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24 Cards in this Set
- Front
- Back
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why is the Na-K ATPase in renal phys important?
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returns Na to circulation
maintain low intracellular Na allows for passive Na entry allows transpot of other substances to be linked to Na reabsorption |
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fanconi syndrome
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deficit in ability to reabsorb Na+ and other key molecules in the proximal tubule
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where is carbonic anhydrase located in the prox tubule?
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in the cell and in the bushboard of the cell in the lumen of the proximal tubule
key role - reabsorption of bicarb |
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bicarb reabsorption in the proximal tubule mechanism
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Na/H exchange reabsorbs Na and secretes H+
H+ combines with the filtered bicarb to form carbonic acid (H2CO3) carbonic acid breaks down to water and CO2 via brush boarder carbonic anhydrase CO2 is reabsorbed passively and transformed back to carbonic acid via intracellular carbonic acid carbonic acid then disassociates into H+ and HCO3- (H+ is recycled and bicarb is reabsorbed) |
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acetazolamide
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carbonic anhydrase ihibitor
limits bicarb reabsorption promotoes NaCl and NaHCO3 excretion limited diuretic effect becuase of DISTAL reclamation of Na+ metabolic acidosis that results further diminishes diuretic effect good use: metabolic alkalosis treatment, use to alkinize the urine, combo therapy with other diuretics |
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functions of the loop of henle
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diluting segment is impermeable to water - establishment of medullary hypertonicity
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NaK2Cl transporter
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site of loop diuretic action - compete for Cl- site - prevents NaCl reabsorption -> reduction of medullary hypertonicity
Ca++ and Mg++ follow NaCl reabsorption K+ leaks back out into tubule |
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furosemide vs ethacrynic acid
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give ethycrynic acid to people with sulfa allergies
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T/F hyponatremia is a common complication of loop diuretics
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FALSE its rare
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side effects of loop diretics
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increased NaCl delivery to distal nephron -> hypokalmia
volume depletion (azotemia) - metabolic alkalosis due to more sodium reabsorption in exchange for H+ ototoxicity (ethacrynic acid) hypocalcemia (bad for osteoperosis - but can treat hypercalemia) hypomagnesemia |
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clinical use for loop diuretics
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edema
hypertension acute renal failure type IV RTA hypercalcemia |
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benefits of loop diuretics continuous infusion
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less toxicity
prevents body from adapting during "diuretic free intervals" |
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Bartter's Syndrome
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defect in NaK2Cl transporter
NaCl wasting, hyper-renin state, hypokalemic, metabolic alkalosis |
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thiazides
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act on NaCl cotransporter - compete for Cl- site - allows for salt wasting and diuresis
does not effect Ca++ reabsorption can cause HYPOnatremia because lose solute in excess of water causes hypokalemia and hypomagnesemia can't use for patients in renal failure (GFR < 30-40) |
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uses of thiazides
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stones and hypercalciuria (enhances Ca++ transport)
nephrogenic DI |
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Gitelman's Syndrome
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NaCl cotransporter defect
see hyponatremia see hypokalemia see hypomagnesmia secondary hyperrenin state |
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K+ sparing diuretics
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amiloride, triamterene - block Na+ channels
spironolactone - aldosterone receptor antagonist use in cases where need to minimize K+ loss - often in combo therapy |
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spironolactone special use
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in high aldosterone states
cirrhosis, chf inhibits myocardial fibrosis (protects against arrhythmia) and improves myocardial uptake of norepinephrine |
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side effects of sprionolactone
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gynecomastia, hirsutism
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amiloride special use
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Li+ induced polyuria
treatment for Mg wasting |
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liddle's syndrome
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defect in Na channels in principle cells
mutation prevents degradation/removal of channel active independent of aldosterone - means always open causes hypernatremia and hypoaldosteronism --> hypertension, hypokalemia, metabolic alkalosis |
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Gordon's syndrome
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aka pseudohypoaldosteronism type II
problem in the NaCl cotransporter - allows for continuous activation causes a chloride shunt -> hyperchloremia, hypertension hyperkalemia metabolic acidosis |
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effect of black licorice
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same as apparent mineralocorticoid excess
inhibition of the enzyme that breaks down 11beta-hydroxysteroid dehydrogenase -> uninhibited cortisol cortisol mimics aldosterone --> hypertension, hypokalemia, metabolic alkalosis |
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diuretic efficacy are modified by
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hypoalbuminemia or nephrotic proteinuria - diuretics are protein bound
first dose is most effective - "tolerence" develops as body adapts takes 2-3 weeks of usage to stablize lower GFR means high dose needed need to limit Na+ intake while on diuretics |
