations exceedingly HY for septic arthritis, but it’s also rare that
students make the connection between the two. Once again, 16F who has a red, hot,
sore knee + she had a kickboxing workout yesterday –> answer = arthrocentesis.
Septic joints are also seen on the peds shelf –> 6M with recurrent joint flares (so
you’re immediately thinking JRA) + today he has a fever of 101F + a hot, red, painful
knee –> answer = joint aspiration. Same deal –> abnormal joint architecture as the
risk factor.

The latter contrasts with toxic synovitis (aka transient synovitis), which is a different
peds diagnosis –> usually a viral infection in kids age 3-8 causing inflammation of the
hip joint. Kids are usually afebrile and will have no Hx of joint trauma or JRA. The kid
can bear weight and the pain improves throughout the course of the day. A hip x-ray
is done early as toxic synovitis is a diagnosis of exclusion. You will not get asked
about arthocentesis regarding toxic synovitis. They merely want you to know the Dx
based on recent URTI in a kid who now has hip pain.

Bacteria In aspirate- staph- oxycillin,nafcillin gonoorrhea- ceftri

G neg- salmonella- osteomyelitis, give ceftriaxone

Still disease- jra- risk factor for septic

HY lecture notes:2 fm

Family med favorite Q: vegan with nutrient deficiency and B12 isn’t listed –> answer
= calcium –> normally present in fish and dairy in high amounts.

Varicocele

• Enlargement of pampiniform venous plexus in the scrotum.

• Presents as a “bogginess” or “bag of worms” –> USMLE will rarely use
buzzwords like that, but there is in fact an FM NBME Q where they say
“bag of worms,” making the question absurdly easy.
• Almost always occurs on the left because the left testicular vein –> left
renal vein –> IVC, whereas the right testicular vein drains straight into the
IVC. The left testicular vein drains into the left renal vein at roughly a 90-
degree angle; the effect of this geometry enables a pressure backup that
results in the varicocele.
• Can increase the risk of infertility due to increased testicular temperature.
• Dx –> valsalva maneuver can make veins more salient on physical exam;
modality-wise, a scrotal ultrasound may be ordered.
• Tx is done for men with pain, infertility, and abnormal semen analysis –>
surgical abalation, embolization or varicocelectomy may be performed.

Testicular torsion vs epididymitis

• Torsion presents with a negative cremasteric reflex (when the thigh is

stroked, the ipsilateral testicle should normally retract toward the inguinal
canal; in testicular torsion, this does not occur; this reflex is driven by the
 sensory fibers of both the genitofemoral and ilioinguinal nerves at L1+L2;
the motor component resulting in testicular movement is the genitofemoral
nerve), whereas it’s positive in epididymitis.
• A congenital malformation of the processus vaginalis (“bell-clapper
deformity”) accounts for 90% of cases of torsion.
• Prehn sign (relief of pain with lifting/elevation of the testis in epididymitis
but not torsion) is not considered reliable.
• For Dx and Tx of torsion: if clinical suspicion is high, do a urologic consult
with immediate surgical exploration. If Dx is questionable, order a Doppler
ultrasound; if reduced blood flow, go to surgery; if unremarkable, torsion is
less likely.
• For Dx of epididymitis: cremasteric reflex (intact) + Doppler ultrasound
(showing intact blood flow) are effective initial approaches.
• Abx Tx for epididymitis depends on age and risk factors.
• Chlamydia and gonorrhea are most common causes in <35
sexually active patients; E. coli is most common in older patients.
• If sexually active, cotreat with ceftriaxone PLUS either
doxycycline or azithromycin to cover chlamydia and gonorrhea.
This cotreatment will be the answer on the USMLE if they ask
you.
• If not sexually active or have BPH or recent urologic
instrumentation, give just a fluoroquinolone to cover E. coli.
• If receptive male anal intercourse as risk factor, give
fluoroquinolone + ceftriaxone.
• Once again, for USMLE, just know the above bolded
cotreatment.

Testicular torsion vs strangulated hernia

• Based on relevance, it should be noted that on the surgery NBME forms,

they ask a few questions with a presentation very similar to testicular
torsion, but the answer is inguinal hernia instead.
• They’ll say there’s a kid with severe scrotal pain + has blue-black
discoloration of the superior pole of the testis + bowel sounds are
decreased + abdomen is rigid –> answer = strangulated hernia, not torsion.
Another question asked very similarly has “surgical exploration” as the
answer; Doppler ultrasound is wrong. For these Qs, they will not mention
the cremasteric reflex having been performed. If they want torsion, they’ll
definitely say the reflex is negative. So essentially what I’ve been able to
gather is that if they give you a presentation similar to torsion but say
anything about bowel sounds being decreased + a rigid abdomen, go with
strangulated hernia.

Testicular torsion vs torsion of appendix testis (a twisting of a vestigial appendage that is

located along the testicle)
 • On the peds forms, they want you to know “blue dot sign” means torsion of
appendix testis.

•
• They will say cremasteric reflex is intact + there is a blue dot on the
superior pole of the testis –> answer = torsion of appendix testis, not
testicular torsion.

Hydrocele vs testicular cancer

• USMLE wants “persistent processus vaginalis” as the embryologic cause of

hydrocele, resulting in serous fluid accumulation around the testis.
• Positive transillumination is seen with hydrocele; it’s negative for cancer.
• Testicular cancer on the Step will present as a rock hard nodule (yolk sac
tumor or mixed germ cell tumor in peds; seminoma most common in teens
and adults).
• Most hydroceles spontaneously resolve before the age of 1. Surgery is only
performed in older patients in select circumstances, as most hydroceles are
aysmptomatic. Testicular cancer requires orchiopexy; seminoma is notably
radiosensitive.

Cryptorchidism

• Undescended testis.
• Increased risk of infertility if bilateral due to increased temperature.
• Hormonal changes may not be seen, but if the USMLE asks you, select up-
arrow for LH + FSH and down-arrow for testosterone + inhibin B.
• Do not perform orchiopexy under the age of 1, as most will spontaneously
descend.
• Risk of testicular cancer is increased even after testis spontaneously descends
or post-orchiopexy –> essentially any added time the testis spends in the
abdomen, risk is permanently increased; however, once again, orchiopexy
under the age of 1 on the USMLE is the wrong answer; choose observation
for these questions.
HY lecture notes:4

Malassezia furfur (tinea versicolor) is an incredibly HY spot-diagnosis on Steps 1 and

2CK (main image for this lecture).

It is a fungal infection that classically causes hypopigmentation on the trunk, back,

and shoulders. This is caused by fatty acid breakdown in the skin.

Treatment is with topical selenium. Once again, super HY.

Scabies + lice (pediculosis) –> treat with permethrin.

USMLE will show you a picture of a guy’s hands that appear to be studded with red
dots (linear burrows) + they’ll say he was living in a homeless shelter for four months
+ they will say topical antifungals were attempted but didn’t work; next best Tx? –>
answer = permethrin.

Scabies-associated pyoderma (scabies + pus) is when a scabies lesions become

infected with S. aureus or Group A Strep (S. pyogenes).

Pediculosis capitis = head lice; pediculosis corporis = body lice. Once again –> Tx with
permethrin.

Tx for tinea capitis (cradle cap) = griseofulvin for patient only (one of the FM NBME
Qs asks pt only vs patient + close contacts; answer is patient only).

Another tinea capitis Q wants “avoidance of hat sharing” as number-one way to

prevent infection. They will have other answers like using anti-fungal shampoo, but
“avoidance of hat sharing” is best way to prevent.

Tx for tinea corporis (ring worm) –> topical miconazole or clotrimazole.

Tx for tinea pedis (athletes foot) –> topical terbinafine or topical -azoles. USMLE
won’t list both as answers for the same Q.

Tx for onychomycosis (fungal nail infection) –> oral terbinafine (6 weeks for
fingernails; 12 weeks for toenails; USMLE won’t ask duration, but I just find that
detail interesting + makes the treatment easier to remember).

USMLE wants you to know diabetes is a bigger risk factor for cutaneous candida than
obesity –> they’ll say 48F + BMI of 67 + has red, moist, 8×12-cm elipse under one of
her breasts; what’s the biggest risk factor? –> answer = “insulin resistance,” not
obesity. This is exceedingly HY.
And it should be made clear that T1DM is equally a risk factor for cutaneous candidal
infections; the USMLE just tends to ask the Q in obese patients with T2DM because
they want to specifically assess you on knowing that dysglycemia/diabetes, period, is
more important than obesity as a risk factor for cutaneous candida.

Chronic mucucutaneous candidiasis (CMC; more IM, but HY tangent) –> T cell
dysfunction –> answer will be “defect in cell-mediated immunity” –> 17F + Hx of
cutaneous candidal infections since childhood + 1-yr Hx of autoimmune thyroiditis +
2-yr Hx of T1DM; what’s the mechanism for her disease? –> answer = “defect in cell-
mediated immunity,” or “T cell” (if they ask which cell is affected).

USMLE likes the concept of “autoimmune diseases to together,” and “autoimmune

diseases and immunodeficiencies go together,” which is why the mention of the
autoimmune thyroiditis and T1DM isn’t an accident; they’re essentially pushing on
you the fact that she certainly has CMC.

Oropharyngeal candidiasis –> use nystatin mouthwash.

Esophageal candidiasis –> oral azole –> odynophagia in immunocompromised patient

is esophageal candidiasis until proven otherwise.

Vaginal candidiasis –> topic nystatin –> if doesn’t work, go to oral azole –> nystatin is
used first because the correct medicine is technically to do LFTs before giving an oral
azole, whereas nystatin has shown efficacy and can be given right away.

HY lecture notes:5

The majority of acne is treated as follows:

1. Topical retinoids first (i.e., topical tretinoin; NOT oral isotretinoin) ; cause
photosensitivity (rash); also used for photoaging; mechanism is decreasing
sebum production; topical tretinoin (not oral isotretinoin) is not a teratogen
and does not have any effect on pregnancy or male sperm.
2. Benzoyl peroxide used second; often coadministered with topic retinoids;
mechanism is the killing of bacteria.
3. Topical clindamycin
4. Oral tetracycline; causes photosensitivity (blistering)
5. Oral isotretinoin; must do beta-hCG in women; recommend barrier
contraception even if on OCP; can cause elevations in LFTs; can cause
dyslipidemia; main complaint is dry skin + peeling; takes several weeks to
really start working but ultra-effective according to most patients; can be
commenced earlier in patients with severe nodulocystic acne; works by
diffusely shutting of sebum production.

There is an NBME question floating around where they say they say a girl is starting
on OCPs at the same time as isotretinoin, and then they ask what else you should do,
and the answer is “recommend barrier contraception.” Students get this wrong
because they say, “Wait, I don’t get it, why two methods?” We can debate it all we
want, but it’s still on the NBME.

Students may ask, “USMLE is actually that pedantic about acne management?” My
answer: 2CK will assume you know #1+2 are used first and that #5 is last resort for
most patients, and that #1 and #4 cause photosensitivity; Step 1 wants you to know
mechanisms of the drugs in terms of how they actually treat the acne (which I’ve
written above).

HY lecture notes:

Carpal tunnel syndrome

Will show up as “median nerve entrapment” as the answer on FM forms –>

characterized by pain and paresthesias of the thenar eminence and lateral 3.5 digits.

CTS is normal in pregnancy (edema) and can also be seen in hypothyroidism (edema +
GAG deposition) and acromegaly (growth of tendons).

USMLE will not ask you how to Dx CTS, but they’ll sometimes describe the diagnostic
maneuver being performed in a vignette:

Dx is with flick sign, Phalen maneuver, Tinel sign, and median nerve compression test
(Durkan test).

Flick sign –> patient awakens in pain and shakes out hand to relieve Sx –> 93%
sensitive and 96% specific for CTS.

Phalen maneuver –> flexion of the wrist to 90 degrees for one minute elicits Sx.

Tinel sign –> tapping over the carpal tunnel induces Sx.

Median nerve compression test (Durkan test) –> compression of carpal tunnel with
the thumbs for 30 seconds elicits Sx.

Treatment (really important for FM):

1. Avoid the provoking activity if at all possible (e.g., typing all day in an
office).
2. Wrist splint (super HY; FM loves conservative therapy first).
3. Triamcinolone (corticosteroid) injection into the carpal tunnel (NOT the
same as IV steroids). This provides relief for about one month and delays
the need for surgery in severe cases for about one year.
 4. Endoscopic + open nerve decompression are performed if conservative
therapy fails after 4-6 months. Never choose these as answers on the
USMLE.

Vignettes will sometimes say the patient has tried acetaminophen or NSAIDs to no
avail. Recent literature says that these drugs have not been proven to be effective for
CTS. On FM NBMEs, I have only ever seen wrist splint and triamcinolone injection as
answers for CTS.

Cubital tunnel syndrome

Ulnar nerve entrapment at the medial elbow (proximal entrapment) –> produces
paresthesias in along the ulnar distribution of the medial forearm, hypothenar
eminence, and medial 1.5 fingers –> classically caused by sleeping with the hands
behind the head with the arms bent; can also be caused by bench pressing.

Tx is with a straight-arm cast to be worn while sleeping (this is HY for the USMLE).

Guyon canal syndrome

Ulnar nerve entrapment at the wrist (distal entrapment) –> caused by hook of hamate
fracture or chronic handlebar compression in avid cyclists.

Meralgia paresthetica

Numbness and burning pain in the lateral thigh –> due to compression of the lateral
femoral cutaneous nerve.

De Quervain tenosynovitis

Pain along the radial aspect of the wrist caused by thickening of the tendon sheaths
of extensor pollicis brevis and abductor pollicis longus –> classically seen in
breastfeeding women due to long periods of keeping the wrist in a cocked position.

Dx is with Finkelstein test (HY) –> (main picture for this lecture) –> 1) place thumb in
the palm of hand, 2) wrap four remaining fingers over the thumb, 3) then ulnar
deviate the wrist. If the patient experiences pain at the lateral wrist when attempting
the ulnar deviation, that is a positive Finkelstein test and is consistent with a
diagnosis of De Quervain tenosynovitis.

The literature says splinting, NSAIDs, and steroid injection are all acceptable as first-
line treatments. On the USMLE, a one-off steroid injection into the wrist will be the
answer.
HY lecture notes: incontinence

MS- t cell mediated destruction of oligodendrocytes, white matter lesions.

B interferon b/w falres, in flares iv methylprednisolone, spasticty with baclofen

Stress incontinence

Answer = “laxity of pelvic floor muscles” or “downward mobility of vesicourethral

junction.” USMLE will have “urethral prolapse” as a distractor answer choice re the
latter descriptor.

Weakened pelvic floor muscles resulting in loss of urine with increased abdominal
pressure (coughing, sneezing, laughing) –> Hx of multiple pregnancies classic, but
often too easy of a descriptor and they won’t say that –> they’ll say there’s
“downward movement of the vesicourethral junction with coughing”; next best step
in Mx? –> pelvic floor (Kegel) exercises –> if ineffective, do mid-urethral sling; do
not give medications for stress incontinence (HY!).

USMLE might ask you which muscle is not strengthened by Kegel exercises –>
student then proceeds to have two thoughts: 1) “wtf, I’m supposed to know Kegel
exercises at that high level of detail?” and 2) couldn’t any muscle not be strengthened
by Kegel exercises; I mean, the deltoid wouldn’t be for instance.” –> answer to this Q
= internal anal sphincter –> even if you have zero clue about Kegel exercises, bear in
mind internal sphincters (urethral + anal) are under sympathetic control – i.e., you
can’t voluntarily strengthen a muscle not under somatic (voluntary) control; in case
you’re curious though, Kegels strengthen levator ani (which comprises
pubococcygeus, puborectalis, and iliococcygeus).

Urge incontinence

Answer = “hyperactive detrusor,” or “detrusor instability” –> needs to run to the

bathroom when sticking a key in the front door; needs to run to bathroom when
opening car door; answer in multiple sclerosis + perimenopausal state (part of
vasomotor Sx); can be idiopathic; answer = give oxybutynin (anti-muscarinic) or
mirabegron (beta-3 agonist); once again, do not give these drugs in stress
incontinence.

Overflow incontinence (neurogenic bladder)

Answer = “hypoactive detrusor” in both diabetes and BPH; sometimes for BPH the
answer will be “bladder outlet obstruction.” In diabetes, neurogenic bladder is caused
by myelin damage from sorbitol (glucose enters myelin, causing osmotic damage),
leading to detrusor denervation; in BPH, merely due to outlet obstruction –> leads to
detrusor burnout; in overflow incontinence, postvoid volume is high (i.e., 300-400
mL in USMLE Qs); normal should be <50-75 mL; for diabetic bladder, answer =
bethanecol (muscarinic agonist); for BPH, insert catheter first always.

Summary tidbits:

82M + dribbling, hesitancy, interruption of urinary stream + suprapubic mass

(bladder) + bacteria in the urine –> answer = insert catheter first, not antibiotics.

Hx of many pregnancies + downward movement of vesicourethral junction –> stress

incontinence.

Tx of stress incontinence –> pelvic floor exercises (Kegel); if ineffective –> mid-
urethral sling.

“Hyperactive detrusor” or “detrusor instability” –> urge incontinence.

Needs to run to bathroom when sticking key in the door –> urge incontinence.

Incontinence in multiple sclerosis patient or perimenopausal –> urge incontinence.

Tx of urge incontinence –> oxybutynin (muscarinic cholinergic receptor antagonist) or

mirabegron (beta-3 receptor agonist).

Incontinence + high post-void volume (usually 3-400 in question; normal is <50 mL) –
> overflow incontinence.

Incontinence in diabetes –> overflow incontinence due to neurogenic bladder.

Tx for overflow incontinence in diabetes –> bethanacol (muscarinic cholinergic

receptor agonist).

Incontinence in BPH –> overflow incontinence due to outlet obstruction –> eventual
neurogenic bladder.

Tx for overflow incontinence in BPH –> insert catheter first; if bacteriuria, give
Abx after the catheter is inserted –> manage BPH with alpha-1 blocker (e.g.,
tamsulosin) or 5-alpha-reductase inhibitor (finasteride, then TURP if necessary.

In contrast (and as discussed above), wrist splinting will indeed by the first answer in
carpal tunnel syndrome, and NSAIDs are not effective in CTS.
HY lecture notes: vaccines 8

There are some 2020 updates to mention for the vaccine schedule (HY for FM and
peds shelves, as well as 2CK in general).

I’ll write out the schedule in timeline form first, followed by when to administer per
organism (depending on whichever you find easier to digest).

Bear in mind persons with special circumstances (i.e., immunodeficiency, asplenia,

living in endemic area, etc.) will receive a modified schedule, but the below is the
normal vaccine schedule assessed on USMLE and shelves.

