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Internal Medicine Exam Answers Explained

The document provides a series of questions and answers related to internal medicine, covering topics such as anemia of chronic disease, autoimmune disorders, multiple sclerosis treatment, hyperkalemia, peripheral edema, heart failure management, chronic kidney disease staging, tuberculosis diagnosis, asthma exacerbation treatment, hypertensive emergencies, acute glomerulonephritis, sepsis management, hepatorenal syndrome, hyponatremia treatment, atrial fibrillation management, and Factor V Leiden mutation. Each answer is accompanied by a detailed explanation and references for further reading. The content is aimed at medical professionals seeking to enhance their knowledge in internal medicine.

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0% found this document useful (0 votes)
25 views115 pages

Internal Medicine Exam Answers Explained

The document provides a series of questions and answers related to internal medicine, covering topics such as anemia of chronic disease, autoimmune disorders, multiple sclerosis treatment, hyperkalemia, peripheral edema, heart failure management, chronic kidney disease staging, tuberculosis diagnosis, asthma exacerbation treatment, hypertensive emergencies, acute glomerulonephritis, sepsis management, hepatorenal syndrome, hyponatremia treatment, atrial fibrillation management, and Factor V Leiden mutation. Each answer is accompanied by a detailed explanation and references for further reading. The content is aimed at medical professionals seeking to enhance their knowledge in internal medicine.

Uploaded by

EMIN3M
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd

Answers with Explanations

INTERNAL MEDICINE

1. Answer: B)- IL-6

Explanation:
Anemia of chronic disease occurs in chronic infections, autoimmune disorders, or
malignancy. It's a normocytic, normochromic anemia that stems not from blood loss or
iron deficiency, but from iron trapping and inhibited erythropoiesis.

 IL-6 stimulates hepcidin, which blocks ferroportin in enterocytes and macrophages →


iron stays trapped intracellularly.
 Hepcidin is a negative regulator of iron availability for erythropoiesis.
 Though IL-1 and TNF-α are also elevated in inflammation, IL-6 is the main driver of
hepcidin-mediated iron blockade.

Tip: IL-6 → Hepcidin ↑ → ↓ Ferroportin → Functional iron deficiency.

Reference:: (Harrison 21st Ed., Ch. 89 | Cecil 27th Ed., Vol 2, p. 1924 | UpToDate)

2. Answer: D)- Anti-Sm

Explanation:

Anti-Sm is highly specific (~98–100%) but low sensitivity (~30%)


Anti-dsDNA: More sensitive and correlates with lupus nephritis activity
ANA: Highly sensitive but non-specific
Anti-Ro: Associated with neonatal lupus, subacute cutaneous lupus, and Sjogren's
syndrome

Remember: Anti-dsDNA = Activity marker | Anti-Sm = Diagnostic marker

Reference: (Harrison 21st Ed., Ch. 349 | Davidson 24th Ed., p. 1064 | Kumar & Clark 10th
Ed., p. 1054)

3. Answer: C)- IV methylprednisolone

Explanation:

 In acute MS relapses, first-line treatment is high-dose IV corticosteroids (e.g.,


methylprednisolone 1g/day for 3–5 days).
 Interferons and Natalizumab are used for long-term disease modification, not acute
attacks.
 Azathioprine is used occasionally as maintenance immunosuppression, not for relapse.

MRI with Dawson's fingers + optic neuritis + relapsing course = MS

Reference ( Harrison 21st Ed., Ch. 458 | Davidson 24th Ed., p. 1170)

4. Answer: C)- Peaked T waves

Explanation:

Hyperkalemia alters cardiac membrane potentials, leading to progressive changes in the


ECG. The changes correlate with rising serum potassium levels.

ECG progression in hyperkalemia:

1. Mild elevation (K⁺ ~5.5–6.5 mEq/L)


→ Tall, narrow-based, peaked T waves (especially in precordial leads)
This is the earliest and most specific ECG finding.
2. Moderate elevation (K⁺ ~6.5–7.5 mEq/L)
→ Flattening or disappearance of P waves, prolonged PR interval
3. Severe hyperkalemia (K⁺ >7.5 mEq/L)
→ Widened QRS, sine wave pattern, ventricular arrhythmias

Common distractors:

 U waves → Classic finding in hypokalemia, not hyperkalemia.

References: (Harrison’s Principles of Internal Medicine, 21st Ed., Ch. 52, UpToDate: "ECG
changes in hyperkalemia")

5. Answer: C)-Medication-induced peripheral vasodilation

Explanation:
 Dihydropyridine calcium channel blockers (e.g., amlodipine) cause preferential
arteriolar dilation, increasing capillary hydrostatic pressure → leading to transudative
peripheral edema.
 This occurs typically within 2–3 weeks of starting or increasing the dose of amlodipine,
and is dose-dependent.
 Clinical studies show it is seen in up to 10–15% of patients on ≥5 mg/day, and more
commonly at 10 mg/day.
 Diuretics are ineffective as it is not due to fluid overload. Management includes dose
reduction, drug switch, or adding ACE inhibitors/ARBs, which dilate post-capillary
venules.

References: (Davidson’s 24th Ed., p. 618, Harrison’s 21st Ed., Ch. 308 ,Krause et al., Am J
Hypertens. 1994;7(9):844–850.)

6. Answer: C)- Spironolactone

Explanation:

 Spironolactone is a mineralocorticoid receptor antagonist (MRA) that blocks the


effects of aldosterone, which contributes to cardiac remodeling, myocardial fibrosis, and
sodium/water retention in heart failure.
 It is proven to reduce all-cause mortality and hospitalization in patients with HFrEF
(LVEF < 35–40%), especially in NYHA class II–IV.

 The RALES trial (1999) showed a 30% reduction in mortality with spironolactone in
severe HFrEF (NYHA III–IV, EF <35%).
 This benefit is independent of diuresis, due to antifibrotic and anti-remodeling actions.

Comparison:

 Loop Diuretics (e.g., furosemide):


→ Provide symptomatic relief by reducing pulmonary and peripheral congestion
→ But do not reduce mortality
 Digoxin:
→ Reduces hospitalizations, especially in patients with concurrent atrial fibrillation
→ No mortality benefit (DIG trial)
 Ivabradine:
→ May reduce hospitalization in selected patients with:
o Sinus rhythm
o HR >70 bpm
o Already on max tolerated beta-blockers
→ Not first-line; mortality benefit is uncertain

References: (Harrison’s Principles of Internal Medicine, 21st Ed., Ch. 252 – Heart Failure,
ESC Guidelines 2022 for Heart Failure, UpToDate: Pharmacologic Therapy for HfrEF)
7. Answer: C)- Stage 3

Explanation:

Chronic Kidney Disease (CKD) staging is based on estimated glomerular filtration rate
(eGFR), which reflects kidney function. The patient has an eGFR of 40 mL/min/1.73m²,
placing them in Stage 3 CKD.

An eGFR of 40 falls within Stage 3b of CKD, associated with progressive symptoms and
risk of complications.

Exam Points:

 CKD = eGFR <60 for ≥3 months or evidence of kidney damage (e.g., albuminuria,
structural abnormalities).
 Stage 3 is when complications (anemia, acidosis, bone-mineral disorders) typically
begin to appear.

Reference: (KDIGO 2024 Clinical Practice Guideline, Harrison’s Principles of Internal


Medicine, 20th Ed., Ch. 338 ,Levey AS et al., JASN 2017 – Epidemiology and impact of
CKD.)

8. Answer: B)- Tuberculosis (TB)

Explanation:
This patient's symptoms of persistent cough, night sweats, weight loss, and upper lobe
cavitary lesions on chest X-ray are classic signs of pulmonary tuberculosis (TB), a chronic
infectious disease caused by Mycobacterium tuberculosis.
 Community-acquired pneumonia often presents with acute symptoms and infiltrates on
chest X-ray.
 Lung cancer can present with weight loss and cough but typically causes a solitary mass
on chest X-ray rather than cavitary lesions.
 COPD presents with chronic cough, sputum production, and dyspnea, but does not
typically cause cavitary lung lesions.

Reference: (Raviglione, MC., et al. Tuberculosis. Lancet, 2016. ,Fauci, AS, et al. Harrison's
Principles of Internal Medicine, 20th ed. McGraw-Hill; 2018.)

9. Answer: B)- Inhaled short-acting beta-agonist (SABA)

Explanation:
The first-line treatment for an acute asthma exacerbation involves the use of an inhaled
short-acting beta-agonist (SABA) such as albuterol to relieve bronchoconstriction. This
medication provides rapid relief by relaxing bronchial smooth muscle.

 Oral corticosteroids (e.g., prednisone) are used for moderate to severe exacerbations but
are not the first-line treatment.
 Antibiotics are not indicated unless there is evidence of a concurrent bacterial infection.
 Oxygen therapy is used in severe exacerbations with hypoxemia but is not the first step in
all cases.
Reference: ( National Heart, Lung, and Blood Institute (NHLBI). Guidelines for the
Diagnosis and Management of Asthma, 2020. ,Fauci, AS, et al. Harrison's Principles of
Internal Medicine, 20th ed. McGraw-Hill; 2018.)

10. Answer: B)- Intravenous antihypertensive medications

Explanation:

This patient presents with signs of hypertensive emergency, which is defined as severe
hypertension (typically >180/120 mmHg) with evidence of end-organ damage (e.g.,
retinopathy, encephalopathy, acute kidney injury). According to the 2025 guidelines, the
most appropriate management is the use of intravenous antihypertensive medications
(e.g., labetalol, nicardipine, nitroprusside) to lower the blood pressure in a controlled
manner.

 Initial blood pressure reduction should aim for a 20-25% reduction in mean arterial
pressure (MAP) over the first hour. This gradual approach helps prevent abrupt decreases
that could lead to ischemic damage to vital organs. Over the subsequent 2–6 hours, further
blood pressure reduction is done to reach a target MAP of approximately 100–110 mmHg.
 Oral antihypertensive medications are appropriate for hypertensive urgency, but they
are not effective in managing the immediate, severe elevations of blood pressure seen in
hypertensive emergencies.
 Observation and lifestyle modification are insufficient for hypertensive emergencies and
should not be used in the acute management of such patients.
 Diuretics, while useful for managing chronic hypertension, are not the first choice for
rapidly lowering blood pressure in hypertensive emergencies. They may be employed for
volume overload but are not sufficient for the immediate and controlled reduction of
severely elevated blood pressure.

References: (Mancia, G., et al. Hypertension in Adults: Current Management. Lancet, 2017.,
Fauci, AS, et al. Harrison's Principles of Internal Medicine, 20th ed. McGraw-Hill;
2018. ,European Society of Cardiology (ESC) 2024 Guidelines on Hypertension, Best
Practice in Hypertension Management, BMJ, 2024.)

11. Answer: C. Acute glomerulonephritis

Explanation:

This patient’s hematuria, proteinuria, and red blood cell casts on urinalysis are
characteristic of acute glomerulonephritis (AGN). AGN is an immune-mediated condition
causing glomerular inflammation. Key features include:

 Hematuria: Often "smoky" or "tea-colored" urine due to red blood cell casts and
dysmorphic red blood cells.
 Proteinuria: Typically <3 g/day (less than in nephrotic syndrome).
 Edema: Periorbital and dependent edema.
 Hypertension: Often >140/90 mmHg due to fluid retention.
 Renal function: Elevated serum creatinine and BUN; decreased GFR (<60 mL/min).

Differential:

 Nephrotic syndrome: Characterized by massive proteinuria (>3.5 g/day),


hypoalbuminemia, and edema, but no hematuria or red blood cell casts.
 Chronic kidney disease: Develops gradually, lacking the acute features of AGN.
 Polycystic kidney disease: Can cause hematuria and hypertension but not red blood cell
casts.

References: (Jennette, JC., et al. Kidney International, 2013. , Fauci, AS, et al. Harrison's
Principles of Internal Medicine, 21st ed., 2020.)

12. Answer: B)- Piperacillin-tazobactam

Explanation:
In the management of sepsis due to Gram-negative bacteria, piperacillin-tazobactam is
often used as an empiric broad-spectrum antibiotic because it covers a wide range of
Gram-negative organisms.

 Vancomycin and ceftriaxone are appropriate for suspected Gram-positive infections or


community-acquired pneumonia but not as broad-spectrum coverage for Gram-negative
sepsis.
 Cefepime and metronidazole are useful for infections like intra-abdominal infections
but may not cover all Gram-negative pathogens as effectively as piperacillin-tazobactam.
 Meropenem is an option in cases of severe infections, but it is reserved for multi-drug-
resistant organisms.

Reference: (Dellinger, RP., et al. Surviving Sepsis Campaign. Journal of the American
Medical Association, 2017. ,Fauci, AS, et al. Harrison's Principles of Internal Medicine, 20th
ed. McGraw-Hill; 2018.)

13. Answer: B)- Low serum albumin

Explanation:

Hepatorenal syndrome (HRS) is a type of functional renal failure that occurs in patients
with advanced liver disease, typically cirrhosis with ascites, and without an alternative
cause for renal dysfunction. The key diagnostic criteria for HRS include:
Low serum albumin (usually <2.5 g/dL) is common in cirrhosis due to decreased hepatic
synthesis, but it is not part of the diagnostic criteria for HRS itself. While low albumin
contributes to fluid retention and ascites, it is not the direct cause of renal dysfunction in HRS.
The renal dysfunction is primarily due to splanchnic vasodilation and renal
vasoconstriction.

References: ( Fauci, AS, et al. Harrison’s Principles of Internal Medicine, 21st ed., Ch.
308. , Schiff, ER, et al. Schiff’s Diseases of the Liver, 12th ed., Vol 2, Ch. 40.)

14. Answer: A)- Fluid restriction

Explanation:

This patient has euvolemic hyponatremia, likely due to SIADH from paraneoplastic
secretion of ADH (common in small cell carcinoma). Urine sodium >40 mEq/L and high
urine osmolality (>100 mOsm/kg) confirm inappropriately concentrated urine.

 In mild, asymptomatic hyponatremia (Na >125 mEq/L and patient alert), fluid
restriction is the first-line treatment.
 Hypertonic saline is reserved for severe symptomatic hyponatremia (e.g., seizures,
altered mental status).
 Normal saline can worsen hyponatremia in SIADH because the kidney excretes the
sodium and retains water.
 Salt tablets are second-line when fluid restriction alone fails.
Reference: ( Harrison’s Principles of Internal Medicine, 21st ed., Ch. 67 ,Goldman-Cecil
Medicine, 26th ed., Vol 1, Ch. 117.)

15. Answer: C)- Warfarin to maintain INR 2–3

Explanation:
This patient has atrial fibrillation (AF) and multiple stroke risk factors. The CHA₂DS₂-
VASc score helps estimate stroke risk:

 C = CHF (1)
 H = Hypertension (1)
 A = Age ≥75 (2)
 D = Diabetes mellitus (1)
 S = Stroke/TIA history (2)
 V = Vascular disease (1)
 A = Age 65–74 (1)
 Sc = Sex category (female = 1)

Patient’s score is 4 (HTN + DM + Age ≥75), indicating high stroke risk, requiring oral
anticoagulation.
For non-valvular AF, either Warfarin (INR 2–3) or a DOAC (e.g., apixaban, dabigatran)
is indicated.
Aspirin alone or dual antiplatelet therapy is inadequate in AF-related stroke prevention
unless anticoagulation is contraindicated.

Reference: (Harrison’s Principles of Internal Medicine, 21st ed., Ch. 270 ,2020 ESC
Guidelines for the diagnosis and management of atrial fibrillation.)

16. Answer C)- Factor V Leiden mutation

Explanation:

 Factor V Leiden mutation is a point mutation (G1691A) in the gene for coagulation
Factor V, which makes it resistant to inactivation by activated protein C (APC).
 It is the most common inherited thrombophilia, particularly in Caucasians (3–8%
prevalence).
 Mode of inheritance: Autosomal dominant
 Homozygotes have 10–80x increased risk of venous thromboembolism (VTE);
heterozygotes ~5x.
 Associated with:
 Deep vein thrombosis (DVT)
 Pulmonary embolism (PE)
o Recurrent miscarriages (especially in young women)

Exam Points:
 Always choose Factor V Leiden over Protein C/S deficiency if asked "most common."
 Protein C/S deficiency more likely to cause warfarin-induced skin necrosis.
 Diagnosed by activated protein C resistance assay or PCR for the mutation.
 Not associated with arterial thrombosis.

Reference: (Harrison’s Internal Medicine, 21st Ed., Ch. 117, Kumar & Clark, Oxford
Handbook of Clinical Medicine.)

17. Answer B)-Conduction System abnormalities

Explanation:

 In systemic sclerosis (SSc), also called scleroderma, cardiac involvement is common but
often subclinical.
 Myocardial fibrosis, affecting both the conduction system and muscle tissue, is the main
pathology.
 The most frequent manifestation is arrhythmia due to conduction system involvement
(SA node, AV node, bundle branches).
 Other cardiac findings include:
o Pericardial effusion/pericarditis
o Pulmonary hypertension → Right heart failure
o Rarely: myocardial infarction (due to coronary microvascular disease)

Exam Points:

 Conduction blocks, bundle branch blocks, and premature beats = most common.
 Sudden cardiac death may occur due to arrhythmias in diffuse SSc.
 Heart disease worsens prognosis in scleroderma.
 Screening: ECG, Holter monitoring, and echocardiography in all suspected cases.

Reference: (Harrison’s 21st Ed., Ch. 351, ACR Guidelines for Systemic Sclerosis.)

SURGERY

18. Answer: B)- NPO, IV fluids, analgesia

Explanation:

This patient has acute pancreatitis, supported by:

 Severe epigastric pain radiating to the back


 Serum lipase >3× upper limit of normal (Normal: <160 U/L → Pancreatitis: typically

Revised Atlanta Classification:


Need 2 of 3: (Typical abdominal pain, Serum lipase or amylase >3× ULN and Imaging
evidence (only if diagnosis is unclear).

Initial Management :

Component Guideline Values & Explanation

Early oral feeding within 24 hrs is now recommended (if no


Feeding ileus/vomiting). Start with low-fat solid meals — better outcomes,
faster recovery.

Start Lactated Ringer’s at 5–10 mL/kg/hr. Titrate to maintain urine


IV Fluids
output ≥0.5–1 mL/kg/hr. Avoid fluid overload.

Use IV opioids (e.g., morphine, fentanyl) for pain control.


Analgesia
Avoid NSAIDs in renal dysfunction.

Not routinely needed:

NPO is outdated unless patient has severe pain, ileus, or vomiting.


Prophylactic antibiotics unless infection is confirmed.
CT scan only if diagnosis is unclear or no improvement in 48–72 hrs.
ERCP reserved for biliary pancreatitis with cholangitis or CBD obstruction (elevated
bilirubin + imaging signs).

References: ( Harrison’s Principles of Internal Medicine, 21st ed., Ch. 344 , Bailey & Love,
27th ed., Ch. 68, Cleveland Clinic Journal of Medicine, 2024; 91(6):341, Clinical Nutrition,
2023; DOI: 10.1016/[Link].2023.11.001.)

19. Answer: D)-Femoral

Explanation:
Femoral hernia passes below the inguinal ligament through the femoral canal, which has
rigid borders (lacunar ligament medially, femoral vein laterally). This makes it narrow and
prone to incarceration and strangulation. Though less common than inguinal hernias, femoral
hernias are more dangerous, especially in elderly females.

References: (Bailey & Love 27th ed., Ch. 59; SRB Surgery 5th ed., Ch. 17; Schwartz 11th
ed., Ch. 38.)

20. Answer: C)-Emergency laparotomy

Explanation:
A patient with blunt trauma and hemodynamic instability (hypotension + tachycardia) with a
positive FAST (fluid in Morison’s pouch = intra-abdominal bleeding) must be taken directly
for exploratory laparotomy. CT is only done in stable patients. Delaying surgery for
imaging in such cases can be fatal.

References: (ATLS 10th ed.; Bailey & Love 27th ed., Ch. 28; Sabiston 21st ed., Ch. 13.)

21. Answer: C)- Ringer lactate

Explanation:
Ringer lactate is preferred during the first 24 hours of burn management. It resembles
plasma and avoids hyperchloremic acidosis associated with normal saline. Dextrose and
colloids like albumin are avoided early as they worsen edema due to increased capillary
permeability.

