16.2 Physiology & Biochemistry Essentials

16.2 Physiology & Biochemistry Essentials

Quick Answer: Lock the control equations and pathway logic first—CO = HR × SV, BP = CO × TPR, right-shifted O₂–Hb unloading with ↑CO₂/H⁺/temp/2,3-BPG, RAAS/ADH for volume–osmolarity, and insulin deficiency → lipolysis → ketones → high anion-gap acidosis. AIAPGET rewards integrated loops over isolated memorization.

Pre-clinical physiology questions on AIAPGET reward equations, feedback loops, and pathway logic over isolated facts. Link each concept to a bedside vignette: shock, dyspnea, oliguria, thyrotoxicosis, or diabetic ketoacidosis.

Cardiovascular Physiology Essentials

Core equations:

Stroke volume determinants: Preload (Frank–Starling—venous return), afterload (arterial impedance), and contractility (inotropy). Starling's law: within limits, increased end-diastolic fiber length increases stroke volume—explains fluid challenge response in hypovolemia.

Cardiac cycle high-yield: Isovolumetric contraction (AV and semilunar valves closed, pressure rises); ejection; isovolumetric relaxation; filling. S1 = AV valve closure; S2 = semilunar closure. Splitting of S2 widens on inspiration (physiologic); fixed splitting suggests ASD.

Baroreceptor reflex: Carotid sinus (CN IX) and aortic arch (CN X) sense stretch → modulate sympathetic/parasympathetic outflow. Carotid massage ↑ parasympathetic → slows AV conduction (used therapeutically in SVT discussion stems).

Mini-case: Narrow pulse pressure with muffled heartsounds and elevated JVP after chest trauma points toward tamponade physiology (impaired filling), not high-output thyrotoxicosis where pulse pressure widens.

Respiratory Physiology & Gas Transport

Lung volumes (simplified): Tidal volume ≈ 500 mL; vital capacity = IRV + TV + ERV; residual volume remains after maximal expiration. FEV₁/FVC falls in obstructive disease, is preserved/↑ in restrictive disease—classic MCQ discriminator.

Oxygen cascade: Atmospheric PO₂ → alveolar PO₂ (PAO₂) → arterial PO₂ (PaO₂) → tissue. A-a gradient widens in V/Q mismatch, shunt, and diffusion limitation.

O₂–Hb dissociation curve:

Carbon monoxide binds Hb with ~200–250× affinity of O₂, shifts curve left, and causes cherry-red tissues—bridging physiology to toxicology.

CO₂ transport: ~70% as bicarbonate (carbonic anhydrase in RBCs), ~20–25% carbamino compounds, remainder dissolved. Haldane effect: deoxygenated Hb carries more CO₂.

Renal Physiology & Acid–Base

GFR & Starling forces: Net filtration = Kf × [(PGC − PBS) − (πGC − πBS)]. Afferent constriction ↓GFR; moderate efferent constriction (angiotensin II) can preserve GFR when renal blood flow falls.

Tubular handling high-yield:

RAAS: Juxtaglomerular renin → angiotensin I → ACE → angiotensin II (vasoconstriction, aldosterone, ADH, thirst). Explains ACE-inhibitor effects and secondary hypertension vignettes.

Acid–base (Henderson–Hasselbalch logic): Metabolic acidosis (↓HCO₃⁻) → compensatory hyperventilation; metabolic alkalosis → hypoventilation; respiratory acidosis (↑PaCO₂) → renal HCO₃⁻ retention. Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻); high AG in ketoacidosis, lactate, uremia, toxins (MUDPILES mnemonic family).

Endocrine Physiology High-Yield

Feedback: Negative feedback dominates (thyroid, cortisol, gonadal axes). Positive feedback examples: oxytocin in labor; LH surge mid-cycle.

Biochemistry Pathways That Score Marks

Carbohydrate metabolism: Glycolysis (cytosol) converts glucose → pyruvate (aerobic) or lactate (anaerobic). Pyruvate dehydrogenase links to acetyl-CoA for Krebs (mitochondria). Rate-limiting glycolytic enzyme: phosphofructokinase-1 (PFK-1), inhibited by ATP/citrate, activated by AMP/fructose-2,6-bisphosphate.

Gluconeogenesis: Liver (± kidney) makes glucose from lactate, glycerol, glucogenic amino acids—critical in fasting >~12–18 hours after glycogen depletes. Cori cycle recycles muscle lactate to hepatic glucose.

Lipid & ketone metabolism: β-oxidation yields acetyl-CoA; excess acetyl-CoA in fasting/diabetes forms ketone bodies (acetoacetate, β-hydroxybutyrate, acetone)—explains fruity breath and high-AG acidosis in DKA. Carnitine shuttle moves long-chain fatty acids into mitochondria.

Protein & nitrogen: Transamination (ALT/AST) funnels nitrogen to glutamate; urea cycle (liver) detoxifies ammonia. Hyperammonemia in urea-cycle defects or severe liver failure causes encephalopathy—classic biochemistry–clinical bridge.

Electron transport & ATP: NADH/FADH₂ donate electrons; oxidative phosphorylation at Complexes I–IV with ATP synthase. Cyanide and CO block cytochrome oxidase (Complex IV)—again overlapping toxicology.

Vitamins as cofactors (quick hits): Thiamine (B1)—PDH and α-KGDH; Niacin (B3)—NAD; Riboflavin (B2)—FAD; Pyridoxine (B6)—transamination; B12/folate—one-carbon/DNA synthesis (megaloblastic anemia).

Integration for Homoeopathic Clinicians

Physiology explains why a constitutional picture shows heat intolerance with weight loss (hyperthyroid metabolic rate), why nocturnal polyuria appears with poorly controlled diabetes (osmotic diuresis), and why shock states demand different remedy and referral urgency. You are not replacing materia medica with equations—you are preventing dangerous misreads of vital signs and lab context that AIAPGET will embed in stems.

Study tip: For every hormone or pathway, write one stimulus, one action, and one disease of excess/deficiency. That triad covers most MCQs without encyclopedic memorization.