Normal vaccine schedule by timeline

At birth:

• Hepatitis B

At 2, 4, 6 months (3 doses total):

• Hepatitis B (new 2020 guidelines: skip at 4 months; so give at birth, 2

months, and 6 months)
• Strep pneumo PCV13
• Rotavirus (oral; live-attenuated)
• Polio (Salk; IM killed)
• TDaP (tetanus, diphtheria, pertussis)
• Haemophilus influenzae type B

At 1 year:

• Strep pneumo (4th dose)

• Haemophilus influenzae type B (4th dose)
• MMRV (mumps, measles, rubella, varicella; 1st dose)
• Hepatitis A (1st dose)

At 18 months:

• Hepatitis A (2nd dose)

• TDaP (4th dose)

At 4-6 years:

• TDaP (5th dose)

• Polio (4th dose)
• MMRV (2nd dose)
Age 9-45:

• HPV (2 doses if first given age 9-14; 3 doses if first given age 15+)

School age 11-13:

• TDaP (6th dose)

• Meningococcal (1st dose)

School age 16:

• Meningococcal (2nd dose)

Vaccines by organism
HepB: birth, 2 + 6 months (3 doses)

Rotavirus (oral; live-attenuated): 2, 4, 6 months (3 doses)

Polio (Salk; IM killed): 2, 4, 6 months; 4-6 years (4 doses)

Strep pneumoniae PCV13: 2, 4, 6 months; 1 year (4 doses)

Haemophilus influenzae type B: 2, 4, 6 months; 1 year (4 doses)

Tetanus, diphtheria, pertussis (TDaP): 2, 4, 6 months; 18 months; 4-6 years; 11-13

years (6 doses)

Hepatitis A: 1 year; 18 months (2 doses)

Mumps, measles, rubella, varicella (MMRV): 1 year; 4-6 years (2 doses)

HPV: 9-45 years (2 doses if first given age 9-14; 3 doses if first given age 15+)

Meningococcal: 11-13 years; 16 years (2 doses)

Special notes
Influenza
 • Two options: either killed (IM) or live-attenuated (intranasal)
• Only give in fall or winter (if they say, e.g., April, the answer is don’t give)
• Give IM killed starting at age 6 months, then every year (annually)
• Live-attenuated may be given annually in the fall or winter only to non-
pregnant, non-immunocompromised persons age 2-49

Strep pneumoniae (additional administrations)

• Give one dose of PCV13 to all persons age 65, then PPSV23 6-12 months
later.
• To patients with asplenia, sickle cell, and cochlear implants, give PPSV23 6-
12 months after last dose of PCV13.

Shingles (herpes zoster; VZV)

• Give at age 60

HY lecture notes: screening 9

A bit of a briefer segment here focusing on a few very high-yield points for the FM
shelf + 2CK.

Colorectal cancer (CRC) screening

• Start colonoscopy at age 50, then do every 10 years.

• Sigmoidoscopy + barium enema combo can be done every 5 years as an
alternative.
• Fecal occult blood (FOB) can be done annually as a second alternative.

If Hx of colon cancer in the family (first degree relative only – i.e., must be parent or
sibling):

• Start colonscopy at age 40, or ten years before the age of Dx in the 1st-
degree family member, then every 5 years.
• For instance:
• Dad was Dx with CRC at age 57; when to start colonoscopy? –>
answer = age 40, then every 5 years.
• Dad was Dx with CRC at age 43; when to start colonoscopy? –>
answer = age 38, then every 5 years.

When to start lipid screening for FM shelf

• Age 20 years, then every 3-5 years.

 • There’s a Q on one of the FM forms where they give healthy 23M and ask
for the appropriate screening; answer = check lipids.

How to make Dx of diabetes mellitus

• Two fasting glucoses 126 mg/dL or greater.

• Any one random glucose measurement of 200 mg/dL or greater.
• Any HbA1c measurement of 6.5 or greater.
• Normal fasting glucose is 72-99 mg/dL.
• Impaired fasting glucose is considered to be 100-125 mg/dL.

HY lecture notes: 10

Asthma (outpatient) –> albuterol (short-acting beta-2 agonist; SABA) inhaler for
immediate Mx –> if insufficient, start low-dose ICS (inhaled corticosteroid) preventer
–> if insufficient, maximize dose of ICS preventer –> if insufficient, add salmeterol
inhaler (long-acting beta-2 agonist; LABA); in other words:

• 1) SABA; then
• 2) low-dose ICS; then
• 3) maximize dose ICS; then
• 4) LABA.

That initial order is universal. Then you need to know last resort is oral
corticosteroids, however they are most effective.

In other words:

12M has ongoing wheezing episodes + is on albuterol inhaler; next best step? –> add
low-dose ICS.

12M has ongoing wheezing episodes + is on albuterol inhaler; what’s most likely to
decrease recurrence –> oral corticosteroids –> student says “wtf? I thought you said
ICS was what we do next and that oral steroids are last resort.” Yeah, you’re right, but
they’re still most effective at decreasing recurrence. This isn’t something I’m
romanticizing; this distinction is assessed on the FM NBME forms.

After the LABA and before the oral steroids, any number of agents can be given in
any order – i.e., nedocromil or cromolyn sodium, zileuton, montelukast, zafirlukast.

MOA of nedocromil and cromolyn sodium –> mast cell stabilizers.

MOA of zileuton –> lipoxygenase inhibitor (enzyme that makes leukotrienes from
arachidonic acid).
MOA of the -lukasts –> leukotriene LTC, D, and E4 inhibitors. LTB4 receptor agonism
is unrelated and induces neutrophilic chemotaxis (LTB4, IL-8, kallikrein, platelet-
activating factor, C5a, bacterial proteins).

16M goes snowboarding all day + takes pain reliever for sore muscles afterward +
next day develops wheezing out on the slopes again; what’s going on? –>
took aspirin + this is Samter triad (now cumbersomely known as aspirin-exacerbated
respiratory disease [AERD]) –> triad of aspirin-induced asthma + aspirin
hypersensitivity + nasal polyps). Just to be clear, other NSAIDs can precipitate Samter
triad, but the literature + USMLE will make it explicitly about aspirin.

16M takes aspirin + gets wheezing; what are we likely to see on physical exam? –>
answer on USMLE = nasal polyps.

“Wait I don’t understand. Why would aspirin cause asthma?” –> arachidonic acid can
be shunted down either the cyclooxygenase or lipoxygenase pathways; if you knock
out COX irreversibly by giving aspirin (or reversibly with another NSAID), more
arachidonic acid will be shunted down the lipoxygenase pathway –> more
leukotrienes –> more bronchoconstriction.

Kid has Hx of AERD; physician considers agent to decrease his recurrence of Sx –>
zileuton, or -lukasts (both are correct; and only one will be listed).

Kid has Hx of AERD; what agent is most likely to decrease his recurrence of Sx –
> oral steroids (sounds wrong, but once again, you need to know oral steroids are
most effective for preventing asthma, period; this is exceedingly HY, especially on
family medicine forms). We simply don’t want to give them because of their nasty
side-effects (Cushing syndrome).

Any weird asthma Txs? –> omalizumab –> monoclonal antibody against IgE –> used
for intractable, severe asthma unresponsive to oral steroids + in patients who have
eosinophilia + high IgE levels (I asked a pulmonologist about this drug years ago when
I was in MS3 and he said he was managing 1000 patients with asthma and just three
were on omalizumab).

Acute asthma Mx (emergencies) –> most important piece of info straight-up is:
USMLE wants you to know that inhaled corticosteroids (ICS) have no role in acute
asthma management. First thing we do is give oxygen (any USMLE Q that shows
depressed O2 sats, answer is always O2) + nebulized albuterol (face mask with
mist); IV steroids are then administered. The Mx algorithm is more complicated, but
that is what you need for the USMLE.

Acid-base disturbance in asthma? –> respiratory alkalosis –> low O2, low CO2, high
pH, normal bicarb.
“Wait, why the low CO2? Aren’t you not able to breathe?” –> low CO2 is due to high
respiratory rate; even if your bronchioles are constricted + filled with secretions, CO2
can diffuse really quickly; in contrast, O2 diffuses slowly and requires healthy
airways; that’s why with a high RR, O2 and CO2 are both low (O2 can’t get in, but
CO2 can still get out); 19 times out of 20 on the USMLE, if your respiratory rate is
high, CO2 is low.

Dry cough in winter + eczema in summer + seasonal allergies in winter; what is the
cough? –> cough-variant asthma (1/3 of asthmatics only have cough).

Young African American woman + dry cough + normal CXR –> asthma (activation of
mast cells), not sarcoidosis.

Young African American woman + dry cough + nodularity on CXR –> sarcoidosis
(non-caseating granulomas).

Electrolyte disturbance in sarcoid? –> hypercalcemia –> LOW PTH (suppressed) +

high calcium. Phosphate can also be elevated because of the high vitamin D, but
there is one Q on a newer CMS form where it’s normal.

Hypercalcemia in sarcoid, why? –> epithelioid (activated) macrophages produce 1-

alpha hydroxylase, thereby activating vitamin D3.

Fecal calcium level in sarcoidosis? –> decreased –> activated D3 increases small
bowel absorption –> this is asked on NBME.

Tx for sarcoid? –> steroids.

COPD management? –> similar to asthma, except muscarinic receptor antagonists

(e.g., ipratropium) inhalers can be used, often mixed with albuterol or steroid. The
literature does not give a very concrete step-wise Mx for COPD because it’s variable
depending on patient risk factors. USMLE wants you to know that smoking cessation
is always the first answer for decreasing severity of someone’s COPD.

If they ask how to best decrease mortality in COPD, if smoking cessation isn’t listed,
choose home oxygen therapy as the answer. Apart from smoking cessation, home
oxygen therapy is the only treatment for COPD shown to decrease mortality.

If the 2CK-level Q is quantitative and they ask you when to commence home oxygen
therapy; answer? –> when patient’s pO2 on room air at rest is <55 mmHg (<88%
saturation).

If you get a patient with COPD who’s already quit smoking and they ask for next best
step + don’t list arterial oxygen values, choose pulmonary rehabilitation over home
oxygen therapy. This is on one of the NBMEs.
Patient with exacerbation of COPD (i.e., acute shortness of breath + decompensation
+ has Hx of COPD), apart from ABCs, USMLE wants you to know that we
give antibiotics, even when patient is afebrile. This is because most exacerbations of
COPD are due to infection.

Acid-base disturbance in acute exacerbation of COPD? –> “acute respiratory acidosis

+ chronic respiratory acidosis”; aka acute on chronic respiratory acidosis. You will see
the RR is 28, pCO2 is 80 mm Hg (super high), bicarb 32-34 mEq/L; O2 50 mm Hg;
and then your thought is, “wait, but if the RR is high, why is the pCO2 high, not low?”
–> Because in COPD, the alveolar surface area for gas exchange is actually
obliterated because of the emphysema, so even though the RR is high (which would
normally cause respiratory alkalosis in patients with, e.g., asthma, PE), the CO2 is still
high in exacerbation of COPD. You’ll be able to infer that it’s chronic respiratory
acidosis as well because the bicarb will be elevated; ordinarily bicarb is unchanged in
acute respiratory disturbances because it takes 12-24 hours to change. When bicarb
is high, it means you either have metabolic alkalosis or chronic respiratory acidosis; in
the case of COPD, it will clearly be the latter.

HY lecture notes:11 fm

This lecture is exceedingly HY for both pediatrics and family medicine shelves. This
lecture is therefore a mandatory crosspost (Pediatrics #4).

You need to be aware of the CENTOR criteria, which is used to differentiate a viral
from bacterial upper respiratory tract infection (URTI).

If 0 or 1 point, the URTI is unlikely to be bacterial (i.e., it’s likely to be viral). If 2-4
points, chance is much greater that URTI is bacterial.

CENTOR: viral and bacterial

1. Absence of cough (i.e., no cough = 1 point; if patient has cough = 0 points).

2. Fever.
3. Tonsillar exudates.
4. Lymphadenopathy (cervical, submandibular, etc.).

There is a version of the criteria that includes age, but on the USMLE it can cause you
to get questions wrong. So just use the simplified above four points.

If 0-1 point, viral, answer = “supportive care”; or “no treatment necessary”; or “warm
saline gargle” (same as supportive care).

If 0-2 points, bacterial, next best step = “rapid Strep test.” If rapid Strep test is
negative, answer = throat culture, NOT sputum culture.
While waiting on the throat culture results, we send the patient home with amoxicillin
or penicillin for presumptive Strep pharyngitis.

If child is, e.g., 12 years old, and develops a rash with the beta-lactam, answer = beta-
lactam allergy.

If the vignette is of a 16-17 year-old who has been going on dates recently (there will
be no confusion; the USMLE will make it clear), the answer = EBV mononucleosis;
therefore do a heterophile antibody test (Monospot test).

EBV is the odd virus out that usually presents with all four (+) CENTOR
criteria.

This is why it’s frequently misdiagnosed as Strep pharyngitis. It is HY to know that

beta-lactams given to patients with EBV may cause rash via a hypersensitivity
response to the Abx in the setting of antibody production to the virus. EBV, in a
patient who does not receive Abx, can cause a mild maculopapular rash. But the rash
with beta-lactam + EBV causes a more intense pruritic response generally 7-10 days
following Abx administration on the extensor surfaces + pressure points.

HY lecture notes:

Tx of otitis media (OM) = simple amoxicillin or penicillin. Augmentin (amoxicillin +

clavulanate) is the wrong answer for first-time OM on the USMLE.

Augmentin is used for recurrent OM or Hx of Abx within the past month; Hx of

recent hospitalization; immunocompromised state; or for patients over age 65.

Tympanostomy tube (grommet) is the answer when the child has had three OM
occurrences within the past 6 months, or four OM occurrences within the past year.

For otitis externa (OE), Tx = topical ciprofloxacin + hydrocortisone drops.

If the question asks about prevention of OE recurrence, the best answer is avoid the
water exposure (if patient is a swimmer, etc.). If the Q doesn’t give this as an option,
the answer is “acetic acid-alcohol drops.” This is an answer on one of the FM forms
where they mention a guy who does crew + has frequent water exposure. Answers
such as “use of ear plugs” are wrong.

Carbamide peroxide is the answer for softening and loosening ear wax in someone
with cerumen (ear wax) buildup.

Tx of Strep pharyngitis = amoxicillin or penicillin, not Augmentin initially.

Tx of sinusitis = go straight to Augmentin. Sinusitis requires broader coverage.

Otitis media with effusion (serous otitis media) = fluid behind the tympanic
membrane in child who recently had one or more OM. Answer = observe. Most
spontaneously resolve within 8 weeks.

UTI antibiotic Tx –> simple trimethoprim; or trimethoprim/sulfamethoxazole

(TMP/SMX; Bactrim); or amoxicillin; or nitrofurantoin.

Nitrofurantoin is classically used for cystitis in pregnant women, however this is an

answer on the NBME for both UTI as well as cystitis in non-pregnant women.

If the Q asks for the best way to prevent recurrent UTI, the answer is “postcoital
voiding,” since sexual activity is the biggest risk factor.

If postcoital voiding has already been attempted, the next best answer is “postcoital
nitrofurantoin prophylaxis.”

If postcoital nitrofurantoin prophylaxis fails, the answer is daily TMP/SMX

prophylaxis. This sounds absurdly wrong but is the correct answer on one of the
obgyn forms. Everyone gets this Q wrong because it sounds incredibly overkill, but
it’s on the obgyn CMS form.

If postcoital voiding has already been attempted + postcoital nitrofurantoin

prophylaxis is not listed as an answer + they mention in the vignette that TMP/SMX
was used successfully in the past for Tx of UTI, go straight to “daily TMP/SMX
prophylaxis” as the answer.

Chronic interstitial cystitis = dysuria +/- bladder pain for at least 6 weeks with no
evidence of infection or pathology. The question might also mention that there’s
anterior vaginal wall pain, which sounds a bit strange, but this refers to the bladder.
Tx is conservative at first – i.e., patient education, stress management, physiotherapy.
Steroids are not recommended anymore.

If the question tells you a girl has UTI-like Sx + urine WBCs + no organisms grow;
answer = check for Chlamydia.

HY lecture notes:13 fm

You need to know standard community-acquired pneumonia (CAP) empiric Tx is a

macrolide, usually azithromycin.

This will cover both Strep pneumo as well as atypicals such as Mycoplasma,
Chlamydia, and Legionella.
Roxithromycin is sometimes used in kids instead of azithromycin, although the
USMLE won’t go there. Just making a point.

If the patient has been on Abx during the past three months or is
immunocompromised, a fluoroquinolone such as levofloxacin may be used instead of
the macrolide. The USMLE won’t make you distinguish. The bottom line is you need
to be aware that azithromycin and levofloxacin are frequently given for CPP empiric
Tx.

If the patient is in sepsis + has strep pneumo infection (confirmed or likely), then
give a third-generation cephalosporin. This is really HY.

If it’s a kid <1 year, cefotaxime is often used. If >1 year, cefriaxone is standard. On
one of the IM forms, cefotaxime was the answer in an 11-month old with sickle cell.
On NBME 8 for 2CK, the answer was ceftriaxone in a 6-year-old.

Likely S. pnuemo infection = kid with sickle cell who missed penicillin prophylaxis
(answer = third-gen ceph, not penicillin to Tx).

Confirmed S. pneumo infection = sputum sample grows gram (+) diplocci.

Sepsis = SIRS + source of infection.

SIRS = 2 or more of the following:

• Temp <36 or >38C.

• WBC <4,000 or >16,000.
• RR 20 or higher.
• HR 90 or higher.

Macrolides can cause GI disturbance (diarrhea or constipation), which is the number-

one reason for non-adherence. They can also prolong the QT-interval. They also
inhibit P-450 (but not azithromycin).

Fluoroquinolones cause cartilage damage (Achilles tendonitis) and cannot be taken

with foods, especially the divalent cations iron and calcium, which decrease oral
bioavailability.

If they say the patient has a pneumonia that presents as right-lower lobe
consolidation with dullness to percussion (lobar), the answer is S. pneumo.

If they say the patient has bilateral interstitial infiltrates, the answer is Mycoplasma.

If they say right-lower lobe interstitial infiltrates seen on CXR, the word “interstitial”
wins over right-lower lobe location; answer = Mycoplasma.
If they say immunocompromised patient who went to a conference recently, the
answer is Legionella. Legionella is also the answer if someone has diarrhea +
hyponatremia alongside the pneumonia.

Summary:

Outpatient empiric Tx for CAP: azithromycin (1st-line) or fluoroquinolone.

If patient is admitted to hospital for CAP (non-ICU): fluoroquinolone, OR beta-lactam

+ macrolide (e.g., azithromycin).

If patient is admitted to hospital for CAP (ICU): beta-lactam, PLUS either macrolide or
fluoroquinolone.

If hospital- or ventilator-acquired pneumonia (HAP/VAP), must cover for S. aureus +

Pseudomonas: Tx = broad-spectrum Abx coverage; various answers are vancomycin +
cefepime; vancomycin + ceftazidime; pipericillin-tazobactam; meropenem. Bottom
line is: know that the difference between CAP and HAP/VAP is that the latter two
require coverage for S. aureus + Pseudomonas.

HY lecture notes:14

Tx for hypertension? –> if patient has pre-diabetes, diabetes, or any

cardiovascular/cerebrovascular disease of any kind, answer = ACEi or ARB
first. These agents decrease morbidity and mortality in these patient groups. If
patient has none of the above (i.e., your typical fat American middle-age male who’s a
little overweight but otherwise just has essential hypertension), the answer = HCTZ
or dihydropyridine CCB. You might think that’s really weird (i.e., “why not just give an
ACEi or ARB anyway to anyone if they’re good for morbidity/mortality?”), but the
basis is: you’re not going to live to 120 just because you start taking a statin when it’s
not indicated; well the same is true here: there’s no evidence of further improvement
or morbidity/mortality benefit in patients without the above risk factors if started on
ACEi or ARB. This knowledge about how to Tx HTN is HY for FM shelves in
particular.

1-2 drinks is permissible for cardiac health, meaning that’s good better than no
drinking.

32F + pedal + forearm edema after commencing anti-hypertensive agent; Dx? –>
answer = fluid retention / edema caused by dihydropyridine CCB (e.g., nifedipine) –>
really HY side-effect of d-CCBs.