References: Bailey & Love 27th ed., Ch. 62; Schwartz 11th ed., Ch. 9

22. Answer: C)- Papillary

Explanation:
Papillary carcinoma is the most common thyroid cancer (~80%), typically affecting young
females. It spreads via lymphatics and has excellent prognosis. Histology shows Orphan
Annie eye nuclei and psammoma bodies. Follicular spreads hematogenously. Medullary
arises from C cells and secretes calcitonin.

References: Bailey & Love 27th ed., Ch. 66; SRB Surgery 5th ed, First Aid 2025
23. Answer: C)- Sacrococcygeal region

Explanation:
Pilonidal sinus is a midline lesion found in the natal cleft of the sacrococcygeal area, usually
in young hirsute males. It is a chronic inflammatory reaction to embedded hair. Treatment is
excision, sometimes with flap coverage.

References: Bailey & Love 27th ed., Ch. 69; SRB Surgery

24. Answer: A)- Traumatic rupture of the aorta

Explanation:
A widened mediastinum in the setting of blunt chest trauma is highly suggestive of aortic
transection, especially at the ligamentum arteriosum.

 It is the most common vascular deceleration injury.


 Further evaluation requires CT angiography.
 This is a life-threatening emergency often requiring surgical or endovascular repair.

Reference: (Harrison’s Principles of Internal Medicine, 19th ed., p. 289e ,Sabiston Textbook
of Surgery, 20th ed., p. 891, Radiology Rounds)

25. Answer: B)- McBurney’s point tenderness

Explanation:
Tenderness at McBurney’s point (1/3rd from ASIS to umbilicus) is the most consistent and
earliest sign of acute appendicitis. Rovsing’s, Psoas, and Obturator are supplementary signs.
Rebound tenderness suggests peritonitis.

References: Bailey & Love 27th ed., Ch. 65; Sabiston 21st ed.

26. Answer: C)- Patent processus vaginalis

Explanation:
Communicating hydrocele occurs due to persistence of processus vaginalis, which connects
peritoneal cavity to tunica vaginalis. Fluid flows freely and the swelling fluctuates with
position. Surgical repair (herniorrhaphy) is needed if it persists beyond 1–2 years.
References: Bailey & Love 27th ed., Ch. 59; Schwartz 11th ed.

27. Answer: B)- Bilateral mammogram

Explanation:
After confirming malignancy via FNAC/core biopsy, the next step is to image both breasts
to rule out multicentric disease and assess the extent. MRI is useful in high-risk or dense
breasts. Tumor markers are not primary tools in diagnosis.

References: Bailey & Love 27th ed., Ch. 72; SRB Surgery; NCCN Guidelines

28. Answer: C)- Doyen’s clamp

Explanation:
Doyen’s clamp is a long, light, non-crushing intestinal clamp used to occlude bowel lumen
temporarily during resection or anastomosis. Kocher’s is a heavy crushing clamp. Allis and
Babcock are tissue-holding forceps.
References: Bailey & Love 27th ed., Surgical Instruments Appendix; SRB Surgery

29. Answer: B)- Clostridium perfringens

Explanation:
Gas gangrene is a rapidly progressive necrotizing soft tissue infection caused by
Clostridium perfringens, an anaerobic Gram-positive bacillus. It produces alpha toxin
causing myonecrosis and gas formation. Urgent debridement and high-dose penicillin are
needed.

References: Bailey & Love 27th ed., Ch. 26; Robbins Pathology; Sabiston 21st ed.

30. Answer: C)- Contraception should continue until two consecutive negative semen
analyses

Explanation:
Vasectomy is not immediately effective. Residual sperm can remain distal to the site of
ligation. Patients are advised to use alternative contraception until two negative semen
samples (usually 12 and 16 weeks post-procedure) confirm azoospermia.

 Spontaneous recanalization is rare but possible.


 Patients must be clearly counseled on this before the procedure.

Reference: (Bailey & Love’s Short Practice of Surgery, 27th ed., p. 1512, Sabiston Textbook
of Surgery, 20th ed., p. 1943.)

31. Answer: A)- Lymphatics

Explanation:
Thromboangiitis obliterans (Buerger’s disease) is a non-atherosclerotic segmental
vasculitis involving:

Small and medium arteries


Veins
Peripheral nerves
Most commonly affects smokers under 45 years.
It does not affect lymphatics.
Diagnosis is clinical and by imaging showing corkscrew collaterals.

References: (Sabiston Textbook of Surgery, 20th Edition, p. 1780 ,StatPearls: Buerger


Disease (Thromboangiitis Obliterans

32. Answer: D)- Ultrasound of the abdomen

Explanation:
This is a classic case of infantile hypertrophic pyloric stenosis (IHPS).
 Ultrasound is the investigation of choice showing a thickened pyloric muscle (>3 mm)
and elongated pyloric canal (>14 mm).
 CT and endoscopy are not required unless the diagnosis is unclear.
 Plain X-ray may show a dilated stomach but is nonspecific.

Reference: (Bailey & Love’s Short Practice of Surgery, 27th ed., p. 128, Nelson Textbook of
Pediatrics, 20th ed., p. 1947.)

33. Answer: C)- Great saphenous vein at SFJ

Explanation:
Trendelenburg procedure is ligation of the great saphenous vein close to its junction with
femoral vein to treat varicose veins. It is often followed by stripping. Small saphenous vein
enters popliteal vein.

References: (Bailey & Love 27th ed., Ch. 54; Schwartz 11th ed.)

OBSTRETICS AND GYNECOLOGY

34. Answer: B)- Start methotrexate chemotherapy

Explanation:
After the evacuation of a molar pregnancy, persistence of β-hCG levels (elevated beyond 6
weeks post-evacuation) can indicate the development of gestational trophoblastic neoplasia
(GTN). The most common form of GTN is invasive mole, and it can progress to
choriocarcinoma. Methotrexate is the first-line treatment for low-risk GTN, especially
when the patient desires to preserve fertility.

 Repeat suction evacuation is generally not performed unless there is incomplete


evacuation or ongoing hemorrhage.
 Total abdominal hysterectomy is reserved for high-risk GTN or patients who no longer
wish to preserve fertility.

Reference: ( Berek JS, Hacker NF. Berek & Hacker's Gynecologic Oncology. 6th ed.
Wolters Kluwer; 2020., Monk BJ, Tewari KS, et al. Clinical Gynecologic Oncology. 9th ed.
Elsevier; 2020.)

35. Answer: C)- Lower uterine segment

Explanation:
In patients with a previous cesarean section (CS) or uterine surgery, the lower uterine
segment (LUS) is the most vulnerable area for rupture, especially during labor. The LUS is
the site of the uterine incision in most previous cesareans. Rupture occurs when the uterine
scar fails under the pressure of labor, leading to catastrophic consequences for both mother
and fetus.

 Fundal rupture is more common in unscarred uteri and tends to happen in obstructed
labor or where there is excessive use of uterotonics (e.g., oxytocin).

Reference: (Cunningham FG, Leveno KJ, et al. Williams Obstetrics. 25th ed. McGraw-Hill
Education; 2018., Spong CY, Berghella V. Preventing Uterine Rupture in Women with
Previous Cesarean Delivery: A Review of Evidence. Obstetrics and Gynecology Clinics.
2014.)

36. Answer: C)- Squamous cell carcinoma

Explanation:
Squamous cell carcinoma accounts for the vast majority of vulvar cancers (around 90%).
Risk factors include HPV infection (types 16 and 18) and chronic conditions like lichen
sclerosus.

Adenocarcinoma and melanoma are rare and have a different histologic pattern.
Basal cell carcinoma is also rare and generally associated with chronic sun exposure in
other skin regions.

Reference: (Berek JS, Hacker NF. Berek & Hacker's Gynecologic Oncology. 6th ed. Wolters
Kluwer; 2020. ,Barton DPJ. Gynecologic Cancer. Elsevier; 2021.)

37. Answer: B)- Hyponatremia and hypokalemia

Explanation:
Hyperemesis gravidarum (HG) is characterized by severe vomiting, resulting in fluid loss,
electrolyte imbalance, and metabolic alkalosis.

 Hyponatremia occurs due to excessive fluid loss, renal retention of water in response to
ADH secretion, and dehydration.
 Hypokalemia is due to vomiting (loss of potassium-rich gastric contents), leading to
hypokalemic metabolic alkalosis.
 A more severe deficiency of thiamine (B1) can result in Wernicke's encephalopathy,
particularly if the vomiting is prolonged.

Reference: ( James DH, Brown MA. High Risk Obstetrics. Elsevier; 2021. , Cunningham
FG, Leveno KJ, et al. Williams Obstetrics. 25th ed. McGraw-Hill Education; 2018.)

38. Answer: C)- History of migraine with aura

Explanation:
Women with a history of migraine with aura are at increased risk of ischemic stroke when
using estrogen-containing combined oral contraceptives (COCs), making it an absolute
contraindication.

 Age >35 is a relative contraindication, but smoking combined with this age factor
significantly raises cardiovascular risks.
 Family history of breast cancer does not automatically contraindicate OCPs, but if the
patient has active breast cancer, COCs are contraindicated.
 Nulliparity is not a contraindication for OCPs.

Reference: (Hatcher RA, Trussell J, et al. Contraceptive Technology. 21st ed. Ardent Media;
2018., Speroff L, Darney PD. A Clinical Guide for Contraception. 5th ed. Lippincott
Williams & Wilkins; 2012.

39. Answer: C)- Immediate laparoscopy

Explanation:
Ovarian torsion is a surgical emergency that occurs when the ovary twists around its
supporting ligaments, compromising its blood supply. The clinical presentation often
includes sudden severe abdominal pain, vomiting, and a cystic mass on ultrasound.

 Doppler flow absent on USG indicates compromised blood supply to the ovary, which
requires urgent laparoscopic detorsion to save the ovary.
 Observation is inappropriate because delayed intervention leads to ovarian necrosis and
loss of fertility.

Reference: ( Berek JS, Hacker NF. Berek & Hacker's Gynecologic Oncology. 6th ed.
Wolters Kluwer; 2020. ,Missmer SA, Nothnagle M, et al. Gynecology and Obstetrics.
Elsevier; 2021.)

40. Answer: C)- Polycystic ovarian syndrome

Explanation:
PCOS is the most common cause of chronic anovulation and is characterized by
oligomenorrhea, hyperandrogenism, and polycystic ovaries on ultrasound.

 Hyperprolactinemia may also cause anovulation but is less common compared to PCOS.
 Asherman syndrome is related to intrauterine adhesions typically after curettage,
leading to infertility, but anovulation is not the primary issue.
 Turner syndrome is characterized by gonadal dysgenesis and primary amenorrhea, but
it is not the primary cause of chronic anovulation.

Reference: (Speroff L, Darney PD. A Clinical Guide for Contraception. 5th ed. Lippincott
Williams & Wilkins; 2012. , McClusky III, A, & Maturu, J. Polycystic Ovarian Syndrome:
Etiology, Pathophysiology, and Management. J Obstet Gynaecol. 2021.)

41. Answer: D)- Nuchal translucency


Explanation:
Nuchal translucency (NT) is the first marker to become abnormal during the first
trimester screening for trisomy 21 (Down syndrome).
An increased NT (>3 mm) has a strong association with aneuploidy.
In later trimesters, other markers like β-hCG and Inhibin A become elevated, and estriol
levels decrease in Down syndrome.

FIGURE 14-5 Sagittal image of a normal, 12-week fetus demonstrating correct caliper
placement (+) for nuchal translucency measurement. The fetal nasal bone and overlying skin
are indicated. The nasal tip and the 3rd and 4th ventricles (asterisk), which are other
landmarks that should be visible in the nasal bone image, are also shown.

Reference: (Cunningham FG, Leveno KJ, et al. Williams Obstetrics. 25th ed. McGraw-Hill
Education; 2018., Spencer K, et al. Antenatal Screening for Down’s Syndrome. Obstetrics
& Gynecology. 2019.)

42. Answer: C)-Endometrial biopsy

Explanation:
Postmenopausal bleeding (PMB) is always abnormal and requires investigation to rule out
endometrial carcinoma. An endometrial thickness of >4 mm on transvaginal ultrasound
warrants an endometrial biopsy to exclude malignancy.

 Progesterone therapy may be indicated in cases of endometrial hyperplasia without


atypia, but this must be confirmed by biopsy.
 Observation or repeating the scan is inappropriate because of the potential for
malignancy.

Reference: (Berek JS, Hacker NF. Berek & Hacker's Gynecologic Oncology. 6th ed.
Wolters Kluwer; 2020., Gaba N, Meher P. Postmenopausal Bleeding: Etiology and
Management. J Gynecol Oncol. 2020.)

43. Answer: C)- McRoberts maneuver

Explanation:
Shoulder dystocia is an obstetric emergency that occurs when the anterior shoulder becomes
impacted behind the pubic symphysis. The first step is to perform the McRoberts
maneuver—flexing the mother's legs toward her abdomen to open the pelvis and release the
shoulder.

 Suprapubic pressure can also be used in conjunction with this maneuver to help
disimpact the shoulder.
 Zavanelli maneuver (reversal of the delivery) is only used if all other methods fail.

Reference: ( Cunningham FG, Leveno KJ, et al. Williams Obstetrics. 25th ed. McGraw-
Hill Education; 2018., ACOG. Shoulder Dystocia and Brachial Plexus Injury. Obstetrics
& Gynecology. 2020.)

44. Answer: A)- Superfetation


Explanation:

Superfetation

 Definition: Superfetation is the fertilization and implantation of a second ovum during


an ongoing pregnancy.
 It results in the development of two fetuses at different stages of gestation—typically
showing a gap of weeks or even a month between their ages on ultrasound.
 For this to happen, ovulation must occur during an already established pregnancy (which is
rare, due to hormonal changes usually preventing further ovulation).
 More commonly described in animals, but extremely rare in humans. However, case
reports do exist, and it is recognized as a possibility when a marked discordance in fetal
gestational age is seen without evidence of intrauterine growth restriction (IUGR) or
anomalies.

Key Point: If the ultrasound shows a significant difference (e.g.,4 weeks) in gestational age
between twins, and no pathology explains this discrepancy, superfetation should be
considered.

Other options:

B. Superfecundation:

 Fertilization of two ova released during the same cycle but by separate acts of coitus,
which may involve different fathers (heteropaternal superfecundation).
 This results in twins of the same gestational age, but possibly different paternity.
 Important difference: In superfecundation, both fetuses are of the same gestational age.

C. Suppositious child:

 A legal/forensic term used to describe a fraudulently claimed child — not biologically


related to the parents. Often falsely introduced for inheritance claims.
 Not a biological or obstetric term for twin gestation.

D. Posthumous child:

 A child born after the death of the biological father.


 Again, this is a legal definition, unrelated to gestational age differences.

References: (DC Dutta's Textbook of Obstetrics, 9th Edition , Williams Obstetrics, 25th
Edition – Chapter 44: Multifetal Gestation, Sridhar Rao's Clinical Obstetrics, 3rd Edition ,
Langman's Medical Embryology, 14th Edition.)

45. Answer: B)- 3 cm Anterior to the Posterior fontanelle

Explanation:
In ventouse (vacuum-assisted) delivery, the correct site for application of the suction cup
is known as the flexion point. This point is located:

 On the sagittal suture,


 Approximately 3 cm anterior to the posterior fontanelle (towards the face),
 And about 6 cm posterior to the anterior fontanelle (glabella),
 This corresponds to just anterior to the lambda.

Applying the cup at this precise location maximizes head flexion, allowing the smallest
possible presenting diameter — the suboccipitobregmatic diameter (9.5 cm) — to pass
through the birth canal.

Incorrect cup placement can lead to:

 Deflexion of the fetal head


 Presentation of larger diameters like occipitofrontal (11.5 cm) or mentovertical (13.5 cm)
 Increased risk of failed vacuum attempt or need for cesarean section.

References: (Williams Obstetrics, 25th Edition, DC Dutta’s Textbook of Obstetrics, 9th


Edition.)

PAEDIATRICS

46. Answer: B)- Hyperinsulinism

Explanation:
Neonatal hypoglycemia can be caused by multiple factors, but hyperinsulinism is a
common cause in neonates, especially in those with increased birth weight (macrosomia),
maternal diabetes, or low birth weight. In these cases, the infant produces excess insulin,
leading to hypoglycemia.

 Inadequate feeding is a possible cause but is less likely in the presence of severe
symptoms and low blood glucose levels.
 Neonatal infections can cause hypoglycemia but are generally associated with other signs
of infection (fever, lethargy).
 Metabolic disorders like galactosemia can also present with hypoglycemia but are rarer.

Reference: (Kliegman, RM, et al. Nelson Textbook of Pediatrics. 21st ed. Elsevier; 2020.,
American Academy of Pediatrics. Hypoglycemia in Newborns. Pediatrics, 2019.)

47. Answer: D)-All of the above

Explanation:
Routine newborn screening typically includes screening for conditions such as
phenylketonuria, cystic fibrosis, and galactosemia. These disorders can cause severe
developmental delays and other health complications if not detected and treated early.

 Phenylketonuria (PKU) is screened because it causes intellectual disability if untreated.


 Cystic fibrosis is a genetic disorder that affects the lungs and digestive system.
 Galactosemia can cause liver failure and cataracts if untreated.

Reference: (Kliegman, RM, et al. Nelson Textbook of Pediatrics. 21st ed. Elsevier; 2020.,
American Academy of Pediatrics. Newborn Screening Practices. 2021.)

48. Answer: B)- Acute chest syndrome

Explanation:
Acute chest syndrome is the leading cause of hospitalization and morbidity in children with
sickle cell disease. It is often triggered by infection, fat embolism, or pulmonary
infarction.

 Stroke is a significant risk, particularly in young children with sickle cell disease, but
acute chest syndrome is more common.
 Osteomyelitis and sepsis are also complications but occur less frequently

Sickle Cell Disease – Major Complications


Important
Complication Frequency Key Features
Values
Acute Chest Most common Fever, chest pain, SpO₂ < 92%,
Syndrome hospitalization cough, hypoxia, ↓ O₂ CXR: new
Important
Complication Frequency Key Features
Values
infiltrate, WBC ↑,
cause sat, lung infiltrates
Hb ↓
Most frequent Hb ↓ (mild), Retic
Pain Crisis Severe bone/joint pain,
complication ↑, LDH ↑,
(VOC) often in limbs or back
overall bilirubin ↑
MRI/MRA:
~11% in children infarct; TCD
Sudden neuro signs,
Stroke <20 yrs; peak at velocity >200
hemiparesis, seizures
2–5 yrs cm/s (risk
marker)
Hb ↓↓, Retic ↑,
Rapid splenomegaly,
Splenic Hypotension,
Common <5 yrs pallor, hypovolemia,
Sequestration Splenic size ↑ on
shock
USG
↑ ESR, ↑ CRP, X-
Fever, localized bone ray/USG/MRI
Osteomyelitis Less common pain, warmth, changes;
tenderness Salmonella often
grown
Occasional Sudden fatigue, pallor, Hb ↓↓, Retic ↓↓,
Aplastic Crisis (Parvovirus no Parvovirus PCR
B19) hepatosplenomegaly +
References: (Nelson Textbook of Pediatrics, 21st Ed., Ch. 467, Ghai Essential Pediatrics,
10th Ed., Ch. 11, NIH Management of Sickle Cell Disease, 2014 & 2019 updates, AAP Red
Book 2021, CDC Sickle Cell Disease Data & Guidelines.)

49. Answer: C)-Respiratory viral infections

Explanation:
Respiratory viral infections, especially those caused by respiratory syncytial virus (RSV),
rhinovirus, and influenza, are the most common triggers for asthma exacerbations in
children.

 Cold air and exercise can trigger symptoms in some children but are less common than
viral infections.
 Allergens such as dust mites or pollen are also triggers but not as frequent as viral
infections.

Reference: (American Academy of Pediatrics. Pediatric Asthma Management. ,Pediatrics.


2019., Kliegman, RM, et al. Nelson Textbook of Pediatrics. 21st ed. Elsevier; 2020.)

50. Answer: C. Antipyretics


Explanation:
Febrile seizures are common in young children, and the primary treatment is the control of
fever with antipyretics (e.g., acetaminophen or ibuprofen). Most febrile seizures do not
require anticonvulsants or intravenous fluids.

 Anticonvulsants may be needed for recurrent seizures but are not typically required for a
single episode.
 Lumbar puncture is not indicated unless there is suspicion of meningitis.

