Disclaimer – very rough, I can’t take any responsibility for what they do and
don’t ask, also pharmacology is not my strong suit (sometimes not sure what
drugs to highlight)
Psychosocial does have high & low-yield, but I have not included it bc I didn’t
properly know it
*** means I need to double-check what’s in this lecture
Module 1
Immunology: (some of this is taught in later gem1 modules)
Innate vs adaptive = B-Cells & T-cells, antibody = Ig (same thing), antibodies
are produced by B-cells only; know where the different Ig's are and
when/where they're produced -> IgM = first-time infection, IgG = B memory
cells in the blood; IgA = mucosal surfaces (eg gut, eyes, mouth, breast milk
(important)); IgE = allergic responses; T-cells = important for viral responses
(and other things); blood tests - neutrophils -> usually bacterial, lymphocytes
-> usually viral; know your autoimmune markers (especially rheumatoid
arthritis, lupus), and know your hypersensitivities
Macrophages for different tissue types (eg liver = kupffer cell, CNS =
microglia, skin = Langerhans cell)
Main things to look for in diagnostic tests –
• FBC, U&Es, LFTs, CRP/ESR, bone profile
• Endocrine tests (see module 6 for more)
O broadly speaking, they all have a HP+organ axis
O if pituitary hormone is raised and target hormone is raised, pituitary
(or hyp) is the problem (applies to HPA axis, HPT axis, tests reflect that)
O if pituitary is low and target is raised, target is the problem (primary)
O with growth hormone, as a screening test, because GH levels go up
and down throughout the day, the first thing they do is check IGF-1, as if GH
activity has been high, this will also be high
O after that -> more involved tests to confirm if it’s a pituitary issue
Module 2
Sympathetic + parasympathetic – alpha receptors -> peripheral
vasoconstriction, and beta receptors – beta-1 = heart, beta 2 = lungs
Anatomy of URT – peanut falling in the lung, recurrent laryngeal nerve +
signs, laryngeal nerves
***Anatomy of ear – glue ear, otitis externa, mastoiditis
Recurrent illness in children – glue ear (clinical years mostly)
Resp histology – type 1 vs type 2 pneumocytes (which ones secrete
surfactant, which ones gas exchange, types of cell (goblet cells or whatever),
(whatever I was thinking)
(you guys know that RBCs carry O2 through Hb by now), CO2 bound to Hb =
carbaminohaemoglobin (left shift right shift not even that tested)
Methaemoglobinaemia -> iron in Hb needs to be fe2+, if it ever ends up as
Fe1+ (eg local anaesthetic gets into the blood stream eg during dental
operation, local injection gone wrong, exposure to certain pesticides/farming
products) can happen, treatment = IV methylene blue or ascorbic acid
Pneumonia – bacterial infection in lungs, crackles + fever/constitutional
symptoms
Obstructive * restrivtive pathologies -> obstruvtive – struggle to expire air
quickly thf FEV goes down a lot. Eg asthma + COPD (chronic bronchitis
and/or emhysema); restrictive – both go down but a similar proportion
(everything other than asthma and COPD afaik), mesothelioma -> rare
cancer of the pleura -> asbestos
Pharm of resp drugs – SABAs = relievers (salbutamol & co), LABAs (only …
can be uses as a SABA because it’s also quick), LAMAs, steroids; some extra
ones – eg mast cell targeting one, + some weird one. If you have time, can
remember the mast cell one, but honestly, main thing is relievers (beta
agonists which act short), musc antagonist (tropiums), steroids to attack
inflammation long term. Bear in mind for module 3 that beta blockers
shouldn’t be used in asthmatics
Eicosanoids – nsaids – block prostaglandins – block inflammation, side effects
inc peptic ulcers and kidneys; aspirin (reduces platelet activity, blocks COX…
(2?))
Clinical imaging of the thorax – look at a couple of pneumothraxes,
consolidations, hyperinflated lung in COPD; PA projection is preferred, but
patient has to stand up and cross arms; if bed bound, AP will probs be used.
Makes heart look bigger than it is
TB – gram-indeterminate stain, Ziehl-Neelsen stain used, acid-fast
bacteria/acid fast bacilli, caseous necrosis, granulomas, macrophages + T-
cells, hardcore antibiotic regimen to treat (rifampicin, isoniazid, other stuff)
*** oncogenesis, neoplasia and cancer
Module 3
*** cardiac muscke, structure, cycle, valve function
***BP and CV regulation – arterioles main source of resistance, in the
resistance equation – radius to the power of 4
Statins – some side effects
ECG – what components of the trace represent (P, QRS, T), can calculate rate
by using rhythm strip (number of peaks in rhythm strip* 6)
Key arrhythmias – atrial fibrillation – irregularly irregular (compare length
from peak to peak), atrial flutter (sawtooth appearance); atrial fibrillation ->
massive massive massive risk factor for stroke and heart attack (is the main
way that thrombi are generated in the left circulation, another one is if there
are plaques in the carotid sinus)
(other risk factors for stroke – high cholesterol, hypertension (I think?),
diabetes, smoking)
***Antiarrhythmics – vaughan williams classification plus examples
(wikipedia has a good table)
Side effects eg verapamil
Clotting and thrombosis – which factors does vitmain k help with, warfarin =
vitamin k antagoinst, reversed by adding more vitamin k(confirm this, could
be wrong), DOACs eg rivaroxaban etc act on factor Xa (hence rivaroXaban),
very rare to give a clotbuster like alteplase (only in MI + stroke once
haemorrhagic stroke ruled out I think)
Oedema …
Heart failure pathophys – RHF, LHF differences
Pharmacology of HF – diuretics, other drugs (reduce heart rate, improve
heart efficiency?)