Side-effects of thiazides –> hyperGLUC –> hyperglycemia, -lipidemia, -uricemia,

calcemia.
Whom should you never give thiazides to? –> pre-diabetics or diabetics –> will push
people into type II DM and make current DMs worse –> one of the worst/frequent
pharmacologic mistreatments. Also don’t give to patients with Hx of gout (bc of
hyperuricemia risk).

Diabetic patient on HCTZ for HTN in FM vignette; what do you do? –> take them the
fuck off the thiazide and put them on an ACEi or ARB.

Important use of thiazide apart from HTN management in select patients –>
decreased risk of calcium nephro- / ureterolithiasis (stones) because they cause
hypocalciuria (and hence hypercalcemia).

So bottom line:

Patient has HTN but no CVD or pre-diabetes / diabetes? –> use either HCTZ or
dihydropyridine CCB (e.g., nifedipine).

Patient has CVD (i.e., intermittent claudication, angina, Hx of MI, etc.) or CVD
equivalent (i.e., diabetes I or II) –> use ACEi or ARB.

If patient has peripheral edema after starting the dCCB, take them off and put them
on HCTZ instead.

If patient has calcium renal stone Hx, give HCTZ, cuz it absorbs calcium from kidneys.

If patient has Hx of gout, use dCCB.

If patient has confusion who’s on HCTZ, check serum calcium –> hypercalcemia can
cause delirium.

If patient has fasting sugars 100 mg/dL or greater (impaired fasting glucose) and HTN,
give ACEi or ARB.

If patient has normal fasting sugars but HbA1c of 6.0 or greater (6.0-6.4 is
prediabetic; 6.5 or greater is diabetic), give ACEi or ARB.

HTN is >140/90 in the general population; in diabetes, >130/80 is considered HTN

and patient needs an ACEi or ARB.

If patient with diabetes has either >130/80 and/or evidence of proteinuria, start ACEi
or ARB.

African Americans tend to have stiffer vessels and propensity of diastolic HTN; if
African American, give dCCB if no other CVD risk factors.
If you start an ACEi or ARB in patient with HTN and the creatinine and/or renin shoot
up, Dx = renal artery stenosis (older patient with atherosclerosis; or any patient with
diabetes) or fibromuscular dysplasia (young woman without CVD).

HY lecture notes:

What is IBS? –> Irritable bowel syndrome à classically constipation +/- diarrhea +/-
other GI Sx like cramping pain or GERD-like Sx that are relieved with defecation –>
there are many ways to Tx IBS, such as starting with psych screen, but if the USMLE
asks about meds, they like lubiprostone, which is used for constipation-predominant
IBS (PGE1 analogue that causes increased Cl secretion in bowel –> Na follows Cl à
water follows Na –> softens stool).

Travel + self-limiting watery or brown/green diarrhea; Dx? –> Traveler diarrhea =

ETEC HL or HS toxin.

Bloody diarrhea + poultry consumption –> Campylobacter jejuni or Salmonella spp.

Abx (clindamycin, beta-lactam, cephalosporin) + diarrhea –> C. difficile.

Dx of C. diff –> stool AB toxin test, not stool culture.

Fever of 104 + abdo distension in C diff –> toxic megacolon –> laparotomy.

Tx of C. diff –> vancomycin, not metronidazole (updated guidelines as of Feb 2018).

Bloody diarrhea + travel –> Entamoeba histolytica.

Tx of E. histolytica –> metronidazole + iodoquinol; can give paromomycin.

Close quarters or military barracks or cruise ship + watery diarrhea –> Norwalk virus.

Child <5 years + watery diarrhea –> rotavirus.

Few organisms causing bloody diarrhea –> Shigella.

Bloody diarrhea + appendicitis-like pain (pseudoappendicitis) in a child –>Yersinia

enterocolitica.

Bloody diarrhea + reactive arthritis in an adult –> Y. enterocolitica, Campylobacter,

Shigella, Salmonella.
Diarrhea + Guillain-Barre syndrome –> Campylobacter.

Vomiting a few hours after eating meat –> aureus preformed heat-stable toxin.

Vomiting (or any unusual Sx like bloody diarrhea) + eating custards, creams, potato
salad –> answer = S. aureus preformed HS toxin –> the type of food in this scenario
“wins” over the weird bloody diarrhea finding –> bear in mind typical bloody-
diarrhea-inducing gram (-) rods like EHEC, Yersinia enterocolitica, Campylobacter,
Shigella, Salmonella have ~1-3-day incubation period) –> iow, if you get sick on the
scale of hours from food, S. aureus preformed toxin is likely.

25F + intermittent bloody diarrhea for 3 months + intermittent fever + weight loss –>
answer IBD (Crohn or UC).

Tx for Crohn + UC –> USMLE wants oral sulfasalazine (or mesalamine) first before
oral steroids; for perianal disease in Crohn, topical agents / enemas can be used;
NBME won’t make you pick between oral and topical distinguish (that’s more Qbank
being pedantic); surgery can be done for UC.

UC + high bilirubin + high ALP –> primary sclerosing cholangitis.

Red shins + Crohn –> erythema nodosum (type III hypersensitivity; panniculitis –>
inflammation of subcutaneous fat, not a rash).

Crater with necrotic debris on forearm + UC –> pyoderma gangrenosum.

IBD + eczematoid plaque on forehead + sore joints –> psoriatic arthritis (HLA-B27 –>
PAIR à Psoriasis, Ankylosing spondylitis, IBD, Reactive arthritis).

IBD + back pain –> sacroiliitis (or ankylosing spondylitis).

Biopsy in Crohn –> non-caseating granulomas; transmural; UC you don’t see these
findings.

Vesicles anywhere on body (not limited for extensors) + Celiac –> dermatitis
herpetiformis.

Biopsy of DH –> IgA deposition at dermal papillae.

Biopsy of small bowel in Celiac –> flattening of intestinal villi.

Dx of Celiac –> IgA anti-tissue transglutaminase, anti-gliadin (aka anti-endomysial).

After Celiac Ab positivity, what’s the next best step (no further intervention
necessary or duodenal biopsy) –> answer = duodenal biopsy (sounds wrong, but it’s
what USMLE wants).

Weird factoid about Celiac –> increased risk of T cell lymphoma.

Biopsy of small bowel in lactose intolerance –> normal villi.

Dx of lactose intolerance –> hydrogen breath test or decreased stool pH.

Vague vignette where it sounds like either Celiac or lactose intolerance but it’s in a
young adult who’s had zero symptoms until now –> lactose intolerance (can be adult-
onset).

Watery diarrhea in immunocompromised patient –> Cryptosporidium parvum.

How is Giardia transmitted (is the answer “water-borne” or “fecal-oral”?); answer –>
water-borne.

Steatorrhea in guy who went swimming or scuba diving –> Giardia.

Tx for Giardia –> metronidazole.

Fever + periorbital edema + muscle aches + went to a BBQ; Dx? –> Trichinella spiralis
–> this is a classic triad seen in trichinosis.

How do you get trichinosis? –> bear meat (yes, Alaska is still in the United States and
people hunt polar bear) or pork (pork nematode, not cestode).

What is nematode vs cestode vs trematode? –> nematode is roundworm; cestode

tapeworm; trematodes are flukes.

Nematode from pork –> Trichinella spiralis.

Cestode (tapeworm) from pork –> Taenia solium.

What does T. solium cause? –> cysticersosis (muscle cysts) or neurocysticercosis

(brain cysts).

“Swiss cheese appearance” of brain in someone who traveled abroad –>

neurocysticercosis.

Single cystic lesion seen on brain CT in someone who went to Mexico –>
neurocysticercosis.
Tx for cysticersosis / neurocysticercosis –> praziquantel or albendazole (the USMLE
will never give you both and make you choose between them; for anti-helminth drugs
questions, the correct answer will be the only anti-helminth drug listed).

HY lecture notes:

The main value of this lecture is the emphasis on the importance psych screening on
the FM shelf.

“Suicidal ideation” on the FM shelf is pretty much always the answer if it’s listed.
Always address psych first for FM, even if the vignette is clearly discussing a salient
diagnosis like hypothyroidism, where your initial gut is to jump on “check serum TSH.”
Once again, if “suicidal ideation” is listed, go with it.

Any patient over the age of 50 who presents with what appears to be cognitive
decline, always check for depression first.

Pseudodementia is depression presenting as cognitive decline (but the patient

doesn’t actually have true dementia). The patient will not try on the mini mental state
exam (MMSE), whereas a patient with true dementia will try. In other words, a patient
with pseudodementia may perform poorly on the MMSE because of apathy, and this
is evidenced by notably poor performance on the reverse serial 7s component, which
requires greater concentration. They may also say that an, e.g., 58M draws a clock
very slowly, but once prompted, is able to finish it quickly.

Another HY point is if they say the patient complains about his or her own memory
loss. In this case, the answer is normal aging, not dementia. Patients with true
dementia don’t complain about their cognitive decline. If they say anything about an,
e.g., 72F who is concerned because she says she walks into rooms and can’t
remember why she went in there, the answer is normal aging. Once again, patients
with true dementia often try to cover it up, rather than complain about it.

So if you get a vignette where a patient over age 50 has cognitive decline + appears
quiet and is not making much eye contact, think pseudodementia. Answer = “check
for suicidal ideation.” Tx for depression = SSRI and/or CBT.

2CK-level hypothyroidism presents much different from Step 1. On Step 1, the

presentation is classically dry hair, brittle skin, constipation, cold intolerance, weight
gain, etc. This is too easy for FM/psych shelf + 2CK. Important presentation
descriptors are:

• Low mood (dysthymia).

• Mood will improve with administration of thyroid hormone.
• Proximal muscle weakness. Hypothyroid myopathy
• Difficulty getting up from chair unassisted +/ increased serum
creatine kinase (CK).
 • Increased serum cholesterol.
• They might say total cholesterol of 300 mg/dL.
• Increased hepatic transaminases.
• You might see AST is elevated and say “wtf?” But this is frequent
in thyroid dysfunction.
• Bradycardia (HR of 55-60).
• Not abnormal per se, as plenty of healthy people can have have
bradycardia, but I’ve observed that this is nevertheless slipped
into hypothyroidism Qs as a frequent detail.

For hypothyroidism Qs, although “check serum TSH” is the correct answer for initial
screening, once again, if “check for suicidal ideation” is listed, this will still be the
answer ahead of TSH. You will always do a simple psych screen ahead of ordering
investigations.

Hashimoto = low T3, low T4, high TSH, decreased radioiodine uptake.

Subclinical hypothyroidism = normal T3, normal T4, high TSH, normal or reduced
uptake.

Euthyroid sick syndrome = decreased T3, high reverse-T3, normal TSH, normal T4.

Graves = high T3, high T4, low TSH, high diffuse uptake.

Toxic multinodular goiter = high T3, high T4, low TSH, high multifocal uptake.

Toxic adenoma = high T3, high T4, low TSH, high uptake isolated to one nodule.

Factitious thyrotoxicosis with levothyroxine (T4) = high T3, high T4, low TSH, low
uptake.

Factitious thyrotoxicosis with triiodothyronine (T3) = high T3, low T4, low TSH, low
uptake. (T4 is converted to T3 peripherally, but not the other way around).

Subacute thyroiditis (subacute granulomatous thyroiditis; DeQuervain) = can be

hyper- or hypo-, but the key is that uptake is decreased always no matter what –> so
if the patient is hyper-, choose high T3, high T4, low TSH, decreased uptake.

HY lecture notes:17 fm: risk factors

Best way to decrease mortality overall –> smoking cessation.

Best way to decrease stroke, TIA, central retinal artery occlusion risk –> HTN control.
72M smoker with BP of 155/90 has stroke, TIA, central retinal artery occlusion; best
way to decrease recurrence? –> answer = lisinopril, not smoking cessation (HY). This
is because emboli from carotid plaques are responsible for most strokes in patients
with HTN. Even though smoking is big risk factor for atherosclerosis, when it comes
to the carotid arteries specifically, the systolic impulse of HTN is more causative of
the plaques.

Best way to decrease stroke in patient with AF + HTN? –> Tx of the AF > Tx of the
HTN.

Best way to decrease BP –> weight loss, not smoking cessation.

Best way to decrease type II diabetes risk –> weight loss, not smoking cessation.

Best way to decrease type II diabetes risk (choose between “low-calorie diet” or “low-
carbohydrate diet”) –> answer = low-calorie diet –> as long as BMI is in the normal
range, type II diabetes risk is reduced.

Best way to decrease complications of diabetes –> good glycemic control, not
smoking cessation.

Best way to decrease risk of MI –> smoking cessation.

Most common risk factor for atherosclerosis –> HTN.

Most acceleratory (worst) risk factor for atherosclerosis –> FIRST diabetes (I or II;
doesn’t matter), THEN SECOND smoking. HTN is most common risk factor across the
population, but of those who are diabetic and/or smokers, they develop
atherosclerotic disease much faster. If the FM Q gives you a patient who is both a
smoker + has HTN, choose smoking cessation as more important in that patient to
decrease atherosclerotic risk.

Most common cause of carotid plaques? –> HTN –> the strong systolic impulse from
the heart pounds the carotids –> endothelial damage –> atherosclerosis.

55M + BP 150/90 + TIA; next best step in Mx? –> carotid duplex USS –> the first
thing you want to think about is, “does this guy have a carotid plaque that has
resulted in a clot embolizing to his brain.”

80M + good blood pressure (e.g., 110/70) + stroke or TIA; next best step in Mx? –>
ECG –> you want to think, “Does he have atrial fibrillation with a LA mural thrombus
that’s now embolized to the brain.”

80M + good blood pressure (e.g., 110/70) + stroke or TIA + ECG shows sinus rhythm
with no abnormalities; next best step in Mx? –> Holter monitor –> when you first see
this scenario you’re probably like, “Wait, the ECG is normal, so it’s not AF?” –> No, it
is likely AF, but AF is often paroxysmal, so in order to detect it in this scenario, the
next best step is a Holter monitor (24-hour wearable ECG). This means that later in
the day when he sits down to have dinner and then pops into AF, the Holter monitor
will pick it up.

What % of people over age 80 have AF? –> 8% of people over age 80 have AF, which
is why age is a huge risk factor. In other words, if the vignette says the guy is 58, AF is
probably less likely just based on shear probability, regardless of hypertensive status.”
And, once again, knowing that AF is often paroxysmal is really important.

Age 50s-60s + high BP + TIA/stroke/retinal artery occlusion; next best step in Dx? –>
answer = carotid duplex ultrasound to look for carotid plaques.

Age >75 + good BP + TIA/stroke/retinal artery occlusion; answer = ECG to look for
AF –> if normal, do Holter monitor to pick up paroxysmal AF.

55M + good BP + carotid bruit heard on auscultation; next best step in Mx? –>
answer = carotid duplex ultrasound to look for carotid plaques –> in this case, if they
are obvious and explicit about the suspected etiology of the stroke, TIA, or retinal
artery occlusion, then you can just do the carotid duplex ultrasound.

How to Mx carotid plaques? –> first we have to ask whether the patient is
symptomatic or asymptomatic. A bruit does not count as symptoms (that’s a sign).
Symptomatic means stroke, TIA, or retinal artery occlusion. According to recent
guidelines: carotid occlusion >70% if symptomatic, or >80% if asymptomatic –>
answer = do carotid endarterectomy. Below these thresholds –> answer = medical
management = statin, PLUS clopidogrel OR dipyridamole + aspirin. The USMLE will
actually not be hyper-pedantic about the occlusion %s (that’s Qbank). They’ll make it
obvious for you which answer they want. They’ll say either 90% –> answer certainly
= carotid endarterectomy, or they’ll say 50% à answer = medical management only.
There’s one NBME Q where they say a guy has a bruit but is asymptomatic, and has
10 and 30% occlusion in the left vs right carotids, respectively, and he’s already on
aspirin + statin, and the answer is “maintain current regimen” –> if he were
symptomatic, even with low occlusion, he’d certainly need statin, PLUS clopidogrel
OR dipyridamole + aspirin.

How to Tx AF? –> we have to consider both arms of management: blood thinning +
treating the actual AF. For blood thinning, CHADS2 score is standard in terms of
evaluating risk (there are variants, but the USMLE won’t ever be borderline with how
this plays into a question; they’ll either give you a full-blown obvious high-risk patient
where all are positive, or they’ll make it clear that the patient is low-risk and merely
just has AF alone).

CHADS2 = CHF, HTN, Age 75+, Diabetes, Stroke/TIA (latter is 2 points; the rest are 1
point).
If 0 or 1 points, give aspirin (anti-platelet therapy).

If 2+ points, give warfarin (anti-coagulation therapy).

If valvular AF (i.e., AF in someone with a mitral or aortic valve lesion), answer =

warfarin.

If non-valvular AF, can give other agents (e.g., dabigatran, apixaban).

For the actual Tx of the AF, we do rate control before rhythm control (the
management is actually heavily involved, but for the USMLE know the following):

Rate control: beta-blocker first-line (metoprolol). If beta-blocker avoided (i.e., severe

or psychotic depression, sexual dysfunction, COPD, Hx of asthma requiring oxygen or
hospitalization, 2nd/3rd-degree heart block), verapamil is the next choice. If rate
control fails, go to rhythm control.

Rhythm control: Flecainide (type-Ic Na channel blocker) first-line in those without

any structural (i.e., LVH or valvular problems) or coronary artery disease (any
symptomatology of CVD or PVD means patient has coronary artery disease). In those
who cannot receive flecainide, other anti-arrhythmics like amiodarone, dronedarone,
and dofetilide may be used.

HY lecture notes:18

82F + tea/toast diet for six months + high MCV; B9 or B12 deficiency? –> answer =
B9 deficiency –> folate stores deplete in about six months.

“Tea and toast” diet was classically taught to us in 7th grade as synonymous with
vitamin C deficiency, but on the FM shelf, they want B9 deficiency in an elderly
patient with poor diet for six months. If the vignette wants vitamin C deficiency,
they’ll say the patient “looks ill” (vague, but they say that) and has easy bruising, or
bleeding from the gums or around hair follicles (perifollicular hemorrhages).

22F + vegan + high MCV + has Hashimoto thyroiditis; cause of B12 deficiency? –>
potentially pernicious anemia (autoimmune diseases go together; this one is HLA-
DR5) –> answer = check Abs to intrinsic factor / parietal cells. If they don’t mention
autoimmune disease, answer would clearly be dietary deficiency from the veganism.

35M on phenytoin for epilepsy + high MCV; Dx? –> folate deficiency –> anti-
epileptics (phenytoin, valproic acid, carbamazepine) all cause folate deficiency.
40M + large tongue + angular cheilitis + high MCV + serum methylmalonyl-CoA is not
elevated; Dx? –> folate deficiency –> serum methylmalonyl-CoA is elevated in B12
deficiency but not folate deficiency.

Vegan + Q asks for nutrient deficiency + B12 isn’t listed; answer = calcium –> sounds
obvious when you consider that vegans don’t eat dairy or fish, but this Q gets a lot of
people. Students frequently and erroneously select folate as the answer here, but
folate found in high amounts of dark green, leafy vegetables.

Point tenderness over a vertebra in older woman –> osteoporosis (compression

fracture).

Point tenderness over a vertebra in younger patient on steroids –> osteoporosis

(compression fracture).

Point tenderness over a vertebra in patient with autoimmune disease –> recognize
patient is on steroids –> osteoporosis (compression fracture).

34F + Hx of SLE (or IBD, or RA, etc.) managed with multiple medications + point
tenderness over vertebra; Dx? –> osteoporosis (compression fracture) –> need to be
able to infer she’s on prednisone.