Febrile Seizure
Parameter Details
Age group 6 months – 5 years (Peak: 18–24 months)
Core temp (≥) ≥38.0°C (100.4°F) before, during, or after seizure
Seizure duration <15 min (Simple) / >15 min or recurrent (Complex)
Type of seizure Generalized tonic-clonic (most common)
Recurrence risk ~30% after 1st seizure; up to 50% if onset <1 yr
Neuro exam (post-
Normal in simple febrile seizure
ictal)
EEG/CT/MRI Not indicated in simple febrile seizures
Done only if suspect meningitis or in infants <12 months with no
CSF analysis
clear infection source
Acetaminophen (15 mg/kg) or Ibuprofen (10 mg/kg) for
Antipyretics
comfort—not proven to prevent recurrence
Not routinely used; Diazepam may be considered in
Anticonvulsants
frequent/recurrent cases

Prognosis Excellent — no increased risk of epilepsy in simple cases

References: (Nelson Textbook of Pediatrics, 21st Edition, Chapter 591: Seizures in


Childhood, Ghai Essential Pediatrics, 10th Edition, Ch. 13, AAP Guidelines: Febrile
Seizures, Pediatrics, 2018, Current Pediatric Diagnosis & Treatment, 24th Ed., Chapter on
Pediatric Neurology.)

51. Answer: A)- Erythema marginatum

Explanation:
Erythema marginatum is one of the major criteria for the diagnosis of rheumatic fever. It
is a non-pruritic, serpiginous rash with a raised border, often found on the trunk and
extremities.

 Cough and abdominal pain are nonspecific and are not diagnostic criteria for rheumatic
fever.
 Skin rashes are common but are not the hallmark of rheumatic fever.
Acute Rheumatic Fever – Diagnostic Criteria
Major Criteria Clinical Description Key Values & Notes
Tachycardia, murmurs Echo: mitral/aortic
Carditis (MR/AR), CHF, regurgitation, PR > 0.20
(clinical/subclinical) cardiomegaly, pericarditis, sec (age-adjusted), ↑
prolonged PR on ECG ESR/CRP
Migratory, painful, large joints
Polyarthritis (knees, ankles, elbows), ↑ ESR, ↑ CRP, WBC ↑
responds to salicylates
Involuntary jerky movements, May appear late (1–6
Chorea (Sydenham’s) emotional instability, worsens months) after infection; no
with stress lab abnormalities
Found on trunk and
Non-pruritic, pink macules
Erythema proximal limbs, not on
with central clearing,
Marginatum face, transient, heat-
serpiginous raised edge
sensitive
Firm, painless, mobile nodules
Subcutaneous Associated with severe
over bony prominences
Nodules carditis, rare (<5%)
(elbow, spine, tibia)

Erythema Marginatum
Feature Description
Color & Shape Pink, annular or serpiginous rash with clear center
Borders Raised, well-defined, snake-like margins
Location Trunk, proximal limbs; spares the face
Pruritus Absent (non-itchy)
Timing Transient; appears early or during active disease
Precipitating Factors May be enhanced by heat or warm bath
Significance Major Jones Criterion – although rare, very specific

References: (Nelson Textbook of Pediatrics, 21st Ed., Ch. 456 – Acute Rheumatic Fever, AHA
Guidelines: Jones Criteria 2015 Revision, Circulation, Ghai Essential Pediatrics, 10th Ed., Ch.
11 – Rheumatic Fever.)

52. Answer: A)- ΔF508

Explanation:
The ΔF508 mutation in the CFTR gene is the most common mutation associated with cystic
fibrosis. It accounts for approximately 70% of all CF cases globally.

 Other mutations like G551D, N1303K, and R117H are less common but can affect the
severity of the disease.
References: (Kliegman, RM, et al. Nelson Textbook of Pediatrics. 21st ed. Elsevier; 2020.,
Cystic Fibrosis Foundation. Genetics of Cystic Fibrosis. 2021.)

53. Answer: A)- Oral rehydration therapy

Explanation:
Oral rehydration therapy (ORT) is the first-line treatment for acute gastroenteritis in
infants, especially if the dehydration is mild to moderate. The goal is to replace lost fluids
and electrolytes.

 Intravenous fluids may be needed if the dehydration is severe or if the infant cannot
tolerate oral fluids.
 Antibiotics are not typically needed unless there is a clear bacterial infection.
 Antiemetics are not usually recommended in infants unless there is severe vomiting.

Reference: (Kliegman, RM, et al. Nelson Textbook of Pediatrics. 21st ed. Elsevier; 2020.,
World Health Organization. Management of Acute Diarrhea in Children.)

54. Answer: A)- Paint

Explanation:
The most common source of lead exposure in children is lead-based paint in homes built
before 1978. Children often ingest lead dust or chips from deteriorating paint.

 While soil, water, and imported toys can also be sources, lead-based paint remains the
most common cause.
Reference: (Kliegman, RM, et al. Nelson Textbook of Pediatrics. 21st ed. Elsevier; 2020.,
American Academy of Pediatrics. Prevention of Lead Exposure in Children.)

55. Answer: B)- Vitamin K deficiency

Explanation:
Vitamin K deficiency can lead to bleeding disorders in newborns, particularly within the
first few days of life. This deficiency results in impaired clotting factor synthesis, leading
to bleeding from mucous membranes, umbilical cord, and intracranial hemorrhage.

 Hemophilia is a genetic bleeding disorder, but it presents with more chronic bleeding.
 Immune thrombocytopenic purpura is unlikely in the first few days of life and typically
presents with purpura.
 Disseminated intravascular coagulation is an acute condition associated with severe
infections.

Reference: (Kliegman, RM, et al. Nelson Textbook of Pediatrics. 21st ed. Elsevier; 2020.,
American Academy of Pediatrics. )

56. Answer: B)- Bacterial meningitis

Explanation:
Bacterial meningitis is a life-threatening infection of the meninges, often caused by Group
B Streptococcus, Escherichia coli, or Streptococcus pneumoniae in neonates. The
symptoms in infants often include fever, vomiting, irritability, and bulging fontanelles. A
positive Brudzinski's sign indicates meningeal irritation.

Paediatric CNS Conditions


Bacterial Viral Febrile
Feature Encephalitis
Meningitis Meningitis Seizure
Acute (hours– Subacute (1–3 Sudden
Onset Acute
1 day) days) (with fever)
Neonates to 6 months–5
Age Group Infants to teens All ages
teens years
High
Fever Mild–moderate High >38°C
(>38.5°C)
↓ in severe
Consciousness Usually normal Altered Normal
cases
Single (<15
Seizures Common Rare Common
min)
May be
Focal Signs Rare Common Absent
present
100–1,000/
100–10,000/ 50–500/mm³ Normal
CSF WBC mm³
mm³ (PMNs) (Lymphs) (<5/mm³)
(Lymphs)
Bacterial Viral Febrile
Feature Encephalitis
Meningitis Meningitis Seizure
CSF Protein >100 mg/dL 50–100 mg/dL 80–150 mg/dL Normal
Normal/slightly
CSF Glucose ↓ <40 mg/dL Normal/↓ Normal

Gram Stain Often +ve Negative Negative Normal
Supportive ± IV Acyclovir, Supportive
Treatment IV antibiotics
Acyclovir ICU only
May cause
Prognosis Excellent Variable Excellent
neuro deficits

High-Yield Tip for Exam:


CSF with PMNs + low glucose = Bacterial Meningitis
CSF with lymphocytosis + normal glucose = Viral Meningitis
Seizures + altered sensorium + MRI temporal changes = Encephalitis (HSV)
Febrile seizure = no focal signs, no CSF changes, age-limited
References: (Nelson Textbook of Pediatrics, 21st Ed., OP Ghai, 10th Ed., Johns Hopkins
Pediatric Infectious Diseases, AAP Red Book, CDC Guidelines.)

57. Answer: A)- Poor diet and lack of physical activity

Explanation:
The most common cause of childhood obesity is a combination of poor diet (high calorie,
low nutrient foods) and lack of physical activity. Overweight children are more likely to
become obese adults and are at increased risk for developing type 2 diabetes, hypertension,
and cardiovascular diseases.

 Endocrine disorders such as hypothyroidism or Cushing's syndrome can cause obesity,


but these are much rarer.
 Genetic conditions and hypothalamic lesions are rare causes of obesity.

Reference: (Kliegman, RM, et al. Nelson Textbook of Pediatrics. 21st ed. Elsevier;
2020,American Academy of Pediatrics. Prevention and Management of Childhood Obesity.)

ORTHOPEDICS

58. Answer: B)- Osteoarthritis

Explanation:
This patient’s symptoms of joint pain that worsen with activity and improve with rest,
along with crepitus and limited range of motion, are highly suggestive of osteoarthritis
(OA). OA is a degenerative joint disease that primarily affects weight-bearing joints such as
the knees.
 Rheumatoid arthritis (RA) typically presents with symmetrical joint involvement and
morning stiffness.
 Gout is characterized by acute attacks of intense pain and redness in joints, usually
starting with the first metatarsophalangeal joint.
 Psoriatic arthritis is often associated with skin psoriasis and may involve both axial and
peripheral joints.
Reference: (McQueen, F., et al. Osteoarthritis: Pathophysiology and Management. Lancet
Rheumatology, 2018., Campbell, W., et al. Campbell's Operative Orthopaedics, 13th ed.
Elsevier; 2017., First Aid Usmle Step 1, 2025)

59. Answer: C. Neer classification

Explanation:
The Neer classification is the most commonly used system to classify proximal humerus
fractures. It divides the fractures into four parts based on the number of fragments and
their displacement. This classification helps guide treatment decisions.
Garden classification is used for hip fractures (femoral neck).
Salter-Harris classification is used for pediatric fractures involving the growth plate.
AO classification is a comprehensive system for long bone fractures, but Neer is
preferred specifically for the humerus.

Reference: (Neer, CS. Fractures of the Proximal Humerus. Journal of Bone and Joint
Surgery, 1970. Campbell, W., et al. Campbell's Operative Orthopaedics, 13th ed. Elsevier;
2017.)

60. Answer: D)- Inability to walk 10 steps

Explanation:
The Ottawa ankle rules help determine whether an X-ray is necessary in the evaluation of
acute ankle injuries. According to these rules, an X-ray is required if the patient has:

1. Tenderness over the posterior malleolus or navicular bone.


2. Inability to bear weight for 4 steps immediately after the injury.

 Inability to walk 10 steps is not part of the criteria for an ankle X-ray decision.
Reference: (Stiell, I.G., et al. The Ottawa Ankle Rules: Prospective Validation of a Decision
Rule for the Use of Radiography in Acute Ankle Injuries. JAMA, 1992., Campbell, W., et al.
Campbell's Operative Orthopaedics, 13th ed. Elsevier; 2017.)

61. Answer: B. Compartment syndrome

Explanation:
This patient’s severe pain, tightness in muscle compartments, and symptoms of numbness
and tingling are characteristic of compartment syndrome, a medical emergency. This
condition occurs when increased pressure within a muscle compartment compromises
blood flow and nerve function, leading to tissue damage.

 DVT presents with swelling and pain but not the tightness and numbness of
compartment syndrome.
 Acute limb ischemia presents with pain, pallor, pulselessness, and paralysis, but not the
compartmental pressure signs.
 Cellulitis presents with skin redness and warmth but not the deep tissue signs of
compartment syndrome.
Reference: (Sundaram, M., et al. Compartment Syndrome. Journal of Orthopaedic Trauma,
2018., Campbell, W., et al. Campbell's Operative Orthopaedics, 13th ed. Elsevier; 2017.)

62. Answer: B)- High-dose corticosteroids

Explanation:
For patients with acute spinal cord injury, high-dose corticosteroids (e.g.,
methylprednisolone) have been shown to improve outcomes when administered within 8
hours of injury, although the benefits are debated. The therapy is believed to help reduce
spinal cord edema and inflammation.

 Immediate surgery is not indicated unless there is structural instability or a


compressive lesion.
 Physical therapy and rehabilitation are important in long-term management but are not
the initial steps in acute care.
 Observation without intervention is inappropriate given the potential for neurological
deterioration.

Reference: (Bracken, MB., et al. Methylprednisolone or Naloxone Therapy for Acute Spinal
Cord Injury. NEJM, 2012., Campbell, W., et al. Campbell's Operative Orthopaedics, 13th ed.
Elsevier; 2017.)

63. Answer: A)- Inflammatory phase, reparative phase, remodeling phase

Explanation:
The bone healing process consists of three main stages:

1. Inflammatory phase: Begins immediately after fracture, characterized by hematoma


formation and inflammation.
2. Reparative phase: Formation of callus, bridging the fracture gap.
3. Remodeling phase: Gradual reshaping of the bone to its original form.
Reference: (Haug, E., et al. Bone Healing and Fracture Repair. Orthopedic Clinics of North
America, 2018., Campbell, W., et al. Campbell's Operative Orthopaedics, 13th ed. Elsevier;
2017.)

64. Answer: B)- Carpal tunnel syndrome

Explanation:
Carpal tunnel syndrome (CTS) results from compression of the median nerve at the wrist
and typically presents with numbness and tingling in the thumb, index, and middle
fingers. Symptoms are often worse at night.

 De Quervain's tenosynovitis causes pain on the radial side of the wrist, typically affecting
the extensor tendons.
 Tennis elbow involves pain over the lateral epicondyle and is related to overuse of the
forearm extensor muscles.
 Rheumatoid arthritis typically presents with symmetrical joint involvement and
morning stiffness.

Reference: (Padua, L., et al. Carpal Tunnel Syndrome. Lancet Neurology, 2018., Campbell,
W., et al. Campbell's Operative Orthopaedics, 13th ed. Elsevier; 2017.)

65. Answer: B)- Paget's disease of bone

Explanation:
Paget’s disease of bone is a chronic disorder that results in abnormal bone remodeling,
leading to bone pain, bone deformities, and enlargement of affected bones. The classic
cotton wool appearance on skull X-rays is characteristic of Paget’s disease.

 Osteosarcoma typically presents with pain and soft tissue mass rather than the specific
X-ray findings of Paget’s disease.
 Osteoporosis causes bone fragility but does not lead to the enlargement or deformities
seen in Paget's disease.
 Multiple myeloma presents with diffuse osteopenia, lytic lesions, and bone pain, but
does not cause the enlargement seen in Paget’s disease.

Reference: ( Roodman, GD. Paget’s Disease of Bone: Pathophysiology and Treatment.


Journal of Clinical Investigation, 2016, Campbell, W., et al. Campbell's Operative
Orthopaedics, 13th ed. Elsevier; 2017.)

66. Answer: A)- Osgood-Schlatter disease

Explanation:

Osgood-Schlatter disease is a traction apophysitis of the tibial tubercle, seen in


adolescents, especially those active in sports.
 It results from repetitive strain and microtrauma at the patellar tendon insertion during
periods of rapid growth.
 Symptoms: Anterior knee pain, worsened by running or jumping, and tender swelling
over the tibial tubercle.
 Seen commonly in boys aged 10–15 years.
 X-ray may show fragmentation or ossicle formation near tibial tubercle.

Reference: (Turek’s Orthopaedics, 7th Edition – Chapter: Pediatric Orthopaedics, Nelson


Textbook of Pediatrics, 21st Edition – Musculoskeletal Disorders, Campbell’s Operative
Orthopaedics, 14th Edition – Volume on Knee and Pediatric Orthopaedics.)

67. Answer: 4. Immobilize wrist in thumb spica cast

Explanation:

 Tenderness in the anatomical snuffbox suggests a scaphoid fracture, even if the initial
X-ray is normal.
 Scaphoid fractures are commonly missed early because the fracture line may not be
visible for up to 2 weeks.
 Untreated scaphoid fractures can lead to nonunion or avascular necrosis due to poor
blood supply (especially to the proximal pole).
 Therefore, the standard approach is immobilization in a thumb spica cast and repeat
imaging (X-ray or MRI) after 10–14 days if symptoms persist.
Reference: (Campbell’s Operative Orthopaedics, 14th Edition – Chapter: Hand and Wrist,
Turek’s Orthopaedics, 7th Edition – Wrist Injuries, Apley’s System of Orthopaedics and
Fractures, 10th Edition – Chapter: Fractures of the Upper Limb.)

EMERGENCY MEDICINE

68. Answer: D)- Perform a non-contrast CT scan of the brain

Explanation:
This patient is presenting with signs of a suspected acute ischemic stroke, as evidenced by
right-sided weakness, dysarthria, and facial drooping. The first step in the management of
suspected stroke is to perform a non-contrast CT scan of the brain to rule out a
hemorrhagic stroke. If the CT scan shows no hemorrhage, further treatment options such as
thrombolysis (IV alteplase) may be considered within the 3-hour window from symptom
onset.

 Intravenous thrombolysis (alteplase) is appropriate if the CT excludes hemorrhage and


the patient is within the therapeutic window. However, thrombolysis cannot be initiated until
the CT scan confirms no bleeding, which is why CT is the first step.
 CT angiogram may be helpful in assessing the vascular anatomy if thrombectomy is
being considered but is not the first diagnostic step.
 Oral anticoagulation is typically used in atrial fibrillation or to prevent further strokes but
is not used during the acute phase of ischemic stroke.

Reference: (Lansberg, M.G., et al. Thrombolysis for Acute Stroke. NEJM, 2015., Powers,
W.J., et al. 2015 American Heart Association/American Stroke Association Guidelines for
the Early Management of Acute Ischemic Stroke. Stroke, 2015., Tintinalli, J.E., et al.
Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9th ed. McGraw-Hill;
2020.)
69. Answer: A)-Benzodiazepines

Explanation:
This patient is experiencing symptoms of acute alcohol withdrawal. The most appropriate
treatment is benzodiazepines, which help prevent seizures and delirium tremens (DTs).
They act by enhancing GABA activity in the central nervous system to decrease withdrawal
symptoms.

 Thiamine should also be administered to prevent Wernicke-Korsakoff syndrome, but


benzodiazepines are the first-line therapy.
 Intravenous fluids may be necessary for hydration but will not address the primary cause.
 Antipsychotics may be considered for agitation or delirium but are not first-line for
alcohol withdrawal.

Reference: (Matz, M., et al. Alcohol Withdrawal: Management and Pharmacological


Approaches. Journal of Clinical Medicine, 2019., Tintinalli, J.E., et al. Tintinalli's
Emergency Medicine: A Comprehensive Study Guide, 9th ed. McGraw-Hill; 2020.)

70. Answer: B)- Acute peritonitis

Explanation:
The patient’s symptoms of sudden onset abdominal pain, rigid abdomen, and rebound
tenderness suggest acute peritonitis, which is inflammation of the peritoneal cavity. This
condition can be caused by various underlying conditions such as perforated peptic ulcer,
bowel perforation, or pelvic inflammatory disease.

 Acute appendicitis would typically present with right lower quadrant pain and may not
have generalized abdominal tenderness.
 Gastroenteritis usually presents with diarrhea and vomiting, and pancreatitis tends to
cause epigastric pain with elevated enzymes.

Reference: (Millikan, K., et al. Peritonitis: Diagnosis and Management. American Journal of
Surgery, 2017., Tintinalli, J.E., et al. Tintinalli's Emergency Medicine: A Comprehensive
Study Guide, 9th ed. McGraw-Hill; 2020.)

71. Answer: A)- IV calcium gluconate

Explanation:
The patient presents with symptoms of acute hyperkalemia (potassium >5.5 mEq/L), and
the ECG changes (tall, peaked T waves) are characteristic of hyperkalemia. The first step
in management is the administration of IV calcium gluconate to stabilize the myocardium
and prevent arrhythmias.

IV insulin and glucose are used to shift potassium into cells, but calcium gluconate is the
immediate priority.
 IV sodium bicarbonate can be used if acidosis is present, but it is not the first line for
hyperkalemia without acidosis.
 Hemodialysis may be needed for refractory cases or severe hyperkalemia but is not the
first intervention.

Reference: (Gennari, F.J., et al. Hyperkalemia: A Review. Journal of the American Society
of Nephrology, 2018., Tintinalli, J.E., et al. Tintinalli's Emergency Medicine: A
Comprehensive Study Guide, 9th ed. McGraw-Hill; 2020.)

OTOLARYNGOLOGY

72. Answer :D)- Vestibular Neuronitis

Explanation:

 Vestibular neuronitis is a peripheral disorder caused by inflammation of the vestibular


nerve.
 Presents with vertigo without hearing loss.
 Central causes include brainstem strokes (PICA), basilar migraines, MS, etc.

