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CARBONIC ANHYDRASE INHIBITOR (3) |
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***act on carbonic anhydrase in the lumen of the proximal tubule, keeps sodium bicarb in the urine and keeps H2O in the PCT acetazolamide methazolamide dichlophenamide |
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THIAZIDES AND THIAZIDE LIKE AGENTS (5) |
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chlorothiazide hydrochlorothiazide hydroflumethiazide metolazone trichlormethiazide |
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bumetanide ethacrynic acid furosemide torsemide |
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amilordide eplerenone spironolactone triamterene |
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chlorpropamide desmopressin lypressin vasopression |
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URICOSURIC AGENT: uSE: gout Mechanism: inhibits xanthine oxidase and not related to nepthron function |
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URICOSURIC AGENT USE: ggout Mechanism: acts on neutrophils that carry uric acid crystals in joints and stop microtubules from forming Adverse effect: bone marrow suppresion |
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SULFINPYRAZONE (ANTURANE) |
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URICOSURIC AGENTS USe: gout Mechanism: antagonize reabsorption and secretion of uric acid with biphasic effect: 1) cause decreased excretion of uric acid and 2) increased excretion with active resorption of uric acid and active anion secretion |
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URICOSURIC AGENTS USe: gout Mechanism: antagonize reabsorption and secretion of uric acid with biphasic effect: 1) cause decreased excretion of uric acid and 2) increased excretion with active resorption of uric acid and active anion secretion Other: preferred drug - Organic acid transporter competitive antagonist in proximal tubule and in the distal tubule |
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ANTIDIURETIC AKA ADH (peptide) USE: Diabetes insipidus mechanism: binds V1 and V2 receptors, stimulates water respor[tion in distal tubule and collecting duct by stimulating the production of aquaporins in the epitjhelium allowing more H2O back into blood, more permeability of distal duct to urea, increased activity of Na/K/2Cl symporter in ascending liumb Adverse effectss: coronary artery constriction in MI, nasal mucosal drying |
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ANTIDIURETICUSE: Diabetes insipidus mechanism: binds V1 and V2 receptors, stimulates water respor[tion in distal tubule and collecting duct by stimulating the production of aquaporins in the epitjhelium allowing more H2O back into blood, more permeability of distal duct to urea, increased activity of Na/K/2Cl symporter in ascending liumb Adverse effectss: coronary artery constriction in MI, nasal mucosal drying |
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ANTIDIURETIC - synthetic analog of arginine vasopressin with little V1 activity USE: Diabetes insipidus mechanism: binds V1 and V2 receptors, stimulates water respor[tion in distal tubule and collecting duct by stimulating the production of aquaporins in the epitjhelium allowing more H2O back into blood, more permeability of distal duct to urea, increased activity of Na/K/2Cl symporter in ascending liumb Adverse effectss: coronary artery constriction in MI, nasal mucosal drying |
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ANTIDIURETIC Use: type II diabetes and increases ADH secretion in diabetes insipidus |
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OSMOTIC AGENT Use: reduce intracranial pressure for acute edmea and acute renal failure by IV only (do not give with intracranial bleed), acute glaucoma to reduce pressure, in dialysis disequilibrium syndrome, acute tubular necrosis and acute renal failure Mechanism: act on tissues by drawing water into the blood and on the kidney by increasing renal blood flow and washing out the medullary salt gradient - primary site of action is the Loop of Henle, secondary site is PCT *K+ wasting diuretic - increase osmotic pressure Effects: Increase Na, K+, Ca, Mg, Cl, HCO3, H2PO4, uric acid Side Affects: pulonary congestion to pulmonary edema, hyponatremia, dehydrtion, contraindicated in anuria, impaired liver, hyperglycemia with glycerin |
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OSMOTIC AGENT Use: stool softener, acute glaucoma to reduce pressure, in dialysis disequilibrium syndrome, acute tubular necrosis and acute renal failure Mechanism: act on tissues by drawing water into the blood and on the kidney by increasing renal blood flow and washing out the medullary salt gradient - primary site of action is the Loop of Henle, secondary site is PCT *K+ wasting diuretic - increase osmotic pressure Effects: Increase Na, K+, Ca, Mg, Cl, HCO3, H2PO4, uric acid Side Affects: pulonary congestion to pulmonary edema, hyponatremia, dehydrtion, contraindicated in anuria, impaired liver, hyperglycemia with glycerin |
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K+ SPARING AGENT INHIBITOR OF RENAL NA CHANNELS Use: in combo with diuretics to block K+ excretion, Liddle's syndropme, can be used in place of a thiazide if a. American with ENac B subunit polymorphism, aerosol in cystic fibrosis Mechanism: small increase in NaCL excretion, act on DCT and collecting duct - blocks luminal Na+ channel and drops K+ secretion as well as inhibits proton secretion by raising intraluminal positive potential Effects: increase Na, and Cl excretion by decrease K, H, Ca and Mg excretion Other: metabolized into active metabolite and given 4x or more daily - folate antagonist and can lead to megaloblastic anemia in cirrhosis (not for pregnant women) Side efefcts: hyperkalemia, cardiac arrhythmia, death, interact with other K sparers, CNS, GI, derm, and hematological, reduced glucose tolerance, photosensitization, interstitial nephritis, renal stones |
