Chapter 24 - The Urinary System Application Questions

What effect would this toxin have on the reabsorption of glucose and bicarbonate ions?

Glucose molecules are reabsorbed with sodium ions as a result of secondary active transport. Bicarbonate ions are reabsorbed as a result of the Na+/H+ antiporter in the PCT. If all sodium ion reabsorption were blocked, the glucose/sodium ion cotransporter and Na+/H+ antiporter would not function, and high amounts of glucose and bicarbonate ions would appear in the urine.

Respiratory conditions can cause hypoventilation that leads to a decreased blood pH. Predict how the kidneys will respond to this change in pH.

Hypoventilation will lead to acidosis, which causes the kidneys to increase their secretion of hydrogen ions and increase the reabsorption of bicarbonate ions.

Inflammation of the peritoneal membranes, or peritonitis, can cause dysfunction of multiple organs in the abdominal cavity. Would you expect peritonitis to affect the kidneys? Explain.

Peritonitis would be unlikely to impact the kidneys as they are retroperitoneal, or located posterior to the peritoneal membranes.

Ms. Douglas has advanced liver disease; because her liver is no longer able to produce plasma proteins, her colloid osmotic pressure has decreased. Predict the effects that this loss of pressure will have on the net filtration pressure and the GFR in her nephrons.

A decrease in colloid osmotic pressure will decrease the force that retains water in the blood in the glomerulus. As a result, the net filtration pressure will increase in favor of filtration, and more filtrate will be produced.

How would a spinal cord injury above the level of S1 - S2 affect micturition in that patient? How would the situation change in the injury were below S1 - S2?

A spinal cord injury above S1 - S2 would prevent voluntary control of micturition, as the impulses would be unable to reach the micturition center in the pons. An injury below S1 - S2 could damage the neurons in the involuntary pathway of the micturition reflex. This could lead to urinary retention, because the signals that trigger the emptying of the urinary bladder would be interrupted.

Drugs called loop diuretics block the Na+/K+/2CL symporters in the thick ascending limb of the nephron loop. a) Predict the effect these drugs will have on the gradient in the renal medulla, and the resulting effect on water reabsorption form the medullary collecting system. How will this impact urine volume? b) Predict what might happen if the drug instead had the opposite effect - it caused more sodium and chloride ions to be reabsorbed into the medullary interstitial fluid.

A) Since less sodium chloride is pumped into the interstitial fluid, the gradient for water reabsorption from the medullary collecting system will be decreased. This will reduce the volume of water reabsorbed and thus increase urine volume. B) If the drug instead stimulated the Na+/K+/2Cl- pumps, a steeper gradient in the renal medulla would be created for water reabsorption. This would cause a person to produce more concentrated urine and retain more water, possibly leading to overhydration.

Predict the potential effects of abnormally narrow renal arteries, a condition called renal artery stenosis, on the ability of the kidneys to carry out their functions.

Anything that decreases the blood flow to the kidneys will lower the rate of filtration of fluid from the blood into the nephrons and therefore decrease the regulation of fluid, electrolyte and acid-base balance performed by the kidneys.

Certain diuretics block the effects of carbonic anhydrase in the proximal tubule. Predict the effects these drugs would hav eon the pH of the blood. How might the kidneys compensate for this?

Blocking carbonic anhydrase will result in the reabsorption of fewer sodium and bicarbonate ions. This will lead to a decreased pH of the blood. The resulting acidosis will cause the kidneys to increase secretion of the hydrogen ions and retain bicarbonate ions from the distal tubule.

Dietary supplementation with creatiine phosphate is popular among athletes for its supposed performance-enhancing effects. What effect would creatine phosphate supplementation have on the amount of creatine in the blood, and therefore the amount of creatinine that the kidneys must exercise?

Creatine phosphate is metabolized to creatinine, and so an increase in consumption of creatine will lead to an increased amount of creatinine in the blood. This will increase the workload of the kidneys, as they must excrete the excess creatinine.

Mr. Adams is taking an ACE inhibitor and an antiotensin-receptor blocker, both drugs that block the RAAS, for his high blood pressure. He complains that when he tries to engage in physical activity, he feels faint. He is asked to exercise on a treadmill, and his blood pressure remains very low when he exercises, rather than rising with his level of physical activity. Explain how his medications could be causing his current problem.

