Which statement best explains why antidiuretic hormone (ADH) increases blood volume?
It promotes water reabsorption in distal tubules.
It enhances sodium retention in the loop of Henle.
It decreases renal artery blood flow.
It stimulates the adrenal cortex to release aldosterone.
The Correct Answer is A
Rationale:
A. It promotes water reabsorption in distal tubules is correct. Antidiuretic hormone (ADH), also called vasopressin, is secreted by the posterior pituitary in response to increased plasma osmolality or decreased blood volume. ADH acts primarily on the distal convoluted tubules and collecting ducts of the kidney, increasing their permeability to water by inserting aquaporin-2 channels into the tubular membranes. This allows water to move from the tubular lumen back into the bloodstream, concentrating the urine and expanding blood volume, thereby helping maintain blood pressure and plasma osmolality.
B. It enhances sodium retention in the loop of Henle is incorrect. Sodium reabsorption is primarily regulated by aldosterone, not ADH. While water follows sodium osmotic gradients, ADH’s effect on water reabsorption is independent of direct sodium regulation.
C. It decreases renal artery blood flow is incorrect. ADH does have vasoconstrictive properties via V1 receptors in high concentrations, but its primary role in normal physiology is water reabsorption, not reducing renal perfusion. Decreased renal blood flow is not the mechanism by which ADH increases blood volume.
D. It stimulates the adrenal cortex to release aldosterone is incorrect. Aldosterone secretion is primarily regulated by the renin-angiotensin-aldosterone system and plasma potassium levels, not by ADH. ADH increases blood volume directly through water retention, not indirectly via aldosterone release.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
Rationale:
A. By promoting vasoconstriction, aldosterone release, and increasing blood volume is correct. The renin-angiotensin-aldosterone system (RAAS) is activated in response to low blood pressure, decreased renal perfusion, or low sodium levels. Renin, released by the juxtaglomerular cells of the kidney, converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor, increasing systemic vascular resistance and blood pressure. It also stimulates aldosterone release from the adrenal cortex, which promotes sodium and water reabsorption in the distal tubules and collecting ducts of the kidney, thereby increasing blood volume and further raising blood pressure.
B. By blocking angiotensin II from binding to its receptors, reducing vasoconstriction is incorrect. This describes the action of angiotensin receptor blockers (ARBs), which lower blood pressure by preventing angiotensin II from exerting its effects. This is the opposite of the RAAS’s natural compensatory mechanism during hypotension.
C. By decreasing blood volume through promoting sodium and water excretion is incorrect. RAAS activation conserves sodium and water, increasing blood volume. Promoting excretion would lower blood volume and exacerbate hypotension, which is contrary to the system’s function.
D. By inhibiting aldosterone production and promoting sodium excretion is incorrect. RAAS stimulates aldosterone production, not inhibits it. Inhibiting aldosterone would lead to sodium and water loss, reducing blood volume and failing to restore blood pressure.
Correct Answer is A
Explanation
Rationale:
A. In emphysema, destruction of alveolar walls and loss of elastic recoil lead to air trapping and hyperinflation of the lungs. Over time, this causes the diaphragm to flatten as the lungs expand, which is a classic radiographic sign of advanced emphysema. This finding correlates with reduced ventilatory efficiency, increased work of breathing, and progressive respiratory compromise.
B. In emphysema, breath sounds are often decreased due to the destruction of alveoli and hyperinflation of the lungs. Loud or increased breath sounds are more typical in conditions such as bronchospasm or pulmonary edema with turbulent airflow.
C. While early emphysema may present with minimal auscultatory findings and a mild cough, advanced disease is associated with hyperinflated lungs, decreased breath sounds, and sometimes wheezing. Clear lung fields alone do not indicate severe or advanced disease.
D. Bradycardia and constricted pupils are incorrect. These findings are unrelated to emphysema. Bradycardia and miosis may suggest medication effects (e.g., opioids) or neurologic conditions, not pulmonary pathology.
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