Physiology Practice Questions

Atrial natriuretic peptide (ANP) is released with atrial stretch. It promotes natriuresis/diuresis by decreasing tubular Na⁺ reabsorption and inhibiting renin/aldosterone/ADH, lowering blood volume and pressure.

Angiotensin-converting enzyme (ACE), largely in pulmonary endothelium, converts angiotensin I to the potent vasoconstrictor angiotensin II.

Edema results from increased capillary hydrostatic pressure, increased permeability, decreased plasma oncotic pressure, or lymphatic obstruction.

Decreased capillary hydrostatic pressure would oppose fluid filtration, not cause edema.

Hypokalemia classically shows prominent U waves (often with flattened T waves and ST depression). Severe cases predispose to arrhythmias.

Changes isolated to QRS, PR, or ST are less specific for hypokalemia.

Mobitz I is typically benign and often asymptomatic. It features gradually lengthening PR intervals before a non-conducted P wave.

High fatality is not characteristic of Mobitz I.

An S3 can be physiologic in youth/pregnancy but in older adults often indicates volume overload states such as congestive heart failure.

COPD and arrhythmias are not typical causes of an S3.

MAP ≈ CO × TPR (central venous pressure is usually negligible in this relation).

The other expressions do not define MAP.

Phase 3 (repolarization) is dominated by K⁺ efflux via delayed rectifier K⁺ channels.

Ca²⁺ influx peaks in phase 2, while fast Na⁺ influx defines phase 0.

Ejection fraction is stroke volume divided by end-diastolic volume.

TPR is not part of the EF calculation.

Bradykinin promotes vasodilation, increased vascular permeability, and pain. It does not increase prothrombin secretion.

Para-aminohippurate (PAH) is actively secreted by proximal tubule cells via organic anion transporters. It’s used to estimate renal plasma flow.

Vasopressin (ADH) is released from the posterior pituitary (synthesized in the hypothalamus). TSH, GH, and prolactin are anterior pituitary hormones.

T3 supports growth (including bone), CNS development, and increases beta-adrenergic responsiveness and basal metabolic rate.

Decreasing calcium reabsorption is not a recognized direct action of T3.

Hypercalcemia is commonly due to primary hyperparathyroidism or malignancy and can occur in granulomatous diseases such as sarcoidosis.

Aldosterone excess is not a typical cause of hypercalcemia.

ACTH is a peptide hormone derived from POMC and is not synthesized from progesterone.

Cortisol, aldosterone, and sex steroids arise from cholesterol via steroidogenic pathways that pass through progesterone intermediates.

Chief cells of the gastric mucosa secrete pepsinogen, which is activated to pepsin in acidic conditions.

CCK from duodenal I cells is the principal stimulus for pancreatic acinar enzyme (zymogen) secretion. Vagal acetylcholine also stimulates.

Secretin mainly stimulates bicarbonate from ductal cells. Somatostatin is inhibitory.

Angiotensin II is a potent vasoconstrictor that increases blood pressure, stimulates aldosterone release, and promotes ADH release from the posterior pituitary.

Vasodilation is not an effect of Ang II.

Progesterone raises basal body temperature, relaxes some smooth muscle, and supports secretory endometrium with spiral artery development.

Estrogen promotes breast/uterine growth, follicular development, and (in much of the cycle) negative feedback that suppresses FSH. It increases hepatic synthesis of many transport proteins, not decreases them.