Diuretics - Hausmann Flashcards
How can we know that a patient is hypovolemic?
Urine concentration <20 (if diluting urine by drinking won’t drop this low)
Double check: plasma sodium, if high can be false d/t diuretics
What are the hypothesized causes for netriuresis in diabetic nephropathy?
- Lots of glucose in the tubular lumen keeps the water there and at first sodium will be reabsorbed but the concentration gradient between the peritubular capillaries and the tubular fluid will cause sodium to come back to the water.
- Hyperosmosis causes vasodilation of vasa recta and the increased flow causes medullary washout which won’t be corrected in the loop of Henle because it is not hypoosmotic. Sodium will stay in ascending limb.
What are the diuretics that act at each section of the tubule?
I. Antagonists at PCT
Acetazolamide = Diamox ®
Carbonic anhydrase inhibitor (loss of bicarbonate, can cause acidosis). Blocks Na/H antiporter–> natriuresis
II. Loop of Henle
Fusid ® = Furosemide
Small molecule, sits on swing at Na/K/2Cl transporter in position of one of the Cl and the whole swing doesn’t work and Na stays in the tubular fluid–> natriuresis
III. Distal Tubule
a. Thiazides
Block Na/Cl cotransporter
Not active with Cr > 2.3
IV. CCD- K+ sparing
a. Na channel blockers- triampterine or amilioride
b. Spironolactone = aldactone ®
Aldosterone receptor blocker
Works on the basolateral side of principal cells
I and III. Metolazone= Metinex ®
Old diuretic-helpful, has a thiazide-like action and blocks the sodium/phosphate cotransporter of the proximal tubule. With one molecule-block 2 sites. (Can add furosemide and block 3 sites).
How are patients on diuretics assessed for drug level in the blood?
By testing uric acid levels in the blood. Uric acid competes with diuretics so blood levels will increase. No risk for gout unless previous history.
What percentage of sodium reabsorption takes place in each section of the kidney?
What is the comparison of potency of diuretics?
Proximal tubule is 65% but only 17% by Na/H antiporter
CCD absorbs 5%
Loop of Henle: 20%
Distal Tubule: 10%
Loop diuretics (given for urgent cases of pulmonary edema in continuous drip) > Thiazide > K+ sparing diuretics > Acetazolamide (not used for natriuresis)
How is calcium connected to K reabsorption?
When Na/K/2Cl channel is blocked, K reabsorption is blocked. Ca is reabsorbed and Mg is not. Furosemide can cause this.
Hypomagnesemia can be a factor in hypokalemia, and needs to be fixed before hypokalemia is fixed.
Check Mg and give if low!
Hypercalcemia will block eith Na/K/Cl cotransporter causing hypercalciuria. (Problem in Bartter’s type A)