Point tenderness over vertebra + patient who has pituitary adenoma; Dx for
adenoma? –> ACTH (Cushing disease) –> osteoporosis.

Point tenderness over a vertebra in IV drug user –> epidural abscess.

“Step-off” of one vertebra relative to another –> spondylolisthesis.

Back pain worse when standing or walking for long periods of time –> lumbar spinal
[Link] change of spine

HY lecture notes:19

Back pain worse in the morning and gets better throughout day in male 20s-40s –>
ankylosing spondylitis.

Bamboo spine –> ankylosing spondylitis., yearly eye exams – anterior uvieits ,
restrivictive lung disease, aortic regurg

Dx of AS –> x-ray of sacroiliac joints.

HLA-B27 associations –> PAIR –> Psoriasis, Ankylosing s pondylitis, IBD, Psoriasis.
Blood in stool in guy with ankylosing spondylitis –> likely IBD (HLA-B27 association).

Lower back pain in someone with psoriasis –> likely sacroiliitis (usually first Sx of
ankylosing spondylitis).

Back pain worse when standing or walking for long periods of time –> lumbar spinal
stenosis.

Back pain worse when walking down a hill –> lumbar spinal stenosis.

Radiculopathy down an arm –> cervical disc herniation.

Radiculopathy down a leg –> lumbosacral disc herniation.

24M lifts a heavy box + gets lower back pain with paraspinal muscle spasm + positive
straight-leg raise test + no radiating pain; next best step in Mx? –> answer = no
further studies indicated; x-ray is the wrong answer here.

Straight-leg raise test should ordinarily be positive in sciatica, but the test is not very
reliable and has false-positives.

For simple lumbosacral strain, do not x-ray. Tx is exercise as tolerated + NSAIDs if

necessary. Bed rest is the wrong answer for Tx.

24M lifts a heavy box + gets lower back pain that radiates down a leg; next best step
in Mx? –> x-ray –> in this case, we think about disc herniation. Although x-ray does
not detect the herniation, it’s still the next best step before MRI in order to rule out
other things like vertebral mal-alignments.

Bilateral paresthesias in the arms in rheumatoid arthritis patient –> atlantoaxial

subluxation.

Bilateral paresthesias in the arms in rheumatoid arthritis patient –> MR of spine to Dx

atlantoaxial subluxation.

Prior to surgery in rheumatoid arthritis patient –> cervical CT or flexion/extension x-

rays of cervical spine to check for atlantoaxial subluxation.

Back pain in elderly patient with hypercalcemia –> multiple myeloma or metastases.

Back in pain in patient with history of other type of cancer –> metastases.

Suspected spinal mets –> MRI.

Metastases to long bones in prostate cancer –> osteoblastic (Dx with bone scan);
spine do MRI.

Bell palsy; next best step in Mx? –> “no further studies indicated” –> the wrong
answer is “nerve conduction studies.”

HY lecture notes:

First-line Tx for diabetic neuropathic pain? –> TCAs (i.e., amitriptyline, nortriptyline).

Important side-effects of TCAs? –> CCC (Coma, Convulsions, Cardiotoxicity) + anti-

“triad”: anti-cholinergic + anti-alpha-1-adrenergic + anti-H1-histaminergic effects.
(Don’t worry, I’ll explain below).

Anti-“triad” is seen with TCAs, anti-psychotics (classically atypicals

[second generation]) and first-generation H1-blockers.

Psych patient is started on new drug + gets prolongation of QT-interval; next best
step? –> stop the TCA –> on one of the psych forms, the TCA was doxepin, which is
quite strange since this drug is LY to the point that it’s essentially unheard of, but this
is the one mentioned on one of the forms.

By anti-cholinergic effects, what are we referring to? –> “opposite of DUMBBELSS” –

> DUMBBELSS is the pneumonic for cholinergic effects –> Diarrhea, Urination,
Myosis, Bradycardia, Bronchoconstriction, Excitation (neuromuscular), Lacrimation,
Salivation, Sweating –> so TCAs can cause the opposite effects due to anti-
cholinergic side-effects –> Constipation, Urinary retention, Mydriasis, Tachycardia,
(not bronchodilaton), (not muscular relaxation), Xerophthalmia, Xerostomia,
Anhydrosis.

The anti-cholinergic side-effects of TCAs, 2nd gen anti-psychotics, or 1st-gen H1-

blockers in elderly exacerbate cognitive decline and more readily precipitate
delirium.

If the Q tells you someone on a TCA has confusion or disorientiation, it’s alluding to
delirium and the answer is discontinue the TCA.

43F + suprapubic mass + hot, dry, red skin on face + started on new drug for
depression; which drug was she started on? –> TCA (urinary retention + anhydrosis
leading to heat retention).

By anti-alpha-1-adrenergic effects, this refers to orthostatic hypotension + fainting.

We don’t want to give TCAs, 2nd gen anti-psychotics, or 1st-gen H1-blockers to
elderly because they can precipitate FALLS.

By anti-H1-histaminergic, this refers to sedation.

If we must give a TCA to an elderly patient, it’s almost always nortriptyline.

Apparently this doesn’t penetrate the BBB to the same extent, so the side-effects are
not as pronounced as with other TCAs.

There’s a Q on one of the FM forms where they tell you an 82M with diabetes is
being treated with carbamazepine + gabapentin for neuropathic pain to no avail; then
they ask for the next best step; answer is give nortriptyline.

Another Q gives a 42M with diabetic neuropathic pain, and the answer was simply
amitriptyline.

Tx for TCA toxicity? –> sodium bicarb –> dissociates drug from myocardial sodium
channels –> sodium as the cation will outcompete the TCA for its own channel + the
alkalinization of the serum causes decreased affinity of the TCA for the channel.

Gabapentin is first-line for neuropathic pain associated with herpetic/post-herpetic

neuralgia + injury + idiopathic. But for diabetes it’s TCAs.

Carbamazepine is first-line for trigeminal neuralgia.

Pediatrics #1

HY lecture notes:1

Juvenile dermatomyositis –> shawl rash (over upper back / back of neck); heliotrope
rash (violaceous eyelids; don’t confuse with malar rush of SLE); Gottron papules over
knuckles, mechanics hands (rough / scaly palms). Proximal muscle weakness; pain and
stiffness not mandatory. High ESR, aldolase, and creatine kinase.

Dx next best step with anti-Jo1 and -Mi2 antibodies. Confirmatory is muscle biopsy.
Tx with oral steroids.

(In contrast, polymyalgia rheumatica is age >55 and has muscle pain and stiffness
without weakness. Associated with temporal arteritis.)

Juvenile rheumatoid arthritis (aka Juvenile idiopathic arthritis) –> recurrent joint pain
in a kid –> high ESR, RF, and/or salmon-pink body rash; associated with anemia of
chronic disease (showed up on one of the peds forms with a decreased MCV, even
though AoCD is typically normocytic 80-100).

They’ll describe multiple joints affected, but must rule out septic arthritis
with arthrocentesis as the next best step if they tell you there’s a warm, tender, red
knee in a kid with JRA, as arthropathy and abnormal joint architecture is a risk factor
septic arthritis.

You’ll see high leukocytes in the joint aspirate. Tx flares with steroids.

Treat sepsis with third-generation cephalosporin. Peds they like cefotaxime over
ceftriaxone because it causes less displacement of bilirubin from albumin, but both
have shown up as answers. One Q on one of the peds forms has 11-month-old with
sickle cell who missed a dose of his penicillin prophylaxis and was septic, and the
answer was cefotaxime. Then there’s a Q on NBME 8 where the kid was a little older
with sepsis, and the answer was ceftriaxone. Bottom line is: if they list both
cefotaxime and cefriaxone as answers for the same Q, go with the former; but both
can be answers depending on the Q.

Kawasaki disease –> aka mucocutaneous lymph node syndrome –> super common
medium-vessel vasculitis in peds –> fever of 5+ days (this is really important); edema
of dorsums of the hands with desquamation of the palms and soles –> cervical
lymphadenopathy; injection of the conjunctiva (red eyes) + red lips or tongue; of
course kid can get coronary artery aneurysms.

Dx is clinical. Tx with aspirin + IVIG. Only thing we give aspirin to kids for (bc we
don’t want Reye syndrome, remember?).

Polyarteritis nodosa hep b +(rare in kids but HY quick tangent) is another medium-
vessel vasculitis –> fibrinoid necrosis w/ immune complex deposition –> associated
with hepatitis B infection –> spares the lungs. Arteriogram may show “beads on a
string” (dilatations/constrictions due to inflammation). Tx most simply with
corticosteroids.

White-eye reflex (leukocoria) –> congenital retinoblastoma; Rb mutation (tumor

suppressor gene but AD condition); kid is at risk of getting osteosarcoma later
on. They like that. They’ll show you image of leukocoria then ask what you’ll see later
–> osteosarcoma.

Kid with 4+ protein in urine + eyelid swelling +/- edema +/- ascites –> minimal
change disease (lipoid nephrosis). Tx with steroids. Very effective.

Minimal change usually due to viral infection, but the 2CK often won’t mention that.

Minimal change can rarely be due to adult with Hodgkin lymphoma (cytokine effect).
Nephrotic syndrome in kid with sickle cell –> focal segmental glomerulosclerosis
(FSGS).

Nephritic syndrome in kid with sickle cell –> renal papillary necrosis.

Red urine 1-3 days after viral (or GI) infection in peds –> IgA nephropathy

Red urine 1-2 weeks after strep throat or skin infection –> PSGN. E.g., impetigo for 7
days –> red urine –> PSGN. USMLE won’t ask PSGN Tx because steroids are often
given but with controversial effect; Tx generally consists of managing hypertension
and edema and giving penicillin to eradicate the nephritogenic strain of Strep.

HY lecture notes:2

Transient tachypnea of the newborn (TTN) is a really HY diagnosis that contrasts with
neonatal respiratory distress syndrome (NRDS).

TTN –> TERM neonate who was born via C-section or fast vaginal delivery –> not
enough time for amniotic fluid to be cleared from lungs. They may or may not say
there are increased fluid markings on chest x-ray.

NRDS –> preterm + dyspnea + low lecithin (dipalmitoyl phosphatidylcholine) to

sphingomyelin ratio. To prevent, two boluses of corticosteroids are given to the mom
if she’s <34 weeks gestation. After 34 weeks, the steroids aren’t given.

Meconium aspiration syndrome –> dyspnea in neonate –> answer if darkly stained
amniotic fluid + meconium visible in/on the airways.

Bronchopulmonary dysplasia –> restrictive lung disease in neonate caused by

receiving oxygen; for instance, neonate born at 28 weeks gestation and on ventilator
+ needed home oxygen –> leading to restrictive lung disease.

Retinopathy of prematurity –> abnormal vascular proliferation on the retina caused

by receiving oxygen after birth.

If you get a vignette of an asymptomatic patient who’s partner tested positive for
chlamydia or gonorrhea, the answer is yes, you treat the asymptomatic
patient (ceftriaxone PLUS azithro or doxycycline; always cotreat). This is a Q on one
of the newer peds forms.

Metronidazole is for trichomoniasis (patient + partner) and bacterial vaginosis

(Gardnerella)

“Absence of ganglion cells in the bowel wall” –> Hirschsprung (Down syndrome)
“Double bubble sign” –> Duodenal atresia (Down syndrome) or annular pancreas;
bilious vomiting in neonate

“Forceful vomiting” –> hypertrophic pyloric stenosis; non-bilious vomiting –> low K,
low Cl, high bicarb, high pH; can be caused by erythromycin (motilin receptor
agonist); also seen in first-born males.

“Exocrine pancreas insufficiency” –> cystic fibrosis –> inspissation of secretions leads
to malsecretion into duodenum.

“Villous atrophy” –> Celiac

If you get a vague vignette where it’s hard to differentiate Celiac from lactose
intolerance, and they tell you the onset is in a teenager or young adult, the answer is
lactose intolerance (can be adult-onset).

Celiac notably presents with iron deficiency anemia. Diagnose with IgA anti-tissue
transglutaminase, anti-gliadin (anti-endomysial) antibodies. After positive antibody
screen, must do duodenal biopsy to confirm; in other words, “no further studies
indicated” is the wrong answer.

Lactose intolerance –> check for decreased stool pH or do hydrogen breath test to
diagnose. Secondary lactose intolerance can be seen after viral gastroenteritis
(classically children with rotavirus infection who get bloating with meals for a couple
weeks following). Do not perform duodenal biopsy, but if it’s done, it’s normal.

Super-high lymphocytes in kid –> usually ALL, but if infection, this is

actually pertussus (which is weird because it’s bacterial, but this is HY).

Pertussis –> lymphocytes, e.g., at 30,000 cells/mm3, paroxysms of cough;

hypoglycemia and vomiting may also be seen; give erythromycin to patient and close
contacts, irrespective of vaccination status.

Strawberry tongue + body rash –> Scarlet fever –> Group A Strep (S. pyogenes) –>
give penicillin to prevent rheumatic fever. Won’t prevent PSGN.

Young child with “spiking fever followed by a rash” –> Roseola –> HHV6 –> self-
limiting

Slapped-cheek appearance –> Parvo B19; can also cause aplastic anemia (do bone
marrow biopsy if all cell lines down); adults can get arthritis + lacy body rash; classic
for daycare centers in Qs; increased risk of aplastic crisis in sickle cell.

Body rash that moves head to toe + suboccipital/post-auricular lymphadenopathy –>

Rubella (German measles)
Body rash that moves head to toe + Koplik spots –> Measles (Rubeola)

“Cough, coryza, conjunctivitis” not specific for measles and more or less just reflect
viral infection.

Meningitis, orchitis, parotitis –> Mumps; rash not characteristic.

HY lecture notes:

3M + midline abdominal mass + HTN + eye movements; Dx? –> neuroblastoma (n myc) eye
movements = opsoclonus-myoclonus syndrome-eye movements dancing eyes (seen in
neuroblastoma).

3M + midline abdominal mass + HTN + eye movements; next best step in Mx? –> USMLE
wants “urinary homovanillic acid (HVA) and vanillylmandelic acid (VMA)”; these are
catecholamine breakdown products. In contrast, for pheochromocytoma in adults, the answer
is “urinary + serum metanephrines”; these are also catecholamine breakdown products.

If they ask imaging for neuroblastoma; answer? –> meta-iodobenzylguanidine scan (mIBG-
avid), which can image >90% of neuroblastomas.

Neonatal male + midline abdo mass; Dx? –> posterior urethral valves (PUV); most common
genitourinary abnormality in neonatal males.

PUV; next best step in diagnosis + Tx? –> voiding cystourethrogram to Dx; Tx = surgery.

3M + painless flank mass + no other info; Dx? –> Wilms tumor.

6M + painless flank mass + seizure + MRI of brain shows periventricular nodules; Dx? –>
Tuberous sclerosis with renal angiomyolipoma.

Anything else about Wilms tumor? –> increased incidence in horseshoe kidney in Turner
syndrome.

Horseshoe kidney key point? –> not only increased risk of Wilms tumor, but the kidney gets
caught under the IMA.

What is WAGR complex? –> Wilms tumor, Aniridia, Genitourinary malformation,

Retardation; caused by WT1 gene mutation.

What is Denys-Drash syndrome? –> Wilms tumor + male pseudohermaphroditism

(secondary sex characteristics are female; primary sex characteristics are male); caused by
WT1 gene mutation.
What is Beckwith-Wiedemann syndrome? –> Wilms tumor + neonatal hypoglycemia +
macrosomia / macroglossia + hemihypertrophy +/- omphalocele; caused by WT2 gene
mutation.

AR vs AD polycystic kidney disease? –> ARPKD is chromosome 6 and a pediatric

condition; it’s associated with hepatic fibrosis. ADPKD is chromosome 16 and presents in
30s or 40s; associated with HTN and circle of Willis saccular (berry) aneurysms.

HY lecture notes:

ToRCHeS:

Toxo –> triad of hydrocephalus, intracranial calcifications, chorioretinitis

Other –> Parvo B19 (aplastic anemia; hydrops), Varicella (zigzag skin lesions, limb
defects, micro-ophthalmia)

Rubella –> patent ductus arteriosus (PDA), cataracts, deafness

CMV –> deafness, intracranial calcifications, hepatomegaly, blueberry muffin rash

(non-specific);

Dx of CMV is diagnosis of exclusion in vignettes –> Q will say “intracranial

calcifications” but won’t mention the other components of the Toxo vignette; there
will also be no mention of classic Rubella, Syphilis, Parvo complications, etc., so you’re
left with CMV. Although deafness is non-specific and can occur in congenital rubella
and syphilis, it’s nevertheless exceedingly HY for congenital CMV and any
pediatrician will drill that.

Herpes/HIV –> if woman has herpetic Sx (i.e., tingling, burning, etc.; she does
not need to have active/visible vaginal lesions), must do C-section on USMLE. For
HIV, give mother HAART during pregnancy (most important way to decrease risk of
vertical transmission), give her intrapartum zidovudine, deliver fetus by C-section,
then give fetus intrapartum zidovudine within 12 hours. The latter is asked
specifically on one of the peds forms (i.e., the answer is literally “give neonate
zidovudine within 12 hours”).

Syphilis –> saddle nose, Hutchinson incisors, saber shins, keratitis, deafness.

Iron deficiency in peds is HY for kids fed more than 24 ounces of cows milk daily.
Why this detail is so HY I don’t know, but it’s asked. Or the vignette will simply
mention a kid is on cows milk + they’ll show you a smear of pale RBCs, and expect
you to know the Dx is iron deficiency. Not super complicated, but important to
mention.
Kids with sickle cell require folic acid supplementation even when MCV is normal. So
you’ll get a vignette of, e.g., 2-year-old with SS + no overt problems; Q asks “what
should he/she be supplemented with?” Answer = folic acid (B9), even when MCV is
normal. This probably is because of increased RBC turnover –> increased folate
requirement.

Turner syndrome –> female, 45XO, coarctation of the aorta, bicuspid aortic valve,
(aortic stenosis later), scattered nevi, cystic hygroma (lymphatic insufficiency +
webbed neck), infertile (streak ovaries, but can reproduce via IVF –> behavioral
science USMLE Qs); Tanner stage 1 (or rarely 2); bone age = chronologic age (genuine
short stature –> usually a girl 4’11”).

Constitutional short stature –> bone age < chronologic age –> i.e., right-shifted
growth curve –> will catch up, but is merely slow to start –> vignette will be 14M
who is 4’10” freshman year of high school + parents are average height; next best
step is getting the parents’ growth charts if possible –> or if that’s not listed, choose
“get bone age.” I have seen one 2CK NBME Q where they didn’t mention bone age
anywhere in the Q or As, but they mentioned the kid was, e.g., 4’11” freshman year of
high school + Tanner stage 2 –> implication being: he clearly has a long way to go in
terms of growth.

Achondroplasia –> postural height is normal –> torso is normal height, but merely
limbs are short. FGFR3 mutation.

HY lecture notes:6

Craniopharyngioma –> answer for pituitary tumor in peds –> can calcify –> can have
cholesterol deposits + “motor oil” appearance on biopsy –> contains squamous
epithelium –> known to recur following resection.

If grows laterally, CN VI (abducens) is affected first due to medial location of the

nerve in the cavernous sinus.

If grows upward, this will cause bitemporal hemianopsia due to impingement on CN II

at the optic chiasm.

Derived from Rathke pouch (so not true pituitary tumor according to some sources).

Most common primary brain tumor overall in peds is pilocytic astrocytoma –> solid +
cystic in appearance on MRI + contains Rosenthal fibers.

