Renal Physiology and Diuretics Flashcards
What is the main indication for use of diuretics?
To maintain normal blood pressure in patients with hypertension.
What are some therapeutically useful extrarenal effects of diuretics?
- Increasing vascular wall compliance (better control of HTN)
- Decreases CSF volume, preventing damage to brain tissue.
- Decreases intraocular fluid volume.
- Improves localized imbalances in lung fluid distribution in children with respiratory disease.
What groups of diuretics acts in the proximal tubule?
The carbonic anhydrase inhibitors and osmotic diuretics.
Why do some diuretics cause an increase in urine potassium?
Decreasing Na reabsorption in an earlier part of the nephron leads to a compensatory increase in Na reabsorption in the late distal tubule and collecting duct. This means more K secretion due to functional coupling.
What group of diuretics act in the thick ascending limb? What do they inhibit?
“High-ceiling” or “loop” diuretics. They inhibit Na/K/2Cl symporters by competing with chloride for occupancy at the transporter.
Which group of diuretics induces the largest diuresis? What induces the smallest?
The loop diuretics (largest) and the potassium-sparing diuretics (smallest).
What group of diuretics act in the cortical thick ascending limb and early distal tubule? What do they inhibit?
The thiazide diuretics and thiazide-like diuretics. They inhibit Na/Cl symport.
What group of diuretics act in the late distal tubule and collecting duct?
The potassium-sparing diuretics: renal epithelial sodium channel inhibitors and aldosterone receptor antagonists.
Why are potassium-sparing diuretics, well…potassium-sparing?
Due to functional coupling, less Na reabsorption means less K secretion. However, this time we are at the very end of the nephron, so there is no place for compensatory actions to take place downstream.
What “negative” effects do loop diuretics have and why does it happen? What are patients at risk for?
- They increase the time it takes to decrease ECF volume in the event of excess fluid intake (due to less solute being reabsorbed, forming less hypotonic urine).
- They compromise the ability of the kidney to take up water during dehydration. (due to decreased counter current multiplication)
Patients are at risk for developing hyponatremia due to less solute reabsorption.
Why do thiazide diuretics have no effect on the concentrating ability of the kidney?
Thiazide diuretics block solute reabsorption in the early distal tubule in the CORTEX, which does not participate in the counter current multiplication process.
Describe the mechanism behind carbonic anhydrase inhibitors.
They inhibit the conversion of carbonic acid to carbon dioxide and water, so it can’t be taken up by the proximal tubule cells. Less intracellular carbonic acid is formed, leading to a decrease in intracellular protons available for the Na/H pump, slowing Na absorption as well.
Carbonic anhydrase inhibitors are contraindicated in what affliction?
Cirrhosis of the liver.
This is because CAIs induce metabolic acidosis, which causes ammonia to accumulate in the ECF, creating a risk for hepatic encephalopathy.
What are the toxicities of carbonic anhydrase inhibitors?
Hypokalemia from increased compensatory K secretion, and alkalinization of the urine from decreased reabsorption of bicarbonate, which also produces metabolic acidosis.
How do osmotic diuretics work?
They are a nonreabsorbable solute, which allows for a larger volume of isotonic tubular fluid with lower Na concentration to leave the proximal tubule.