Exam Highlight:

 Vestibular neuronitis = peripheral


 Always rule out central signs when vertigo is atypical.

Reference:( Dhingra 8th Ed., p. 44: )

73. Answer B)- Malleus

Explanation:
Malleus is the anatomical landmark used to classify central perforations into anterior,
posterior, and inferior types. This classification is essential f or choosing the appropriate
type of tympanoplasty.

 Central perforations are seen in tubotympanic CSOM, also known as the safe type.
 It’s important to identify the site of perforation because:
o Posterior perforations often affect ossicular movement more.
o Anterior perforations are harder to access surgically.

Highlight:

 Malleus = key landmark for central perforation classification.


 Helps in tympanoplasty type decision-making.
Reference: (Logan Turner ENT , Dhingra 8th Ed., p. 79.)

74. Answer : C)- Luc Abscess

Explanation:

 Luc’s abscess is a subperiosteal mastoid abscess, often seen in children with CSOM.
 It occurs when pus breaks through the lateral wall of the mastoid into the soft tissue over
the temporal bone, pushing the pinna outward.

 It is the most common complication of mastoiditis in children.


 Bezold’s abscess – pus escapes through mastoid tip into neck.
 Zygomatic abscess – anterior spread.
 Citelli’s abscess – posterior extension into digastric groove.

Highlight:

 Luc’s abscess = postaural swelling + CSOM + pinna displaced


o Most common in children

Reference:(Dhingra 8th Ed., p. 88:, Logan Turner ENT)

75. Answer D)- Profuse mucoid discharge

Explanation:

Tubotympanic (Safe) vs. Atticoantral (Unsafe) CSOM


Feature Tubotympanic Type (Safe) Atticoantral Type (Unsafe)
Also Known As Safe type Unsafe type
Affects the anterior inferior Affects the attic (epitympanum)
Location of Disease part of the middle ear, and posterior part, especially
typically pars tensa pars flaccida
Tympanic Central perforation – Attic perforation – located in the
Membrane located in the pars tensa of pars flaccida (top portion of the
Perforation the eardrum eardrum)
Mucoid or mucopurulent – Purulent, foul-smelling due to
Discharge non-foul-smelling, often infected material and
clear to yellowish cholesteatoma
Present – cholesteatoma
Presence of
Absent – no cholesteatoma (keratinized skin cells) leads to
Cholesteatoma
bone erosion
High risk – complications like
Risk of Low risk – easily managed, bone erosion, mastoiditis, facial
Complications rare complications nerve palsy, and intracranial
infections
Feature Tubotympanic Type (Safe) Atticoantral Type (Unsafe)
Treated medically with Requires surgical intervention
antibiotics and ear drops, (e.g., modified radical
Treatment
surgery (e.g., tympanoplasty) mastoidectomy) to avoid
if needed complications

References: (Dhingra: Diseases of Ear, Nose and Throat, 8th Edition, pp. 77–78, Logan
Turner: Diseases of the Nose, Throat, and Ear, 11th Edition, pp. 148–149, Cummings:
Otolaryngology: Head and Neck Surgery, p. 658–660.)

76. Answer : C)- Fixed direction

Explanation:

Central vs. Peripheral Nystagmus


Feature Central Nystagmus Peripheral Nystagmus
Absent – Immediate onset Present – Delayed (a few
Latency of Onset
with position change seconds after movement)
Non-fatigable – Persists with Fatigable – Weakens or
Fatigability
repeated testing disappears on repetition
Direction of Multidirectional – May Unidirectional – Fast phase
Nystagmus change with gaze direction always in the same direction
Duration of
> 1 minute or persistent < 1 minute, usually brief
Nystagmus
Suppression with Not suppressed by visual
Suppressed with visual fixation
Visual Fixation fixation
Associated Often present – Ataxia, Absent – No central
Neurologic Signs diplopia, dysarthria, etc. neurological signs
Severe, often with
Severity of Vertigo Mild or absent
nausea/vomiting
Central Nervous System – Peripheral Vestibular System –
Site of Lesion
Brainstem or cerebellum Labyrinth or vestibular nerve

References: (Dhingra: Diseases of Ear, Nose and Throat, 7th Edition – pp. 88–89, Logan
Turner: Diseases of the Nose, Throat and Ear, 11th Edition – pp. 197–198, Harrison’s
Principles of Internal Medicine, 21st Edition – Ch. 455 (Adams & Victor’s Principles of
Neurology, 11th Edition – Ch. 13.)

77. Answer: D)- Closure of oval window

Explanation:
Conductive hearing loss (CHL) arises when sound conduction from the outer ear to the
cochlea is disrupted. Among the listed conditions, closure of the oval window( e.g.,
otosclerosis, tympanosclerosis ) results in the maximum average hearing loss due to
complete blockade of mechanical sound energy entering the inner ear. Also described as
“Third window pathology

Condition Average Hearing Loss


Closure of oval window ~60 dB (Maximum CHL)
Ossicular interruption with perforation ~45–50 dB
Ossicular discontinuity with intact drum ~30–40 dB
Complete obstruction of canal (e.g., wax/cotton) ~25–30 dB
Loose cotton in EAC ~10–15 dB

Highlights:

 Conductive hearing loss ≥60 dB is rarely exceeded—indicates oval window pathology.


 Obstruction (wax/cotton) causes mild CHL—important clinical differential.
 Audiometry helps differentiate outer/middle ear lesions.

References: (Dhingra, Diseases of ENT, 8th Ed. – p. 34–35, Logan Turner, Diseases of the
Nose, Throat and Ear, 11th Ed. – CHL ,Cummings Otolaryngology – Head and Neck
Surgery, 7th Ed., Vol. 4 – Evaluation of Hearing Loss ,K.J. Lee’s Essential Otolaryngology,
11th Ed. – External Ear & Hearing chapter.)

78. Answer: D)- Carcinoma of the vocal cord


Explanation:

The clinical picture is classic for early-stage glottic carcinoma, commonly seen in middle-
aged male smokers. The main symptoms include:

Persistent hoarseness >2 weeks(often the only early symptom)


Unilateral vocal cord lesion
Impaired mobility or fixation of vocal cord due to tumor invasion of intrinsic muscles
or cricoarytenoid joint

Diagnostic Importance:

 Glottic carcinoma arises from the true vocal cords, usually from the anterior 2/3, and
presents early because of voice change.
 Early glottic cancers (T1–T2) do not typically present with lymphadenopathy due to
limited lymphatic drainage of the glottis.

Cord Malignant
Condition Laterality Appearance Cause/Association Common in
Mobility Potential
Vocal Smooth,
Usually Voice
Cord translucent, Voice overuse Normal None
unilateral professionals
Polyp pedunculated
Reinke’s Bilateral Gelatinous Chronic voice Middle-aged Normal None
Edema swelling of abuse, smoking women
Cord Malignant
Condition Laterality Appearance Cause/Association Common in
Mobility Potential
cords (fluid in
Reinke’s
space)
Small nodules
Vocal at junction of
Bilateral, Chronic Teachers,
Cord anterior 1/3 Normal None
symmetric phonotrauma singers
Nodules and posterior
2/3

High-Yield Points:

Hoarseness >2 weeks in smokers = Laryngeal carcinoma until proven otherwise


True vocal cords have sparse lymphatic supply → late nodal spread
Most common site of laryngeal cancer = Glottis
Early symptom = Hoarseness; Late symptoms = Stridor, dysphagia, pain, weight loss
Best diagnostic test = Direct laryngoscopy with biopsy

References: (Dhingra, 8th Edition – Page 249–252, Cummings Otolaryngology, 6th Ed –


Vol. 3, Laryngeal Tumors, Pg. 1502–1512, Scott-Brown’s Otorhinolaryngology, 8th Ed –
Volume 2, Chapter: Laryngeal Carcinoma ,Bailey & Love’s Short Practice of Surgery, 27th
Ed – Head & Neck section.)

79. Answer: B)- Anterior ethmoidal

Explanation:

 Agger nasi = most anterior ethmoidal air cell


 Important in frontal sinus drainage pathway.
 Obstruction can lead to frontal sinusitis.

Exam Highlight:

 Agger nasi = key landmark in FESS


 Drains into middle meatus

Reference: (Dhingra 8th Ed., p. 212)

80. Answer C)- Nasal obstruction

Explanation:

 Used to test for nasal valve collapse.


 Patient breathes in; examiner pulls cheek laterally.
 If breathing improves = positive Cottle’s test

Exam Highlight:

 Cottle’s test = nasal valve competency


 Helps decide on septoplasty or spreader graft

Reference:(Dhingra 8th Ed., p. 169.)

OPHTHALMOLOGY

81. Answer D)- Tear secretion

Explanation:

 The Schirmer I Test is used to measure total tear secretion, including both basal and
reflex components.
 A Whatman filter paper (5x35 mm) is folded at 5 mm and placed in the lower fornix at
the junction of lateral 1/3 and medial 2/3 of the eyelid.
 The patient keeps eyes open and avoids blinking. After 5 minutes, the length of wetted
paper is measured.

Interpretation:

 >15 mm = Normal
 5–10 mm = Mild to moderate dry eye
 <5 mm = Severe dry eye / Sjögren’s syndrome

Exam Highlight:

 Schirmer I without anesthesia = total tear secretion


 Used in KCS, Sjögren's, ocular cicatricial pemphigoid

Reference:: (Khurana, 6th Ed., p. 389–390, Parson's Diseases of the Eye, 22nd Ed.)

82. Answer D)- Patient with corneal thickness of 400 µm

Explanation:

 LASIK eligibility requires:


o Age >20 years
o Stable refraction for ≥12 months
o Absence of corneal ectasia, scars, infections
o Minimum corneal thickness >450 µm
A cornea <450 µm is contraindicated due to risk of ectasia, flap complications, and poor
healing.

LASIK Eligibility and Contraindications

Category Details

Eligibility Criteria

Minimum Age ≥18 years (ideal: 20+ years)


Stable Refraction No significant change for ≥12 months

Refractive Errors Myopia (up to -10 D)Hypermetropia (up to +4


D)Astigmatism (up to ±5 D)

Corneal Health Clear cornea with no ectasia (e.g., keratoconus), scars, or


infections

Corneal Thickness Minimum >480 µm preferred<450 µm = absolute


contraindication
- No active ocular disease- No pregnancy/lactation- No
Other Criteria
collagen vascular/autoimmune diseases

Absolute Contraindications
Keratoconus / Corneal ectasia High risk of progression post-LASIK
Severe dry eye Poor healing, worsened symptoms
Autoimmune / Connective
e.g., SLE, RA — impaired healing
tissue disease
Active Herpetic eye disease Risk of reactivation and complications
Pregnancy / Lactation Hormonal changes affect corneal shape
Corneal thickness <450 µm Risk of ectasia, flap complications
Alternatives to LASIK (for thin cornea or contraindications): PRK – No flap; better for thin
corneas and ICL (Implantable Collamer Lens) – For high refractive errors or corneal
limitations

Reference:: (Khurana, 6th Ed., p. 53, Kanski Clinical Ophthalmology, 9th Ed.)

83. Answer B)- Geniculate body

Explanation:

Visual pathway:
o 1st-order: Photoreceptors → bipolar cells
o 2nd-order: Bipolar → retinal ganglion cells
o 3rd-order: Lateral geniculate body (LGN) → optic radiations to visual cortex
 Lesions in LGN result in contralateral homonymous hemianopia.

Reference:: (Khurana, 6th Ed., p. 312, Snell's Clinical Neuroanatomy)

84. Answer A)- Gatifloxacin

Explanation:

 Gatifloxacin and Moxifloxacin are fourth-gen fluoroquinolones.


 They act on both DNA gyrase and topoisomerase IV.
 Have broad Gram +ve and –ve coverage, ideal for bacterial keratitis.

Exam Highlight:

 Gatifloxacin = MCQ favorite for eye infections


 Fourth-gen = dual action (DNA gyrase + topo IV)

Reference:: Khurana, 6th Ed., p. 446, Kanski, Clinical Ophthalmology.)

85. Answer A)- Granulomatous uveitis


Explanation:

 Mutton-fat KPs are large, waxy, greasy-looking deposits on the endothelium of cornea.
 Composed of epithelioid cells and macrophages
 Classic in granulomatous anterior uveitis (e.g., TB, sarcoidosis, VKH).

Exam Highlight:

 Granulomatous uveitis = mutton-fat KPs


 Nongranulomatous = fine KPs

Reference:: (Khurana, 6th Ed., p. 154, Parson’s, Intraocular Inflammation chapter.)

86. Answer D)-Inferonasal

Explanation:

 Typical colobomas result from incomplete closure of the embryonic fissure, which is
located inferonasally.
 Atypical colobomas can occur in other locations but are rare.

Exam Highlight: Colobomas always occur inferonasally if typical.

Reference: (Khurana, 6th Ed., p. 149, Parson’s, Congenital Eye Anomalies.)

87. Answer D)- Body

Explanation:

 Pterygium parts:
o Head: Apex on cornea
o Neck: Transition zone at limbus
o Body: On sclera (between limbus and canthus)
o Cap: Semilunar area just anterior to head

Exam Highlight:

 Body = scleral part


 Cap = seen just before head

Reference:: (Khurana, 6th Ed., p. 88)

ANESTHESIA
88. Answer: B)- Compound A production and nephrotoxicity

Explanation:

 Sevoflurane reacts with dry soda lime and baralyme to form Compound A, which is
nephrotoxic.
 It is dose- and flow-dependent, so low-flow systems increase risk.
 This reaction can lead to renal tubular injury, especially in animal studies.

Exam Highlight:
Avoid low-flow anesthesia with Sevoflurane.
Use fresh soda lime and higher flows to prevent toxic compound buildup.

References: (Ajay Yadav, p.94, Morgan & Mikhail’s Clinical Anesthesiology, 6th
ed ,Miller’s Anesthesia, 9th ed.)

89. Answer: B)- 3.0 – 3.5 mm

Explanation:

 For infants <1 year, usually we don’t use formulas but follow general size ranges.
 A 2-month-old should typically have a 3.0 – 3.5 mm uncuffed tube.
 Always prepare one size smaller and larger than expected.

Exam Highlight:
ETT formula for children ≥1 year: (Age/4) + 4
References: (Ajay Yadav, p.38, Nelson Pediatrics, 21st ed, APLS Guidelines.)

90. Answer: B)- Pancuronium

Explanation:

 In ICU tetanus management, a long-acting non-depolarizing muscle relaxant is


preferred.
 Pancuronium provides prolonged control and is cardiac stable.
 Succinylcholine is contraindicated due to risk of hyperkalemia.

Exam Highlight:
Avoid depolarizing agents like suxamethonium in tetanus.
Use long-acting relaxants like Pancuronium for spasm control.
Muscle Relaxants in Tetanus

Use in Extra Key


Drug Type Duration Onset
Tetanus Points
Long-acting,
vagolytic →
Non- 60–100
Pancuronium 2–3 min Preferred ↑HR; renal
depolarizing min
excretion

Hofmann
elimination →
Non- 30–40 organ-safe;
Atracurium 2–3 min
depolarizing min mild histamine
release

Fasciculations,
5–10 min risk of
Succinylcholine Depolarizing (ultra- 30–60 sec Avoid hyperkalemia,
short) bradycardia

Fast onset; good


Non- 30–40 1–1.5 intubation drug;
Rocuronium Alternative
depolarizing min min reversed with
sugammadex

References: (K.D. Tripathi – Essentials of Medical Pharmacology, 8th Ed, Goodman &
Gilman’s – Pharmacological Basis of Therapeutics, 13th Ed, Morgan & Mikhail – Clinical
Anesthesiology, Katzung – Basic & Clinical Pharmacology.)

91. Answer: A)- Edmund Boyle

Explanation:

 Boyle’s machine was introduced by Edmund Boyle in 1917.


 It's a continuous flow system for administering gases and anesthetic vapors.
 Still forms the basis of modern anesthesia workstations.

Exam Highlight:
Boyle = Continuous flow machine, foundational to modern anesthesia practice.

References: (Ajay Yadav, p.15, Morgan & Mikhail.)

92. Answer: B)- Heliox

Explanation:
 Heliox = Helium + Oxygen
 Color code: Black body, brown & white shoulder
 Used in obstructive airway diseases to reduce airway resistance.

Exam Highlight:
Heliox reduces airway resistance due to low density.

References: (Ajay Yadav, p.18, KDT Pharmacology ,Morgan & Mikhail)

93. Answer: B)- Epidural anesthesia

Explanation:

 Epidural anesthesia causes sympathetic block → vasodilation → decreased venous


return → ↓ CVP.
 Other conditions (tamponade, fluid overload) increase CVP.

Exam Highlight:
CVP decreases = hypovolemia, vasodilation (spinal/epidural), hemorrhage.
Normal CVP = 3–10 cm H₂O

References: (Ajay Yadav, p.58–59, Miller’s Anesthesia ,Harrison’s Internal Medicine.)

94. Answer: D)- 24 hours

Explanation:

 Dextran, a colloid, expands plasma volume and has a 24-hour half-life.


 Used for hypovolemia, but risk of anaphylaxis and coagulopathy exists.

Exam Highlight:
Dextran = Long half-life (24 hrs), not first-line fluid resuscitation.

References: (Ajay Yadav, Morgan & Mikhail, KDT Pharmacology)

PYSCHIATRY

95. Answer: C)- High thyroxine levels

Explanation:

This is a classical presentation of rapid cycling bipolar disorder, defined as ≥4


episodes/year.
 It's more common in females, Bipolar II subtype, thyroid dysfunction, and those on
antidepressants, especially tricyclics.
 The correct association is hypothyroidism, not hyperthyroidism (i.e., high thyroxine
levels).

Tricyclics and SSRIs may destabilize mood, triggering rapid switches.

Important for Exams:

 Always assess thyroid profile in rapid cyclers.


 Consider lithium and valproate for mood stabilization.
 Avoid TCAs unless carefully monitored.

References: (Ahuja Psychiatry, 7th ed, p.74, Kaplan & Sadock’s Comprehensive Textbook,
11th ed, DSM-5, p.130–135.)

96. Answer: A)- Amok

Explanation:

 Amok is a culture-bound syndrome, mainly in Southeast Asia, characterized by


unprovoked sudden aggression followed by amnesia and fatigue.
 It may be linked to underlying psychosis, depression, or dissociation.
 Considered a dissociative disorder in ICD-10.

References: (Ahuja, p.111, ICD-10, F44.89, Kaplan & Sadock, 11th ed.)

97. Answer: C)- Psychogenic vomiting


Explanation:

 Psychogenic vomiting is seen in conversion disorders or anxiety-related disorders.


 Vomiting occurs without nausea, retching, or physical causes, and may be attention-
seeking or stress-related.
 Bulimia has body image concerns + binge-purge cycles.
 In contrast, this case lacks body image disturbance or food binges.

Important for Exams: Absence of physical findings + vomiting = psychogenic etiology.

References: (Ahuja, p.145, Kaplan & Sadock, 11th ed, Oxford Textbook of Psychiatry,
p.412.)

98. Answer: A)- Bipolar I

Explanation:

 Bipolar I disorder involves at least one manic episode, which may or may not be
followed by depression.
 Bipolar II requires hypomania + major depression.
 Bipolar III and IV are unofficial variants or research terms.

Important for Exams: Mania without depression = Bipolar I

References: (DSM-5, p.126, Ahuja, p.72, Kaplan, 11th ed.)


99. Answer: B)- Alexithymia

Explanation:

 Alexithymia is the inability to identify or describe feelings. Common in psychosomatic


disorders, PTSD, depression, and some personality disorders.
 Ambivalence: coexistence of opposing impulses.
 Ambitendency: hesitation between opposing actions.

Important for Exams:


Alexithymia is often seen in somatizing patients or those with flat affect.

References: (Ahuja, p.246, Kaplan, 11th ed)

100. Answer: D)- Logoclonia

Explanation:

 Logoclonia is a speech disorder characterized by repetition of the final syllables of


words, typically seen in patients with neurodegenerative conditions, especially
Parkinson’s disease dementia and Alzheimer’s disease.
o In this case, the patient repeats the final syllables “tic tic tic” after saying “fantastic,” which
is typical of logoclonia.
 Alogia refers to poverty of speech or content and is commonly seen in schizophrenia or
other psychiatric disorders with negative symptoms. It does not involve repetition.
 Dysarthria is a motor speech disorder caused by impaired movement of the muscles
used for speech, often due to neurologic injury or disease (e.g., stroke, Parkinsonism). It
causes slurred or slow speech, not syllable repetition.
 Echolalia is the meaningless repetition of another person’s spoken words, typically
seen in autism spectrum disorders, catatonia, or schizophrenia. The repetition in this
case is self-generated syllables, not someone else’s words.

