Fellowship of the Royal College of Anaesthetists (FRCA) Physiology and Biochemistry Flashcards

24 sample cards from the Physiology and Biochemistry deck

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

1. How is plasma osmolality calculated and what is its normal range?

   $Osm = 2[Na^+] + [glucose] + [urea]$ (mmol·L⁻¹). Normal $\approx 275\text{–}295\ \text{mOsm·kg}^{-1}$. An osmolar gap >10 suggests unmeasured solutes (e.g. ethanol, methanol).

2. Write the Henderson-Hasselbalch equation for the bicarbonate buffer system.

   $pH = pK_a + \log_{10}\dfrac{[HCO_3^-]}{0.03 \times P_aCO_2}$, with $pK_a = 6.1$. Normal arterial $pH = 7.35\text{–}7.45$.

3. Classify the four primary acid-base disturbances by $pH$, $P_aCO_2$ and $HCO_3^-$.

   Respiratory acidosis: low pH, high $P_aCO_2$. Respiratory alkalosis: high pH, low $P_aCO_2$. Metabolic acidosis: low pH, low $HCO_3^-$. Metabolic alkalosis: high pH, high $HCO_3^-$. Compensation moves the other variable in the same direction.

4. Define the anion gap and give causes of a raised anion gap metabolic acidosis.

   $AG = [Na^+] - ([Cl^-] + [HCO_3^-])$, normal $8\text{–}12\ \text{mmol·L}^{-1}$. Raised AG causes (MUDPILES): methanol, uraemia, DKA, propylene glycol, isoniazid, lactate, ethylene glycol, salicylates.

5. State the Nernst equation and the equilibrium potential for $K^+$.

   $E_{ion} = \dfrac{RT}{zF}\ln\dfrac{[ion]_o}{[ion]_i} \approx 61\log_{10}\dfrac{[ion]_o}{[ion]_i}\ \text{mV at 37°C}$. For $K^+$, $E_K \approx -90\ \text{mV}$; resting membrane potential $\approx -70\ \text{mV}$ (nerve).

6. Describe the ionic phases of a neuronal action potential.

   Depolarisation: voltage-gated $Na^+$ channels open ($Na^+$ influx). Repolarisation: $Na^+$ channels inactivate, voltage-gated $K^+$ channels open ($K^+$ efflux). Hyperpolarisation: slow $K^+$ closure. Absolute then relative refractory periods follow.

7. Outline the sequence of events in chemical synaptic transmission.

   Action potential depolarises terminal → voltage-gated $Ca^{2+}$ entry → vesicle fusion and neurotransmitter release → diffusion across cleft → postsynaptic receptor binding → EPSP/IPSP. Transmitter removed by reuptake, enzymatic breakdown or diffusion.

8. State the determinants of cerebral perfusion pressure and the autoregulation range.

   $CPP = MAP - ICP$ (or CVP if higher). Cerebral autoregulation keeps CBF (~50 mL·100g⁻¹·min⁻¹) constant over MAP $\approx 50\text{–}150\ \text{mmHg}$. CBF rises with $P_aCO_2$ and falls with hypocapnia.

9. State the Monro-Kellie doctrine.

   The skull is a rigid box containing brain (~80%), blood (~10%) and CSF (~10%). An increase in one component must be offset by a decrease in another, or ICP rises. Initial compensation buffers volume, then ICP rises steeply.

10. Compare first (fast) and second (slow) pain fibres.

    Fast/first pain: $A\delta$ fibres, myelinated, sharp/well-localised, fast conduction. Slow/second pain: C fibres, unmyelinated, dull/burning/poorly localised. Both synapse in dorsal horn and ascend mainly via the spinothalamic tract.

11. Explain the gate control theory of pain.

    Activity in large $A\beta$ (touch) fibres excites inhibitory interneurons in the dorsal horn substantia gelatinosa, 'closing the gate' and reducing transmission of nociceptive ($A\delta$/C) input to projection neurons. Descending pathways also modulate the gate.

12. Contrast sympathetic and parasympathetic preganglionic/postganglionic transmitters and receptors.

    Both: preganglionic release ACh acting on nicotinic receptors. Parasympathetic postganglionic: ACh on muscarinic receptors. Sympathetic postganglionic: noradrenaline on adrenoceptors (exception: sweat glands use ACh/muscarinic; adrenal medulla releases adrenaline).

