Pre-clinical Sciences: Anatomy, Physiology and Biochemistry
NEET PG treats the pre-clinical subjects as applied science, not pure recall. Anatomy questions hinge on relations, nerve supply, embryological derivatives and imaging landmarks; physiology on renal, respiratory and cardiovascular regulation with simple calculations; biochemistry on rate-limiting enzymes, vitamin cofactors and inborn errors. A stem gives one clinical clue and expects you to trace it back to the mechanism.
Core rules
- Anatomy: Erb palsy is C5-C6 with waiter's tip posture; Klumpke is C8-T1 with claw hand and Horner syndrome. Common peroneal nerve injury causes foot drop. Femoral triangle contents lateral to medial: nerve, artery, vein, empty space, lymphatics.
- Physiology: renal glucose threshold about 180 mg/dL, Tm about 375 mg/min; filtration fraction is GFR divided by renal plasma flow, roughly 0.2.
- Biochemistry: rate-limiting steps are PFK-1 (glycolysis), FBPase-1 (gluconeogenesis), HMG-CoA reductase (cholesterol) and carbamoyl phosphate synthetase I (urea cycle). Thiamine is the cofactor for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase and branched-chain ketoacid dehydrogenase.
Worked example
A patient in diabetic ketoacidosis has Na 130, Cl 100, HCO3 10 and glucose 500 mg/dL. Anion gap = 130 minus (100 plus 10) = 20, against a normal of 8-12. Delta ratio = change in AG divided by change in HCO3 = (20-12)/(24-10) = 0.57. A ratio below 1 indicates a coexisting normal-anion-gap acidosis such as diarrhoea or large-volume saline; 1-2 is pure high-AG acidosis; above 2 suggests coexisting metabolic alkalosis. Corrected sodium = measured sodium plus 1.6 mEq for every 100 mg/dL glucose above 100.
Traps
- Reporting the anion gap without albumin correction; it falls about 2.5 for every 1 g/dL fall in albumin.
- Swapping the C5-C6 and C8-T1 lesion patterns.
- Quoting PFK-1 regulation backwards: activated by AMP and fructose-2,6-bisphosphate, inhibited by ATP and citrate.