Reference: (Adams and Victor’s Principles of Neurology, 11th Edition, Chapter 26 – The
Dementias, pp. 1238–1240. ,Kaplan and Sadock’s Synopsis of Psychiatry, 12th Edition.)

101. Answer: C)- Awareness that leads to behavioral change

Explanation:

 Emotional insight means understanding your condition in a deep, emotional, and


motivational way that leads to behavioral improvement.
 This contrasts with intellectual insight, where the patient may understand their illness but
fail to act accordingly.
Important for Exams:
Emotional insight → good prognosis in psychotherapy.
Used to assess readiness for change.

References: (Ahuja, p.15, Kaplan, p.78)

RADIOLOGY

102. Answer: C) Crazy paving pattern

Explanation:
Pulmonary Alveolar Proteinosis (PAP) is a rare lung disorder caused by the accumulation of
proteinaceous material within the alveoli. On High-Resolution CT (HRCT), the classic
finding is the “crazy paving” pattern, which is a combination of ground-glass opacities
and interlobular septal thickening, giving an appearance similar to irregular stone paving.
While this pattern is highly suggestive of PAP, it can also be seen in conditions like:

 Acute Respiratory Distress Syndrome (ARDS)


 Pneumocystis pneumonia
 Lipoid pneumonia
 Bronchioloalveolar carcinoma
Common Causes Less Common Causes
Pulmonary edema (most common) Drug-induced pneumonitis
Pulmonary alveolar proteinosis
Radiation pneumonitis
(PAP)
Acute respiratory distress syndrome
Pulmonary hemorrhage / Diffuse pulmonary hemorrhage
(ARDS)
Bacterial pneumonia Acute interstitial pneumonia (ARDS of unknown etiology)
Pneumocystis jirovecii pneumonia
Goodpasture syndrome
(PCP)
Tuberculosis Chronic eosinophilic pneumonia
Usual interstitial pneumonia (UIP) with superimposed
Mycoplasma pneumonia
diffuse alveolar damage
Obstructive pneumonia
Pulmonary infections (various
etiologies)

References: (Grainger & Allison, 6th ed, Vol 2, p.355, Sutton’s Radiology, 7th ed,
Radiopaedia:, Harrison’s Internal Medicine, 21st ed.)

103. Answer: C)- Plain MRI

Explanation:

 Plain (non-contrast) MRI is the gold standard for evaluating intracapsular silicone
implant rupture.
 Key MRI signs:
o Linguine sign: Wavy collapsed shell inside silicone (intracapsular rupture).
o Snowstorm appearance: Extracapsular rupture.
 Ultrasound has lower sensitivity and operator dependence; CT lacks soft tissue contrast.

MRI with contrast is only needed if you are also evaluating for malignancy, not just rupture.

Key Exam Points:

 MRI > US > CT in silicone implant evaluation.


 No contrast needed for rupture diagnosis.

References: (Grainger & Allison, Vol 4, p.1682, Radiopaedia: "Silicone breast implant
rupture", Breast Imaging Reporting and Data System (BI-RADS).)

104. Answer: A)-Renal TB (Putty kidney)

Explanation:
 Putty kidney is a radiological term used for end-stage renal tuberculosis, where the
kidney becomes shrunken, non-functioning, and completely calcified.
 Seen in chronic untreated renal tuberculosis, especially in immunocompromised or late-
diagnosed cases.
 Calcifications may be lobar, linear, or amorphous, with a classic putty-like appearance
on X-ray or CT.

Differentials like RCC or XGP will show mass or asymmetry, not a uniformly shrunken and
calcified kidney.

Key Exam Points:

 Putty kidney = End-stage TB


 Common in TB-endemic areas
 Confirmed with CT and urinary AFB if needed

References: (Grainger & Allison, Vol 3, p.852, Radiopaedia: “Putty kidney”, Sutton
Radiology, 7th ed.)

105. Answer: A)- Bochdalek hernia

Explanation:

 Anterior mediastinal masses classically include the 4 Ts:


o Thymoma
o Teratoma
o Thyroid goiter
o Terrible lymphoma
 Bochdalek hernia is a posterolateral diaphragmatic hernia, more common on the left,
presenting in neonates and in contrast, Morgagni hernia is anterior diaphragmatic, and
thus may present as an anterior mass.
Key Exam Point:
Bochdalek = posterior
Morgagni = anterior → may mimic anterior mediastinal mass

Reference:: (Grainger & Allison, Vol 2, p.1799, Sutton Radiology, p.375)

106. Answer: C)- Submucosal thickening

Explanation:

 “Thumbprinting” refers to rounded, thickened mucosal folds seen in colon loops,


especially the ascending colon.
 Seen in:
o Ischemic colitis
o Infective colitis
o Inflammatory bowel disease
 Represents edema or hemorrhage in the submucosa, mimicking thumb imprints.

Key Exam Point: Thumbprinting + pain + bloody diarrhea → suspect ischemia

Reference:: (Grainger & Allison, p.603, Radiopaedia: "Colonic thumbprinting")

107. Answer: A)- CTPA

Explanation:

 CT Pulmonary Angiography (CTPA) is the current gold standard for diagnosing acute
PE.( Sensitivity: ~83%; Specificity: ~96%)
 Visualizes filling defects in the pulmonary arteries.
 D-dimer is sensitive but non-specific; used to rule out PE in low-risk patients.

CTPA Findings in Pulmonary Embolism


Category CTPA Finding Explanation / Description
Classic sign of PE – appears as
Intraluminal filling
Direct Signs central/layered clot surrounded by contrast
defect
(polo mint sign).
Cut-off of pulmonary Abrupt end of contrast column due to
artery embolus blocking vessel.
Embolus at bifurcation of main pulmonary
Saddle embolus
artery into left and right branches.
Indirect Wedge-shaped peripheral opacity
Pulmonary infarct
Signs (Hampton’s hump).
Decreased vascular markings (Westermark
Regional oligemia
sign).
Often small; nonspecific but commonly
Pleural effusion
seen.
Collapse or volume loss in lung areas distal
Atelectasis
to embolus.
Elevated hemidiaphragm Due to adjacent atelectasis or infarction.
Right Heart RV dilation (RV/LV
Suggests increased RV afterload due to PE.
Strain ratio > 1)
Interventricular septum bulges into LV –
Septal bowing
marker of RV pressure overload.
Contrast reflux into
Indicates elevated right atrial pressure.
IVC/hepatic veins
Areas of alternating increased and decreased
Other Mosaic perfusion pattern
attenuation due to variable perfusion.
Subsegmental filling
Seen in smaller arteries – may be subtle.
defects
References: ( Harrison’s Internal Medicine, 21st Ed, Ch. 246., Grainger & Allison’s Diagnostic
Radiology., Felson’s Principles of Chest Roentgenology, 4th Ed., Radiopaedia – Pulmonary
Embolism.)

108. Answer: B)- Esophageal varices

Explanation:

 On barium swallow, varices appear as serpiginous, longitudinal filling defects.


 Seen in portal hypertension, often in cirrhotic patients.
 Can mimic other mucosal irregularities but distinguished by appearance and clinical
context.

Reference::( Grainger, Vol 2, p.472 , Radiopaedia: “Esophageal varices”)

109. Answer: C)- Ultrasound abdomen


Explanation:

 Ultrasound is safe, quick, and non-invasive.


 Shows:
o Pyloric muscle thickness >3 mm
o Channel length >15 mm
 HPS = non-bilious projectile vomiting in infants ~3–6 weeks of age.

References: (Bailey & Love, 27th ed, p.128 ,Radiopaedia: “Pyloric stenosis”)

110. Answer:A)- Interstitial edema

Explanation:

 Kerley B lines = short horizontal lines at the lung periphery, especially lung bases.
 Caused by interlobular septal thickening, usually due to pulmonary edema, CHF.

Feature Kerley A Lines Kerley B Lines Kerley C Lines


Central → upper lobes Peripheral lower
Location Diffuse/lower lungs
(from hilum) zones (esp. bases)
Length 2–6 cm 1–2 cm Short, reticular
Horizontal,
Orientation Oblique perpendicular to Mesh-like
pleura
Deep lymphatics/septa Interlobular septal Superimposed septal
Cause
thickened thickening lines
Feature Kerley A Lines Kerley B Lines Kerley C Lines
Seen in advanced Classic in cardiogenic Suggests widespread
Clinical Use
interstitial edema pulmonary edema interstitial disease

Reference:: Grainger, p.166 ,Sutton Radiology, Felson’s Principles of Chest Roentgenology,


3rd ed. , Grainger & Allison’s Diagnostic Radiology, 6th ed.)

DERMATOLOGY

111. Answer: A) Streptococcal infection

Explanation:
Erythema nodosum (EN) is an inflammatory condition characterized by painful, red
nodules typically on the shins. The most common cause of erythema nodosum is
streptococcal infection, particularly following a throat infection caused by Group A
Streptococcus. Other causes can include Mycoplasma pneumoniae, sarcoidosis, and
tuberculosis, but streptococcal infection remains the most prevalent trigger.

Key Points:

 Streptococcal infection is the most common trigger for erythema nodosum.


 Erythema nodosum is often associated with other systemic conditions like sarcoidosis
and tuberculosis, but they are less common triggers.
 Mycoplasma pneumoniae can also cause EN, particularly in children, but it is secondary
to streptococcal infections.

References: (Fitzpatrick's Dermatology in General Medicine, 9th Edition, p. 2487, Rook's


Textbook of Dermatology, 9th Edition, p. 1631.)

112. Answer: C)- Herpes Simplex Virus (HSV)

Explanation:
The most common cause of recurrent erythema multiforme (EM) is Herpes Simplex Virus
(HSV), particularly HSV-1. Recurrent outbreaks of HSV can trigger EM, especially when
the virus affects the skin or mucosal areas.

In EM minor, lesions typically affect the skin and sometimes the lips. EM major (EMM)
involves mucosal involvement, which distinguishes it from the minor form. The typical
presentation includes target lesions, which are pathognomonic for EM.

 Target lesions are a distinctive feature and are often used to identify the condition.
 Antiviral therapy, such as acyclovir, can reduce the frequency of recurrences by
controlling HSV outbreaks.
 Although Mycoplasma pneumoniae can also trigger EM, especially in children, HSV
remains the primary cause of recurrent EM, particularly in adults.

Key Points:

 HSV (especially HSV-1) is the most common cause of recurrent erythema multiforme.
 Target lesions are characteristic of EM.
 Antiviral prophylaxis reduces recurrence by managing HSV outbreaks.
 Mycoplasma pneumoniae is associated more with children than with adults.

References: (Fitzpatrick's Dermatology in General Medicine, 9th Edition, p. 72 , Bolognia's


Dermatology, 4th Edition, p. 1150.)

113. Answer: B)-Topical clotrimazole

Explanation:
The first-line treatment for tinea corporis (ringworm), a superficial fungal infection caused
by dermatophytes, is topical antifungal agents such as clotrimazole, miconazole, or
terbinafine. These are highly effective in treating localized infections and have minimal side
effects.

Key Points:

 Topical clotrimazole is the first-line treatment for localized tinea corporis.


 Oral antifungals (e.g., terbinafine or fluconazole) are used for extensive or refractory
cases, but topical agents are preferred for localized infections.
 Topical hydrocortisone is contraindicated as it can worsen fungal infections by
suppressing local immunity.

References: (Fitzpatrick's Dermatology in General Medicine, 9th Edition, p. 2331,


Bolognia’s Dermatology, 4th Edition, p. 740.)

114. Answer: C) X-linked ichthyosis

Explanation:
The most likely diagnosis in this case is X-linked ichthyosis. This is a genetic disorder that
typically presents with dry, rough skin and large, dark brown scales, usually seen on the
trunk and neck while sparing the face and palms. The presence of a maternal uncle with
similar skin suggests an X-linked inheritance pattern, which is characteristic of X-linked
ichthyosis.

 X-linked ichthyosis results from mutations in the steroid sulfatase gene (STS), leading to
a deficiency of the enzyme steroid sulfatase, which is responsible for breaking down
cholesterol sulfate in the skin. The accumulation of cholesterol sulfate leads to scaling.
 Ichthyosis vulgaris typically presents with smaller, fine scales over the extremities,
especially in the flexural areas, and is often associated with dry skin. It is more common in
both males and females and does not typically follow the X-linked inheritance pattern.
 Lamellar ichthyosis is a more severe form of ichthyosis, presenting with thick, large
scales covering the entire body from birth, including the face and palms. It is usually
associated with a more generalized presentation and is not typically sparing the face and
palms.
 Atopic dermatitis presents with itchy, red, inflamed skin (often involving the flexures,
like the elbows and knees), but it does not present with the same type of thick, brown scales
seen in X-linked ichthyosis. The scaling in atopic dermatitis is not as prominent or thick.

References: (Fitzpatrick's Dermatology in General Medicine, 9th Edition, p. 2717,


Bolognia's Dermatology, 4th Edition, p. 1934.)

115. Answer C)- Lower back and sacrum

Explanation:
Mongolian spots are congenital dermal melanocytosis.
Seen at sacrum/lumbosacral region, usually fade by early childhood.

Key Points:

 Blue-grey macules.
 Benign.
 Can be extensive in metabolic disorders like mucopolysaccharidosis.

Reference:: Fitzpatrick’s Dermatology, 9th Ed., p. 1357

116. Answer C)- 30 days

Explanation:
In healthy skin, the normal process of skin cell migration from the basal layer (the deepest
layer of the epidermis) to the cornified layer (the outermost layer) takes about 30 days. This
process, known as epidermal turnover, ensures the constant renewal of the skin's outermost
layer, which is essential for protecting the body from environmental damage.

In psoriasis, a chronic inflammatory skin condition, the turnover rate is significantly


accelerated. Typically, psoriatic skin turnover occurs in about 3-5 days rather than the
normal 30-day period. This rapid turnover leads to the formation of thick, scaly plaques, a
hallmark of psoriasis. The excessive production of skin cells and their premature shedding
results in the formation of plaques and inflammation.

Retinoids help reduce keratinocyte proliferation and promote the differentiation of skin
cells, thus slowing down the excessive skin cell turnover and improving the skin's
appearance.
Additionally, hyperkeratosis, which is the thickening of the skin, is a common feature of
psoriasis and other disorders of epidermal turnover. The retinoids and other treatment
options aim to restore normal keratinocyte function, improving the skin barrier function
and reducing inflammation.

Key Points:

 Basal keratinocytes in healthy skin take about 30 days to migrate to the cornified layer.
 In psoriasis, this migration process is sped up to 3-5 days, contributing to the development
of plaques and scaling.
 Retinoids help normalize rapid skin turnover by slowing down keratinocyte
proliferation and promoting differentiation.

References: (Rook’s Dermatology, 9th Edition, Dermatology: A Practical Approach, by N.


L. Draelos, 3rd Edition, p. 77, Fitzpatrick's Dermatology in General Medicine, 9th Edition,
p. 1036, Bolognia's Dermatology, 4th Edition, p. 1236.)

117. Answer C)- Fixed drug eruption

Explanation:

 Well-demarcated, dusky red lesions at same site after drug intake = Fixed Drug
Eruption (FDE).
 Trigger: NSAIDs, sulfonamides, tetracyclines.
 Lesions heal with hyperpigmentation and recur at same location with re-exposure to the
drug.

Key Features Comparison


Stevens-
Erythema
Fixed Drug Johnson
Feature Multiforme Urticaria
Eruption (FDE) Syndrome
(EM)
(SJS)
Drugs (NSAIDs, Infections Drugs
Foods, drugs,
Trigger sulfonamides, (HSV) or (sulfonamides,
infections
tetracyclines) drugs NSAIDs)
30 min – 8 hrs after 1–2 days after 1–3 weeks after Minutes to
Onset
drug infection/drug drug hours
Well-demarcated, Blisters + Wheals,
Target lesions
Lesion dusky red, same site necrosis, raised, pale
(3 zones)
recurrent widespread center
Anywhere,
Common Extremities, Mucosal sites,
Lips, genitals, hands moves
Sites face eyes, trunk
quickly
Mucosal Possible (lip, genital Severe, multiple
Rare Rare
Involvement ulcers) sites
Stevens-
Erythema
Fixed Drug Johnson
Feature Multiforme Urticaria
Eruption (FDE) Syndrome
(EM)
(SJS)
No
Postinflammatory Heals with no Scarring
Healing pigmentation
hyperpigmentation pigmentation possible
change
Same site with same Rare if drug Yes, but not
Recurrence Not site-fixed
drug avoided site-specific

References: (Fitzpatrick’s Dermatology, 9th Ed., Bolognia Dermatology, 4th Ed., Rook’s
Textbook of Dermatology, 9th Ed.)

118. Answer C)- Paraneoplastic pemphigus

Explanation:

Erythema
Bullous
Paraneoplastic Pemphigus Multiforme
Feature Pemphigoid
Pemphigus (PNP) Vulgaris (PV) Major
(BP)
(EMM)
Post-
Malignancy (esp.
Idiopathic, Idiopathic, infection
Trigger NHL, CLL,
autoimmune elderly (HSV) or
Castleman)
drugs
Severe painful
Common (flaccid
Oral Lesions stomatitis, crusting Rare Present
mucosal erosions)
lips
Polymorphic: Tense
bullae, Flaccid bullae, bullae, Target
Skin Lesions
erosions, EM- erosions urticarial lesions
like, lichenoid base
Against
None
desmoplakin,
BP180, (immune
Autoantibodies envoplakin, Desmoglein 1 & 3
BP230 complex–
periplakin,
mediated)
BP230
IgG/C3 in Linear
IgG in intercellular Usually
DIF intercellular IgG/C3 at
spaces ("fishnet") negative
& BM zone BMZ
Key Hint Cancer + Flaccid bullae + oral Elderly + HSV history
desmoplakin erosions tense bullae + targetoid
antibody + lesions
Erythema
Bullous
Paraneoplastic Pemphigus Multiforme
Feature Pemphigoid
Pemphigus (PNP) Vulgaris (PV) Major
(BP)
(EMM)
polymorphic
mucocutaneou
s lesions
Poor, often Good with
Good with Usually self-
Prognosis resistant to immunosuppressant
steroids limited
treatment s

Key Point:

Painful mucosal erosions + polymorphic skin lesions + IgG against desmoplakin in


lymphoma = Paraneoplastic pemphigus.

References:(Fitzpatrick’s Dermatology, 9th Edition – Chapter: Paraneoplastic Autoimmune


Multiorgan Syndrome (PAMS), Harrison’s Principles of Internal Medicine, 21st Edition,
Bolognia: Dermatology, 4th Edition – Immunobullous Diseases.)

ANATOMY

119. Answer B)- Domes pulled inferiorly

Explanation:

 During inspiration, the diaphragm contracts and flattens, pulling the central tendon
downward.
 This increases thoracic volume, creates negative pressure, and draws air into lungs.
 Flattening of the diaphragm (seen in COPD/emphysema) reduces efficiency of inspiration.

Key Points:

 Domes pulled downward


 Thoracic volume increases
 Air enters lungs passively due to pressure gradient
Refer
ence:: (Moore’s Anatomy, Physiology of Respiration)

120. Answer B)- Right hepatic artery

Explanation:

 The cystic artery supplies the gallbladder and usually arises from the right hepatic
artery.
 It is located in the Calot’s triangle bounded by the cystic duct, common hepatic duct, and
inferior liver edge.
 Knowledge of this anatomy is critical to avoid bleeding during gallbladder surgery.

Key Points:

 Branch of right hepatic artery


 Lies in Calot’s triangle
 Must be clipped before cholecystectomy
Reference:: (Gray’s Anatomy, Bailey & Love)

121. Ans: B)- Cervix size = uterus at puberty

Explanation:

 In children, the cervix is relatively longer than the body (ratio 2:1).
 At puberty, body length increases, and the uterus becomes longer than the cervix (ratio
~1:2).
 The uterine artery crosses lateral to cervix, an important surgical landmark.
 Lymph drainage:
o Cervix → internal/external iliac, sacral
o Fundus → para-aortic

Key Points:

Cervix is NOT same size as uterus at puberty


Uterine artery crosses above ureter (“water under the bridge”)
Reference: ( Moore’s Anatomy, Shaw’s Gynecology.)