Medulloblastoma is second-most common in peds –> grows from

the cerebellum, not medulla –> aggressive (in contrast to pilocytic astrocytoma).
Posterior urethral valves are most common genitourinary abnormality in neonatal
males –> valves within the urethra face the wrong direction –> causes inability to
urinate.

Dx of PUV is voiding cystourethrogram. Tx is surgical.

They will tell you an 24-hour-old male has a suprapubic mass –> full bladder –>
answer = voiding cystourethrogram, or simply, posterior urethral valves.

If they tell you there’s a painless flank mass in a 3-4 year-old, answer = Wilms tumor.
Sounds obvious, but I see this mistake in students a lot: Wilms tumor won’t develop
until a few years of age. PUV is literally in neonates (first several days of life).

Wilms tumor can present alone or in constellation with various syndromes:

WAGR –> Wilms tumor, Aniridia, Genitourinary abnormalities, Retardation.

Denys-Drash syndrome –> Wilms tumor + pseudohermaphroditism (WT1 mutation).

Beckwith-Weidemann syndrome –> macrosomia (>4000g birth weight), hemi-

hypertrophy, macroglossia, neonatal hypoglycemia –> go on to develop Wilms tumor
(WT2 mutation)

Wilms tumor can present in horseshoe kidney of Turner syndrome.

Do renal ultrasound to Dx Wilms tumor. (extraordinarily rare to do CTs on kids).

Neuroblastoma –> usually n-myc gene; grows from median sympathetic chain (in the
midline) –> will present usually as midline mass in a kid 3-8 years old.

Reiteration: Neuroblastoma is midline; Wilms is lateral flank mass. Not difficult, but I
see students mess this up.

Neuroblastoma can present classically with “dancing eyes” (opsoclonus-myoclonus

syndrome) –> weird, but HY.

Neuroblastoma can also present with hypertension –> Dx with urinary homovanillic
acid (HVA) and vanillylmandelic acid (VMA).

This is contrast to pheochromocytoma in adults, for instance, which is diagnosed with

urinary or serum metanephrines (you’ll often see this as another answer choice).

Weird but important detail: neuroblastoma can present in THE POSTERIOR

MEDIASTINUM –> there’s a Q on one of the peds forms where they say there’s a
mass in the posterior mediastinum; the kid didn’t have HTN or any other typical
findings of neuroblastoma, but it was the answer. Thymoma was wrong, as this is in
the anterior, not posterior, mediastinum. Apparently neuroblastoma can be in the
posterior mediastinum as this is still consistent with the median sympathetic chain.

Failure to pass meconium at birth –> cystic fibrosis –> answer = “exocrine pancreas
insufficiency.”

Hirschsprung –> “failure of migration of neural crest cells” –> seen in Down
syndrome, no stools, single streak of bowel

Duodenal atresia –> also seen in Down syndrome –> bilious vomiting + double-
bubble sign seen on AXR.

HY lecture notes:7

Recurrent varicella infections; what is the immunologic defect? –> answer = T cell
dysfunction (defect in cell-mediated immunity).

T cell deficiency –> Q may mention absent thymic shadow.

B cell deficiency –> Q may say absent or scanty lymph nodes + tonsils.

Bruton X-linked agammaglobulinemia –> B cell deficiency –> bacterial infections only
since ~6 months of age.

Severe combined immunodeficiency (SCID) –> X-linked (more common) or AR.

X-linked SCID = common gamma chain mutation, or IL-2 receptor deficiency.

AR SCID = adenosine deaminase deficiency.

SCID is classically all different types of infections (bacterial, viral, fungal, protozoal)
from birth.

Note the contrast with Bruton.

However one of the Qs on a newer Peds form says “bacterial infections since
birth” for a Bruton Q. This is “outrageous” because the timeframe has always been a
classic means to distinguish Bruton from SCID, but we can’t argue with the
NBME/USMLE. The key to this Q was that the infections were limited to bacterial,
whereas in SCID, there will certainly be a variety of infections.
For Bruton, supply immunoglobulins to Tx. Bone marrow transplant is definitive. For
SCID, must do bone marrow transplant.

Sometimes the answer for Bruton is “deficiency of humoral immunity.”

Chronic granulomatous disease (CGD; aka respiratory burst; aka NADPH oxidase
deficiency) –> susceptibility to catalase (+) organisms –> SPACES

• Serratia/Staph, Pseudomonas, Actinomyces/Aspergillus, Candida, E. coli.

The bolded ones are ultra-HY as more specific for NADPH oxidase deficiency. In
other words, if Q mentions Hx of Serratia sepsis, you’re likely dealing with CGD.

Dx with dihydrorhodamine test; tetrazolium blue assay is now obsolete and

the WRONG answer. They have both answer choices on NBME 15 or 16 for Step 1
and dihydrorhodamine test is correct.

Newer CGD Qs on the peds forms are now giving recurrent Staph infections as the
presentation.
IgA deficiency is probably the highest yield immunodeficiency for the 2CK and peds
shelf.

Presentation is always recurrent sinopulmonary infections in a teenager or young

adult. I will always tell students you can Dx this one because the presentation is “not
that bad,” which means the vignette won’t give you a a young, sick kid as with the
Bruton and SCID vignettes.

Usually a 16-35-year-old with Hx of a few pneumonias and/or several instances of

sinusitis, treated with antibiotics. Patient now presents with sore cheeks (sinusitis).

Classic /easy Step 1 detail is Hx of anaphylaxis with blood transfusion, but for 2CK,
you need to know IgA deficiency also presents with:

• Atopy (asthma, seasonal allergies, eczema).

• Giardia infection in the Hx
• Other autoimmune diseases (e.g., vitiligo).
• False (-) antibodies for Celiac screen, since anti-tissue transglutaminase, -
gliadin/-endomysial are IgA.

Answer for IgA deficiency will be “defect in humoral immunity,” or “deficiency of

mucosal immunoglobulin.” Note the former can be correct for either Bruton or IgA
deficiency, but the latter would be wrong for Bruton.

HY lecture notes:8

Chronic mucocutaneous candidiasis (CMC) –> one of the highest-yield conditions for
both 2CK and the peds shelf.

They’ll say theres a 17-year-old girl who has a one-year Hx of autoimmune

thyroiditis, a 2-year Hx of type I diabetes mellitus, and a Hx of cutaneous candidal
infections since childhood; what’s the Dx?

Initial thought could be, “Well doesn’t diabetes increase risk of candida?” Yeah, but if
the infections have been since childhood, they clearly aren’t specifically due to the
T1DM here.

Autoimmune diseases and immunodeficiencies are often linked, same as with IgA
deficiency often presenting with atopy or vitiligo.

Answer for CMC = “defect in cell-mediated immunity”; this answer is exceedingly

HY.

Tx cutaneous candida with oral fluconazole.

This is in contrast to tinea corporis (ring worm), which is Tx with topical clotrimazole
or miconazole.

Tinea pedis is Tx with topical terbinafine or -azole.

Tinea capitis is Tx with oral griseofulvin.

Wiskott-Aldrich syndrome (X-linked recessive) presents with the triad of

thrombocytopenia, eczematoid skin lesions, and immunodeficiency.

So you’ll get a 6M with epistaxis/petechiae, eczematoid skin lesions on the, e.g.,

forehead or trunk, and recurrent infections.

For WAS, you need to know the answer is “T cell dysfunction.” Yes, this is for
2CK/peds. They will give you the vignette of the triad in a boy, and then the answer
is just “T cell” for which cell is dysfunctional.

Hyper IgM syndrome = deficiency of CD40 ligand on T cells (normally binds to CD40
on B cells, causing isotype class switching).

Hyper IgE syndrome (Jobs syndrome) = FATED = abnormal Facies, recurrent

staphylococcal cold Abscesses, retained primary Teeth, hyper IgE, Dermatologic
abnormalities.

Leukocyte adhesion deficiency = deficiency of LFA-1/CD18 integrin –> always

presents with delayed separation of umbilical cord + recurrent infections with absent
pus; answer will be “defective chemotaxis” or “defective leukocyte adhesion.”

IL-12 receptor deficiency = recurrent TB infections; Tx is with IFN-gamma

HY lecture notes:

Rubella (German measles; three-day measles)

Presentation1

• Classically pediatric viral illness, with peak incidence age 5-9.

• Three-day prodrome of fever, malaise, and anorexia.
• As the fever abates, a maculopapular rash starts at the head and descends to
cover the whole body.
• Suboccipital and/or postauricular lymphadenopathy (exceedingly HY)
• Adults may present with arthritis
Vaccine

• Rubella is rare in the United States because of the Mumps-Measles-Rubella

(MMR) live-attenuated vaccine.1
• First dose given at age 12-15 months; second dose given age 4-6 years.2
• MMR and varicella/zoster are the only live-attenuated vaccines approved for use
in HIV patients (CD4 must be >200 cells/mm3).3

Congenital rubella1

• Disease occurs secondary to first-trimester in utero infection in non-immune

mother.
• As mentioned above, pregnant adult female may present with arthritis.
• Neonatal deafness, meningoencephalitis, cataracts
• Patent ductus arteriosus (PDA) in neonate (exceedingly HY)

Rubeola (measles)

• High fever, cough, coryza, conjunctivitis (3Cs).4

• Koplik spots 2-3 days after symptoms begin and are described as punctate white
spots on an erythematous background on the buccal mucosa.5
• As the fever abates, a maculopapular rash starts at the head and descends to
cover the whole body (similar to rubella).4

Mumps6

• Classically presents as parotitis; orchitis and meningitis may also be seen (POM).
• Rash is not part of the classic disease presentation.

Roseola infantum (exanthem subitum; Sixth disease)7

• Caused by HHV6 (human herpes virus 6)

• High-grade fever (i.e., up to 104F) for 3-5 days.
• This is followed by a rapid defervescence of the fever with an accompanying
maculopapular rash.
• For the USMLE, just remember: “spiking fever followed by a rash.”

Fifth disease (erythema infectiosum; Fifth disease)8

• Characteristic facial rash described as a “slapped cheek” appearance

• By the time the rash appears, the virus is no longer infectious (i.e., cleared by the
immune system). For behavioral science USMLE questions, you can tell the
worried parent that the child will be okay.
• Can cause aplastic anemia (↓ RBCs + ↓ WBCs + ↓ platelets – i.e., all are
decreased); more common in children with RBC conditions associated with
shortened lifespan, i.e., sickle cell.
• Associated with daycare centers.
• Can present as arthritis and lacy rash in adult.
Pityriasis rosea is a self-limiting cutaneous eruption with a very characteristic
presentation:

• Begins as a herald patch, or mother patch, which is an erythematous, round to

oval, scaly patch or plaque, 2-10 cm in diameter, with a depressed center and
raised border.1

HY lecture notes:11

Tx of community-acquired sepsis –> if USMLE asks you for one drug, the answer =
third-generation cephalosporin –> ceftriaxone is almost always the answer; if the
presentation is a young kid, the answer will be cefotaxime.

Cefotaxime is preferred over ceftriaxone because it doesn’t displace bilirubin from

albumin as much as ceftriaxone.

One of the 2CK peds forms gives a 12-month-old girl with sickle cell who missed a
dose of penicillin prophylaxis (for S. pneumo) + had septic shock –> answer is
cefotaxime, not penicillin or ceftriaxone –> consideration is: “yes, penicillin is given
for prophylaxis, but once the kid already has sepsis, we must give the third-
generation cephalosporin instead for broader coverage.”

One of the Qs on NBME 8 for 2CK gives sepsis in a 6-year-old; answer was
ceftriaxone; they didn’t list cefotaxime –> consideration is: “if they list both
ceftriaxone and cefotaxime as answers for sepsis in a kid, choose cefotaxime; if they
only list ceftriaxone, just go with that.”

For quick refresh: sepsis = SIRS (systemic inflammatory response syndrome) + source
of infection.

SIRS = 2 or more of the following:

• Temperature <36 or >38 C.

 • WBCs <4,000 or >16,000.
• RR 20+.
• HR 90+.

Septic shock then just = sepsis + low BP.

Asplenia / sickle cell vaccines = Neisseria meningitides, Haemophilus influenzae type

B, Strep pneumoniae.

When peds shelf / 2CK asks “which organism are we most trying to protect against
when we give cefriaxone/cefotaxime?” the student thinks, “Um can’t it just be all
three; I don’t understand.” –> USMLE wants S. pneumo.

Third-generation cephalosporins are good for community-acquired sepsis, but they’re

also notably good against S. pneumo. The reason we don’t give them, however, for
empiric Tx in community-acquired pneumonia (CAP) is because they’re too broad-
spectrum and are overkill; azithromycin is standard CAP empiric Tx (in peds,
roxithromycin is often used clinically, although this won’t specifically show up on
NBME forms).

Myotonic dystrophy

Caused by CTG repeat expansion

• Myotonic dystrophy is an AD disease on chromosome 19, with an

expansion of CTG (MyoTonic dystrophy).
• This leads to abnormal expression of a myotonin-protein kinase, a type of
serine-threonine kinase.

Presentation is generally easy on the USMLE

• Characterized by sustained muscle contraction, muscle wasting, baldness,

cataracts, and testicular atrophy.
• The key feature is the sustained muscle contraction, where the
individual will demonstrate an inability to relax his or her muscles.
• This shows up in questions as an extra-long handshake or not being able to
let go of the golf club or doorknob.

Friedreich ataxia

Caused by GAA repeat expansion

• Friedreich ataxia is an AR disorder on chromosome 9, with an expansion of

GAA (Friedreich AtaxiA).
• USMLE wants you to know the gene is called frataxin. Do NOT confuse
this with Fragile X, which is the FMR1 gene.
HY findings

• May present with cardiomyopathy. Sources differ as to whether

hypertrophic or dilated is more common. But the USMLE will give you a
clear presentation as to which one they’re referring to.
• If hypertrophic, the patient will have a severely thickened LV and (often) an
S4 heart sound; there will be diastolic dysfunction (↑ diastolic filling
pressure + preserved ejection fraction). If dilated, there will be a lateralized
apex beat / apical impulse, a dilated cardiac silhouette, and an S3 heart
sound.
• Early-onset T2DM is a notable feature.
• Kyphoscoliosis and pes cavus (high-arched foot) are HY.
• The disorder is characterized by (obviously) ataxia, Babinski
reflexes, dysarthria, and hammer toes (contraction deformity of toes).

Inheritance pattern and molecular understanding are really HY for USMLE

• Both Duchenne and Becker are X-linked recessive.

• Caused by mutations in the dystrophin gene (DMD).
• Dystrophin is a large cytoskeletal protein inside skeletal muscle that
stabilizes the cytoskeleton with the extracellular matrix.
• Dystrophin binds to a transmembrane protein called beta-dystroglycan.
• The dystroglycan-dystrophan complex is necessary for normal skeletal
muscle cell integrity.

USMLE wants you to know that Duchenne is usually caused by a frameshift

mutation (i.e., 1 or 2 bp deleted or inserted).

In contrast, Becker is usually not caused by a frameshift (i.e., a missense

mutation, or deletion/insertion in repeats of 3 bp, etc.).

Age of onset and the Gower maneuver

• You need to know that Duchenne is worse than Becker.

• Questions on Duchenne will almost always mention a young boy, whereas
for Becker they’ll almost always mention a teenager or adult.
• Boys who have Duchenne classically exhibit the Gower maneuver. This is
described as walking backwards with the arms in order to stand up. You
will not see the Gower maneuver being described in a patient with Becker;
on the Step1, this is Duchenne only.

Psuedohypertrophy and affected muscles

• All hypertrophy that occurs is followed by pseudohypertrophy, which

is fibroadipose deposition in the muscle.
 • Despite the seemingly enlarged muscle size, patients progress to profound
weakness.
• Asymmetrical weakening of paraspinal muscles leads to kyphoscoliosis.
• The USMLE-tested cause of death from both diseases
is cardiomyopathy/heart failure.

Pseudohypertrophy = fibroadipose replacement of the muscle.

Biopsy shows fibrous and fatty tissue; it also shows variation in fiber
diameter and ↑ # of internalized nuclei + fiber regeneration / degeneration.

• The muscular dystrophies tend to affect pelvic girdle muscles and calves
first.
• If they ever ask you which location the weakness starts first, and calves and
hips are both answers, hips are correct over calves.
• Most students get this wrong because these patients are classically
photographed for having massively hypertrophied calves, but the calves are
typically not the first place affected.

Miscellaneous
 • One last point about the DMD gene is that it is the longest human gene.
This means if they ever ask you which gene would be most likely to
undergo a spontaneous mutation, the answer is DMD.

Infants of diabetic moms –> five classic disturbances are possible in the neonate:

• Hypoglycemia
• Hypocalcemia
• Hypomagnesemia
• Hyperbilirubinemia
• Polycythemia

Calcium derangement is associated with QT prolongation in the neonate.- hypo

Hypoglycemia in the neonate is the answer when he/she has jittery movements.

HY lecture notes:

Pathologic jaundice in peds = must have at least one of the following:

1. Any jaundice on the first day of life (first 24 hours of life), period =
pathologic.
2. Jaundice present after one week if term, or after two weeks if preterm =
pathologic.
3. Total bilirubin >15 mg/dL.
4. Direct bilirubin >10% of total bilirubin, even if total bilirubin is <15 mg/dL.
5. Rate of change of increase in bilirubin >0.5 mg/dL/hour.

Most common vignette in peds regarding this stuff is biliary atresia.

They’ll give you a neonate who has a total bilirubin of, e.g., 13 mg/dL, with a direct
(conjugated) bilirubin of 12 mg/dL.

At first you might be like, “Wait, but total bilirubin is fine isn’t it?” Yeah, but the direct
bilirubin is >10% of total. Direct bilirubin should be under 1.3 mg/dL if this were
physiologic jaundice.

When you get this type of vignette, choose “liver biopsy” as the next best step; if
they ask for the treatment, go straight to “liver transplant.”
If neonate has pathologic jaundice (not due to biliary atresia) and they ask for
treatment, choose “phototherapy” first, followed by “exchange transfusion” if they
tell you they already tried phototherapy to no avail.

Breastmilk jaundice vs breastfeeding jaundice:

Breastmilk jaundice = due to beta-glucuronidase in breast milk, which leads to de-

conjugation of intestinal bilirubin + increased enterohepatic circulation –> jaundice
that starts on day 3-5 and peaks at 2-3 weeks –> Tx = stop breastfeeding for ~48
hours (and do bottle feeding), which leads to a rapid decrease in bilirubin; once
breastfeeding is resumed, bilirubin might rise, but not back to pathologic levels.

Breastfeeding jaundice = insufficient feeding (e.g., failure of suckling, etc.) +

decreased milk intake leads to reduced intestinal clearance of bilirubin –> increased
enterohepatic circulation –> jaundice that peaks at 3-5 days –> Tx = formula feeding
(fluid + caloric supplementation).

Before even telling you what G6PD is or why it’s significant, you need to know this:

A USMLE question writer’s obsession: G6PD deficiency is X-linked recessive.

Ok cool. Now that that’s out of the way, the reason the USMLE gives a fuck about
G6PD is because it’s used to generate NADPH.

Why is NADPH important? Because it’s production ultimately leads to the mopping
up of free radicals and the neutralizing of oxidizing agents and H2O2.

Presence of G6PD → means NADPH production → ↑ protection against

oxidizing agents + H2O2
Adding an extra piece of info, NADPH helps convert oxidized glutathione into
reduced glutathione. The latter is a reducing agent that neutralizes oxidizing agents.

