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A patient drinks a large amount of water and soon produces a high volume of dilute urine. What hormone’s activity has decreased, and why?
ADH secretion decreases because plasma osmolarity falls, reducing water reabsorption and leading to dilute urine.
A marathon runner becomes dehydrated after prolonged exercise in heat. How do the kidneys and brain respond to restore homeostasis?
Increased plasma osmolarity stimulates hypothalamic thirst and ADH release → more water intake and reabsorption → concentrated urine and restored osmolarity.
A patient with central diabetes insipidus presents with excessive urine output. Which renal mechanism is impaired?
ADH secretion is deficient, so the distal tubules and collecting ducts remain impermeable to water, preventing concentration of urine.
A patient with chronic kidney disease develops anemia. Explain the renal basis of this symptom.
Damaged kidneys produce less erythropoietin (EPO), decreasing RBC production in bone marrow and reducing oxygen-carrying capacity.
A trauma patient loses significant blood volume. How does the renin-angiotensin-aldosterone system (RAAS) help stabilize blood pressure?
↓ Renal perfusion → renin release → ↑ angiotensin II and aldosterone → vasoconstriction, Na⁺ and water retention → restored blood volume and pressure.
A person on ACE inhibitors shows decreased blood pressure and mild hyperkalemia. What renal processes explain these effects?
Blocking ACE reduces angiotensin II and aldosterone → ↓ Na⁺ reabsorption and ↓ K⁺ secretion → lower blood volume and elevated K⁺.
A patient with hypocalcemia is given vitamin D supplements. How does renal activation of vitamin D help correct calcium levels?
Kidneys convert vitamin D to calcitriol under PTH control → ↑ intestinal Ca²⁺ absorption and renal Ca²⁺ reabsorption → restored calcium balance.
In a patient with respiratory acidosis, how do the kidneys compensate over time?
They increase H⁺ secretion and generate new HCO₃⁻ via ammonium buffering, helping restore normal plasma pH.
A patient has an obstruction in one ureter due to a kidney stone. What reflex limits urine production from that kidney, and why?
The ureterorenal reflex causes sympathetic constriction of renal arterioles, decreasing urine formation and preventing pressure buildup.
A patient with benign prostatic hyperplasia experiences dribbling and incomplete emptying of the bladder. What type of incontinence is this and what’s the mechanism?
Overflow incontinence; obstruction prevents normal outflow, so bladder overfills and urine leaks dropwise.
A spinal cord injury above the sacral region results in uncontrolled bladder emptying. Which neural control mechanism is lost?
Voluntary cortical inhibition of the micturition reflex is lost, causing reflexive (automatic) bladder emptying.
A patient on a high-salt diet has chronically elevated blood pressure. How do the kidneys attempt to normalize it?
They increase urine and sodium excretion through pressure diuresis and natriuresis, lowering blood volume and arterial pressure.
A patient with chronic acidosis from renal failure has reduced ability to excrete hydrogen ions. What consequence occurs?
Plasma H⁺ accumulates, bicarbonate buffering is overwhelmed, and metabolic acidosis develops.
During hemorrhage, why is angiotensin II release critical for survival?
Ang II constricts systemic and renal arterioles and stimulates aldosterone and ADH, preserving blood pressure and circulating volume.
A patient with severe dehydration shows elevated plasma sodium and osmolarity. Which two mechanisms correct this imbalance?
Increased thirst and ADH secretion → more water intake and reabsorption → restored plasma osmolarity.
A patient with a spinal cord lesion loses voluntary control of urination but retains reflex contractions. What term describes this condition?
Automatic bladder (reflex bladder) — micturition reflex functions without cortical regulation.
A patient with hyperkalemia and normal renal function will likely have increased secretion of which hormone, and what effect will it have?
Aldosterone; it enhances K⁺ secretion and Na⁺ reabsorption in distal nephron to normalize plasma K⁺.
How does increased arterial pressure promote long-term regulation of blood volume?
It enhances renal excretion of water and sodium (pressure diuresis/natriuresis), reducing ECF volume and returning pressure to normal.
A patient on diuretics for hypertension experiences increased urine output and decreased plasma osmolarity. Which renal mechanism explains this?
Diuretics inhibit Na⁺ reabsorption → less osmotic water retention → increased urine volume and lower osmolarity.
A PT notes a patient with orthostatic hypotension after dehydration. How does RAAS activation help stabilize their pressure?
Renin release → angiotensin II and aldosterone → increased vascular resistance and water retention → restores perfusion and BP.