122. Answer: C)- Right ventricle

Explanation:

 The bulbus cordis contributes to the formation of the right ventricle and the outflow
tracts (conus arteriosus and aortic vestibule).
 The primitive ventricle gives rise to the left ventricle, while the primitive atrium forms
parts of both atria.
Reference: (Moore (9th Ed, Ch. 13) and AK Dutta (Ch. 5), First Aid Step 1 2025)

123. Answer: B)- Facial nerve

Explanation:

 The second pharyngeal arch gives rise to the muscles of facial expression and is
innervated by the facial nerve (CN VII).
 Facial asymmetry and drooping indicate dysfunction in these muscles, pointing to CN VII.
R
eference: (Moore (9th Ed, Ch. 10) and AK Dutta (Ch. 9), Rahul Bangla ENT Book.)

124. Ans: D)- Suction of diaphragm

Explanation:

 The liver is held in position by:


o Coronary & falciform ligaments (peritoneal folds)
o Hepatic veins anchoring it to IVC
o Intra-abdominal pressure
 Diaphragmatic suction is a myth, not a real stabilizer of the liver.

Key Points:

 Suction of diaphragm ≠ liver support


 Hepatic veins = strong anchoring

Reference: (A.K. Dutta, Gray’s Anatomy)

125. Ans: D)- Right renal vein is shorter

Explanation:

 Right renal vein is shorter and drains directly into IVC


 Left renal vein crosses in front of aorta, beneath SMA
 Renal arteries originate from abdominal aorta, not iliac
 Renal vein entrapment (nutcracker syndrome) can occur on left side

Key Points:

 Left renal vein: longer, crosses aorta anteriorly


 Artery from abdominal aorta, not internal iliac

Reference : (BDC Vol 2, Gray’s Anatomy)

126. Answer D)- Apical

Explanation:

 The apical group of axillary lymph nodes lies at the apex of the axilla, medial to the
axillary vein and superior to pectoralis minor.
 It receives drainage from all other axillary groups (anterior, posterior, lateral, and central
nodes).
 These nodes also communicate with the supraclavicular nodes and may form a pathway
for metastasis to systemic circulation.

Key Points:

 Apical = terminal group in axilla


 Receives lymph from all other groups
 Clinically important in breast cancer staging (level III nodes)

A) Three surgical levels of axillary lymph nodes, relative to the pectoralis minor muscle
(Pm). (B) Five groups of axillary lymph nodes. Level I contain 3 main groups of axillary
nodes: 1. Anterior (pectoral) 2. Posterior (subscapular) 3. Lateral (brachial), Level II
contains the 4. Central (and interpectoral nodes) and Level III contains the Apical
(Infraclavicular) nodes (5).

Reference:: (BDC Vol 1, Gray’s Anatomy, [Link] )


127. Ans: C)- L5

Explanation:

 The trans-tubercular plane runs horizontally through the iliac tubercles and crosses L5
vertebra.
 It is one of the horizontal planes used to divide the abdomen into 9 regions (with subcostal
and interspinous planes).

Key Points:

 L5 level, passes through iliac tubercles


 Used in 9-region abdominal division

 Reference: Moore’s Clinical Anatomy

128. Ans: D)- Brachiocephalic trunk

Explanation:

 The right subclavian artery arises from the brachiocephalic trunk, while the left
subclavian arises directly from aortic arch.
 Important during central line insertion or thoracic surgeries.

Key Points:
 Right: brachiocephalic trunk
 Left: aortic arch

Reference: (Moore’s Anatomy, Vascular and Interventional Radiology (Second Edition),


Philadelphia: W.B. Saunders, pp. 182–203.)

PHYSIOLOGY

129. Answer A)- Slow oxidative

Explanation:

 Type I fibers are slow-twitch, fatigue-resistant, and use aerobic metabolism.


 Contain high myoglobin and mitochondria → red color
 Important for endurance activities
 Low ATPase activity, small diameter
Reference:: (Ganong 25th Ed., p.108, Khan Academy Physiology)

130. Answer D)- Norepinephrine acts as NT in periphery and neuromodulator in CNS

Explanation:

Norepinephrine (NE) serves as a neurotransmitter (NT) in the peripheral nervous


system (PNS), specifically within the sympathetic nervous system (SNS). In the periphery,
NE is involved in the fight-or-flight response, regulating essential functions such as heart
rate, blood pressure, and vasoconstriction. It activates alpha- and beta-adrenergic
receptors to elicit these physiological changes.

In contrast, within the central nervous system (CNS), NE acts primarily as a


neuromodulator rather than a traditional neurotransmitter. In this context, NE does not
directly trigger action potentials but modulates the strength and efficacy of synaptic
transmission, influencing processes like mood, attention, and arousal. This neuromodulatory
role is important for regulating alertness and emotional responses.

In addition to NE, neurotransmitters can be categorized into two types:

 Small molecules: These include classical neurotransmitters like acetylcholine (ACh),


dopamine, and glycine, which play direct roles in synaptic transmission.
 Larger molecules (neuropeptides): These include substance P, vasopressin, and other
neuropeptides, which primarily function as neuromodulators influencing broader neural
processes.

Key Features of Norepinephrine:

 Acts as a neurotransmitter in the sympathetic nervous system (SNS).


 Functions as a neuromodulator in the central nervous system (CNS), modulating mood,
attention, and arousal.

References: Ganong's Review of Medical Physiology, 25th Edition, p. 147-148, Guyton &
Hall's Textbook of Medical Physiology, 13th Edition, p. 292, Harrison's Principles of
Internal Medicine, 21st Edition, p. 2409 ,Cecil Medicine, 25th Edition, p. 1047.)

131. Answer: B)- Saturation of glucose transporters in the proximal tubule

Explanation:

 Glucose is freely filtered at the glomerulus but completely reabsorbed in the proximal
tubule by SGLT transporters, up to a threshold (~180 mg/dL).
 At plasma glucose >180–200 mg/dL, transporters get saturated → glucosuria results.
 This patient’s plasma glucose = 180 mg/dL, at threshold → likely just enough to
saturate some transporters.

Important Points:

 Glucosuria occurs only when transport maximum (Tm) is exceeded


 GFR is normal (creatinine clearance = 110 mL/min) → rules out ↓GFR
 No structural barrier defect is needed for glucose leakage
 Glucose is not secreted, only filtered and reabsorbed
Reference: Guyton & Hall, 14th ed., p. 326–327, Ganong’s Physiology, 26th ed., p. 661,
First Aid 2024)
132. Answer: D)- 1.7 mmol/L (~30 mg/dL)
Explanation :

CNS Effects of Hypoglycemia


Plasma Glucose
Effect on CNS Symptoms
(mmol/L)
Counterregulatory hormone Tremor, sweating, tachycardia
3.3 – 3.9
release begins (adrenergic)
Early neuroglycopenic Irritability, confusion, blurred
2.5 – 3.3
symptoms vision
Severe neuroglycopenia → Unconsciousness, seizures, brain
< 1.7
coma, seizures injury if prolonged

Key Points:

 Brain cannot store glucose and depends on plasma glucose


 Hypoglycemia first triggers autonomic symptoms → later CNS symptoms
 Coma usually occurs < 1.7 mmol/L, equivalent to ~30 mg/dL
 Treatment: IV dextrose or glucagon ASAP to prevent brain damage

References: Ganong’s Review of Medical Physiology, 25th ed., p. 439,Guyton and Hall,
14th ed., Ch. 76 (Pancreatic hormones),Harrison’s Principles of Internal Medicine, 21st ed.,
Vol. 2, Ch. 417.)
133. Answer: C)- RQ = 0.8, protein
Explanation:
 RQ = CO₂ produced / O₂ consumed = 200 / 250 = 0.8
 RQ of 0.8 indicates protein or mixed substrate metabolism
 Key values:
o 1.0 → Carbs
o 0.7 → Fats
o 0.8 → Proteins
o >1.0 → Anaerobic state

Highlight:
RQ = VCO₂ / VO₂ → reflects fuel type used for energy
Used in ICU, exercise testing, and nutrition planning.

Respiratory Quotient (RQ) – Summary


RQ Clinical/Physiological
Substrate Metabolic Insight
Value Examples
Equal CO₂ produced and After high-carb meals, early
Carbohydrate 1.0
O₂ consumed exercise
Less CO₂ produced per
O₂ consumed due to Fasting state, prolonged
Fat 0.7
higher oxygen exercise, low-carb diet
requirement
Intermediate; depends on
Protein ~0.8 amino acid deamination Starvation, high-protein diet
and urea formation
Most normal individuals
~0.82–
Mixed Diet consuming balanced Resting state in healthy adults
0.85
diets fall here
Indicates buffering of
>1.0 lactic acid → excess Intense exercise, early sepsis,
>1.0
(Anaerobic) CO₂ generation (via anaerobic threshold reached
HCO₃⁻ buffering)
Clinical Applications:

 RQ is measured in indirect calorimetry (ICU nutrition, metabolic rate assessments)


 RER (Respiratory Exchange Ratio) ≈ RQ during steady-state conditions
 RER > 1.0 → often seen during anaerobic exercise, hyperventilation, or lactic acidosis
 VO₂ and VCO₂ are used to calculate energy expenditure and fuel utilization

References: Guyton and Hall Textbook of Medical Physiology, 14th ed., p. 854–855,
Ganong’s Review of Medical Physiology, 26th ed., p. 661, ACSM’s Resource Manual for
Guidelines for Exercise Testing and Prescription, 10th ed., Ch. 7, Murray & Nadel's
Textbook of Respiratory Medicine, 7th ed., Vol. 1, p. 125–128 (Gas exchange).)

134. Answer C)- Jejunum > ileum > colon > feces
Explanation:
Approximate
Water
Region Details Water Absorbed
Absorption
(mL/day)
The jejunum is the primary site for
water absorption. It absorbs water
Most water
Jejunum through osmosis, driven by active 3,000–4,000 mL
absorbed
transport of electrolytes like
sodium.
The ileum absorbs the remaining
Secondary water, though less than the
Ileum 1,500–2,000 mL
absorption jejunum. It also absorbs bile salts
and vitamin B12.
The colon absorbs a smaller
Minimal volume of water and electrolytes
Colon 1,400–1,500 mL
absorption from undigested food, forming
solid stool.
Feces contain minimal water,
Very little usually around 100–200 mL per
Feces 100–200 mL
water day, as the majority has been
absorbed by the intestines.

References: (Ganong's Review of Medical Physiology, 25th Edition, p. 464, Guyton & Hall's
Textbook of Medical Physiology, 13th Edition, p. 907, Harrison's Principles of Internal
Medicine, 21st Edition, p. 2641, Cecil Medicine, 25th Edition, p. 305.)

135. Answer C)- SGLT-1

Explanation:

Transporter Function Location Clinical Relevance


Glucose + Na⁺ co- Mutation → Glucose-
Small intestine
SGLT-1 transport into Galactose Malabsorption,
(apical side)
enterocytes osmotic diarrhea
Deficiency: Fanconi–Bickel
Facilitated diffusion of Basolateral
GLUT-2 syndrome (not osmotic
glucose/fructose membrane
diarrhea)
Proximal
Na⁺-glucose Inhibited by SGLT2
SGLT-2 tubule of
reabsorption inhibitors in diabetes
kidney
Fructose transporter Small intestine Fructose malabsorption (not
GLUT-5
(facilitated diffusion) (apical) glucose)

Clinical Highlight:

 SGLT-1 is sodium-dependent, located on the apical surface of enterocytes


 Its dysfunction leads to osmotic diarrhea due to malabsorbed glucose and galactose
 Symptoms improve with IV feeding, confirming enteric transport defect

References: (Ganong’s Review of Medical Physiology, 25th ed., p. 433, Guyton and Hall,
14th ed., Ch. 65, Harper’s Illustrated Biochemistry, 31st ed., Ch. 21.)

136. Answer B)- CSF absorption rate

Explanation:

CSF is produced at a constant rate (~500 mL/day) by choroid plexus.


CSF is absorbed via arachnoid villi into dural venous sinuses.
CSF pressure is not regulated by how much is formed, but by how much is absorbed.
oAbsorption is pressure-dependent: ↑ ICP → ↑ absorption
In conditions like communicating hydrocephalus, absorption is impaired, leading to ↑
CSF pressure.

CSF Formation vs. Absorption


Feature CSF Formation CSF Absorption
Choroid plexus (mainly in lateral Arachnoid villi → superior
Site
ventricles) sagittal sinus
Rate ~20 mL/hr (~500 mL/day) Passive, pressure-dependent
Variable, main regulator of CSF
Regulation Minimal, relatively constant
pressure
Clinical Overproduction rare (e.g., Impairment → ↑ ICP
Relevance papilloma) (hydrocephalus)

References: Ganong’s Review of Medical Physiology, 25th ed., p. 603,Guyton and Hall,
14th ed., p. 758, Snell's Clinical Neuroanatomy, 8th ed., p. 510, Nolte’s Neuroanatomy, 8th
ed., Ch. 12.)

PATHOLOGY

137. Answer: D) G2

Explanation:

Drugs that inhibit microtubule polymerization (like vinca alkaloids) or depolymerization


(like taxanes) block cells in M phase, where mitotic spindle assembly is crucial.

However, tubulin, the protein that forms microtubules, is primarily synthesized during the
G2 phase of the cell cycle. This phase prepares the cell for mitosis by synthesizing key
proteins like tubulin needed for spindle formation.
Cell Cycle Phases & Key Events
Phase Key Activities Chemotherapy Targets
Resting phase (non-dividing
G0 Not targeted by most chemotherapeutics
cells)
Cell growth, organelle
G1 Some drugs like steroids may act here
duplication
S DNA replication Antimetabolites (e.g., methotrexate, 5-FU)
Protein synthesis (e.g., Vinca alkaloids & taxanes act in M phase
G2
tubulin), pre-mitotic prep but rely on G2 tubulin
Mitosis (spindle formation,
M Mitotic inhibitors (vinca alkaloids, taxanes)
chromosome separation)

References: K.D. Tripathi, Essentials of Medical Pharmacology, 7th Ed, Pg 857–860,


Robbins & Cotran Pathologic Basis of Disease, 10th Ed – Chapter on Cell Growth &
Neoplasia, Lehninger Principles of Biochemistry, 7th Ed – Cell cycle regulation.

138. Correct Answer: B) Hemangioma

Explanation:

 Hemangiomas are benign tumors of blood vessel endothelium, commonly seen in skin,
mucosa, and liver.
 Capillary hemangioma is most common in children (e.g., "strawberry hemangioma") and
often regresses with age.
 Cavernous hemangiomas are larger, can involve brain/liver.
 Kaposi sarcoma (HHV-8) and angiosarcoma are malignant.

Exam Point:

 Hemangioma = most common benign vascular neoplasm


 Angiosarcoma = malignant, aggressive
 Kaposi = intermediate, seen in immunosuppressed (AIDS)

Reference: (Robbins Basic Pathology, 10th Ed, Pg 396, Goljan Rapid Review Pathology, 5th
Ed, Pg 58.)

139. Answer: A)-t(15;17)

Explanation:

Acute Promyelocytic Leukemia (APL), a subtype of acute myeloid leukemia (AML), is


primarily characterized by the t(15;17) translocation. This translocation leads to the
formation of a PML-RARα fusion gene that plays a central role in the pathophysiology of
APL.
 PML-RARα Fusion Protein:
The PML gene on chromosome 15 and the RARα gene on chromosome 17 fuse, resulting in
the production of the PML-RARα fusion protein. This fusion protein acts as a
transcriptional repressor, preventing the differentiation of promyelocytes into mature
myeloid cells. The block in differentiation is a hallmark of APL, leading to the accumulation
of undifferentiated promyelocytes in the bone marrow and peripheral blood.
 Targeted Treatment with ATRA:
All-trans retinoic acid (ATRA), a derivative of vitamin A, has a specific therapeutic role
in APL due to its ability to target the PML-RARα fusion protein. ATRA binds to the
RARα domain of the fusion protein, inducing conformational changes that allow the
release of transcriptional repression. This results in the differentiation of promyelocytes
into mature granulocytes. ATRA therapy has dramatically improved the prognosis of APL,
making it one of the most curable forms of leukemia when treated appropriately.
 Cytogenetic and Clinical Implications:
The presence of the t(15;17) translocation is diagnostic of APL and correlates with a
favorable prognosis when treated with ATRA and chemotherapy. This contrasts with
other forms of AML, which may not respond as well to ATRA.
 Other Genetic Abnormalities:
o t(8;21): Associated with a different subtype of AML, AML with maturation, and
typically has a better prognosis but is not responsive to ATRA.
o inv(16): Typically seen in AML with monocytic differentiation, associated with a
relatively good prognosis but also does not respond to ATRA.
o t(9;22) (Philadelphia chromosome): This is characteristic of chronic myelogenous
leukemia (CML) and some forms of AML, but does not involve the PML-RARα fusion
protein and is treated with tyrosine kinase inhibitors (e.g., imatinib), not ATRA.

Reference: Harrison’s Principles of Internal Medicine, 21st Ed, Pg, Williams Hematology,
10th Ed, Chapter on Acute Myeloid Leukemia , Mendelsohn's Principles of Cancer Therapy,
8th Ed, Chapter on Leukemias.

140. Answer: C)-Alkalosis

Explanation:

This patient presents with respiratory alkalosis, a condition commonly seen in panic
attacks due to hyperventilation. Respiratory alkalosis leads to a series of compensatory
changes in the body, one of which is hypokalemia.

 Mechanism of Hypokalemia in Alkalosis: In respiratory alkalosis, the increase in pH


(alkalosis) causes shifting of potassium from the extracellular space into cells. This
happens as a result of the body's attempts to maintain electrical neutrality during alkalosis.
The alkalotic state increases the activity of the Na+/K+ ATPase pump, which drives
potassium into the cells, causing hypokalemia in the blood.
 Why the Other Options Are Incorrect:
o Vomiting: Vomiting typically causes hypokalemia due to loss of potassium in gastric
contents. However, this patient has no signs of vomiting or diarrhea, making this option
unlikely.
o Glucosuria: Glucosuria typically occurs in diabetes mellitus or other conditions causing
renal glucose loss, but it is not associated with alkalosis or hypokalemia in this context.
o Laxative abuse: Laxative abuse leads to electrolyte imbalances due to diarrhea, which
causes hypokalemia. However, this patient has no signs of diarrhea, so this option is also
unlikely.

Reference: (Harrison’s Principles of Internal Medicine, 21st Ed, Pg 1563, Kumar & Clark's
Clinical Medicine, 9th Ed, Pg 1189.)

141. Answer: B) 10%

Explanation:

In adults, acute hepatitis B infection progresses to chronic hepatitis B in approximately 5–


10% of cases.
The risk of developing chronic infection is heavily dependent on the age at the time of
infection and the immune status of the individual.

 In newborns (neonates) infected at birth, the risk of chronicity is extremely high, with
over 90% developing chronic infection.
 In children aged 1–5 years, about 20–30% progress to chronic hepatitis.
 In healthy adults, only 5–10% of infections become chronic.
 Individuals who are immunocompromised have a significantly higher chance of
developing chronic hepatitis, even if infected later in life.

The immune response plays a major role: a strong immune system clears the virus
effectively, whereas an immature or weakened immune system fails to do so, leading to
chronic infection.

Points to Remember:

Adults: ~5–10% risk of chronic hepatitis B.


Children (1–5 years): 20–30% risk.
Neonates: >90% risk.
Stronger immune response = less risk of chronicity.
Weaker or immature immune response (newborns, immunocompromised) = higher
chronicity.

References: Harrison’s Principles of Internal Medicine, 21st Edition, Sleisenger and


Fordtran’s Gastrointestinal and Liver Disease, 11th Edition, CDC Hepatitis B Guidelines.

142. Answer: D)- Obesity


Explanation:
Macroglossia (enlarged tongue) is associated with conditions causing tissue infiltration or
growth, such as:

 Amyloidosis: protein deposition


 Acromegaly: GH excess → tissue overgrowth
 MEN IIb: neural hyperplasia
 Myxedema: mucopolysaccharide accumulation

Obesity may make the tongue appear large but does not cause true pathological
enlargement.

