Membership of the Royal College of Surgeons (MRCS) Physiology and Applied Surgical Science Flashcards

24 sample cards from the Physiology and Applied Surgical Science deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. How do thyroid hormones $T_3$ and $T_4$ differ in potency and origin?

   $T_4$ (thyroxine) is the main secreted form but is a prohormone; $T_3$ (triiodothyronine) is several times more potent and is largely produced by peripheral deiodination of $T_4$.

2. What are the three main hormones regulating calcium, and their net effects on serum calcium?

   Parathyroid hormone (PTH) raises serum calcium (bone resorption, renal $\ce{Ca}$ reabsorption, activates vitamin D); calcitriol (active vitamin D) raises it (gut absorption); calcitonin lowers it.

3. Through what mechanisms does PTH raise serum calcium?

   It stimulates osteoclastic bone resorption, increases renal distal tubular calcium reabsorption (and phosphate excretion), and activates renal $1\alpha$-hydroxylase to produce active vitamin D, increasing gut calcium absorption.

4. Describe the ebb and flow phases of the metabolic response to surgery/trauma.

   The ebb phase (first ~24--48 h) features hypovolaemia, reduced metabolic rate and cardiac output; the flow (catabolic) phase shows increased metabolic rate, catabolism, negative nitrogen balance, hyperglycaemia and a later anabolic recovery phase.

5. What hormonal and metabolic changes characterise the catabolic surgical stress response?

   Increased cortisol, catecholamines, glucagon, ADH and aldosterone; insulin resistance with hyperglycaemia; protein breakdown with negative nitrogen balance; lipolysis; and sodium/water retention.

6. Outline the intrinsic and extrinsic coagulation pathways and where they converge.

   Extrinsic pathway: tissue factor + factor VII (measured by PT). Intrinsic pathway: factors XII, XI, IX, VIII (measured by APTT). Both converge on the common pathway activating factor X, then prothrombin to thrombin, and fibrinogen to fibrin.

7. Which clotting factors are vitamin K-dependent?

   Factors II, VII, IX and X, plus the anticoagulant proteins C and S.

8. What is the basis of the ABO blood group system and which is the universal donor?

   ABO groups are defined by A and B surface antigens with naturally occurring IgM antibodies against absent antigens. Group O (no A/B antigens) red cells are the universal donor; group AB is the universal recipient.

9. Why does Rhesus D status matter in transfusion and pregnancy?

   RhD-negative individuals can form anti-D IgG antibodies after exposure to RhD-positive blood, causing haemolytic transfusion reactions and, in pregnancy, haemolytic disease of the newborn; hence RhD-negative recipients should receive RhD-negative blood.

10. Contrast innate and adaptive immunity.

    Innate immunity is rapid, non-specific, has no memory (e.g. neutrophils, macrophages, complement, barriers); adaptive immunity is slower, antigen-specific, generates immunological memory, and is mediated by T and B lymphocytes.

11. What are the four types of graft based on donor-recipient relationship?

    Autograft (self to self), isograft (genetically identical, e.g. identical twin), allograft (same species, different genotype), and xenograft (different species).

12. Classify transplant rejection by timing and mechanism.

    Hyperacute (minutes--hours, preformed antibodies), acute (days--weeks, T-cell mediated and/or antibody-mediated), and chronic (months--years, fibrosis and vascular changes).

13. Describe the structure of the cell membrane (fluid mosaic model).

    A phospholipid bilayer with hydrophilic heads outward and hydrophobic tails inward, interspersed with cholesterol, and integral/peripheral proteins, glycoproteins and glycolipids that provide transport, signalling and recognition functions.

14. Contrast primary and secondary active transport with an example of each.

    Primary active transport directly uses ATP (e.g. $\ce{Na+}/\ce{K+}$-ATPase pumping $3\ \ce{Na+}$ out for $2\ \ce{K+}$ in). Secondary active transport uses an ion gradient set up by primary transport (e.g. $\ce{Na+}$-glucose co-transport, SGLT).

15. What is the typical resting membrane potential of a neuron, and what mainly sets it?

    About $-70\ \text{mV}$, set principally by the high resting permeability to $\ce{K+}$ (approaching the $\ce{K+}$ equilibrium potential) maintained by the $\ce{Na+}/\ce{K+}$-ATPase.

16. Give the Nernst equation for the equilibrium potential of an ion.

    $E_{ion} = \frac{RT}{zF}\ln\frac{[\text{ion}]_{out}}{[\text{ion}]_{in}}$, approximately $E_{ion} = \frac{61}{z}\log_{10}\frac{[\text{ion}]_{out}}{[\text{ion}]_{in}}\ \text{mV}$ at $37^{\circ}\text{C}$.

17. Outline the ionic basis of the neuronal action potential.

    Depolarisation to threshold opens voltage-gated $\ce{Na+}$ channels (rapid upstroke); these inactivate while voltage-gated $\ce{K+}$ channels open, causing repolarisation and a brief hyperpolarisation, before the resting potential is restored.

18. Describe the steps of skeletal muscle excitation-contraction coupling.

    Action potential travels down the T-tubule, triggering $\ce{Ca^2+}$ release from the sarcoplasmic reticulum; $\ce{Ca^2+}$ binds troponin C, moving tropomyosin to expose actin binding sites, enabling myosin cross-bridge cycling (sliding filament) powered by ATP.

19. Name the four main gastrointestinal hormones and their key actions.

    Gastrin (stimulates gastric acid secretion), secretin (stimulates pancreatic/biliary bicarbonate), cholecystokinin (CCK; gallbladder contraction and pancreatic enzyme secretion), and gastric inhibitory peptide/GIP (incretin, stimulates insulin).

20. What stimulates and inhibits gastric acid secretion by parietal cells?

    Stimulated by gastrin, histamine (via $H_2$ receptors) and acetylcholine (vagal); the $\ce{H+}/\ce{K+}$-ATPase proton pump is the final step. Inhibited by somatostatin, secretin, and low luminal pH (negative feedback).

21. How is core body temperature regulated, and what is the controlling centre?

    The hypothalamus acts as the thermostat; heat loss is via radiation, conduction, convection and evaporation. Cold triggers vasoconstriction, shivering and thyroid/catecholamine-driven thermogenesis; heat triggers vasodilatation and sweating.

22. Classify the types of shock by underlying mechanism.

    Hypovolaemic (fluid/blood loss), cardiogenic (pump failure), obstructive (e.g. tamponade, tension pneumothorax, PE), and distributive (septic, anaphylactic, neurogenic — loss of vascular tone).

23. Contrast the haemodynamic profile of septic (distributive) shock with hypovolaemic shock.

    Septic shock: low systemic vascular resistance, high/normal cardiac output, warm peripheries early. Hypovolaemic shock: high SVR, low cardiac output, low preload, cold/clammy peripheries with compensatory tachycardia.

24. What are the four classes of haemorrhagic shock by blood loss volume (ATLS)?

    Class I: $<15\%$ ($<750\ \text{mL}$), minimal signs. Class II: $15\text{--}30\%$, tachycardia, narrowed pulse pressure. Class III: $30\text{--}40\%$, hypotension, altered mental state. Class IV: $>40\%$, life-threatening, marked hypotension and oliguria.

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