Circulatory changes at birth/congenital heart disease – foramen/fossa ovale,
ductus arteriosus/ligamentum arteriosum, the one that connects from liver to
navel
Module 4 (incomplete)
Bone pathologies + telling them apart
PTH – mainly the different hyperparathyroidisms
For anatomy please refer to 100 concepts and see what slides there are
relevant to the region you’re trying to study
Eg Humeral fractures, radial fractures, klumpke Vs erbs palsy, cauda equina
syndrome, piriformis syndrome, foot drop & peroneal nerves
TBC
Module 5
Causes of anaemia – megaloblastic (b12 and/or folate), iron deficiency
Peptic ulcers – h pylori, triple therapy
B12 deficiency – intrinsic factor, pernicious anaemia (if taking too long move on)
barrett’s oesophagus
Anatomy – spaces for fluid collection (lying down vs upright, also in 100 concepts),
boundaries of foregut, midgut and hindgut, source of blood supply, arterial supply of
stomach,
sites of visceral pain (epigastric, umbilical, hypogastric), appendix (umbilical pain ->
sharp mcburney’s pain); default position of appendix (in most people
RETROCAECAL), retro vs intraperitoneal (a sad pucker for retroperitoneal; use in
conjunction with alternation trick – oesophagus (r), stomach (i), duodenum (r),
jejunum & ileum (i), ascending c (r), transverse (i), descending (r), sigmoid (i),
rectum (r)); appendix is intraperitoneal; watershed area of colon, venous drainage
of intestines (which ones go into the splenic vein, s or I mesenteric veins; which
ones go straight into the HPV), internal and external haemorrhoids, dental pectinate
line
Salivary glands (innervation, blockage (submandibular most frequent), parotid
(Stenson) duct emptying behind upper 2 nd molar))
nausea pharmacology – jenny’s drugs + which receptors they target, side effects
whole slide on malabsorption in chemical digestion and absorption of food
(“maladsorption of carbohydrates” (typo is in wayne’s slide)) (discusses GGM &
using fructose, pancreatic insufficiency (cystic fibrosis and schwachman-diamond
syndrome))
liver&biliary – pre, intra, and post hepatic jaundice, liver function tests; hepatitis
(osmosis video “viral hepatitis: pathology review” = really good and explains
hepatitis b markers at different stages of the vaccination/infection process!)
pancreas – pancreatitis causes and presentations, blood results
IBD – crohn’s and UC – differentiating the two; coeliac’s disease
Colorectal cancer – right-sided vs left-sided cancer differences, symptoms of rectal
cancer
Paracetamol overdose -> glutathione is depleted -> NAPQI no longer conjugated,
free to damage cells
Treatment -> acetylcysteine to replenish glutathione
anatomy/pathology - differentiating cholecystitis (inflamed gall bladder) from
ascending cholangitis and head of pancreas tumour
module 6
diabetes medications – different types, where their targets are, which drugs are
ideally suited to which patients, cautions/adverse reactions/side effects
pituitary hormones –
· general rule = hypothalamus stimulates pituitary stimulates organ provides
negative feedback (HP_ axis); if excess hormone suspected -> suppression
test; if deficiency suspected -> stimulation test; these are used in both
growth hormone axis and HPA axis (adrenal))
· suppression test – inhibit the axis and see what happens (eg high glucose to
inhibit GH release, dexamethasone to inhibit acth secretion), stimulation test
= stimulate the axis and see what happens
· HPG axis -> has to be pulsatile, continuous GnRH analogue will inhibit the
axis; usually negative feedback except LH surge = brief period of positive
feedback in, activity of different axes can vary throughout the day which is
why testing can be quite involved
· HPA axis, Cushing’s syndrome and causes, dexamethasone suppression test;
adrenal insufficiency – primary (addison’s) and secondary; dangers of steroid
withdrawal (addisonian crisis); side effects of steroids!
thyroid – pathologies (graves (high t4, autoimmune stimulation) vs hashimotos
(autoimmune destruction)
how it’s tested (T4 and TSH), use negative feedback principles to figure out if high
or low thyroid levels are a pituitary vs thyroid issue, if it’s a thyroid issue -> use
knowledge of graves and hashimoto’s markers to f
Pituitary tumours (eg benign adenoma, craniopharyngioma), pituitary basic
embyology (origin location wise + tissue-type wise)
Growth hormone – pulsatile release, fluctuates -> so initial test, test IGF-1 & IGFBP;
afterwards can do suppression/stimulation tests as needed to confirm where the
issue is
adrenal