Drugs that block the RAAS will inhibit overall vasoconstriction, and this can reduce the vasoconstriction that normally occurs with physical activity. Without this normal vasoconstriction, the blood pressure remains low, even when it would normally rise.

Predict what would happen if the epithelium of the urinary tract were made of simple squamous epithelium instead of transitional epithelium.

Simple squamous epithelium is very thin and would not protect the underlying connective and muscle tissue of the ureters and urinary bladder. In addition, the simple squamous cells would not be as able to change shape with the changing size of these structures, and would be more prone to tears and other structural disruptions.

Certain drugs that treat high blood pressure cause vasodilation of systemic arteries and arterioles, including those in the kidneys. What effect would these drugs have on the GFR? How would the myogenic mechanism and tubuloglomerular feedback respond to this change in the GFR?

Such drugs would increase the GFR temporarily by increasing the glomerular hydrostatic pressure due to the dilation of renal arteries and afferent arterioles. However, these changes would be countered very rapidly by the myogenic mechanism and tubuloglomerular feedback, both of which would trigger constriction of the afferent arterioles to decrease the GFR.

Glomerulonephritis, or inflammation of the glomerulus, results in excessively leaky glomerular capillaries and damaged glomeruli. The damaged and destroyed glomeruli cause the GFR to decrease. Which compensatory mechanisms would you expect to be triggered, and what effects would they have?

The decreased GFR would trigger the RAAS and tubuloglomerular feedback, both of which would lead to increased glomerular hydrostatic pressure and a slight increase in the GFR.

You discover a new toxin that blocks the reabsorption of all sodium ions from the proximal tubule. What effect would this drug have on the reabsorption of water and other electrolytes from this tubule?

The drug would significantly decrease the amount of water and certain electrolytes reabsorbed from the PCT. If fewer sodium ions are reabsorbed, there will be a smaller electrical gradient for reabsorbing chloride, a smaller osmotic gradient for reabsorbing water, and therefore a smaller osmotic gradient for reabsorption of other electrolytes.

Explain why a patient with long-term renal failure might have a decreased number of erythrocytes in his or her blood.

The kidneys produce the hormone erythropoietin, which stimulates erythrocyte production. In renal failure, all aspects of kidney function decrease, including production of erythropoietin. The lower levels of the hormone cause decreased rates of erythropoiesis.

Predict the effects of a condition that results in gradual loss of microvilli from the proximal tubule.

The microvilli of the PCT increase the surface area available for absorption of water and other solutes. If the number of microvilli decreases, the cells will be unable to reabsorb the same amount of water and solutes. As a result, urine volume would increase and solutes such as glucose and amino acids would be found in the urine.

Rory presents with a staghorn calculus, a huge kidney stone that forms in the renal pelvis and extends into the major and minor calyces. Rory's staghorn calculus is preventing urine from draining from his renal pelvis into the ureter. How do you think this is affecting the GFR of the affected kidney? Why? (Hint: How do you think a staghorn calculus would affect the capsular hydrostatic pressure? What would that do to net filtration pressure and thus the GFR?)

The staghorn calculus is causing a "backup" in the kidney by preventing urine from draining from the major and minor calyces into the renal pelvis. The backup is increasing the amount of filtrate in the collecting system and nephron, which in turn increases the amount of filtrate that remains in the capsular space. This increases the capsular hydrostatic pressure, a force that opposes filtration. An increased capsular hydrostatic pressure causes the net filtration pressure to fall, which leads to a drop in the GFR.

Alcohol inhibits the release of ADH. Predict how this inhibition will influence urine volume and concentration.

With lower levels of ADH, less water will be absorbed from the DCT and collecting system. This will incrrease urine volume and decrease urine concentration.

Metabolic acidosis is characterized by decreased blood pH from the accumulation of metabolic acids. Predict the effects this condition will have on the pH of the urine. What effect would you expect the opposite condition, metabolic alkalosis, to have on the urine pH?

With metabolic acidosis, you would expect the pH of the urine to be low; however, it will not likely drop below 4.5 irrespective of the degree of acidosis. With metabolic alkalosis, the urine pH will rise as more hydrogen ions are retained and bicarbonate ions are excreted.