True macroglossia = infiltrative or growth disorders, not simple obesity.

Reference: Goljan Pathology, Pg 469

143. Answer: C)- Type III hypersensitivity

Explanation :

Type III
Type IV
Type I (IgE Type II (Immune
Key Point (Delayed-
mediated) (Cytotoxic) Complex-
Type)
mediated)
Antigen- T-cell
Antibodies
antibody mediated
IgE antibodies (IgG, IgM)
complexes immune
bind to mast bind to cell
form, deposit response. T-
cells and surface
in tissues, and helper cells
basophils, antigens,
Mechanism activate (CD4) activate
triggering activating
complement, macrophages,
histamine complement
causing leading to
release and and causing
inflammation inflammation
inflammation. cell lysis or
and tissue and tissue
phagocytosis.
damage. injury.
Examples Anaphylaxis, Hemolytic Arthus Contact
Type III
Type IV
Type I (IgE Type II (Immune
Key Point (Delayed-
mediated) (Cytotoxic) Complex-
Type)
mediated)
anemia,
reaction,
Goodpasture dermatitis,
allergic serum
syndrome, tuberculin
rhinitis, sickness,
Graves' test, graft
asthma, lupus,
disease, rejection,
urticaria. rheumatoid
myasthenia poison ivy.
arthritis.
gravis.
Antibodies CD4+ T-cells,
Immune Mast cells, Neutrophils,
(IgG, IgM), macrophages,
Cells basophils, complement,
complement, cytotoxic T-
Involved eosinophils. macrophages.
phagocytes. cells (CD8).
Symptoms like Delayed
Rapid onset of
Symptoms of inflammation, symptoms (24-
symptoms like
tissue pain, swelling 72 hours), skin
hives,
destruction at the injection rash,
Clinical swelling,
(e.g., site (e.g., induration
Features airway
hemolysis, Arthus (e.g., contact
constriction
kidney reaction), or dermatitis,
(e.g.,
damage). systemic tuberculin
anaphylaxis).
disease. test).
Immune
T-cell
complex
activation and
IgE-mediated, Cell damage deposition
macrophage
rapid onset, caused by leads to
recruitment,
Key often triggered antibodies inflammation
leading to
Characteristics by allergens binding to cell and necrosis.
chronic
(e.g., pollen, surface Arthus
inflammation
food). antigens. reaction is a
and tissue
classic
injury.
example.
4–10 hours
Minutes to
Minutes to after antigen 24-72 hours
Onset of hours after
hours after exposure (e.g., after antigen
Symptoms exposure to
exposure. vaccine exposure.
the antigen.
booster).
References: (Robbins Basic Pathology, 10th Ed, Pg 135, Harrison's Principles of Internal
Medicine, 21st Ed, Pg 1635, Kumar & Clark's Clinical Medicine, 9th Ed, Pg 1153, Basic
Immunology, 6th Ed, Pg 184.)

144. Answer: C)-Both


Explanation:

Helicobacter pylori infection is associated with two significant complications:

1. Gastric Adenocarcinoma:
o H. pylori is a Class I carcinogen, and long-standing infection can lead to gastric
adenocarcinoma through mechanisms like intestinal metaplasia (a process where gastric
epithelium transforms into a form resembling intestinal epithelium), dysplasia, and chronic
inflammation.
o This is a well-established risk factor for the development of gastric cancer.
2. MALT Lymphoma:
o Chronic H. pylori infection leads to chronic B-cell stimulation within the mucosa-
associated lymphoid tissue (MALT), which can eventually result in the development of
MALT lymphoma.
o Interestingly, this lymphoma is often reversible with eradication therapy targeting H.
pylori, demonstrating that the infection is a direct contributor to the malignancy.

Key Points:

 H. pylori is associated with gastric adenocarcinoma through chronic gastritis, intestinal


metaplasia, and dysplasia.
 MALT lymphoma is linked to chronic B-cell activation due to prolonged H. pylori
infection.
 Both conditions are part of the known sequelae of chronic H. pylori infection, highlighting
the importance of timely eradication therapy to reduce these risks.

References: (Harrison's Principles of Internal Medicine, 21st Ed, Pg 1272-1275:, Robbins


Basic Pathology, 10th Ed, Pg 804:, Kumar & Clark's Clinical Medicine, 9th Ed, Pg 987-
988:)

PHARMACOLOGY

145. Answer: D) Respiratory depression

Explanation:

Fentanyl is a highly potent synthetic opioid analgesic, approximately 80–100 times more
potent than morphine, and acts mainly on mu (μ)-opioid receptors in the central nervous
system.

It is commonly used for severe pain and chronic cancer pain, often via transdermal
patches for sustained delivery. It is also used IV in anesthesia and ICU settings due to its
rapid onset.

Most Dangerous Adverse Effect: Respiratory Depression


 Mechanism: Fentanyl causes dose-dependent respiratory depression by suppressing
the medullary respiratory centers' sensitivity to carbon dioxide (CO₂).
 This is the most serious and life-threatening side effect, especially in: (Opioid-naïve
patients, using long-acting preparations like patches (drug accumulation risk), Patients on
concurrent CNS depressants (e.g., benzodiazepines, alcohol).

Important Points for Exams:

 Unlike morphine, fentanyl causes minimal histamine release, so hypotension and


pruritus are less frequent.
 Chest wall rigidity (a rare but notable adverse effect of rapid IV fentanyl) can impair
ventilation and make intubation difficult — known as "wooden chest syndrome".
 Fentanyl has no ceiling effect for respiratory depression — as dose increases, risk
increases proportionally.
 Naloxone is the antidote for fentanyl toxicity, but higher or repeated doses may be
needed due to fentanyl’s potency and possible long duration (especially in patches).
 Respiratory depression may be delayed in onset with transdermal systems — monitor
patients closely for 24–72 hours.

References: (K.D. Tripathi, Essentials of Medical Pharmacology, 7th Ed, Pg 382, 384, Rang
& Dale’s Pharmacology, 9th Ed, Pg 286–288 –Goodman & Gilman’s The Pharmacological
Basis of Therapeutics, 13th Ed, Pg 259–262 –, Harrison’s Principles of Internal Medicine,
21st Ed, Vol 2, Pg 2742 .)

146. Answer: D) Palonosetron

Explanation:

Cisplatin is a highly emetogenic chemotherapy agent that induces both acute (within 24
hrs) and delayed (after 24 hrs, especially on day 2–5) phases of chemotherapy-induced
nausea and vomiting (CINV).

All 5-HT₃ antagonists (like ondansetron, granisetron, dolasetron) are effective against
acute emesis, but their efficacy in delayed-phase CINV is limited.

Why Palonosetron is Best for Delayed Vomiting:

 Palonosetron is a second-generation 5-HT₃ antagonist with:


o High receptor affinity
o Long half-life (~40 hours)
o Allosteric binding and receptor internalization, giving it prolonged action even beyond
48–72 hours.
 It is particularly effective for delayed CINV, especially when combined with NK1
antagonists (e.g., aprepitant) and corticosteroids.

Important Exam Points:


 Ondansetron, granisetron, and dolasetron are more effective for acute-phase CINV
(first 24 hours).
 Palonosetron is the only 5-HT₃ antagonist FDA-approved for delayed nausea and
vomiting due to its unique properties.
 It is given as a single IV dose before chemotherapy and maintains effect for several days.
 It is part of the triplet regimen for highly emetogenic chemotherapy:
Palonosetron + Dexamethasone + NK1 antagonist (e.g., aprepitant/fosaprepitant).

References: (K.D. Tripathi, Essentials of Medical Pharmacology, 7th Ed, Pg 115–116,


Goodman & Gilman’s Pharmacological Basis of Therapeutics, 13th Ed, Pg 1057–1059,
Harrison’s Principles of Internal Medicine, 21st Ed, Vol 2, Pg 542–543, NCCN Guidelines,
Antiemesis, 2023.)

147. Answer: C) Carmustine

Explanation:

Carmustine is a nitrosourea alkylating agent used in the treatment of high-grade gliomas,


including glioblastoma multiforme, because it can cross the blood-brain barrier (BBB)
effectively.

A hallmark toxicity of carmustine is its delayed-onset myelosuppression, with the nadir in


blood counts typically seen 4–6 weeks after administration. This delayed toxicity profile
helps differentiate it from other agents causing earlier marrow suppression.

Chemotherapeutic Agents and Myelosuppression


Onset of
CNS
Marrow
Drug Main Use Penetratio Key Toxicity
Suppressio
n
n
Myelosuppressio
Glioblastoma
Crosses Delayed (4– n (delayed),
Carmustine , CNS
BBB 6 weeks) pulmonary
tumors
fibrosis
Lymphomas, Myelosuppressio
Early (7–10
Vinblastine testicular Poor n (early),
days)
cancer neurotoxicity
Testicular, Nephrotoxicity,
Cisplatin ovarian, Minimal Mild/early ototoxicity,
bladder CA neurotoxicity
Hemorrhagic
Breast CA,
Cyclophosphamid Early (7–14 cystitis,
lymphoma, Poor
e days) myelosuppressio
leukemia
n
References: (K.D. Tripathi, Essentials of Medical Pharmacology, 7th Ed, Pg 862–864,
Goodman & Gilman’s Pharmacological Basis of Therapeutics, 13th Ed, Pg 1130–1131,
Harrison’s Principles of Internal Medicine, 21st Ed, Vol 1, Pg 522. DeVita, Hellman, and
Rosenberg’s Cancer: Principles & Practice of Oncology, 11th Ed.)

148. Answer: A) Have no CNS effects


Explanation:

Neuromuscular blocking agents (NMBAs) are used to produce muscle paralysis during
surgical procedures, rapid sequence intubation, and mechanical ventilation. These agents act
at the nicotinic acetylcholine receptors at the neuromuscular junction.

They do not cross the blood-brain barrier because of their quaternary ammonium
structure, making them highly polar. Therefore, they do not produce any central nervous
system effects such as sedation, analgesia, or altered consciousness.

Table: Neuromuscular Blocking Agents


Feature Details
CNS penetration None (do not cross BBB)
Effect on voluntary muscles Cause flaccid paralysis
Route of administration IV/IM only (not effective orally)
Use in spasticity Not used (centrally acting agents are preferred)
Examples Succinylcholine, Rocuronium, Vecuronium
Clinical uses Anesthesia, rapid intubation, mechanical ventilation

References:( K.D. Tripathi, Essentials of Medical Pharmacology, 7th Ed, Pg 122–


125,Goodman & Gilman, 13th Ed, Pg 266–268, Harrison’s Internal Medicine, 21st Ed –
Neuromuscular pharmacology.)

149. Answer: C) Hofmann elimination

Explanation:
Atracurium undergoes organ-independent metabolism by Hofmann elimination, a
spontaneous chemical breakdown in plasma at physiological pH and temperature. It does not
rely on renal or hepatic function for elimination, making it ideal for patients with renal or
hepatic impairment. Its metabolite laudanosine may accumulate but is generally not toxic at
clinical doses.

Neuromuscular Blocking Agents: Metabolism and Use in Organ Dysfunction


Use in
Excretio Use in Renal Special
Drug Metabolism Hepatic
n Failure Notes
Failure
Atracurium Hofmann elimination Minimal Safe Safe Produces
& ester hydrolysis renal laudanosi
Use in
Excretio Use in Renal Special
Drug Metabolism Hepatic
n Failure Notes
Failure
ne (risk of
seizures in
high
doses)
Less
Safer than laudanosin
Hofmann Minimal
Cisatracurium atracuriu Safe e→
elimination renal
m preferred
in ICU
Prolonged
Renal& Cautio action in
Vecuronium Hepatic metabolism Accumulates
biliary n liver/kidne
y failure
Fast onset;
Biliary ± used for
Use with
Rocuronium Hepatic metabolism some Caution rapid-
caution
renal sequence
intubation
May cause
Mainly
Pancuronium Hepatic metabolism Avoid Avoid tachycardia
renal
(vagolytic)
Not Risk of
Plasma
Succinyl(Depolrizi organ hyperkalemia,
pseudocholinester Safe (usually) Safe
ng) dependen malignant
ase
t hyperthermia
References: (K.D. Tripathi, Essentials of Medical Pharmacology, 8th Ed., Ch. 18, Morgan &
Mikhail's Clinical Anesthesiology, 6th Ed., Ch. 11, Goodman & Gilman's, 13th Ed.,
Neuromuscular Junction chapter, Harrison’s Principles of Internal Medicine, 21st Ed., ICU
Management Section.)

150. Answer: B) Ergotamine

Explanation:

Most α-adrenergic blockers cause vasodilation by inhibiting α₁ receptors on vascular


smooth muscle. However:

Ergotamine:

 Is not a pure alpha-blocker.


 It is an ergot alkaloid with:
o Partial agonist and antagonist actions at multiple receptors:
 5-HT₁/₂ (serotonin receptors)
 α-adrenergic receptors
 Dopamine receptors
 Despite weak α-blockade, it stimulates vascular smooth muscle, mainly through
serotonergic and direct vasoconstrictor effects → leading to vasoconstriction.

This makes ergotamine unique among these options — it causes vasoconstriction rather
than vasodilation, especially in cranial vessels, which is why it's used to abort migraine
attacks.

Effect on
Drug Mechanism
Vessels
Phenoxybenzamine Vasodilation Irreversible non-selective α-blocker
Prazosin Vasodilation Selective α₁-blocker
Non-selective α-blocker with histamine-
Tolazoline Vasodilation
like activity

References: (K.D. Tripathi, Essentials of Medical Pharmacology, 8th Ed., Pages 137–143,
Goodman & Gilman’s, 13th Ed., Rang & Dale’s Pharmacology, 9th Ed.)

151. Answer: A) ↓ K⁺ concentration

Explanation:

Captopril is an angiotensin-converting enzyme (ACE) inhibitor that:

 Inhibits conversion of Angiotensin I to Angiotensin II


 ↓ Angiotensin II → ↓ Aldosterone secretion
 ↓ Aldosterone → ↓ Na⁺ reabsorption, ↑ K⁺ retention

Result: ↑ serum K⁺ (hyperkalemia) is a known side effect, especially in renal impairment

Other Important Adverse Effects of Captopril:


Adverse Effect Mechanism / Notes
Hyperkalemia ↓ Aldosterone-mediated K⁺ excretion
Proteinuria Common in patients with underlying renal disease
Dry Cough Due to accumulation of bradykinin
Angioedema Bradykinin-mediated, potentially life-threatening
Neutropenia / Agranulocytosis Rare, more likely in collagen vascular diseases
Taste disturbances, rash Less common, reversible
References: (K.D. Tripathi, Essentials of Medical Pharmacology, 8th Edition, Pages 500–502,
Rang & Dale’s Pharmacology, 9th Edition,, Harrison’s Principles of Internal Medicine, 21st
Edition, Volume 2 , BNF and NICE Guidelines.)
152. Answer: A) Heparin

Explanation:

Heparin is a large, negatively charged molecule that does not cross the placenta, making it
safe in pregnancy for anticoagulation. All others (warfarin, etc.) are oral anticoagulants, cross
the placenta and can cause fetal bleeding and malformations.

Comparison of Anticoagulants in Pregnancy


Placental Pregnancy Preferred in Important
Drug Fetal Risk
Transfer Safety Pregnancy Notes
Requires aPTT
monitoring;
risk of
osteoporosis
(UFH) No Safe None Yes
and
thrombocytope
nia with long-
term use
Predictable
pharmacokineti
cs; less
(LMWH) No Safe None Yes monitoring
needed;
preferred over
UFH
Teratogenic
(nasal May be used
hypoplasia, only in selected
Unsafe (esp. stippled high-risk cases
Warfarin Yes 1st epiphyses, No (e.g.,
trimester) CNS mechanical
malformatio heart valves) in
ns, fetal 2nd trimester
bleeding)
Potential
Avoid in
Not fetal
pregnancy due
DOACs Likely recommend toxicity; No
to lack of
ed insufficient
safety data
human data
Fondaparin Minim Use with Limited Possibly Reserved for
ux al caution human data patients with
HIT; use only
when heparin
is
Placental Pregnancy Preferred in Important
Drug Fetal Risk
Transfer Safety Pregnancy Notes
contraindicated
Conditional Low dose
Aspirin Sometim Used to prevent
Yes (low-dose safe; high
(low-dose) es preeclampsia
only) dose risks
References : (K.D. Tripathi, Essentials of Medical Pharmacology, 8th Edition, Pages 618–
620, Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 13th Edition,
Williams Obstetrics, 25th Edition, Chapter 52, Harrison’s Principles of Internal Medicine,
21st Edition, Volume 2, , British National Formulary (BNF) & NICE Guidelines .)

153. Answer: B) V2

Explanation:

Desmopressin (DDAVP) is a synthetic analog of arginine vasopressin (antidiuretic


hormone, ADH) that exhibits selective agonism at V2 receptors in the renal collecting
ducts.

 V2 Receptor Activation (Kidney):


Located on the basolateral membrane of principal cells in the renal collecting ducts,
stimulation leads to insertion of aquaporin-2 water channels, increasing water reabsorption
and reducing urine output.
Used in: Central Diabetes Insipidus (deficiency of ADH)
 V2 Receptor Activation (Endothelium):
Desmopressin also promotes release of von Willebrand factor (vWF) and Factor VIII
from endothelial cells.
Used in:
o Mild Hemophilia A
o Type 1 von Willebrand Disease
 Selectivity Advantage:
Unlike natural ADH, desmopressin does not activate V1 receptors, so it avoids
vasoconstriction and related adverse cardiovascular effects.

References: (K.D. Tripathi’s Essentials of Medical Pharmacology, 8th Edition, Page 596,
Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 13th Edition, ,
Harrison’s Principles of Internal Medicine, 21st Edition, Volume 2.)

BIOCHEMISTRY

154. Answer: C)- Leucine


Explanation:
Amino acids can be classified as:

 Glucogenic: give rise to glucose via gluconeogenesis


 Ketogenic: give rise to ketone bodies
 Both: some amino acids can be both

Leucine and lysine are the only purely ketogenic amino acids, meaning they cannot
contribute to glucose synthesis.

 Serine, Threonine, and Alanine are all glucogenic.


 Alanine is especially important during fasting (glucose-alanine cycle).

Reference: Satyanarayan Biochemistry, 4th Ed., Pg 373, First Aid 2025.

155. Answer: A) HMP shunt

Explanation:
Metabolic pathways based on location:

 Cytoplasm: HMP shunt (Pentose phosphate pathway), glycolysis, steroid and fatty acid
synthesis
 Mitochondria: TCA (Krebs) cycle, β-oxidation, oxidative phosphorylation
 Both: Urea cycle (part in mitochondria, part in cytosol), gluconeogenesis

Reference: USMLE Step 1 First Aid, Pg 72


156. Answer: B)- Alanine
Explanation:

The muscle plays a crucial role in the transport of ammonia to the liver for processing
through the urea cycle. The amino acid responsible for carrying ammonia from the muscle
to the liver is alanine, in a process known as the alanine cycle or glucose-alanine cycle.

 Alanine is synthesized in the muscle by the transamination of pyruvate, which accepts


the ammonia group from the amino acids released during muscle metabolism.
 Alanine then travels via the bloodstream to the liver, where it is converted back to
pyruvate, releasing the ammonia in the process. This ammonia enters the urea cycle for
detoxification and excretion in the form of urea.
 Glutamine also transports ammonia, but it primarily comes from other tissues such as the
brain and kidneys, rather than the muscle.

Key Points:

 Alanine is the key amino acid involved in the transport of ammonia from muscle to liver.
 The process helps regulate ammonia levels by converting it into urea, which is then
excreted by the kidneys.
 Glutamine also carries ammonia but is involved in other processes, mainly in the brain
and kidneys.

References: Harrison's Principles of Internal Medicine, 21st Ed, Pg 2331: ,Robbins Basic
Pathology, 10th Ed, Pg 1234:, First Aid 2024 )

157. Answer: D)-All

Explanation:
Cystinuria is a renal tubular transport defect of dibasic amino acids:

COLA: Cystine, Ornithine, Lysine, Arginine


This leads to excess cystine in urine, which forms insoluble crystals → cystine stones in
kidneys.
The condition is autosomal recessive and often benign except for stone formation.

COLA mnemonic → common for cystine stones Qs

Reference: Harper Biochemistry, 30th Ed., Pg 85

158. Answer: C) Vmax is lowered


Explanation:

Non-competitive inhibitors bind to an allosteric site, not the enzyme's active site. This
causes a conformational change in the enzyme, rendering it less effective regardless of how
much substrate is present.

