NBDE Part I study materials
NBDE Part I study resources

NBDE Part I: Biochemistry and Physiology: Metabolism, Organ Systems, and Regulation

NBDE Part I · Work through your exam, one topic at a time.

All guide sections

Biochemistry and Physiology: Metabolism, Organ Systems, and Regulation

Enzymes and energy

Understand Michaelis-Menten behavior: Km is the substrate concentration at half-maximal velocity and is an inverse measure of enzyme affinity; Vmax reflects enzyme amount. Competitive inhibitors raise Km with Vmax unchanged; noncompetitive inhibitors lower Vmax with Km unchanged. Track ATP yield through glycolysis (net 2 ATP, 2 NADH), pyruvate dehydrogenase, the TCA cycle, and oxidative phosphorylation. Know when gluconeogenesis, glycogenolysis, and ketogenesis are active, and that the Cori cycle moves lactate from muscle to liver.

Hormones and organs

Pair each hormone with its trigger and effect: insulin lowers glucose; glucagon and cortisol raise it; parathyroid hormone raises serum calcium while calcitonin lowers it; ADH increases collecting-duct water permeability; aldosterone increases sodium reabsorption and potassium excretion. In the kidney, know glomerular filtration, clearance, and the countercurrent mechanism. In the lung, the oxyhemoglobin dissociation curve shifts right with increased CO2, decreased pH, and increased temperature (Bohr effect).

Neurophysiology

The resting membrane potential depends on the Na+/K+ ATPase and potassium leak. Depolarization reflects sodium influx; repolarization reflects potassium efflux. Muscle contraction follows the sliding filament model, with calcium binding troponin C to uncover actin-binding sites.

Traps

Students most often invert Km and Vmax effects for inhibitors, confuse ADH with aldosterone, or forget that the Na+/K+ pump is electrogenic and consumes ATP.

Rule of thumb

“Substrate at half-speed” defines Km. When an inhibitor is described, ask first whether the asymptote (Vmax) moved or only the approach to it (Km).