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38 Cards in this Set
- Front
- Back
- 3rd side (hint)
Proximal tubule
-solute reabsorption |
--70% of filtered Na reabsorbed here
--85% of filtered bicarbonate reabsorbed here --80% of filtered phosphate reabsorbed here --80% of filtered K reabsorbed here |
pg 69
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Proximal tubule
-diuretics |
--carbonic anhydrase inhibitors
1. Acetazolamide 2. Methazolamide* --osmotic diuretics |
pg 75
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Medullary portion of TALH
-solute reabsorption -reabsorptive capacity -contribution to gradient |
--active Na, Cl, and K reabsorption here (Na/K/2Cl transporter)
--reabsorptive capacity can be increased to 50% of the filtered Na load when proximal reabsorption is decreased --NaCl reabsorption increases medullary osmotic gradient |
pg 70
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Cortical portion of TALH
-solute reabsorption -reabsorptive capacity -contribution to gradient |
--active Na, Cl, and K reabsorption here (Na/K/2Cl transporter)
--reabsorptive capacity can be increased to 50% of the filtered Na load when proximal reabsorption is decreased --does NOT contribute to the medullary osmotic gradient |
pg 70
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Medullary portion of TALH
-diuretics |
Na/K/2Cl co-transporter blockers
1. Furosemide 2. Bumetanide 3. Torsemide |
pg 76
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Cortical portion of TALH
-diuretics |
Na/K/2Cl co-transporter blockers
1. Furosemide 2. Bumetanide 3. Torsemide |
pg 76
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Distal tubule
-solute reabsorption -reabsorptive capacity |
--5% of filtered NaCl reabsorbed (thiazide sensitive Na/Cl transporter)
--most of remaining bicarbonate is reabsorbed between here and the late distal tubule (8%) --limited capacity for further increasing NaCl reabsorption |
pg 70
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Distal tubule
-diuretics |
1. Thiazides
2. Chlorthalidone 3. Metolazone 4. Indapamide 5. Osmotic diuretics |
pg 76
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Cortical collecting tubule
-solute reabsorption -reabsorptive capacity |
**important site for control of K secretion into final urine
--3% of filtered Na reabsorbed here --fixed reabsorptive capacity --site of aldosterone dependent Na reabsorption |
pg 70
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Cortical collecting tubule
-diuretics |
K sparing diuretics
1. Spironolactone -- aldosterone antagonist 2. Eplerenone 3. Triamterene -- blocks epithelial Na channel 4. Amiloride -- blocks epithelial Na channel |
pg 76
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Proximal tubular diuretics (acetazolamide)
-MOA |
MOA: inhibition of luminal and intracellular carbonic anhydrase --> inhibition of Na/H exchange at apical membrane and basolateral bicarbonate reabsorption
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pg 77
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Proximal tubular diuretics (acetazolamide)
-diuretic potency |
mild potency
--sites downstream reabsorb Na and H2O --the blocking of carbonic anhydrase is incomplete --only 30% of Na is reabsorbed with bicarb, most is reabsorbed as NaCl --development of hyperchloremic metabolic acidosis changes physical properties of carbonic anhydrase, rendering the diuretic ineffective |
pg 78
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Proximal tubular diuretics (acetazolamide)
-effects on urine and plasma composition (3) |
1. Increased urinary excretion of bicarb (alkaline urine)
2. normal anion gap metabolic acidosis (loss of bicarb and inhibition of proximal H secretion) 3. increased K excretion |
pg 78
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Proximal tubular diuretics (acetazolamide)
-use in non-edematous states (2) |
1. Glaucoma -- decreases formation of aqueous humor by blocking carbonic anhydrase in the ciliary body (methazolamide is perferred)
2. to alkalinize the urine -- treat renal stones or metabolic alkalosis |
pg 78
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Loop diuretics
-MOA |
MOA: block active Na/K/2Cl co-transport in the TALH
--secreted into the proximal tubule via organic acid pathway and transported to site of action --potency dependent on urinary concentration of diuretic, not plasma concentration --tubular secretion is potentiated by albumin; hypoalbuminemia decreases potency |
pg 80
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Loop diuretics
-potency |
--HIGH
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pg 80
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Loop diuretics
-effects on urine and plasma composition (5) |
1. Increase Na, K and Cl excretion
2. Increase fractional excretion of Ca by 30% 3. Increase fractional Mg excretion by 60% 4. may increase or decrease uric acid excretion 5. decrease free H2O reabsorption and free H2O clearance by impairing the medullary gradient |
pg 80
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Loop diuretics
-use in edematous states (3) |
*Diuretic of choice for:
1. pulmonary edema 2. edema in patients with renal failure 3. nephrotic syndrome |
pg 81
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Loop diuretics
-use in non-edematous states (5) |
1. HTN
2. hypercalcemia 3. acute renal failure (treatment of oliguria) 4. acure hyperuricemia 5. severe hyponatremia |
pg 81
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Loop diuretics
-adverse effects (7) |
1. volume depletion
2. hypokalemia 3. metabolic acidosis 4. hypocalcemia 5. hypomagnesemia 6. acute interstitial nephritis (allergic) 7. **deafness in patients with renal fail |
pg 81
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Osmotic diuretics (mannitol, glucose, urea)
-MOA and site of action |
MOA:
