Cardio
Which artery is most commonly occluded in an anterior STEMI?
The left anterior descending (LAD) artery
Explain how thyroid hormone is released (5 steps of the HPA axis)?
The hypothalamus (paraventricular nucleus) secretes thyrotropin-releasing hormone (TRH).
TRH is released into the hypophyseal portal system — a specialised venous network that carries hypothalamic hormones directly to the anterior pituitary without entering systemic circulation first, allowing very low concentrations to act with high local potency.
TRH stimulates thyrotrope cells in the anterior pituitary to secrete thyroid-stimulating hormone (TSH).
TSH enters systemic circulation and binds TSH receptors on the thyroid follicular cells, stimulating synthesis and release of T4 (thyroxine, ~90% of output) and T3 (triiodothyronine, more biologically active).
Circulating T3/T4 exert negative feedback at both the hypothalamus (suppressing TRH) and the anterior pituitary (suppressing TSH), maintaining homeostatic hormone levels.
Deficiency of which two vitamins causes megaloblastic anaemia and why?
Vitamin B12 (cobalamin) and folate. Both are essential cofactors for DNA synthesis — specifically for the synthesis of thymidine (via the methylation cycle) needed for purine and pyrimidine production.
Without adequate B12 or folate, cells struggle to synthesize DNA efficiently, but RNA and protein synthesis continue relatively normally.
This creates asynchronous maturation: the nucleus lags behind while the cytoplasm continues to mature and grow.
The result is abnormally large red cell precursors with immature-looking nuclei relative to their cytoplasm — megaloblasts in the bone marrow, and macrocytic red cells (high MCV) in the peripheral blood.
B12 deficiency additionally causes neurological features (subacute combined degeneration of the spinal cord) because B12 is also required for myelin synthesis, which folate deficiency does not cause.
What is a normal GFR?
Normal GFR: ~90–120 mL/min (this reflects the rate of plasma filtration, not total blood flow).
what is the only mammal that is capable of true flight?
Bat
Name two haemodynamic effects of digoxin
Increased contractility (positive inotropy) — digoxin inhibits the myocyte Na⁺/K⁺-ATPase pump. This raises intracellular Na⁺, which reduces the gradient driving the Na⁺/Ca²⁺ exchanger to remove calcium from the cell. Intracellular Ca²⁺ accumulates, increasing the calcium available for excitation-contraction coupling and boosting contractile force.
Slowed AV conduction (negative dromotropy) — digoxin increases vagal (parasympathetic) tone at the AV node, slowing conduction velocity and increasing the AV nodal refractory period. This is why it's useful for rate control in atrial fibrillation, though it has less effect at rest and is less effective during exertion when sympathetic tone dominates.
What is the classic triad of Graves disease?
Hyperthyroidism — the autoantibodies mimic TSH, binding thyroid follicular cell TSH-receptors and continuously stimulating T3/T4 synthesis and release, independent of the normal negative feedback loop. Because the antibodies aren't subject to hypothalamic-pituitary suppression, hormone output stays persistently elevated.
Diffuse goitre — the same TSH-receptor stimulation also drives follicular cell hyperplasia and hypertrophy, causing the thyroid gland to enlarge diffusely (as opposed to the nodular enlargement seen in toxic multinodular goitre or a solitary toxic adenoma).
Exophthalmos (Graves' ophthalmopathy) — this is technically a separate autoimmune process rather than a direct consequence of excess thyroid hormone. Orbital fibroblasts share a cross-reactive antigen with the TSH receptor. TSI antibodies (and associated T-cell mediated inflammation) target these orbital fibroblasts, causing them to proliferate and secrete excess glycosaminoglycans (mainly hyaluronic acid). These are hydrophilic and draw water into the retro-orbital tissue, along with lymphocytic infiltration and expansion of extraocular muscle and fat — pushing the globe forward within the fixed bony orbit.
Name two features of haemolytic anaemia on labs
Elevated reticulocyte count — the bone marrow compensates for accelerated red cell destruction by increasing red cell production, releasing immature reticulocytes into circulation earlier than normal.
Elevated LDH and unconjugated bilirubin — released from lysed red blood cells (LDH is present intracellularly in RBCs), and haem breakdown from destroyed cells increases bilirubin production faster than the liver can conjugate and excrete it, causing unconjugated hyperbilirubinaemia.
Accept decreased haptoglobin too.