Oxidizing agents = damage DNA = bad

Reducing agents = neutralize oxidizing agents → therefore good

Presence of G6PD → production of NADPH → more reduced glutathione →

more (H2O2 → H2O)

In turn, G6PD deficiency can lead to hemolysis secondary to oxidative stress.

Sulfa drugs (e.g., furosemide, sulfonamides, sulfonylureas) are notorious for

causing hemolysis in G6PD.

Questions classically mention an African-American boy with decreased hematocrit

after receiving a drug (e.g., dapsone, primaquine, sulfonamides).

But hemolysis can also occur with consumption of fava beans (favism).

Questions also love to you to know bite cells and Heinz bodies are characteristic
of G6PD deficiency.

Heinz bodies = denatured/oxidized hemoglobin inside RBCs

Bite cells (degmacytes) = RBCs with tiny, semicircular pieces missing that are
formed when the spleen removes the Heinz body but allows the rest of the RBC
to remain in the circulation. These RBCs nevertheless have decreased lifespan.

The reduced lifespan of a bite cell RBC = ↑ RBC turnover = ↑ resistance to malaria.

G6PD deficiency and sickle cell trait/disease both confer resistance to malaria
because shorted RBC lifespan → impedance of malaria lifecycle

The last factoid:

Two most common causes of hemolytic anemia secondary to enzyme deficiency:

1) G6PD deficiency; 2) Pyruvate kinase deficiency

Pyruvate kinase is the last enzyme of glycolysis (PEP → pyruvate). ATP is produced in
this step.
Pyruvate kinase deficiency → decreased ATP → decreased RBC Na/K ATPase
activity → Na builds up inside RBC → RBC swelling + lysis.

HY lecture notes:13

Random point for pediatrics is that pregnancy can occur before one’s first period, so
if they give you, e.g., a 13F who’s never had a menstrual period but who presents
with signs and symptoms suggestive of pregnancy (i.e., nausea/vomiting, suprapubic
mass, etc.), consider pregnancy as an answer. One of the pediatric forms has a Q
where the answer was “beta-hCG” in this scenario.

HY is differentiating polycystic ovarian syndrome (PCOS) from hypothyroidism from

Cushing syndrome. This applies to pediatrics as well and there are many questions on
it.

High BMI female + irregular menstrual cycles –> anovulation.

Anovulation + hirsutism –> PCOS.

Anovulation. Cause USMLE wants? –> insulin resistance –> causes abnormal GnRH
pulsation.

Why hirsutism in anovulation –> abnormal GnRH pulsation causes high LH/FSH ratio.

Why high LH/FSH ratio important in anovulation/PCOS –> ovulation stimulated

when follicle not ready –> no ovulation (anovulation) –> follicle retained as cyst.

What’s LH do? –> Stimulates theca interna cells (females) and Leydig cells (males) to
make androgens.
What’s FSH do? –> Stimulates granulosa cells (females) and Sertoli cells (males) to
make aromatase; also primes follicles.

Tx for PCOS –> if high BMI, weight loss first always on USMLE.

Tx for PCOS if they ask for meds and/or weight loss already tried –> OCPs (if not
wanting pregnancy); clomiphene (if wanting pregnancy).

PCOS increases risk of what –> endometrial cancer (unopposed estrogen).

PCOS will present on the USMLEs + various shelf exams as missed periods, not
gradually prolonged periods. The cysts are the result of follicles that literally did not
rupture, meaning ovulation does not occur.

14F + low mood + gradually increasing fatigue + menstrual cycles gradually increasing
in length + BMI 26; Dx? –> hypothyroidism (Hashimoto).

16F + proximal muscle weakness + increased creatine kinase + low mood + fatigue;
Dx? –> Hashimoto.

15MM + decreased ability to get up from chair unassisted + HR 60; Dx? –>
Hashimoto.

17M + total cholesterol 300 mg/dL + high hepatic AST + HR 55; Dx? –> Hashimoto
(hypothyroidism can cause bradycardia, high cholesterol, and high AST [the latter is
weird, correct]).

Hashimoto parameters –> high TSH, low T3, low T4, decreased iodine uptake

Mechanism for Hashimoto –> antibodies against thyroperoxidase + thyroglobulin;

anti-microsomal.

Histo of Hashimoto –> lymphocytic infiltrate (asked on one of the 2CK NBME forms
weirdly enough).

Tx for Hashimoto = levothyroxine (synthetic T4).

Key point regarding menstruations is that periods gradually increase in length +

become heavier; although hypothyroidism and PCOS can present with amenorrhea,
PCOS won’t present with gradually increasing length + heaviness the same way
hypothyroidism will.

Cushing disease Qs can present with either increased length of menstrual cycle +
heaviness of periods, or missed periods altogether (insulin resistance –>
anovulation/PCOS). However you’ll be able to differentiate in the vignette because
they’ll throw in other signs of Cushing like purple striae.

One Cushing Q on a 2CK form gave just gradually increasing heaviness of periods +
acanthosis nigricans –> the reason the answer wasn’t PCOS is because, once again,
we’d expect missed periods with PCOS.

It is suspected that the mechanism for menstrual dysfunction in hypothyroidism is as

follows: low T3/T4 –> decreased negative feedback at hypothalamus –> increased
TRH –> increased prolactin release –> GnRH dysfunction. It should be noted that
prolactin is regulated two ways: 1) dopamine inhibits prolactin release, and 2) TRH
(not TSH) directly stimulates it.

Should also be noted that Cushing disease in children can present as precocious
puberty and/or stunted growth, rather than as Cushingoid appearance.

HY lecture notes:14

Person who’s vomiting; what’s the biochemical disturbance? –> hypokalemic

hypochloremic metabolic alkalosis –> low K, low Cl, high pH, high bicarb, low H, anion
gap normal (even though it’s alkalosis, not acidosis, the USMLE will still ask an arrow
for the anion gap here).

2-week-old male + forceful non-bilious vomiting; Dx? –> hypertrophic pyloric

stenosis.

Dx of pyloric stenosis? –> abdominal ultrasound to show olive-shaped hypertrophied

pylorus.

Tx of pyloric stenosis? –> myomectomy.

Who gets pyloric stenosis? –> first-born males (weird, but it’s on an old NBME) +
neonates taking oral erythromycin for chlamydial ophthalmia neonatorum
(erythromycin is a motilin-receptor agonist). Oral to cover chlamydia pheumoniae. But
even after oral is given , develops dyspnea – chlmaydia trachomatis pneumoniae

2-week-old male + bilious vomiting; Dx? –> duodenal atresia, annular pancreas,
congenital midgut volvulus, or Hirschsprung (correct, Hirschsprung can present with
bilious vomiting).

2-week-old + Down syndrome + bilious vomiting + passed meconium ok; Dx? –>
duodenal atresia.

2-week-old + Down syndrome + bilious vomiting + slow to pass meconium; Dx? –>
Hirschsprung.
How do you Dx duodenal atresia? –> abdominal x-ray (AXR) showing double-bubble
sign (very HY).

2- week-old + bilious vomiting + triple bubble sign; Dx? –> jejunal atresia.

Triple bubble sign

How do you Dx Hirschsprung? –> rectal manometry, followed by confirmatory rectal
biopsy showing absence of ganglion cells.

Mechanism for Hirschsprung? –> failure of migration of neural crest cells distally to
the rectum.

How do you Dx congenital midgut volvulus? –> upper-GI series (AXR + contrast
follow-through of esophagus, stomach, and duodenum with barium or gastrografin).

Failure to pass meconium at birth. Most likely cause overall? –> cystic fibrosis.

18-month-old + intermittent abdominal pain + crying + blood in stool; Dx? –>

intussusception.

18-month-old + intermittent squatting + crying + FOBT positive; Dx? –>

intussusception.

18-month-old + occasionally brings legs to chest + vomits + FOBT positive; Dx? –>
intussusception.

18-month-old + occasionally brings legs to chest + vomits + FOBT negative; Dx? –>
volvulus –> this is congenital midgut volvulus.

Presentation sounds like intussusception but no blood per rectum –> answer =
congenital midgut volvulus.
Cause of intussusception? –> >99% are in kids under age 2; caused by lymphoid
hyperplasia due to viral infection (e.g., rotavirus) or recent vaccination; if in adult
(usually elderly), it is caused by colorectal cancer.

Dx and Tx of intussusception? –> USMLE wants enema as the answer. Even though
ultrasound can be done which shows a target sign, the USMLE always wants enema.
And it can be any type. I’ve seen “air contrast enema”, “air enema,” “contrast enema,”
all as answers. I also had a student simply get “water-soluble contrast enema” on the
exam, which means gastrografin. Barium would refer to regular contrast

Surgery #1

HY lecture notes:1

Choledocholithiasis

High direct bilirubin + high ALP + high amylase (or lipase) = gallstone pancreatitis =
choledocholithiasis (stone in biliary tree)

Diagnose and Tx with ERCP.

High direct bilirubin + high ALP + NORMAL amylase (or lipase) in patient with history
of intermittent epigastric pain (cholelithiasis; stone in gallbladder) =
choledocholithiasis, just simply the stone hasn’t descended distal to where the
pancreatic duct enters the common bile duct, so there’s no gallstone pancreatitis in
this case; do ERCP to diagnose and Tx gallstone pancreatitis; MRCP is a non-invasive
and equally effective option, but the USMLE wants ERCP. In fact I don’t think I’ve
ever seen an NBME or clinical mastery series question where MRCP was ever the
answer.

USMLE really wants you to know that a patient who has a cholecystectomy and then
a week later has either of the above presentations –> choledocholithiasis –>
sometimes a patient has a retained stone in the cystic duct that will descend after the
procedure.

If the USMLE tells you a patient had a cholecystectomy a week ago and
intraoperative cholangiography was not performed, that’s an obvious giveaway for
choledocholithiasis –> same situation –> likely cystic duct stone that descended into
common bile duct. If USMLE mentions the bold detail, it quite frankly makes the
question too easy. You should be aware mere recent cholecystectomy should be
sufficient info to get the answer.

Sphincter of Oddi dysfunction

Will sound just like gallstone pancreatitis, except they’ll tell you there’s a remote
history of cholecystectomy, so you know there’s no way it’s a stone lodged there.

Cholelithiasis

Hx of colicky epigastric pain in woman in: Fat, forties, female, fertile + NO increase in
bilirubin or ALP + epigastric pain + NO fever = cholelithiasis; do abdominal ultrasound
to diagnose; treat with cholecystectomy; in patients who don’t want surgery or who
are pregnant, can give ursodiol (ursodeoxycholic acid).

Fat, forties, female, fertile + NO increase in bilirubin or ALP + epigastric pain + YES
fever = cholecystitis; do abdominal ultrasound; if equivocal or negative, do HIDA scan
–> involves injecting radiologically visible substance that is taken up by the liver and
secreted into bile. Cholecystitis is almost always due to gall bladder outlet
obstruction, so if the gallbladder does not light up on HIDA scan, that means an
obstruction is indeed present and is confirmatory for cholecystitis.

Cholecystitis has positive Murphy sign –> epigastric pain + sudden voluntary guarding
when epigastric pressure is applied during inspiration.

Pregnancy increases risk for cholesterol stones because estrogen increases HMG-
CoA reductase activity + progesterone slows biliary peristalsis (sludging).

USMLE likes hemolytic disorders or conditions associated with increased RBC

turnover (i.e., sickle cell) as causes of pigment stone cholelithiasis. Black stones are
calcium bilirubinate. Brown stones are often infective origin. Bacteria will de-
conjugate the bilirubin and make it less water soluble –> precipitation.

Chronic cholecystitis (caused by recurrent bouts of acute) can lead to porcelain

gallbladder –> circumferential calcification of gallbladder walls –> 1/3 go on to get
gallbladder cancer (90% are adenocarcinoma). Prognosis is obnoxiously poor.

Pancreatic cancer presents in a few different ways on the USMLE:

History of smoking always helps but isn’t specific for pancreatic cancer.

1) Middle-age patient with high direct bilirubin + high ALP + NORMAL pancreatic
enzymes + history of cholecystectomy performed 25 years ago (i.e., they give you an
absurdly remote history, meaning there’s zero chance there’s a stone) –> answer =
head of pancreas cancer obstructing common bile duct.

2) Standard Courvoisier sign –> painless, palpable gallbladder in a jaundiced, afebrile

patient = head of pancreas cancer till proven otherwise.
3) Image of a jaundiced abdomen (USMLE will increase yellow saturation of image to
make it clear the patient is jaundiced) + visible epigastric bulge; they’ll tell you the
patient is afebrile and not in pain –> head of pancreas cancer till proven otherwise.

4) They might say patient had abdominal x-ray (AXR) in the setting of high direct
bilirubin + high ALP + NORMAL pancreatic enzymes and that the pancreas is poorly
visualized due to overlying gas –> answer is do CT next to look for head of pancreas
cancer.

If you get one of the three vignettes above, the answer is abdo CT with contrast,
NOT ultrasound, because you’re trying to visualize the pancreas.

Cholangiocarcinoma

You’ll get a vignette that sounds like pancreatic cancer (often in a smoker), then
they’ll go ahead and tell you that the CT was done and was negative. So you’re like,
“Wait, this vignette sounds just like pancreatic cancer, so I don’t understand why the
CT is negative.” Answer = bile duct cancer (cholangiocarcinoma). CT might not pick it
up. Must do ERCP or MRCP to diagnose. But as I’ve said, the USMLE wants ERCP,
and this is Q I believe on one of the newer surgery forms.

If the CT does pick it up and shows non-cystic mass of common bile duct,
cholangiocarcinoma is the answer.

If an ultrasound is performed in select patients, there’s dilatation of the intrahepatic

and/or extrahepatic ducts due to the cancer, but the USS itself isn’t diagnostic of
cholangiocarcinoma.

Choledochal cyst

They’ll give you standard presentation that sounds similar to pancreatic cancer, but
when the CT is performed, shows a cystic mass of the common bile duct –> answer =
simple excision of cyst.

Primary biliary cirrhosis

If you get a vignette of a woman 20s-50s who has high direct bilirubin, high ALP, high
cholesterol, and generalized pruritis, this is really HY for primary biliary cirrhosis –>
do anti-mitochondrial antibody screen. After that, confirmatory is with liver biopsy.

They might tell you there’s a stone visualized in the gallbladder. This confuses so
many students unnecessarily. If a patient has high cholesterol, isn’t it possible he or
she also has a cholesterol stone or two? But the rest of the vignette will still scream
PBC.
If they say there’s history of autoimmune disease, e.g., thyroiditis, SLE, etc., in the
patient or in a family member, that’s a giveaway that the USMLE is saying
“autoimmune diseases go together.”

Post-operative bile leak

This is now showing up in UWorld apparently. I’ve seen it as a distractor on one of

the surgery forms, but not as a correct answer yet. But basically if a patient has a
cholecystectomy and then goes on to get abdominal pain and fever, think post-op bile
leak.

Patient will have just had a laparoscopic cholecystectomy for

cholelithiasis/cholecystitis –> during procedure, there’s oblivious damage to bile
ducts, failure to adequately ligate the cystic duct stump, or leakage from the liver
bed/drainage site. –> causes biliary peritonitis.

On the USMLE, the answer is treat with ERCP to stent / make repairs as necessary.

Cholecystoduodenal fistula

In patients with chronic gall bladder obstruction, you can get a fistula/connection to
the duodenum, leading to small bowel obstruction (high-pitched bowel sounds).
They’ll say there’s air visualized in the bile ducts + liver in someone who has had
variable history of biliary pathology, i.e., high direct bilirubin, high ALP, etc. These
patients often have small bowel obstruction from the stone. Essentially just
memorize “air visualized in the bile ducts + liver.” Patient will need endoscopic
removal of stone.

HY lecture notes:2

Sitz bath is the answer for Tx of anal fissure, which occurs posterior in the midline
below the pectinate line –> can present with adjacent skin tag (why I don’t know, but
I’ve seen it on the surgery NBME) –> described as exquisitely and extraordinarily
painful to the point that the patient will refuse the rectal exam –> vignette will often
say a rectal exam cannot be performed.

For Hirschsprung –> Dx = abdominal x-ray (AXR) looking for obstruction, followed by
rectal manometry, followed by definitive rectal biopsy.

They’ll tell you a young child (age can range from neonates up until age ~10ish [there
are varying severities apparently based on the degree of neural crest cell non-
migration]) has chronic constipation + passes one string-like stool every four days
despite maximum fiber + laxative therapy; they’ll also say there’s no stool palpable in
the rectal vault. Answer sequence should go: AXR –> rectal manometry –>
confirmatory biopsy.
AXR in Hirschsprung will show multiple loops of dilated small bowel with air-fluid
levels, which suggests a distal bowel obstruction.

Don’t order an abdominal x-ray unless you’re looking for gas, which may be used to
diagnose a potential obstructive pathology (e.g., Hirschsprung) or conditions such as
toxic megacolon. It can also be used for pneumatosis intestinalis, which is air in the
bowel wall / portal vein seen in necrotizing enterocolitis (generally neonates born
<32 weeks gestation). Obstipation is inability to pass stool and flatus. This is often an
indication for an AXR secondary to the suspicion of obstruction.

For hiatal hernia, do a CXR showing an air fluid-level posterior to the cardiac
silhouette, and then a barium swallow will show the proximal stomach herniating
through the esophageal hiatus, and then definitive Dx is made via endoscopy.

Charcot triad for cholangitis –> fever + RUQ/epigastric pain + jaundice

Primary biliary cirrhosis –> woman 20s-50s with high direct bilirubin + high ALP +
high cholesterol + diffuse pruritis + usually has personal Hx of autoimmune disease
(or in the family) –> autoimmune diseases go together, meaning if a patient has one
(e.g., RA, IBD, SLE), then he or she has increased risk of another. Dx with anti-
mitochondrial antibodies, followed by confirmatory liver biopsy.

Diabetic gastroparesis = new-onset “GERD” in a diabetic with severe disease such as

peripheral neuropathy up to the knees or peripheral edema due to renal failure.
Pathophys is sorbitol-induced myelin damage of the nerves of the GI tract, leading to
delayed gastric emptying (can also cause both diarrhea + constipation; I’ve seen both)
–> the wrong answer is “trial of PPIs” based on the assumption this is regular GERD;
you nee to identify this as diabetic gastroparesis –> first step is endoscopy to rule
out physical obstruction –> if endoscopy negative, do a gastric-emptying
scintigraphy –> if it shows delayed gastric emptying, this confirms the diagnosis. The
Tx is smaller meals –> if insufficient and they want a medication, choose
metoclopramide. Erythromycin (which agonizes motilin receptors) may be added after
metoclopramide.

Empyema = pus in a previously existing space (i.e., pleural space or peritoneal space).

Abscess = pus in a place where there wasn’t a pre-existing cavity (e.g., your forearm).

USMLE wants you to know for empyema that it doesn’t just happen randomly. It
happens as a result of worsening pneumonia:

Pneumonia –> progresses to parapneumonic effusion –> empyema.

Parapneumonic effusion is an exudative pleural effusion (increased LDH, protein,

WBCs; low glucose in the setting of infective exudates). Low pH of the fluid (<7.1) is
the most important indicator of a potential progression to empyema. This is really
HY.

For empyema and abscess, always, always, always drain the fluid/pus before giving
Abx. Even if you’re like, “Well yeah we’d drain, but wouldn’t we at least start the
patient on Abx first?” No. We always drain first.

If skin abscess, the collection will need to be kept open to the air by stuffing it with
sterile gauze, which will gradually be pulled out a little each day, until the space has
closed. If you’re learning this for the first time, that might sound really weird, but it’s
not and is HY. If you drain an abscess and then the area is sealed over or sutured shut
via primary intention, bacterial proliferation may not cease.