--proximal tubule: decreased Na reabsorption due to decreased H2O reabsorption --descending loop of henle: decreased H2O reabsorption secondary to osmotic effect --**desecnding thin limb of loop: major effect here, decreased tubular fluid osmolality results in greater passive influx of Na from the interstitium and increased Na excretion and tubular fluid flow rate -- disrupts gradient --collecting tubule: decreased urea reabsorption from collecting tubule which further decreases interstitial osmolality --vasa recta: increased vasa recta blood flow dissipates gradient -- may account for majority of diuretic effect |
pg 82
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Osmotic diuretics (mannitol, glucose, urea)
-potency |
--highest peak urine flow of all diuretics
--Na excretion greater than thiazides and less than loop diuretics |
pg 83
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Osmotic diuretics (mannitol, glucose, urea)
-effect on plasma and urine composition |
1. increase Na excretion
2. increase K excretion 3. increase bicarb excretion 4. increase free H2O excretion |
pg 83
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Osmotic diuretics (mannitol, glucose, urea)
-uses (5) |
***NOT used to treat edeam because they expand ECF
1. acute renal failure 2. cerebral edema* 3. severe hyperuricemia 4. dialysis disequilibrium syndrome (prevents #2) 5. intoxications* |
pg 83
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Osmotic diuretics (mannitol, glucose, urea)
-adverse effects (5) |
1. volume depletion
2. hypernatremia (enhances free H2O loss) 3. hyponatremia (dilutes Na present in the ECF by enhancing H20 movement from ICF) 4. hypokalemia 5. acute renal failure |
pg 83
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Coritcal TALH and early distal tubule diuretics (Thiazides)
-MOA -potency |
MOA: inhibit active NaCl transport in the cortical thick ascending limb and early distal tubule (major site of action)
--blocks 40% of NaCl reabsorption --moderate potency |
pg 83/84
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Coritcal TALH and early distal tubule diuretics (Thiazides)
-effects on plasma and urinary composition (6) |
1. increase Na excretion --hyponatremia
2. increase K excretion -- large K losses may occur if combined with loop diuretic 3. increase Cl excretion 4. decrease Ca excretion* 5. decrease uric acid excretion 6. decrease in free H2O excretion |
pg 84
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Coritcal TALH and early distal tubule diuretics (Thiazides)
-use in edematous states (3) |
1. CHF
2. edematous conditions in patients with normal renal function 3. potentiate action of loop diuretics |
pg 85
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Coritcal TALH and early distal tubule diuretics (Thiazides)
-use in non-edematous states (3) |
1. HTN (1st line) -- volume contration and arteriolar vasodilation
2. hypercalciuria in Ca stone formers -- increase Ca absorption 3. diabetes insipidus -- impaired dilution, less free H2O loss |
pg 85/86
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Coritcal TALH and early distal tubule diuretics (Thiazides)
-adverse effects (8) |
1. hyponatremia
2. hypokalemia 3. metabolic alkalosis 4. carbohydrate intolerance 5. hyperuricemia 6. hypercalcemia 7. hypersensitivity rxn 8. increased plasma lipids and decreased HDL |
pg 86
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Collecting tubule diuretics (K sparing)
-aldosterone antagonists (spironolactone, eplerenone); MOA, site of action |
MOA: competitive inhibition of aldosterone at cortical collecting tubule (principal cell) -- decreased Na/K-ATPase activity, decreased luminal Na-K permeability
--effect reversed by aldosterone --no effect in the absence of aldosterone |
pg 88
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Collecting tubule diuretics (K sparing)
-aldosterone antagonists (spironolactone, eplerenone); effect on plasma and urine electrolytes |
1. increase Na excretion
2. decrease K excretion** 3. increase urine volume 4. increase plasma K 5. little effect on free H2O excretion or reabsorption |
pg 88
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Collecting tubule diuretics (K sparing)
-aldosterone antagonists (spironolactone, eplerenone); uses |
1. potentiate action of other diuretics in the treatment of edema
2. patients with edema and ascites due to liver disease 3. prevent diuretic induced urine K losses** 4. diagnosis and treatment of hyperaldosteronism (non-edematous use) |
pg 88
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Collecting tubule diuretics (K sparing)
-aldosterone antagonists (spironolactone, eplerenone); adverse effects |
1. hyperkalemia
2. man boobs |
pg 88
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Collecting tubule diuretics (K sparing)
-aldosterone independent (triamterene, amiloride); MOA and site of action |
MOA: decrease luminal Na entry by blocking epithelial Na channel (ENaC) --> decreased gradient for basolateral Na/K ATPase --> less K lost on apical membrane
--coritcal collecting tubule (principal cell) |
pg 88
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Collecting tubule diuretics (K sparing)
-aldosterone independent (triamterene, amiloride); adverse effects |
1. hyperkalemia
2. renal calculi (Triamterene) 3. acute renal failure when Triamterene is used with NSAIDs |
pg 89
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Diuretic resistance
-diuretic braking effect -prevention |
--prolonged administration of a diuretic results in a platuea in weight loss and subsequently return of weight to previous level
--results from an increased stimulus for Na retention created by diuretic induced reduction in ECF --prevented by Na restriction diet or increased dosing |
pg 89
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Diuretic resistance
-"other" causes (6) |
1. volume contraction
2. decreased renal blood flow 3. decreased GFR 4. inadequate dosing 5. inadequate GI absorption (NSAIDs) 6. compliance |
pg 90
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