Km (Michaelis constant) remains unchanged because substrate binding is unaffected.


Vmax (maximum reaction velocity) decreases because fewer functional enzymes are
available to catalyze the reaction.

Visual Insight:

Imagine an assembly line where the workers (enzymes) are functioning properly. A non-
competitive inhibitor is like someone tying one hand behind some workers' backs—they’re
still at their stations (substrate can bind), but they can’t work as fast (reduced Vmax).

References: (Lehninger Principles of Biochemistry, 8th Ed, Pg 203–205, Lippincott's


Illustrated Reviews: Biochemistry, 7th Ed, Pg 74–75, First Aid 2025)

159. Answer: B) Carbamoyl phosphate synthetase II

Explanation:
 CPS II is the rate-limiting enzyme for pyrimidine synthesis, located in the cytosol.
 CPS I, on the other hand, is in the mitochondria and involved in the urea cycle.
 PRPP amidotransferase is rate-limiting in purine synthesis.

Reference: First Aid USMLE Step 1, Pg 34

160. Answer: C) Vitamin B3

Explanation:
Hartnup disease is a defect in neutral amino acid transport, especially tryptophan in the
intestine and kidney.
Tryptophan is a precursor of niacin (Vitamin B3). Thus, deficiency results in pellagra-like
symptoms:

 Diarrhea
 Dermatitis
 Dementia

Exam Highlight: Tryptophan → Niacin → Hartnup = Pellagra → look for 3 D’s!

Reference: Harper Biochemistry, 30th Ed., Pg 308

161. Answer: D) Friedreich ataxia

Explanation:
Trinucleotide repeat expansions cause several neurogenetic disorders. For Friedreich ataxia,
the repeat is GAA in the frataxin gene.

 Causes mitochondrial dysfunction, ataxia, cardiomyopathy


 Other disorders:
o Huntington’s = CAG
o Myotonic dystrophy = CTG
o Fragile X = CGG

Reference: Harper Biochemistry, 30th Ed., Pg 378, First Aid 2025

162. Answer: C)- Phenylalanine hydroxylase

Explanation:
This is a classic presentation of Phenylketonuria (PKU). It is caused by:

Deficiency of phenylalanine hydroxylase, which converts phenylalanine to tyrosine.


Alternatively, a deficiency in tetrahydrobiopterin (BH4) or its regeneration enzyme (e.g.,
dihydropteridine reductase) can also cause PKU-like features.
Refer
ences: (Harper’s Biochemistry, 31st Ed, Pg 200 Lippincott’s Biochemistry, 7th Ed, Pg
176 ,First Aid 2025)

163. Answer: D)- Both a and c

Explanation:

 Pyruvate kinase (in glycolysis) converts phosphoenolpyruvate (PEP) to pyruvate, an


irreversible step.
 During gluconeogenesis, this step is bypassed in 2 stages:
1. Pyruvate → Oxaloacetate (via Pyruvate carboxylase)
2. Oxaloacetate → PEP (via PEP carboxykinase)

Together, pyruvate carboxylase and PEP carboxykinase (PEPCK) bypass this irreversible
step, enabling gluconeogenesis to proceed in the liver.
References: ( Lehninger Biochemistry, 8th Ed, Pg 582, Lippincott’s Biochemistry, 7th Ed,
Pg 140, First Aid 2025)

MICROBIOLOGY

164. Answer: D) Lungs

Explanation:
The clinical features point to leprosy (Hansen’s disease), caused by Mycobacterium
leprae, which prefers cooler areas of the body. It commonly involves:

 Skin: Hypopigmented, anesthetic patches


 Peripheral nerves: Thickening, neuropathy
 Eyes: Corneal ulcers, iritis
 Nasal mucosa: Epistaxis, septal perforation

Lungs are not affected, as M. leprae does not grow well at core body temperatures.

Reference:: Apurba Sastry, Pg 379

165. Answer: a) Not influenced by hormones

Explanation:
Innate immunity is the first line of defense and is non-specific. While it is genetically
determined and does not require previous exposure to a pathogen, it can be influenced by
hormonal status. For example, diabetes and endocrine disorders impair innate immunity,
increasing susceptibility to infections.
Includes physical barriers (skin, mucous membranes), cellular defenses (NK cells,
macrophages), and humoral components (complement).

Reference:: Jawetz Microbiology 27th Ed., Pg 123; Apurba Sastry, Pg 97–98

166. Answer: A) Acute hepatitis B with high infectivity

Explanation:

 HBsAg = Current infection (either acute or chronic)


 HBeAg = Active viral replication → high infectivity
 Anti-HBc IgM = Indicates recent (acute) infection

This combination clearly indicates acute, highly infectious hepatitis B.

Reference:: Jawetz Microbiology, Pg 508

Exam Highlight:

HBsAg + HBeAg + Anti-HBc IgM = Acute and infectious HBV → crucial for infection
control questions.

167. Answer: B) Kidney

Explanation:
Hyperacute rejection occurs minutes to hours after transplantation, due to preformed
recipient antibodies against donor antigens (Type II hypersensitivity).
It leads to vascular thrombosis and necrosis of the graft.
Most common in kidney and skin grafts, as they are highly vascular.
Reference:: Jawetz, Pg 123; Apurba Sastry, Pg 194

168. Answer: D) Resistant to bacitracin

Explanation:

Streptococcus pyogenes is a Beta-hemolytic, Group A, Produces M protein, a major


virulence factor that resists phagocytosis, Sensitive to bacitracin, which helps differentiate
it from Group B Streptococcus (S. agalactiae)

S. pyogenes = bacitracin sensitive, M protein, necrotizing fasciitis ("flesh-eating bacteria").


Reference:: Jawetz Pg 210; Apurba Sastry Pg 194,First Aid 2025

169. Answer: C)- Francisella tularensis

Explanation:

 Category A agents are the highest priority for bioterrorism because they are easily
disseminated, have high mortality, and cause public panic.
 Francisella tularensis:
o Gram-negative coccobacillus
o Causes tularemia (most common form is ulceroglandular tularemia).
o Requires cysteine-enriched media (e.g., Buffered Charcoal Yeast Extract (BCYE) agar
or Chocolate agar with cysteine) for growth.
o Highly infectious — only 10-50 organisms can cause disease.

References: Harrison’s Principles of Internal Medicine, 21st Edition, (Page 1313–1316),


Jawetz, Melnick & Adelberg’s Medical Microbiology, 28th Edition, (Page 222–224), CDC
Bioterrorism Agent List (Updated guidelines, 2024).
170. Answer: C)- Deafness is common

Explanation:
Congenital rubella syndrome (CRS) occurs when a non-immune woman contracts
rubella in 1st trimester.
Classic triad:

 Sensorineural deafness (most common)


 Cataracts
 Congenital heart defects (PDA)

Vaccination with MMR prevents CRS effectively.

Highlight: Deafness = most common feature in CRS.

Ref: Jawetz Microbiology, Pg 609,First Aid 2025

171. Answer: A) Skin and mucous membrane

Explanation:
Leptospira enters via skin abrasions or intact mucosa when a person is exposed to
contaminated water (urine of infected animals).

 Risk groups: farmers, sewage workers, swimmers.


 Can cause Weil’s disease – a severe form with jaundice, renal failure, hemorrhage.

Reference:: Jawetz, Pg 337

172. Answer: A) Is enveloped

Explanation:
Coronaviruses are:

 Enveloped
 Have non-segmented, positive-sense ssRNA
 Replicate in cytoplasm
 Cause respiratory illnesses, including SARS, MERS, and COVID-19

They appear “crowned” under EM due to spike (S) glycoproteins.

Reference:: Jawetz Pg 412–413, First Aid 2025

173. Answer: C)- FTA-ABS

Explanation:

 The presentation is classic for primary syphilis caused by Treponema pallidum.


 VDRL and RPR are nonspecific screening tests.
 FTA-ABS (Fluorescent Treponemal Antibody Absorption test) is highly specific for
treponemal antibodies and used for confirmation.
 Dark-field microscopy can detect spirochetes directly from the lesion but requires
expertise and immediate processing.

Reference:: Jawetz Medical Microbiology, 28th Ed | CDC Syphilis Guidelines, First Aid
174. Answer: C)- Exotoxin

Explanation:

 Diphtheria is caused by Corynebacterium diphtheriae.


 The hallmark pseudomembrane and systemic toxicity (e.g., myocarditis, neuropathy) are
due to the diphtheria exotoxin.
 The exotoxin inhibits EF-2 → halts protein synthesis → cell death.
 Vaccination with DTaP provides protection by inducing neutralizing antibodies against the
toxin.

Reference:: Jawetz Microbiology, 28th Ed | Harrison’s Internal Medicine, 21st Ed, First Aid

FORENSIC MEDICINE

175. Answer: B) -VNTRs and STRs

Explanation:

 Variable Number Tandem Repeats (VNTRs) and Short Tandem Repeats (STRs) are
used in DNA fingerprinting.
 Highly polymorphic → excellent for individual identification & paternity disputes.
 Mitochondrial DNA is maternally inherited and useful when nuclear DNA is degraded,
but not ideal for paternity.

Important Point:
"STRs + VNTRs = gold standard for identity & paternity"
Reference: Reddy 34th Ed | Knight | Parikh | FBI CODIS Manual
176. Answer: A)- Arsenic

Explanation:

 Acute arsenic poisoning mimics cholera: vomiting, rice-water stools, hypotension.


 Later: hemolysis, renal failure, CNS toxicity.
 Classic garlic odor in breath and body fluids.

Important Point:
"Arsenic → garlic breath + rice-water stools + hemolysis"
Reference: Parikh 7th Ed | Reddy 34th Ed | Modi | WHO Arsenic Toxicity Guidelines

177. Answer: C)- Severe hypothermia

Explanation:

 Suspended animation: body functions are so depressed that signs of life may not be
detected.
 Seen in hypothermia, drowning, electrocution, drug overdose.
 Important medicolegal implication: should not declare death hastily.

Important Point:
"In hypothermia, always warm before pronouncing dead"
Reference: Reddy | Knight | Parikh

178. Answer: B)- Repeat clinical examination by two doctors 6 hours apart

Explanation:

 Nepal Medical Council guidelines (aligned with international standards) require:


o Absent brainstem reflexes
o Positive apnea test
o Re-confirmation by two physicians, 6 hours apart
 EEG is supportive but not mandatory if full clinical exam is conclusive.

Important Point:
"Declaration must follow protocol – 2 doctors, 6 hrs apart"
Reference: NMC Guidelines | Reddy | Knight

179. Answer: C)- Livor mortis

Explanation:

 Livor mortis (postmortem staining) appears within 30 mins – 2 hrs, fully develops in 6–
8 hrs.
 It shifts with body position in early hours, then becomes fixed.
 More reliable than algor (affected by environment) or rigor (variable onset).
 ECG may continue for some minutes even after true death.

Important Point:
"Shifting lividity = body moved before livor fixed"

References: Reddy | Parikh | Knight | WHO Autopsy Protocols/ osmosis

COMMUNITY MEDICINE AND STATSTICS

180. Answer:C)- Median

Explanation:

 In skewed distributions, the mean is pulled toward the tail due to extreme values
(outliers), making it less representative of the central location.
 Median, being the middle value, is not affected by outliers and better represents the
central tendency in such cases.
 Example: In income distribution, where most earn less but a few earn excessively more,
median income gives a more realistic picture than the mean.

Reference: Park’s PSM 27th Ed., Ch. 8 – Biostatistics, Mahajan’s Methods in Biostatistics

181. Answer: C)- 25

Explanation:

 Variance = (Standard Deviation)²


 Given SD = 5, so Variance = 52=255^2 = 25
Standard deviation gives a measure of spread around the mean in original units, while
variance gives the average squared deviation.

Reference: Park’s PSM, Ch. 8 – Biostatistics, Principles of Biostatistics by Pagano &


Gauvreau

182. Answer: B)- Case-control study

Explanation:

 Case-control studies start with the outcome (e.g., lung cancer) and look backward to
assess exposure (e.g., smoking).
 Commonly used for rare diseases.
 Efficient and cost-effective but prone to recall bias.

Reference:: Park’s PSM | Gordis Epidemiology | Harrison’s 21st Ed, Pg 243

183. Answer: C)- Randomized controlled trial (RCT)

Explanation:

 RCTs are considered the gold standard for evaluating interventions.


 Random allocation reduces selection bias.
 Allows for causal inference and controls for confounders.
 Positioned Level I evidence in most hierarchies.

References: (Oxford Centre for Evidence-Based Medicine (CEBM) | Harrison's 21st Ed |


Park’s PSM.)
184. Answer: C)- Infant parasite rate

Explanation:

 Infant parasite rate reflects recent transmission because infants are unlikely to have had
prior exposure.
 Spleen rate and slide positivity rate are useful but less sensitive for recent transmission.

References: Park’s PSM, 27th Ed., Ch. 6, WHO Malaria Surveillance Guidelines

185. Answer: D)-Net reproductive rate (NRR)

Explanation:

 NRR < 1 implies that each generation is producing fewer daughters, i.e., replacement-level
fertility has been achieved.
 Nepal’s NRR (NDHS 2022) is nearing 1, suggesting effective FP coverage.

References: Park’s PSM, Ch. 5, Nepal Demographic and Health Survey (NDHS) 2022

186. Answer: D)- All of the above

Explanation:

Nepal’s IDSP (formerly EWARS) tracks multiple epidemic-prone diseases including


dengue, malaria, kala-azar, JE, and measles.

References: EDCD Nepal Guidelines, WHO SEARO Surveillance Manual

187. Answer: B)- Free tertiary care for all

Explanation:

 The policy ensures essential health services are free, but tertiary care may not be
universally free.
 Focus is on equity, federalism, and digital health.

Reference: Nepal National Health Policy 2019 – MoHP

188. Answer: A)-Primary Health Care Approach

Explanation:

Nepal’s service delivery is rooted in PHC, with Health Posts (HPs) as the primary point of
contact, especially in rural areas.
References: Park’s PSM, Ch. 22, Nepal Health Sector Strategy 2015–2020

189. Answer: B)- NS1 Antigen test

Explanation:

 NS1 is preferred in the first 5 days of dengue fever.


 Dengue is endemic in Terai districts like Kailali; early detection is crucial.

Reference: EDCD Nepal Guidelines on Dengue, WHO Dengue Management Guidelines

190. Answer: B)- Index case

Explanation:

 Index case is the first case that brings attention of authorities to the disease.
 Important in surveillance and contact tracing.

Reference: Park’s PSM, Ch. 4 – Epidemiology, WHO COVID-19 Surveillance Protocol

191. Answer: C)- Immediate results

Explanation:

 VIA (Visual Inspection with Acetic acid) is a low-cost, same-day test suitable for rural
screening in Nepal.
 Ideal in low-resource settings.

Reference: Nepal’s National Strategy for Cervical Cancer, WHO Cervical Cancer Screening
Guidelines

192. Answer: B)- HIV

Explanation:

Nepal's PMTCT program under NCASC focuses on HIV prevention during pregnancy,
labor, and breastfeeding.

Reference: NCASC Nepal, WHO HIV PMTCT Guidelines

193. Answer: A)- Research ethics

Explanation:
The Declaration of Helsinki, adopted by the World Medical Association (WMA) in 1964 and
revised multiple times, provides internationally accepted guidelines for conducting medical
research involving human subjects. It emphasizes informed consent, ethical review boards,
respect for individuals' autonomy, and the right to withdraw from research. In Nepal, this is a
mandatory component in CPD to ensure all health professionals conducting or participating
in research uphold ethical standards, especially in clinical trials and community-based
studies.

Reference: WMA Declaration of Helsinki, Park PSM 23rd Ed., Ethics in Public Health

194. Answer: B)- Try to find out why he missed the month

Explanation:
The correct public health approach is to understand the underlying cause of non-adherence,
which could be due to side effects, stigma, poor access to medication, or socio-economic
barriers. The CPD module emphasizes empathetic communication and problem-solving
rather than punitive responses. Re-engaging the patient with counseling and support
improves compliance and TB control. Scolding or blaming may lead to further default and
disease spread.

Reference: CPD Module – Counseling in Public Health, NTCC Guidelines Nepal, Park PSM
27th Ed., Ch. 6

195. Answer: D)- Entertainment

Explanation:
Social influencing skills in healthcare communication involve techniques to support
behavioral change, such as reframing negative beliefs, gently challenging irrational
thoughts, or using limited self-disclosure to build rapport. Entertainment, however, is not a
recognized clinical communication tool and can distract from patient care. CPD emphasizes
these structured interpersonal skills as part of motivational interviewing, especially in
managing NCDs, addiction, and mental health.

Reference: CPD Clinical Communication Skills Module, Park PSM Ch. 8 – Counseling and
Behavior Change

196. Answer: A)- Encouraging

Explanation:
Encouraging is an active listening skill used in doctor-patient communication. It involves
verbal and non-verbal cues (like nodding, saying “I see”, or repeating keywords) to prompt
the patient to continue talking. This creates a safe space for patients to share more about
their symptoms, concerns, and expectations (ICE model). CPD in Nepal now includes this as
a core skill in medical interviewing, especially for primary care and public health settings.

Reference: CPD Communication Skills Handbook, Calgary-Cambridge Guide, Park PSM –


Communication Skills

197. Answer: D)- Tell her it violates patient confidentiality


Explanation:
Carrying patient-sensitive data like OT schedules outside the hospital without authorization
is a breach of medical ethics and confidentiality. The intern should be advised about
ethical obligations under the NMC’s Code of Ethics. CPD modules highlight that protecting
patient identity and data is essential in building trust and professionalism. A reminder or
corrective guidance is preferred before disciplinary action in educational settings.

Reference: NMC Code of Medical Ethics, CPD Medical Law & Ethics Module

198. Answer: B)- Proceed with surgery under implied consent

Explanation:
In emergency settings where a patient is unconscious, unable to provide consent, and
delay in treatment may endanger life, doctors are ethically and legally permitted to
proceed with life-saving treatment under implied consent. Waiting for relatives or legal
clearance can lead to deterioration or death.

Implied consent is recognized when a reasonable person would have consented in such a
situation to save life or prevent serious harm. Documentation of the patient's status, need for
emergency intervention, and inability to obtain consent should be thorough and done
promptly.

Key points: Emergency = Implied consent valid and Life-threatening = Treat without
delay

Document clearly when patient is unconscious and no surrogate is available.

Reference: (Nepal Medical Council Code of Ethics (2023), Chapter 2, Beauchamp and
Childress: Principles of Biomedical Ethics, 8th Ed, pp. 128–130.)

199. Answer: C)- Arrange a private setting and gently inform the patient directly

Explanation:

Patients have the right to know their diagnosis, including cancer. While it is understandable
that family members may want to protect a loved one from emotional distress, withholding
diagnosis without the patient’s consent violates autonomy and ethical standards. The
process of breaking bad news should be conducted with sensitivity, privacy, and support.

You may use structured protocols like SPIKES (Setting, Perception, Invitation, Knowledge,
Emotions, Strategy/Summary) to guide the conversation. After giving the news, provide
psychological support, clarify next steps, and allow time for questions.

Key points:

 Truth-telling is essential unless patient previously declined disclosure.


 Use empathetic communication strategies (like SPIKES).
 Do not allow family members to override patient rights without valid reasons.

Reference: (NMC Code of Ethics, Section on Doctor–Patient Communication, Baile WF et


al. SPIKES Protocol: The Oncologist 2000;5(4):302-311, WHO Guide to Effective
Communication in Cancer Diagnosis.)

200. Answer: C)- Politely explain and maintain the original priority list

Explanation:
Healthcare resources must be allocated fairly and equitably, based on clinical need and
urgency, not personal or political influence. Giving preferential treatment to someone due to
their position or connection is a clear violation of medical ethics and professionalism.

Even in hierarchical systems, a doctor must uphold justice and integrity. It is appropriate to
explain the situation respectfully to the person in authority and ensure transparency in
scheduling. If pressure continues, one can escalate the matter through proper institutional
channels.

Key points:

 Clinical priority > personal influence


 Uphold fairness and professional integrity
 Be firm yet respectful when declining undue requests

Reference: (NMC Ethics Code (2023), Chapter on Justice in Healthcare, World Medical
Association Declaration of Geneva .)

THANK YOU

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