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51 Cards in this Set
- Front
- Back
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% Na filtered
PCT TAL DCT CT |
PCT>60
TAL<25 DCT<10 CT<4 |
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Where do the CA inhibitors work?
Osmotic? Thiazides? K sparing? Loops? Aldosterone antagonists? |
CA inhibitors - proximal convoluted tubule
Osmotic - proximal convoluted tubule and the thin descending limb and also in the coll. duct Thiazides - distal convoluted tubule K sparing - collecting tubule Loops - Thick ascending limb of Loop Aldosterone antagonists - collecting duct |
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What is the main example of a CA inhibitor?
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azolamide
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What are the osmotic diuretic drugs?
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mannitol
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What is the mechanism of osmotic diuretics
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draws water to it anywhere it is in the body and thus can be used to decrease intraocular pressure and intracerebral pressure
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how is mannitol given
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IV
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What are the carbonic anhydrase inhibitors?
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acetazolamide
dorzolamide |
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How is most sodium reabsorbed in the proximal tubule?
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NA/H pump - where the H protons being pumped out originate from Carbonic anhydrase
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What are the two things that CA inhibitors are giong to effect the absortpion of?
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Na and bicarbinate
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What are the uses of CA inhibitors?
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GLAUCOMA (carbonic anhydraese is in the eye and needed to form aqueous humor), mountain sickness, metabolic alkalosis, elimination of acidic drugs
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What is the target for loop diureteics?
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2Cl, Na, K cotransporter on the luminal membrane of TAL
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How is Mg and Ca reabsorbed?
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the K buildup in the cells via the Cl, Na, K transporter and the Na/K pump causes some of the K to diffuse across the luminal membrane and create a positive potential across this membrane. This postive potential drives the reabsorption of Mg anc Ca in the spaces between the cells and the Thick ascending limb
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What is the mechanism for a look diuretic?
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in addition to the direct consequence of having more Cl, Na, and K in the urine, the loss of positive potential on the luminal membrane due to K will result in loss of absorption of Mg and Ca also. Thus you will have more Na, Cl, K, Mg, and Ca in the urine
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What are the results of loop diuretics.
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the increase in Na in the collecting duct wil lead to hypokalemia (loss of K) and alkalosis (loss of H)
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What are the loop diuretic drugs?
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furosemide and ethacrynic acid
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how do loop diuretic get into the lumen?
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filtered and secreted in proximal tubule
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What are some nonintuitive adverse effects of loop diuretics?
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hyperuricemia, ototoxicity (ethacrynate>furosemide) especially with aminoglycosides, decreased clearance of lithium
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What is the target for the thiazide diuretics?
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Na/Cl co-transporter on luminal membrane of DCT
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What is the normal ionic physiology of the distal convoluted tubule?
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Normally, na is exchanged for K via a pump on the basolateral membrane, K returns to blood by back-diffusion. Ca diffuses across luminal membrane via channels (PTH regulated) and returns to blood by a Ca/Na antiporter
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What are the adverse effects of thiazide diuretics?
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increased levels of Na and Cl due to inhibition of the cotransporter leads to hypokalemiz and alkalosis due to the Na load downstream
-the lack of intracellular Na increases the activity of the Na/Ca antiporter and thus there is increased reabsorption of Ca and hypercalcemia. so overall thiazides increase urinary levels of Na, K, and Cl, and decrease levels of Ca |
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What is the target for loop diureteics?
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2Cl, Na, K cotransporter on the luminal membrane of TAL
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How is Mg and Ca reabsorbed?
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the K buildup in the cells via the Cl, Na, K transporter and the Na/K pump causes some of the K to diffuse across the luminal membrane and create a positive potential across this membrane. This postive potential drives the reabsorption of Mg anc Ca in the spaces between the cells and the Thick ascending limb
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What is the mechanism for a look diuretic?
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in addition to the direct consequence of having more Cl, Na, and K in the urine, the loss of positive potential on the luminal membrane due to K will result in loss of absorption of Mg and Ca also. Thus you will have more Na, Cl, K, Mg, and Ca in the urine
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What are the results of loop diuretics.