Primary closure means sutured closed; secondary closure means kept open and
allowed to close on its own, leading to worse scar formation, but as we said, the latter
has its utility.

HY lecture material:3 surg

Fat embolism –> long bone fracture(s) + petechiae on the chest (thrombocytopenia
from fat binding platelets).

Pulmonary contusion vs myocardial contusion:

MVA + rib fractures + underlying infiltrates in lung + low O2 sats –> pulmonary
contusion.

MVA + no rib fractures + non-central chest pain + pulmonary infiltrates underlying

the painful area –> pulmonary contusion (resources will say “white out of the lung”
for pulmonary contusion, but this is buzzywordy and never shows up on actual NBME
material).

MVA + pulmonary infiltrates + low O2 sats + bolus of normal saline given, resulting in
worsening of O2 sats –> pulmonary contusion (contused lung is very sensitive to fluid
overload).

MVA + bruising/pain over the sternum +/- rib fractures –> myocardial contusion.

MVA + bruising/pain over sternum + pulmonary infiltrates + O2 sats get worse when
saline is given –> answer = myocardial contusion (“Wait, but I thought you said that
latter finding means pulmonary contusion” –> it does, and it’s HY for pulmonary
contusion, but “bruising/pain over the sternum” wins if it’s listed; this is on a 2CK
NBME).
Important point about Mx of myocardial contusion –> do troponins + must monitor
for arrhythmia.

thoracic aortic rupture

MVA + widened mediastinum seen on CXR –> answer = thoracic aortic

rupture. Super HY. You need to know this is the most common cause of death after
deceleration injury (i.e., falls, MVAs).

MVA + widened mediastinum seen on CXR; next best step in Mx? –> labetalol (must
give beta-blocker to decrease shearing forces). Sodium nitroprusside is
the wrong answer. Labetalol is the specific beta-blocker that shows up repeatedly for
the med you give in dissection + thoracic aortic rupture.

MVA + widened mediastinum seen on CXR; next best step in Mx? –> (you don’t see
labetalol listed; all the answers are interventions) –> aortic arteriography
(aortography), then surgery.

“Dissection” implies a false lumen within the vascular wall secondary to hypertension
or a connective tissue disorder as the etiology; traumatic aortic rupture is literally a
traumatic rupture; it’s not a dissection. Regardless, choose labetalol.

Hypertensive emergency = BP >180/120 (if either number is exceeded PLUS end-

organ damage secondary to the hypertension) –> i.e., hypertensive retinopathy w/
AV nicking; high Cr from renal damage, etc. –> answer = sodium nitroprusside (don’t
decrease BP more than 25% in first six hours; bottom line is, don’t reduce too much
too soon) + IV nicardipine (hard-hitting dihydropyridine CCB) + fenoldopam (D1
agonist that keeps renal afferent arterioles dilated + kidneys perfused in the setting of
dilating arterioles with former two drugs that could otherwise reduce renal
perfusion).

Hypertensive urgency = severe hypertension without end-organ damage (i.e., you just
record the BP) –> Tx with oral captopril. This was asked in UWorld for Step 3 twice.

Aortic regurg –-> decrescendo holodiastolic murmur (aka decresendo pan-systolic)

that can radiate down left sternal border –> bounding pulses + head-bobbing –> wide
pulse-pressure (big difference between systolic and diastolic BP) –> question will
usually say BP is 160/60 or 120/40. I point this out because often times if students
miss an AR question, I’ll say, “What do you make of the BP?” So pay attention to BP in
AR.

Pulses in AR will often be described as “brisk upstroke with precipitous downstroke,”

which reflects the bounding pulses. The basis for it is that blood quickly leaves the
arterial circulation after entering. Bounding pulses can also be seen in arteriovenous
fistulae (i.e., Paget disease of bone, hereditary hemorrhagic telangiectasia, or dialysis
patients).
So bounding pulses on the USMLE, you should think: AR or AVF.

AR is associated with fluid overload on the left ventricle –> increased preload +
eccentric hypertrophy.

AR is caused by connective tissue disorders (e.g., Marfan, Ehlers-Danlos) or aortic

root dilation (e.g., ascending aortic arch dissection, tertiary syphilis, Takayasu
arteritis).

Aortic stenosis –> crecendo-decrescendo systolic murmur (aka mid-systolic) that can
radiate to the carotids –> slow-rising pulses (“pulsus parves et tardus”) –> can
sometimes be described as “late-peaking systolic murmur with an ejection click” –>
this can fuck with some students who are like, “wait, I thought ‘systolic click’ meant
mitral valve prolapse”; what you need to know is: mid-systolic click = MVP; ejection
click = AS.

AS is associated with pressure overload on the left ventricle –> increased afterload +
concentric hypertrophy –> can result in S4 heart sound (stiff LV).

Classic triad for AS is SAD –> Syncope + Angina + Dyspnea; but by all means Qs don’t
have to mention them.

AS is usually caused by bicuspid aortic valve (autosomal dominant familial, or Turner).

Murmurs get worse with more volume in the heart –> lying down, squatting, leg raise
while supine, hand-grip.

HOCM and MVP are the two murmurs that get worse with less volume in the heart –
> nitrates, standing/sitting up, Valsalva.

USMLE likes Qs about oxygen at different locations in the heart / vena cava, where
they want you to infer the heart defect. For instance:

If blood oxygen goes up from SVC –> RA, then answer is ASD.

If blood oxygen goes up from RA –> RV, then answer is VSD.

HY lecture notes:4 surg

Alcoholic + pancreatitis –> do contrast CT to Dx –> may be negative depending on

stage, but still performed to visualize degree of necrosis + fluid collections.

Drain pancreatic fluid collections percutaneously (through the skin).

Frank necrotic pancreas visualized on CT requires either necrosectomy (excision of
necrotic pancreas) or aggressive percutaneous drainage (the latter is becoming
increasingly favored due to high mortality rate associated with necrosectomy).

Pancreatic abscess is rare (about 3% of patients) and requires the visualization of

thick, enhancing walls on CT.

Pancreatic pseudocysts have thin walls visualized on CT and occur in 2-18% of

patients ~4 weeks after the acute pancreatitis. <40% will spontaneously resolve. The
majority will remain stable in size. A small fraction will grow in size. For those with
persistent pseudocyst, internal drainage is the answer on the USMLE. I have
seen ERCP as the answer on one of the surgery NBME forms (as I’ve mentioned in
this lecture’s audio). That is, the pseudocyst is drained internally via some form of
endoscopic procedure. The literature also says endoscopic ultrasound with
cystgastrostomy can be performed, which is draining the cyst internally via making a
hole through the stomach to the cyst.

(I used this article in regard to the above information.)

45F with diffuse abdo pain + tachy + high leukocytes + hasn’t passed bowel
movement in several days –> order AXR –> toxic megacolon –> looking for gas –> if
pt stable, give IV steroids. If free air under the diaphragm, shock, peritonitis, or
hemorrhage –> laparotomy.

Venous disease:

Dx of lower limb venous disease = duplex venous ultrasound

Venous ulcer = ulcer at medial malleolus + large, irregular, sloughed appearance

Surgery forms like you knowing when to give low-dose prophylaxis heparin dose vs
higher-dose therapeutic heparin dose.

Higher-dose therapeutic heparin dose: when there is an active clot (DVT or

superficial thrombophlebitis) –> if a leg is painful and swollen, think DVT; if the
vignette says there is a painful, palpable, 1-cm cord at the ankle, that’s superficial
thrombophlebitis; the vignette might also say there’s a thick, visible, painful vein that
runs from the ankle to the knee –> answer = subcutaneous thrombophlebitis. Once
again, in DVT or ST, give therapeutic heparin dose.

Low-dose prophylaxis dose: prior to surgery in patients with venous disease – i.e.,
duplex USS of lower limb shows occlusive disease but there is not an active DVT or
ST.
Patients with varicose veins don’t necessarily have venous occlusive disease. Varicose
veins is often familial from incompetent venous valves, but the patient doesn’t
actually have any occlusion visualized on duplex USS. Treatment of varicose veins on
the USMLE = compression stockings.

Now this is where it gets tricky: the first-line treatment for venous occlusive disease
(in the absence of DVT or ST) is still compression stockings. So if you get a vignette
of a guy with a venous ulcer (medial malleolus) +/- “brawny edema” +/- status
dermatitis (pigmentation of lower limbs from hemosiderin deposition secondary to
chronic venous leakage), the first-line Tx is compression stockings, HOWEVER, in this
same patient, if they say there’s an ST (painful palpable cord at the ankle), and you
see both compression stockings and subcutaneous enoxaparin as answers, the
subcutaneous enoxaparin is correct.

In other words:

Varicose veins –> answer = compression stockings

55M + medial malleolus ulcer +/- “brawny edema” +/- status dermatitis –> answer =
compression stockings

55M + medial malleolus ulcer +/- “brawny edema” +/- status dermatitis + has painful,
palpable cord at ankle or tracking up to the knee –> answer = therapeutic dose
subcutaneous enoxaparin, not compression stockings.

55M + active DVT or SV = therapeutic dose heparin

55M + medial malleolus ulcer +/- “brawny edema” +/- status dermatitis + prior to
surgery –> answer = low-dose heparin prophylaxis

55M + varicose veins + duplex venous USS of legs shows occlusive disease + prior to
surgery –> low-dose heparin prophylaxis

55M + varicose veins + duplex venous USS of legs shows nothing + prior to surgery –
> answer = compression stockings

Arterial / peripheral vascular disease:

Arterial ulcer = punched-out appearance, generally smaller and more distal on the
feet/toes.

Presentation is in patient with severe atherosclerotic disease (i.e., diabetes,

hypertension, Hx of coronary artery bypass grafting, pain in the buttocks/thighs with
ambulation [intermittent claudication], renal artery stenosis, etc.).
Dx of lower limb arterial disease = ankle-brachial index (ABI) –> always the answer
first. Then do arteriography to Dx. Doppler ultrasound is a non-invasive (but less
specific and sensitive) alternative to arteriography that is sometimes the answer. So
for Dx of arterial disease, do ABI first, then either arteriography or Doppler
ultrasound (the Q won’t list both; it will only list one or the other; but if they ask
about which is more effective, do arteriography).

Tx of arterial disease always = exercise therapy first BEFORE cilostazol

(phosphodiesterase inhibitor used as vasodilator therapy). Students will often jump on
cilostazol, but it’s exceedingly HY to know the answer is exercise therapy first.

But then it gets even more annoying: before doing the exercise therapy, you must do
a stress test to ascertain the patient’s exercise tolerance first. In other words, you
can’t recommend the patient attempt to walk 30 minutes per day if he or she is going
to get ST-segment depressions due to ischemia after seven minutes on a treadmill.

So for arterial disease: ABI for initial Dx –> then do confirmatory arteriography or
Doppler ultrasound –> then do stress testing to determine patient’s exercise
tolerance –> then Tx with exercise therapy/regimen –> next best Tx is cilostazol
(vasodilator therapy).

Empyema vs abscess:

(From Surgery #2 lecture):

Empyema = pus in a previously existing space (i.e., pleural space or peritoneal space).

Abscess = pus in a place where there wasn’t a pre-existing cavity (e.g., your forearm).

USMLE wants you to know for empyema that it doesn’t just happen randomly. It
happens as a result of worsening pneumonia:

Pneumonia –> progresses to parapneumonic effusion –> empyema.

Parapneumonic effusion is an exudative pleural effusion (increased LDH, protein,

WBCs; low glucose in the setting of infective exudates). Low pH of the fluid (<7.1) is
the most important indicator of a potential progression to empyema. This is really
HY.

For empyema and abscess, always, always, always drain the fluid/pus before giving
Abx. Even if you’re like, “Well yeah we’d drain, but wouldn’t we at least start the
patient on Abx first?” No. We always drain first.

If skin abscess, the collection will need to be kept open to the air by stuffing it with
sterile gauze, which will gradually be pulled out a little each day, until the space has
closed. If you’re learning this for the first time, that might sound really weird, but it’s
not and is HY. If you drain an abscess and then the area is sealed over or sutured shut
via primary intention, bacterial proliferation may not cease.

Primary closure means sutured closed; secondary closure means kept open and
allowed to close on its own, leading to worse scar formation, but as we said, the latter
has its utility.

HY lecture notes:6 surg

For majority of electrolyte disturbance Qs on the USMLE, answer will be simple

normal saline (0.9% NaCl or Ringer lactate).

For low K (normal range 3.5-5.0 mEq/L), simply give K. You will see flattened T-
waves or U-waves on ECG. Hypokalemia is classically seen in vomiting and diarrhea.
It can also be caused by low magnesium. Low K is also the most common cause of
death (arrhythmia) in eating disorders.

For high K, if there are ECG changes (peaked T waves classic, but can progress to PR
and QRS abnormalities), answer = IV calcium to stabilize myocardium; do not choose
mere saline first in this setting. Literature and previous resources fixate on
specifically IV calcium gluconate, but there’s a new NBME Q for 2CK where the
answer was IV calcium chloride (calcium gluconate wasn’t listed). So the bottom line
is, just give IV calcium for hyperkalemia if there are ECG changes. In this above
lecture I say calcium carbonate, but I meant to say calcium chloride.

If you get high K and no ECG changes, just give normal saline.

In short, regarding potassium, it causes cardiac changes most classically.

If you get any Q where the patient (usually an alcoholic) has low calcium or potassium
not responding to supplementation, the answer = check serum magnesium
levels. Alcoholics tend to get low Mg from dietary deficiency; the low Mg levels have
nothing to do with malabsorption. Mg is permissive for ca and k

For low and high Na (normal range 135-145 mEq/L), give normal saline. Na needs to
be corrected very very slowly (no more than 12-24 mEq / 24 hours) to prevent
central pontine myelinolysis (correcting hyponatremia too quickly with hypertonic 3%
saline) or cerebral edema (correcting hypernatremia too quickly with hypotonic 0.45%
saline). Severe sodium disturbance leading to coma can be corrected with very small
amounts of dilute or concentrated saline, but I’m yet to see it as an answer on the
NBME. I’ve seen in the literature that up to 150 mL of hypertonic saline can be given
super slowly in patients who have coma and hyponatremia.
Low Na is classic in diarrhea, SIADH, and psychogenic polydipsia. It can also be
caused via a dilutional effect in hyperglycemia. High Na is classic in diabetes insipidus.
In short, be aware that whilst K disturbance causes cardiac changes, Na disturbance
causes CNS changes such as confusion and coma.

Low calcium (normal range 8.4-10.2 mEq/L) causes hypertonia and tetany (Chvostek
sign: spasm of masseter muscle with palpation; or Trousseau sign: carpopedal spasm
with inflated BP cuff). It is also seen in DiGeorge syndrome. Once again, low Ca that
does not correct with supplementation, especially in an alcoholic, the answer = check
serum Mg. Hypomagnesemia is a cause of low Ca and low K refractory to
supplementation. Low Ca can also be due to rickets + osteomalacia (vitamin D
deficiency in children vs adults, respectively) and in secondary hyperparathyroidism in
renal failure. Black widow spider bites can also cause low Ca (HY for surg for some
magical reason). To correct low Ca, simply supplement it.

High Ca is most of the time caused by primary hyperparathyroidism or metastatic

malignancy leading to bone lysis. It can also be seen in multiple myeloma. High
vitamin D due to granulomatous disease (sarcoidosis) is an important cause of high Ca
(increased 1-alpha-hydroxylase activity by epithelioid macrophages). If Ca is 10.2-12
mEq/L, give saline; if 12-14, give saline and then add a bisphosphonate if
symptomatic (confusion); if >14, give a bisphosphonate after the saline. Answers such
as calcitonin and loop diuretics are almost always distractors. Calcitonin has a slight
analgesic effect and can be given in someone who has hypercalcemia and bone pain.

Low phosphate (normal range 2.5-4.5 mEq/L) is seen in refeeding syndrome. Patient
need not have a low BMI; it must simply be the case that patient has not eaten in
awhile (anorexia; or if normal BMI, someone lost in the wilderness, etc.). The latter
example is on the USMLE.

High phosphate is seen in tumor lysis syndrome. It’s also seen in renal failure with
secondary hyperparathyroidism.

HY lecture notes:

Shelf and 2CK will want you to know how to manage thyroid nodules. Firstly, if the Q
tells you a patient walks in and asks about thyroid cancer screening, and they ask you
for the next best step, the wrong answer = TSH; the correct answer = “palpation of
thyroid nodule.” Sounds incredibly vague and basic, but it’s the answer they want.
You’re simply going to palpate / do a physical exam before you automatically order a
TSH on someone.

After palpation detects a nodule, next step is ordering TSH. Our management is then
determined by the TSH level.
Cancer is 99% of the time “cold,” meaning it’s hyposecretory and the patient will not
be hyperthyroid. So in turn, the TSH of that patient should not be suppressed
because T3 and T4 should be normal or low.

So if TSH normal or high, answer = do fine-needle aspiration (FNA) of the nodule to

detect possible thyroid cancer. Ultrasound in isolation is always the wrong
answer. Rarely you might see “ultrasound-guided FNA” or “ultrasound-guided
biopsy,” but “ultrasound” alone is wrong. FNA is correct is correct.

If TSH is low, then the patient must be hyperthyroid because the T3 and T4 would be
elevated, therefore suppressing it. Some students will read between the lines here
and ask, “Well what about if TSH is low because of secondary hypothyroidism, such
as due to pituitary insufficiency from Sheehan syndrome, or due to impingement
secondary to prolactinoma?” And it’s true, TSH could be low in secondary
hypothyroidism, but when the USMLE and shelf exams ask about thyroid nodule
evaluation, they are referring to primary thyroid derangement (i.e., problems with the
thyroid gland itself).

So if TSH is low, the nodule is likely “hot” and secreting thyroid hormone, so it’s not
likely to be cancer. So rather than doing FNA, we do radioiodine uptake scan, which
will often confirm the diagnosis of toxic adenoma (as opposed to common malignant
variants such as papillary, follicular, medullary, and anaplastic thyroid cancer).

If the uptake scan shows multiple nodules rather than an isolated one, the diagnosis is
toxic multinodular goiter, not toxic adenoma. Toxic multinodular goiter is the most
common cause of hyperthyroidism in elderly. Yes, Graves occurs in elderly as well,
but if you get a 79-year-old with hyperthyroidism, the Dx is likely TMG, whereas in a
29-year-old, it’s more likely to be Graves.

If the scan shows diffuse uptake, the Dx is Graves.

So in summary, for cancer screening:

1) Palpate thyroid gland.

2) If nodule palpated, order TSH.

3a) If TSH normal or high, order FNA. In this case the cold nodule may be cancer.

3b) If TSH low, order radioiodine uptake scan. In this case the hot nodule is unlikely
to be cancer and more likely to be a simple toxic adenoma.

Reidels- fibrosis extending into esophagus, mimic anaplastic thyroid ca

HY lecture notes:8
Medial malleolus ulcer + hyperpigmentation of lower legs; Dx? –> chronic venous
insufficiency.

Punched-out ulcer on foot + intermittent claudication; Dx? –> arterial insufficiency

(peripheral vascular disease).

What causes venous insufficiency? –> valvular incompetence (most commonly

familial), resulting in venous reflux + insufficiency.

What causes arterial insufficiency –> atherosclerosis (diabetes, followed by smoking,

are the two most acceleratory risk factors; hypertension is the most common risk
factor).

How do you Dx venous insufficiency? –> duplex ultrasound of the calves showing
stasis and/or occlusive disease (the latter may result from venous insufficiency or
cause it).

