Ch 31 Diuretics & Kidney Disease

Question 1

What is the target and mechanism of action of osmotic diuretics (mannitol)?

Answer 1

Proximal tubules
Inhibits water and solute reabsorption by increasing osmolarity of tubular fluid

Question 2

What is the target and mechanism of action of loop diuretics (furosemide)? Since these are common, expand a bit more on the action

Answer 2

Thick ascending loop of henle
Inhibit Na/K/Cl co-transport in the luminal membrane.
–>Decreases active reabsorption, VERY powerful.
-Incr amount of solutes delivered to the distal nephron to prevent water reabsorption from the urine
-Disrupt the countercurrent multiplier by decreasing ion reabsorption
-Impairs renal concentrating AND diluting abilities

Question 3

What is the target and mechanism of action of thiazide diuretics?

Answer 3

Early distal tubules
Inhibit Na/Cl cotransport in luminal membrane

Question 4

What is the target and mechanism of action of carbonic anhydrase inhibitors (acetazolamide)?

Answer 4

Proximal tubules
Inhibit H+ secretion and HCO3 reabsorption, which reduces Na reabsorption

Question 5

What is the target and mechanism of action of aldosterone antagonists (spironolactone etc)?

Answer 5

Collecting tubules.
Inhibit action of aldosterone on tubular receptor, decreasing Na reabsorption and K secretion
“K+ sparing”

Question 6

What is the target and mechanism of action of sodium channel blockers (amiloride, triamterene)?

Answer 6

Collecting tubules.
Block Na entry into Na channels of luminal membrane, decr Na reabsorption, and decrease K+ secretion
“K+ sparing”

Question 7

What are the 3 main categories of azotemia (acute renal failure)?

Answer 7

-Prerenal, from hypovolemia/decr perfusion to kidneys
-Renal: affecting kidney itself
-Postrenal: due to obstruction further down

Question 8

Briefly, how does acute tubular necrosis lead to renal azotemia?

Answer 8

Ischemia to the renal tubular epithelial cells or toxic action directly to the tubular epithelial cells themselves causes cells to slough off and plug the tubules. If the basement membrane is damaged, new cells cannot regenerate. If the BM is intact, new cells can grow in 10-20 days

Question 9

What is the most common inciting factor for acute glomerulonephritis?

Answer 9

Infection with group A beta streptococci. As antibodies develop against the strep antigen, the antibodies and antigen react with each other to form insoluble immune complexes that are trapped in the glomeruli.

The glomerulus becomes plugged with WBCs and immune complexes and other parts become excessively permeable.

Question 10

What are the overall physiological effects of acute renal failure?

Answer 10

Retention of lytes water, and waste products. Edema and hypertension can develop, as well as hyperkalemia and metabolic acidosis, which can aggravate the hyperK.

Question 11

Which adaptations/maladaptations occur with primary chronic renal disease?

Answer 11

A reduced number of nephrons leads to increased arterial pressure and the surviving nephrons hypertrophy or develop vasodilation
Glomerular pressure then increases and/or filtration
This leads to glomerular sclerosis, which further reduces the number of functional nephrons

Question 12

What changes culminate in isosthenuria in patients with chronic renal failure?

Answer 12

1. Rapid flow of tubular fluid impairs ability to reabsorb water
2. Rapid flow through LoH impairs proper countercurrent mechanism function and the kidneys cannot concentrate urine
3. Number of nephrons decreases so the diluting capacity is impaired

Question 13

What are some of the major sequelae to chronic renal failure?

Answer 13

1. uremia
2. anemia
3. water retention and edema formation
4. osteomalacia
5. hypertension