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the increase in Na in the collecting duct wil lead to hypokalemia (loss of K) and alkalosis (loss of H)
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What are the loop diuretic drugs?
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furosemide and ethacrynic acid
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how do loop diuretic get into the lumen?
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filtered and secreted in proximal tubule
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What are some nonintuitive adverse effects of loop diuretics?
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hyperuricemia, ototoxicity (ethacrynate>furosemide) especially with aminoglycosides, decreased clearance of lithium
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What is the target for the thiazide diuretics?
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Na/Cl co-transporter on luminal membrane of DCT
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What is the normal ionic physiology of the distal convoluted tubule?
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Normally, na is exchanged for K via a pump on the basolateral membrane, K returns to blood by back-diffusion. Ca diffuses across luminal membrane via channels (PTH regulated) and returns to blood by a Ca/Na antiporter
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What are the adverse effects of thiazide diuretics?
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increased levels of Na and Cl due to inhibition of the cotransporter leads to hypokalemiz and alkalosis due to the Na load downstream
-the lack of intracellular Na increases the activity of the Na/Ca antiporter and thus there is increased reabsorption of Ca and hypercalcemia. so overall thiazides increase urinary levels of Na, K, and Cl, and decrease levels of Ca |
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What are the transporters and channels present in the collecting duct?
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Luminal side:
Na Channel K channel Na/ (H or K) antiporter H energy dependent transporter (intercalated cell) basil side: Na/K pump becarb/Cl antiporter (intercalated cell) |
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What is the mechanism of aldosterone?
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increase formatino of Na channels on luminal membrane (principal cell) and increase antivity of Na/ (k or H) exchangers
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What happens when there is increased Na concentration in the tubular lumen?
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increased intracellular positive charge leads to extrusion of K into the lumen
the Na entry increases energy dependent extrusion of H across luminal membranes (intercalated cell) |
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What are the ionic changes in the urine due to a K sparing diuretic?
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small increase in urinary Na but marked decrease in urinary K and H (hyperkalemia and acidosis)
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What are the K sparing agents (weak diuretics)?
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spironolactone, amiloride, and triamterene
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What is the mechanism of spironolactone?
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aldosterone receptor antagonist
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What is the mechanism of amiloride and triamterene
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Na channel blockers
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What is an unusual use of spironolactone?
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reduces hirsutism in women due to androgen clocking effect
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what are the main uses of K sparing diuretics?
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adjunctive with other diuretics to decrease K loss
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what are the negative side effects of the K sparing agents?
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spironolactone - gynecomastia
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What are the antihyperlipidemic drugs?
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bile acid sequestrants, HMG--CoA inhibitors ("statins"), niacin, and gemfibrozil
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What are the bile acid sequestrants?
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cholestyramine and colestipol
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What is the mechanism of cholestyramine and colestipol
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complex bile salts preventing reabsorption from GI tract, thus decreasing feedback inhibition of 7-alpha hydroxylase and increasing synthesis of bile salts from cholesterol
the decreased liver cholesterol leads to increased LDL receptors and decreased plasma LDL |
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When are the bile acid sequestrants not used?
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hypertriglyceridemias since they encrease VLDLs and TGs
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What are the HMG-CoA reductase inhibitors?
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Lovastatin and other "statins"
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What is the mechanism of the statins?
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inhibit the rate limiting step in cholesterol synthesis and thus decrease liver cholesterol, and thus increase LDL receptors, decrease plasma LDL and decrease synthesis of VLDL and apoproteinB
they cause a small increase in HDL and a decrease in TGs they also release NO (vasodilate) and decrease synthesis of ET-1 (potent vasoconstrictor) |
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What are the adverse effects of the statins?
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diarrhea, myalgia, rhabdomyolysis (especialy with other antihyperlipidia drugs),
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What are the effects of niacin?
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inhibit synthesis of VLDL and apoprotein in hepatocytes, thus decreaseing VLDL, LDL, Tgs and increaseing HDL
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What is the main adverse effect of nicotinic acid (niacin)?
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flushing and pruritis
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What drug activates lipoprotein lipases?
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gemfibrozil
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What are the thiazide drugs?
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hydrochlorothiazide, indapamide, metolazone
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