13. List the steps of excitation-contraction coupling in skeletal muscle.

    Action potential travels down T-tubule → dihydropyridine receptor activates ryanodine receptor → $Ca^{2+}$ released from sarcoplasmic reticulum → $Ca^{2+}$ binds troponin C → tropomyosin moves → actin-myosin cross-bridge cycling (ATP-dependent) → contraction; $Ca^{2+}$ reuptake causes relaxation.

14. Describe neuromuscular transmission at the motor end-plate.

    Action potential → presynaptic $Ca^{2+}$ entry → ACh vesicle release → ACh binds postjunctional nicotinic receptors → $Na^+$ influx → end-plate potential → muscle action potential. ACh is hydrolysed by acetylcholinesterase. A large safety margin exists (~70% receptor block before failure).

15. Name the anterior pituitary hormones and a key target/action of each.

    GH (growth/IGF-1), ACTH (adrenal cortisol), TSH (thyroid hormone), LH and FSH (gonads), prolactin (lactation). Posterior pituitary (stored, not made there): ADH (water reabsorption) and oxytocin.

16. Compare the actions of insulin and glucagon on glucose metabolism.

    Insulin (β-cells): lowers blood glucose—promotes glucose uptake (GLUT4), glycogenesis, lipogenesis, protein synthesis; inhibits gluconeogenesis. Glucagon (α-cells): raises blood glucose—promotes glycogenolysis and gluconeogenesis.

17. Describe the hormonal control of plasma calcium.

    PTH (low $Ca^{2+}$): raises $Ca^{2+}$ via bone resorption, renal reabsorption and activation of vitamin D ($1\alpha$-hydroxylase), increasing gut absorption; lowers phosphate. Calcitonin lowers $Ca^{2+}$. Vitamin D (calcitriol) increases gut $Ca^{2+}$ and phosphate absorption.

18. Match key gastrointestinal secretions to their source cells.

    Parietal cells: HCl and intrinsic factor. Chief cells: pepsinogen. G cells: gastrin. Mucous/neck cells: mucus and $HCO_3^-$. Pancreas: bicarbonate (ductal) and enzymes (acinar). I cells: CCK; S cells: secretin.

19. Summarise the synthetic and metabolic functions of the liver.

    Synthesis of albumin, clotting factors (except VIII and vWF) and bile; glucose homeostasis (glycogen storage, gluconeogenesis); lipid and protein metabolism; urea cycle (ammonia detox); bilirubin conjugation; drug metabolism (phase I CYP450 and phase II conjugation); storage of vitamins and iron.

20. State the basal metabolic rate value and the equation linking $\dot{V}O_2$ to energy expenditure.

    BMR $\approx 1\ \text{kcal·kg}^{-1}\text{·h}^{-1}$ (~70 kcal·h⁻¹, oxygen consumption ~250 mL·min⁻¹). Respiratory quotient $RQ = \dfrac{\dot{V}CO_2}{\dot{V}O_2}$: 1.0 for carbohydrate, ~0.7 for fat, ~0.8 mixed diet.

21. Describe red cell physiology: lifespan, production control and key features.

    Erythrocytes are biconcave, anucleate; lifespan ~120 days; produced in marrow under erythropoietin (renal, hypoxia-driven); rely on anaerobic glycolysis and the pentose phosphate pathway; broken down in the spleen with iron recycling and bilirubin formation.

22. Outline the coagulation cascade pathways and their common convergence.

    Intrinsic pathway (XII→XI→IX→VIII, monitored by APTT) and extrinsic pathway (tissue factor + VII, monitored by PT) converge at factor X activation (common pathway): $X\to Xa$ converts prothrombin (II) to thrombin, which converts fibrinogen (I) to fibrin, stabilised by XIII.

23. State the ABO and Rh blood group compatibility rules for red cell transfusion.

    Group O = universal red cell donor (no A/B antigens); group AB = universal recipient. Anti-A/anti-B are naturally occurring IgM. RhD-negative recipients (especially females of childbearing age) should receive RhD-negative blood to avoid anti-D sensitisation.

24. List the major cardiovascular and respiratory changes of normal pregnancy at term.

    Cardiac output rises ~40% (↑HR and SV), plasma volume rises ~50% (dilutional anaemia), SVR and BP fall in mid-pregnancy. Minute ventilation rises ~50% (↑tidal volume) causing a compensated respiratory alkalosis ($P_aCO_2 \approx 4.1\ \text{kPa}$); FRC falls ~20%.

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