Physiology and Biochemistry
Physiology and Biochemistry tests how the body maintains homeostasis and how biochemical pathways explain clinical signs. High-yield areas include membrane potentials, acid-base balance, renal handling, hormone action, enzyme kinetics, and energy metabolism.
Core rules
- Resting membrane potential depends mainly on potassium permeability; the Na/K ATPase maintains gradients.
- Acid-base: the body compensates but does not fully correct pH; compensation is respiratory or renal depending on the primary disorder.
- High anion gap metabolic acidosis is caused by retained acids such as ketones, lactate, or uremic toxins.
- Enzyme inhibitors: competitive inhibitors raise Km without changing Vmax; noncompetitive inhibitors lower Vmax.
- Insulin lowers blood glucose and shifts potassium into cells.
Worked example
A patient with poorly controlled type 1 diabetes presents with deep rapid breathing, glucose 30 mmol/L, pH 7.18, bicarbonate 10 mmol/L, and positive ketones. The primary disorder is high anion gap metabolic acidosis from diabetic ketoacidosis. Kussmaul breathing is respiratory compensation that lowers PaCO2 by hyperventilation. Treatment requires fluids, insulin, and potassium replacement because insulin drives potassium intracellularly and total body potassium is already depleted.
Traps
- Do not label any low bicarbonate as renal tubular acidosis; check the anion gap and clinical context.
- A normal pH does not exclude a mixed disorder.
- Competitive inhibition can be overcome by more substrate; noncompetitive cannot.
- In diabetic ketoacidosis, serum potassium may look normal or high despite total body depletion.