How do you Dx arterial insufficiency? –> USMLE always wants ankle-brachial indices
(ABI) first –> after this is done, the answer is Doppler ultrasound of the calves
(duplex ultrasound is the answer for venous) or arteriography; both of these latter
answers are correct; they will not give you both; it will be one or the other.

Tx for venous insufficiency –> compression stockings.

Tx for varicose veins –> compression stockings.

Varicose veins and venous insufficiency same thing? –> varicose veins are one of the
mere presentations of venous insufficiency, so yes, patients with varicose veins have
venous insufficiency.

47F has varicose veins + painful palpable cord by the ankle (is the treatment
compression stockings or subcutaneous enoxaparin; both are listed) –> answer =
subcutaneous enoxaparin because this is superficial thrombophlebitis.

Tx for arterial insufficiency –> exercise regimen first, THEN cilostazol

(phosphodiesterase 3 inhibitor).

What must you do before starting the exercise regimen in the Tx of arterial
insufficiency –> ECG stress test to ascertain patient’s exercise tolerance.

What is patient has abnormal baseline ECG (e.g., BBB) –> do echo stress test instead.

What if the patient can’t exercise –> do dobutamine-echo stress test.

82M + Hx of atrial fibrillation + acutely painful lower limb; Dx + Tx? –> acute limb
ischemia due to embolus to lower limb; Dx is clinical (presentation), but arterial
Doppler ultrasond an be performed; Tx = heparin + oxygen + morphine.
Embolectomy / percutaneous intervention may be performed.

82M + Hx of intermittent claudication + acutely painful lower limb; Dx? –> also acute
limb ischemia –> rather than an embolus, caused by thrombosis from ruptured
atherosclerotic plaque. Tx as per above.

HY lecture notes:9

Most common cause of carotid plaques? –> HTN –> the strong systolic impulse from
the heart pounds the carotids –> endothelial damage –> atherosclerosis.

55M + BP 150/90 + TIA; next best step in Mx? –> carotid duplex USS à the first thing
you want to think about is, “does this guy have a carotid plaque that has resulted in a
clot embolizing to his brain.”

80M + good blood pressure (e.g., 110/70) + stroke or TIA; next best step in Mx? –>
ECG –> you want to think, “Does he have atrial fibrillation with a LA mural thrombus
that’s now embolized to the brain.”

80M + good blood pressure (e.g., 110/70) + stroke or TIA + ECG shows sinus rhythm
with no abnormalities; next best step in Mx? –> Holter monitor –> when you first see
this scenario you’re probably like, “Wait, the ECG is normal, so it’s not AF?” –> No, it
is likely AF, but AF is often paroxysmal, so in order to detect it in this scenario, the
next best step is a Holter monitor (24-hour wearable ECG). This means that later in
the day when he sits down to have dinner and then pops into AF, the Holter monitor
will pick it up.

What % of people over age 80 have AF? –> 8% of people over age 80 have AF, which
is why age is a huge risk factor. In other words, if the vignette says the guy is 58, AF is
probably less likely just based on shear probability, regardless of hypertensive status.”
And, once again, knowing that AF is often paroxysmal is really important.

Age 50s-60s + high BP + TIA/stroke/retinal artery occlusion; next best step in Dx? –>
answer = carotid duplex ultrasound to look for carotid plaques.

Age >75 + good BP + TIA/stroke/retinal artery occlusion; answer = ECG to look for
AF –> if normal, do Holter monitor to pick up paroxysmal AF.

55M + good BP + carotid bruit heard on auscultation; next best step in Mx? –>
answer = carotid duplex ultrasound to look for carotid plaques –> in this case, if they
are obvious and explicit about the suspected etiology of the stroke, TIA, or retinal
artery occlusion, then you can just do the carotid duplex ultrasound.

How to Mx carotid plaques? –> first we have to ask whether the patient is
symptomatic or asymptomatic. A bruit does not count as symptoms (that’s a sign).
Symptomatic means stroke, TIA, or retinal artery occlusion. According to recent
guidelines: carotid occlusion >70% if symptomatic, or >80% if asymptomatic –>
answer = do carotid endarterectomy.

Below these thresholds –> answer = medical management = statin, PLUS clopidogrel
OR dipyridamole + aspirin.

The USMLE will actually not be hyper-pedantic about the occlusion %s (that’s Qbank).
They’ll make it obvious for you which answer they want. They’ll say either 90% –>
answer certainly = carotid endarterectomy, or they’ll say 50% –> answer = medical
management only.

There’s one NBME Q where they say a guy has a bruit but is asymptomatic, and has
10 and 30% occlusion in the left vs right carotids, respectively, and he’s already on
aspirin + statin, and the answer is “maintain current regimen” –> if he were
symptomatic, even with low occlusion, he’d certainly need statin, PLUS clopidogrel
OR dipyridamole + aspirin.

Below 70%- Statin+ Clpidogrel or (dipiradamole+aspirin)

HY lecture notes:10

Recurrent bouts of acute pancreatitis cause chronic pancreatitis –> pancreatic

enzymes will usually be normal on the NBME/USMLE because of exocrine pancreas
burn out – i.e., recurrent tissue damage leads to defective enzyme secretion. Patients
need pancreatic enzyme replacement as the Tx.

Patients with chronic pancreatitis will present with steatorrhea because of decreased
lipase secretion –> impaired fat absorption –> can also lead to fat-soluble vitamin
deficiencies.

On one of the IM or Surg forms, they have “pancrelipase” as the answer.

44M + fasting glucose of 112 mg/dL + dark skin on forearms + arthritis; Dx? –>
hereditary hemochromatosis –> AR, chromosome 6, HFE gene, C282Y or H63D
missense mutations account for 90% –> “Bronze diabetes” –> hyperpigmentation
(from hemosiderin deposition) + diabetes due to iron deposition in tail of pancreas
(normal fasting glucose is 72-99 mg/dL; impaired fasting glucose [pre-diabetic] is
100-125 mg/dL; diabetic is two fasting glucoses 126 or greater, or a single HbA1c
>6.5%, or any random glucose >200 mg/dL) + third finding such as arthritis,
cardiomyopathy, or infertility.

44M + fasting glucose of 130 mg/dL + hands are sore + x-ray of hands shows DIP
involvement; what’s the Dx for the type of arthritis? –> answer = pseudogout, not
osteoarthritis. Student says wtf? The two most common etiologies for pseudogout
are hemochromatosis and primary hyperparathyroidism (pseudogout is calcium
pyrophosphate deposition disease, and will present as either a monoarthritis of a
large joint such as the knee, or as an osteoarthritis-like presentation of the hands.

Tx of hereditary hemochromatosis –> serial phlebotomy, not chelation therapy.

44M patient above + USMLE asks what’s the mechanism for his disease –> answer =
“increased intestinal absorption of iron.”

44M above + next best step in Dx? –> check serum ferritin (>300 ug/L in men + post-
menopausal women; or >200 in premenopausal women; USMLE will always say >300
so don’t worry).

Why do men get hemochromatosis younger + with worse Sx than women? –>
menstruation slows progression of disease.

What is secondary hemochromatosis? –> aka transfusional siderosis (amazing to

remember if you want to sound sophisticated) –> due to chronic blood transfusions –
> each transfusion of RBCs contains iron –> seen classically in beta-thalassemia major
or any other patients receiving ongoing transfusions.

Tx for secondary hemochromatosis (transfusional siderosis) –> chelation therapy (e.g.,

deferoxamine), not serial phlebotomy.

Blind loop syndrome

Normally bacterial growth in small bowel is limited by peristalsis + normal flow of

digestive contents. In the case of physical or peristaltic disruption, bacterial
overgrowth in the small bowel may ensue, leading to diarrhea and malabsorption.
Blind loop syndrome may be seen in the setting of surgery, strictures, fistulae,
achlorhydria. Treatment is with doxycycline or rifaximin.

Dumping syndrome

In the setting of roux-en-y procedure (gastric bypass), hyperosmolar chyme from the
stomach may enter the duodenum too quickly, leading to a spike in insulin secretion
and hypoglycemia. This also can be accompanied by diarrhea. On the USMLE: gastric
bypass Hx + hypoglycemia + diarrhea = Dumping syndrome.
Pseudomembranous colitis

For C. difficile, choose “ingestion of spores” as the etiology, not “bacterial

overgrowth.” The latter refers to Blind loop syndrome.

Patient takes Abx for several days + has watery diarrhea; Dx? –> difficile
(pseudomembranous colitis).

Patient takes Abx for several days + has crampy LLQ pain + bloody diarrhea; Dx? –>
difficile à this is on a 2CK NBME –> Yersinia enterocolitica was also listed and was
wrong; this is a good distractor because Y. enterocolitica causes pseudoappendicitis
due to ileitis / mesenteric adenitis, but is RLQ pain, not LLQ.

Which Abx cause C. diff overgrowth? –> clindamycin, cephalosporins, ampicillin are
highest yield.

Dx of C. difficile? –> answer = stool AB toxin test, not stool culture (exceedingly HY).

Tx of C. difficile? –> guidelines as of Feb 2018 say oral vancomycin first-

line, not metronidazole –> apparently UW is updated on this too now –> note that
vanc is given orally –> apart from C. diff, it’s always given IV because it has terrible
oral bioavailability, but in the case of C. diff, where we want the drug confined to the
lumen of the colon, that makes sense.

Mechanism of colonic necrosis in C. diff colonic necrosis? –> answer = “cytoskeletal

disruption.”

Patient is treated with vanc for C. diff but gets recurrence weeks later; why? –>
answer = “regermination of spores.”

C. diff + fever of 104F + tachy + diffuse abdominal pain; next best step in Mx? –>
AXR –> look for toxic megacolon –> Tx w/ NPO (nothing by mouth), NG
decompression + rectal tube (decompression) + Abx (vancomycin or fidaxomicin) +
steroids (if UC) + correct any electrolyte imbalances (sometimes low K) –> if patient
doesn’t improve with conservative therapy, must do surgery (subtotal colectomy +
ileostomy); do not do a colonoscopy on a patient with toxic megacolon as this will
cause perforation.

HY lecture notes:11

87F + coffee bean sign on AXR + obstipated; Dx? → sigmoid volvulus.

Tx for sigmoid volvulus? → answer on surgery NBME = “sigmoidoscopy-guided

placement of rectal tube.”
How do you Dx congenital midgut volvulus? → upper-GI series (AXR + contrast
follow-through of esophagus, stomach, and duodenum with barium or gastrografin).

Where do most colonic ischemic ulcers occur? → watershed areas → splenic flexure
(watershed of SMA and IMA) + sigmoidal-rectal junction (watershed of IMA and
hypogastric artery).

72M + advanced CVD + bloody stool; Dx? → ischemic colitis (due to ischemic ulcer).

79M + Hx of atrial fibrillation + severe, acute, diffuse abdo pain; Dx? → acute
mesenteric ischemia caused by mural thrombus embolizing to SMA or IMA.

Above 79M; next best step in Mx? → mesenteric arteriography.

Above 79M; Tx? → antibiotics (for necrotic bowel) then laparotomy (to remove
necrotic bowel) → they will tell you in last line of vignette that IV Abx are
administered and then ask for the next step, which is just laparotomy. It should be
noted that the literature mentions various Txs like embolectomy, but the USMLE
wants resection of nonviable bowel as the answer.

52F + short episode of ventricular fibrillation + defibrillated + now has severe abdo
pain; Dx? → acute mesenteric ischemia due to ischemia caused by VF, not an
embolus → antibiotics; CT if stable; if unstable go straight to laparotomy.

55F diabetic + Hx of intermittent claudication + Hx of abdo pain 1-2 hours after

eating meals; Dx? → chronic mesenteric ischemia (CMI) caused by severe
atherosclerosis of SMA or IMA (essentially angina of the bowel).

55F diabetic + Hx of CABG + Hx of abdo pain 1-2 hours after eating meals; next best
step in Dx? → mesenteric arteriography (CMI).

55F diabetic + Hx renal artery stenosis + Hx of abdo pain 1-2 hours after eating
meals; Tx? → angioplasty + stenting (CMI) to restore blood flow.

Patient with CMI who has a 2-day Hx of severe abdo pain + fever; Dx? → acute
mesenteric ischemia (acute on chronic due to a thrombosis; essentially akin to an “MI”
of the bowel) → do mesenteric arteriography to Dx; Tx with Abx + laparotomy to
remove necrotic bowel.

69M + LLQ pain + fever = diverticulitis → Dx with CT with contrast of abdomen →

Tx w/ Abx (metronidazole, PLUS fluoroquinolone or Augmentin; USMLE won’t ask
you the exact Abx, but you should be aware that metro covers anaerobes below the
diaphragm) → never do a colonoscopy on someone with suspected diverticulitis, as
you may cause perforation. However, after the diverticulitis is fully treated + cleared,
patient will need a follow-up colonoscopy to rule out malignancy.
 High-yield Transfusion Reactions
[Link] Signs/Symptoms Mechanism Management Notes

“Pre-formed
antibodies Acetaminophen
against is the answer Coombs
Febrile Non-hemolytic Fever, chills,
leukocyte on IM form 5; test is
Transfusion reaction malaise
antigens” steroids is negative
(answer on wrong answer
NBME exam)

ABO
Fever, incompatibility; Stop
Coombs
chills, flank pain, pre-formed transfusion +
Hemolytic Transfusion Reaction test is
hypotension, antibodies administer IV
positive
hemoglobinuria against donor fluids
RBC antigens

Prior
transfusion
or
pregnancy
results in
Presence of
Ab
amnestic
production;
antibodies
↓Hb + hemolysis
Delayed Transfusion Reaction against minor Supportive care
↑bilirubin not
RBC antigens
immediate
(i.e., Kell,
because Ab
Duffy, Kidd)
titers
against
minor Ag
usually
very low

Donor
Alveolar
Bilateral antibodies Stop
damage
Transfusion-Related Lung Injury pulmonary against MHC transfusion +
caused by
(TRALI) infiltrates, I/II or provide airway
activated
dyspnea neutrophil support
neutrophils
antigens
 Dyspnea, Usually
Supportive;
pulmonary Rapid seen in
Transfusion-Associated diuretics;
edema, expansion of elderly
Circulatory Overload (TACO) prevent with
peripheral plasma volume with heart
slower infusion
edema failure

C diff + fever of 104F + tachy + diffuse abdominal pain; next best step in Mx? →
AXR → look for toxic megacolon → Tx w/ NPO (nothing by mouth), NG
decompression + rectal tube (decompression) + Abx (vancomycin or fidaxomicin) +
steroids (if UC) + correct any electrolyte imbalances (sometimes low K) → if patient
doesn’t improve with conservative therapy, must do surgery (subtotal colectomy +
ileostomy); do not do a colonoscopy on a patient with toxic megacolon as this will
cause perforation.

HY lecture notes:

Short clip, but some hard transfusion concepts, so the brevity is warranted.

Antiphospholipid syndrome (APS) will normally present as in vivo thromboses

despite in vitro increase in aPTT. This paradoxical presentation is how you make the
Dx.

Phospholipid is needed for the in vitro aPTT test to run, so if there are Abs against it,
then the test is prolonged (i.e., it cannot run as smoothly). However antibodies against
phospholipid will also cause platelet clumping intravascularly, resulting in thrombotic
events.

Antiphospholipid syndrome can be caused by different types of antibodies, such as

anti-beta-2-microglobulin or anti-cardiolipin. If the disease occurs in SLE, then the
antibodies are simply called “lupus anticoagulant.”

Antiphospholipid syndrome is a notable cause of recurrent miscarriage due to

thromboses in placental vasculature (uteroplacental insufficiency).

Patients with APS can have a false (+) VDRL, the serological screening test for syphilis
(secondary and later).

Where things get hard for Surg shelf:

There’s a Q on one of the forms where they give you a 22-year-old male with
thromboses. They give you no other information. Answer is antithrombin III
deficiency. APS is also listed but is wrong.
AT III deficiency normally presents in patients with chronic nephrotic syndrome (e.g.,
diabetic glomerulonephropathy) who lose AT III in the urine, often leading to renal
vein thromboses. But AT III deficiency can also be an inherited condition.

In order to make the contrast, presumably the question will tell you that aPTT is
elevated (normal 25-40 seconds) if they want APS.

If they don’t mention aPTT elevation, APS will be the answer if they mention (as
discussed above):

• Recurrent miscarriage and/or

• Patient who has lupus and/or
• False (+) VDRL.

HY lecture notes:15

• 32M + pneumothorax that does not resolve following placement of a chest

tube; Dx? –> ruptured bronchus or rupture of intrathoracic trachea.

• 32M + pneumothorax with a persistent air leak despite chest tube placement;
Dx? –> ruptured bronchus or rupture of intrathoracic trachea.

• 32M + contralateral tracheal deviation + low BP; Dx? –> tension

pneumothorax; Tx = needle decompression followed by chest tube. If out in
the field (i.e., not in hospital), if there is penetrating chest trauma, tape over
the wound on three sides only, so air can exit but not enter. Tension
pneumothorax need not be associated with penetrating chest trauma, but this
is one of the most common etiologies.

• Mechanism of low BP in tension pneumothorax? –> answer = compression of

venous structures (IVC).

• 25M + tall +/- uses cocaine + has dyspnea + air in pleural space; mechanism? –
> rupture of subapical bleb causing spontaneous pneumothorax; Tx = can
technically observe if very small and patient stable; however answer on
USMLE will still be needle decompression followed by chest tube.

• 35F + C-section 24-48 hours ago + crackles at both lung bases; Dx? –
> atelectasis; normally the fever is within 24 hours, but a Q on one of the
forms says “two days after surgery.”

• 48M + motor vehicle accident (MVA) + rib fractures + paradoxical breathing

(i.e., chest wall moves outward with exhalation and inward with inhalation);
Dx? –> flail chest.
• 48M + MVA + has severe pain and/or bruising over the sternum; Dx? –
> myocardial contusion –> do an ECG + monitor in hospital due to high risk of
arrhythmia. Get troponins.

• This is where things get hard for the surg shelf:

• 48M + MVA + rib fractures + underlying infiltrates + no other info given in the
stem; Dx? –> pulmonary contusion. The Q will not say “white-out of the lung”
–> too easy / buzzwordy of a description.

• 48M + MVA + no rib fractures + lobar infiltrates + no other info given in the
stem; Dx? –> pulmonary contusion –> need not have rib fractures for
pulmonary contusion.

• 48M + MVA +/- rib fractures + O2 sats decrease when 2L of fluid is given; Dx?
–> pulmonary contusion –> contused lung is very fluid sensitive.

• 48M + MVA +/- rib fractures + severe pain/bruising over the sternum + O2
sats decrease when 2L of fluid is given; Dx? –> myocardial contusion, not
pulmonary contusion –> weird, because the stem said the O2 sats decreased
with fluid, but the pain/bruising over the sternum “wins.”

• Pulmonary contusion isn’t a diagnosis of exclusion per se, but I’ve noticed
across NBME Qs that the presentation is fairly non-specific.

• Essentially:

• Is there paradoxical breathing? Yes? Ok, flail chest. No? Ok, not flail chest.

• Do they mention a persistent air leak despite a chest tube? Yes? Ok, ruptured
bronchus. No? Ok, not ruptured bronchus.

• Do they say bruising/pain over the sternum? Yes, Ok, myocardial contusion.
No? Ok, not myocardial contusion.

• Do they say pulmonary infiltrates on CXR in the setting of trauma and I’ve
eliminated the above three Dx? Yes? Ok, pulmonary contusion is likely answer.