Name two effects of ADH on the kidney.
Increased water reabsorption in the collecting duct — ADH (vasopressin) is released from the posterior pituitary in response to increased plasma osmolality (sensed by hypothalamic osmoreceptors) or decreased blood volume (sensed by baroreceptors)
Insertion of aquaporin-2 channels — ADH binds V2 receptors on the basolateral membrane of principal cells in the collecting duct, triggering a cAMP-mediated signalling cascade that causes aquaporin-2 channels to be inserted into the apical membrane from intracellular vesicles. This makes the collecting duct permeable to water, allowing water to move down its osmotic gradient (out of the tubule, following the concentrated medullary interstitium established by the countercurrent multiplier) — concentrating the urine and conserving body water.
What is the longest international land border?
US - Canada
Name the two types of ventricular hypertrophy and explain why each pattern develops the way it does.
Concentric hypertrophy — caused by chronic pressure overload (e.g. hypertension, aortic stenosis). Increased systolic wall stress drives sarcomeres to be added in parallel within existing myocytes, thickening the wall without enlarging the chamber. Per Laplace's law (wall stress = pressure × radius ÷ 2 × wall thickness), thickening the wall is the mechanism that reduces wall stress against a chronically elevated pressure load.
Eccentric hypertrophy — caused by chronic volume overload (e.g. mitral or aortic regurgitation). Repeated diastolic overfilling stretches the myocytes, so sarcomeres are added in series, lengthening the fibres. This allows the chamber to dilate to accommodate the extra volume, with wall thickness increasing only proportionally — keeping wall stress roughly normalized against the elevated volume load.
What triggers the Wolff–Chaikoff effect?
An acute excess iodine load transiently inhibits thyroid peroxidase-mediated organification of iodine, reducing T3/T4 synthesis as a protective autoregulatory mechanism. The thyroid normally escapes within a few days by downregulating the Na⁺/I⁻ symporter (NIS).
What are the two types of thalassemia and what is the difference between the two.
alpha-thalassaemia results from gene deletions affecting 4 possible gene copies (giving a graded severity spectrum)
beta-thalassaemia results from point mutations affecting only 2 possible gene copies (giving a more binary trait-vs-major distinction).
Name three non-filtration functions of the kidney.
Erythropoietin production — peritubular fibroblasts in the renal cortex produce erythropoietin in response to hypoxia, stimulating red blood cell production in the bone marrow. This is why chronic kidney disease commonly causes anaemia.
Vitamin D activation — the kidney performs the final hydroxylation step, converting 25-hydroxyvitamin D to the biologically active 1,25-dihydroxyvitamin D (calcitriol) via 1-alpha-hydroxylase, which is essential for intestinal calcium absorption and bone mineralisation.
Acid-base regulation — the kidney reabsorbs filtered bicarbonate (mainly in the proximal tubule) and generates new bicarbonate through ammoniagenesis and titratable acid excretion (mainly in the distal tubule/collecting duct), maintaining systemic pH homeostasis over a timescale of hours to days, complementing the more rapid respiratory compensation.
What was the first country to grant women the national vote?
New Zealand in 1893
List four ECG features distinguishing atrial fibrillation from atrial flutter.
Rhythm — AF: irregularly irregular ventricular rhythm. Flutter: typically regular (often with a fixed conduction ratio, e.g. 2:1)
P waves — AF: absent, replaced by chaotic fibrillatory activity. Flutter: absent, replaced by regular "sawtooth" flutter waves
Atrial rate — AF: chaotic, disorganized atrial activity (~350–600/min, not discretely countable). Flutter: organized re-entrant circuit at a fixed rate, classically ~300/min
Baseline appearance — AF: irregular, chaotic undulating baseline. Flutter: regular, uniform sawtooth pattern, most visible in the inferior leads (II, III, aVF)
List four causes of hypothyroidism
Hashimoto's thyroiditis — autoimmune destruction via anti-TPO/anti-thyroglobulin antibodies, the most common cause in iodine-sufficient regions
Iodine deficiency — impaired substrate availability for hormone synthesis, most common cause worldwide
Postpartum thyroiditis — transient autoimmune inflammation following delivery, often biphasic (hyperthyroid phase followed by hypothyroid phase)
Drug-induced — amiodarone (high iodine content, direct thyroid toxicity) or lithium (inhibits hormone release)
List four causes of pancytopenia
Aplastic anaemia — bone marrow failure with loss of haematopoietic stem cells, leading to hypocellular marrow and reduced production of all three cell lines
Marrow infiltration by malignancy — leukaemia, lymphoma, or metastatic solid tumours physically crowd out and disrupt normal haematopoiesis in the marrow
Chemotherapy — cytotoxic drugs suppress rapidly dividing haematopoietic precursor cells, causing marrow suppression
Vitamin B12/folate deficiency — impaired DNA synthesis affects all proliferating cell lines in the marrow (not just red cells), so severe deficiency can suppress white cell and platelet production too, alongside megaloblastic anaemia
List four causes of pre-renal AKI.
