Pre-clinical Sciences: Anatomy, Physiology and Biochemistry
INI CET tests the pre-clinical block through mechanism rather than isolated recall: anatomy appears as nerve lesions and surgical corridors, physiology as integrated regulation (renal handling, cardiac output, gas exchange), and biochemistry as rate-limiting enzymes, cofactor requirements and the consequences of their deficiency.
Core rules and high-yield facts
- Anatomy: localise a lesion by the muscle paralysed plus the sensory strip lost. Erb's palsy (C5–C6, upper trunk) gives the waiter's-tip posture; Klumpke's (C8–T1, lower trunk) gives claw hand, often with Horner's syndrome.
- Physiology: clearance = (urine concentration × urine flow) ÷ plasma concentration. The oxygen–haemoglobin curve shifts right (lower affinity, higher P50) with rising CO2, H+, temperature and 2,3-BPG.
- Biochemistry: the committed, regulated step of each pathway is what gets asked - PFK-1 for glycolysis, pyruvate dehydrogenase for entry into the TCA cycle, HMG-CoA reductase for cholesterol synthesis.
Worked example
A competitive inhibitor (methotrexate at dihydrofolate reductase, statins at HMG-CoA reductase) binds the active site. Reasoning: with substrate and inhibitor competing, the apparent Km rises, Vmax is unchanged, and inhibition is reversed by raising substrate concentration. A non-competitive inhibitor binds elsewhere, so Vmax falls while Km is unchanged and extra substrate does not help. Mixed inhibition changes both. Read the stem for the word "reversible by increasing substrate" - that phrase alone identifies competitive kinetics.
Traps that cost marks
- A lower Km means higher affinity. Candidates routinely reverse this.
- Brachial plexus order is roots C5–T1, trunks, divisions, cords, branches; cords are named for their relation to the axillary artery, not for the nerve they become.
- Net ATP from anaerobic glycolysis is 2, not 4. The old "38 ATP" figure for aerobic oxidation is obsolete; use 30–32 per glucose.
- Thiamine pyrophosphate, not thiamine, is the cofactor for pyruvate dehydrogenase, α-ketoglutarate dehydrogenase and transketolase.