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51 Cards in this Set

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% Na filtered
PCT
TAL
DCT
CT
PCT>60
TAL<25
DCT<10
CT<4
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
What is the main example of a CA inhibitor?
azolamide
What are the osmotic diuretic drugs?
mannitol
What is the mechanism of osmotic diuretics
draws water to it anywhere it is in the body and thus can be used to decrease intraocular pressure and intracerebral pressure
how is mannitol given
IV
What are the carbonic anhydrase inhibitors?
acetazolamide
dorzolamide
How is most sodium reabsorbed in the proximal tubule?
NA/H pump - where the H protons being pumped out originate from Carbonic anhydrase
What are the two things that CA inhibitors are giong to effect the absortpion of?
Na and bicarbinate
What are the uses of CA inhibitors?
GLAUCOMA (carbonic anhydraese is in the eye and needed to form aqueous humor), mountain sickness, metabolic alkalosis, elimination of acidic drugs
What is the target for loop diureteics?
2Cl, Na, K cotransporter on the luminal membrane of TAL
How is Mg and Ca reabsorbed?
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
What is the mechanism for a look diuretic?
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
What are the results of loop diuretics.
the increase in Na in the collecting duct wil lead to hypokalemia (loss of K) and alkalosis (loss of H)
What are the loop diuretic drugs?
furosemide and ethacrynic acid
how do loop diuretic get into the lumen?
filtered and secreted in proximal tubule
What are some nonintuitive adverse effects of loop diuretics?
hyperuricemia, ototoxicity (ethacrynate>furosemide) especially with aminoglycosides, decreased clearance of lithium
What is the target for the thiazide diuretics?
Na/Cl co-transporter on luminal membrane of DCT
What is the normal ionic physiology of the distal convoluted tubule?
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
What are the adverse effects of thiazide diuretics?
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
What is the target for loop diureteics?
2Cl, Na, K cotransporter on the luminal membrane of TAL
How is Mg and Ca reabsorbed?
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
What is the mechanism for a look diuretic?
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
What are the results of loop diuretics.
the increase in Na in the collecting duct wil lead to hypokalemia (loss of K) and alkalosis (loss of H)
What are the loop diuretic drugs?
furosemide and ethacrynic acid
how do loop diuretic get into the lumen?
filtered and secreted in proximal tubule
What are some nonintuitive adverse effects of loop diuretics?
hyperuricemia, ototoxicity (ethacrynate>furosemide) especially with aminoglycosides, decreased clearance of lithium
What is the target for the thiazide diuretics?
Na/Cl co-transporter on luminal membrane of DCT
What is the normal ionic physiology of the distal convoluted tubule?
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
What are the adverse effects of thiazide diuretics?
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
What are the transporters and channels present in the collecting duct?
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)
What is the mechanism of aldosterone?
increase formatino of Na channels on luminal membrane (principal cell) and increase antivity of Na/ (k or H) exchangers
What happens when there is increased Na concentration in the tubular lumen?
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)
What are the ionic changes in the urine due to a K sparing diuretic?
small increase in urinary Na but marked decrease in urinary K and H (hyperkalemia and acidosis)
What are the K sparing agents (weak diuretics)?
spironolactone, amiloride, and triamterene
What is the mechanism of spironolactone?
aldosterone receptor antagonist
What is the mechanism of amiloride and triamterene
Na channel blockers
What is an unusual use of spironolactone?
reduces hirsutism in women due to androgen clocking effect
what are the main uses of K sparing diuretics?
adjunctive with other diuretics to decrease K loss
what are the negative side effects of the K sparing agents?
spironolactone - gynecomastia
What are the antihyperlipidemic drugs?
bile acid sequestrants, HMG--CoA inhibitors ("statins"), niacin, and gemfibrozil
What are the bile acid sequestrants?
cholestyramine and colestipol
What is the mechanism of cholestyramine and colestipol
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
When are the bile acid sequestrants not used?
hypertriglyceridemias since they encrease VLDLs and TGs
What are the HMG-CoA reductase inhibitors?
Lovastatin and other "statins"
What is the mechanism of the statins?
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)
What are the adverse effects of the statins?
diarrhea, myalgia, rhabdomyolysis (especialy with other antihyperlipidia drugs),
What are the effects of niacin?
inhibit synthesis of VLDL and apoprotein in hepatocytes, thus decreaseing VLDL, LDL, Tgs and increaseing HDL
What is the main adverse effect of nicotinic acid (niacin)?
flushing and pruritis
What drug activates lipoprotein lipases?
gemfibrozil
What are the thiazide drugs?
hydrochlorothiazide, indapamide, metolazone