Hypovolaemia — from haemorrhage, dehydration, or GI losses, reducing effective circulating volume and renal perfusion pressure
Heart failure — reduced cardiac output (or in some cases venous congestion) impairs effective renal perfusion despite normal or increased total body fluid
Sepsis — systemic vasodilation and capillary leak reduce effective circulating volume and renal perfusion, despite this often being classified separately as a mixed pre-renal/intrinsic mechanism as it progresses
NSAID/ACE-inhibitor use — NSAIDs inhibit prostaglandin-mediated afferent arteriolar vasodilation, while ACE inhibitors block angiotensin II-mediated efferent arteriolar vasoconstriction; both reduce the compensatory mechanisms that maintain glomerular filtration pressure when renal perfusion is already compromised (particularly dangerous in combination, or in a volume-depleted patient).
What is the one letter that’s missing from the periodic table?
J
List five features that differentiate stable angina, unstable angina, and STEMI along the ACS spectrum and what diagnostics would you use to differentiate between the three?
Stable angina
Unstable angina
STEMI
Key diagnostics to differentiate them: History, ECG, and serial troponins.
List five clinical features of thyroid storm and the physiology behind it?
Fever (often >39°C) — due to thyroid hormone's effect of increasing basal metabolic rate and thermogenesis
Tachycardia (often severe, may include AF) — from upregulation of cardiac beta-adrenergic receptors by thyroid hormone, increasing sensitivity to circulating catecholamines
Agitation/delirium — from excess thyroid hormone's stimulatory effects on the CNS
GI symptoms (vomiting/diarrhoea) — from increased gut motility and, in severe cases, hepatic dysfunction
Heart failure — from sustained tachycardia and increased myocardial oxygen demand outstripping supply, leading to high-output failure
List five steps of the Plasmodium falciparum erythrocytic cycle.
Merozoites invade red blood cells — released from the liver (after the pre-erythrocytic/hepatic stage) or from a ruptured schizont, merozoites attach to and invade RBCs via specific surface receptors
Trophozoite development — inside the RBC, the merozoite matures into a ring-form trophozoite, then a more developed trophozoite, feeding on haemoglobin and generating haemozoin pigment as a byproduct
Schizont formation and rupture — the trophozoite undergoes asexual multiplication (schizogony), forming a schizont containing multiple new merozoites; the infected RBC ruptures, releasing merozoites to invade new RBCs and perpetuate the cycle (this rupture is what causes the classic cyclical fevers)
Cytoadherence via PfEMP1 — P. falciparum expresses PfEMP1 (Plasmodium falciparum erythrocyte membrane protein 1) on the surface of infected RBCs, which mediates adherence to endothelial receptors (e.g. ICAM-1, CD36)
Sequestration in the microvasculature — cytoadherence causes infected RBCs to sequester in small vessels of organs like the brain, placenta, and other tissues, avoiding splenic clearance — this is central to the pathophysiology of severe/cerebral malaria and distinguishes P. falciparum from other Plasmodium species, since mature trophozoites and schizonts are rarely seen on peripheral blood film (they're sequestered), unlike in less severe malaria species
List five features of a complicated urinary tract infection, including risk factors and clinical significance.
Occurs in a structurally or functionally abnormal urinary tract (e.g. obstruction, stones, catheter)
More common in males, pregnant women, and immunocompromised or diabetic patients
Higher risk of progression to pyelonephritis or urosepsis
Often involves a broader or more resistant range of organisms than uncomplicated UTIs (e.g. Pseudomonas, ESBL-producing organisms)
Requires longer treatment courses and, often, further investigation (e.g. imaging) to identify the underlying structural or functional abnormality.
Which country has the most time zones in the world—more than Russia?
France. It has 12 due to its overseas territories!