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SPIRONOLACTONE (ALDACTONE) |
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K+ sparing agent MINERALOCORTICOID ANTAGONIST Use: combo with thiazides and loop diuretics to spare K+, treat primary hyperaldosteronism in adenomas and hyperplasia, cardiac failure, cirrhosis, nephrotic syndrome and severe ascites, treatment of choice for ascites and edema from cirrhosis Effects: Increase Na, , Cl and decreased K, H, and Mg Mechanism: competitively bind the mineralocorticoid receptor and block function Other: major drug in the class Side Effects: hyperkalemia, decreased efficiency with salciylates, cross reacts leading to feminization, diarrhea, gastritis, gastric blleeding, don't use with peptic ulcers, CNS, rash, some possible malignancies |
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K+ sparing agent MINERALOCORTICOID ANTAGONIST Use: combo with thiazides and loop diuretics to spare K+ Effects: Increase Na, , Cl and decreased K, H, and Mg Mechanism: competitively bind the mineralocorticoid receptor and block function Side Effects: hyperkalemia, cross reactions with other steroid receptors for feminization, diarrhea, gastritis, gastric bleeding, dont use with peptic ulcers, CNS, rash, interacts with CYP34A inhibiotrs and get low clearance rates |
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K+ SPARING AGENT INHIBITOR OF RENAL NA CHANNELS Use: in combo with diuretics to block K+ excretion, Liddle's syndropme, can be used in place of a thiazide if a. American with ENac B subunit polymorphism, aerosol in cystic fibrosis Mechanism: small increase in NaCL excretion, act on DCT and collecting duct - blocks luminal Na+ channel and drops K+ secretion as well as inhibits proton secretion by raising intraluminal positive potential Effects: increase Na, and Cl excretion byt decrease K, H, Ca and Mg excretion - daily dosing and removed by the kidney Side effects: hyperkalemia, interact with other K sparing diuretics, CNS< GI, derm, hematological effects, nausea, vomit, leg cramps, dizziness |
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LOOP AGENT Use: diuretic when patient has renal disease (does not decrease renal blood flow) Side Effects: few, hyponatremia, hypokalemia, arrythmia, ototoxicity, not used in hypovolemia, sulfonamide sensitivity, aminoglycosides, interacts with anticoagulants, propranolol, lithium, NSAIDS, cisplatin, probenecid, synergistic with amphotericin B |
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LOOP AGENT Use: Acute pulmonary edema, CHF, hypertension, nephrotic syndrome, edema, ascites, chronic renal failure Side Effects: few, hyponatremia, hypokalemia, arrythmia, ototoxicity, not used in hypovolemia, sulfonamide sensitivity, aminoglycosides, interacts with anticoagulants, propranolol, lithium, NSAIDS, cisplatin, probenecid, synergistic with amphotericin B Mechanism: inhibit the Na+/K+/2Cl- symporter in the ascending thick loop of henle, water stays with it in the urine and medullary ion gradient diminishes, urine flow increases and is more concentrated **K+ wasting agent - enters the urine via organic transporters in proximal tubules Effects: increase Na+, K+, H, Ca, Mg, Cl, HCO3, H2PO4, uric acid Other: short half life with high ceiling (remove lots of fluids) ***major drug, weak inhibitor, increases sstemic venous capacitance, glucuronidated in the KIDNEY |
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ETHACRYNIC ACID (EDECRIN) |
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LOOP AGENT Use: Acute pulmonary edema, CHF, hypertension, nephrotic syndrome, edema, ascites, chronic renal failure Side Effects: few, hyponatremia, hypokalemia, arrythmia, ototoxicity, not used in hypovolemia, sulfonamide sensitivity, aminoglycosides, interacts with anticoagulants, propranolol, lithium, NSAIDS, cisplatin, probenecid, synergistic with amphotericin B |
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LOOP AGENT Use: Acute pulmonary edema, CHF, hypertension, nephrotic syndrome, edema, ascites, chronic renal failure Side Effects: few, hyponatremia, hypokalemia, arrythmia, ototoxicity, not used in hypovolemia, sulfonamide sensitivity, aminoglycosides, interacts with anticoagulants, propranolol, lithium, NSAIDS, cisplatin, probenecid, synergistic with amphotericin B |
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TRICHLORMETHIAZIDE (NAQUA) |
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THIAZIDE Use: hypertension, edema with CHF, daily dosing, treat calcium nephrolithiasis and osteoporosis, nephrogenic diabetes insipidus by decreasing urine volume Mechanism: block Na/Cl symport but not K+ and act on distal collecting tubule **K+ wasting and common, safe Effects: increae Na, K, H, Mg, Cl, HCO3, H2PO4, uric acid; DECREASE CA Other: good for people in danger of dehydration because its not too strong, increase plasma Ca with chronic use, medullary concentration not affected so water retention preserved Side Effecs: small risk of sudden death and renal cell carcinoma, hypovolemia, hypotension, hypokalemia, hyponatremia, metbaolic acidosis, hypercalcemia, hyperuremia, decrease glucose tolerance, allergies to sulfonamides, interact with probenecid, increase anesthesia, vertigo, headache, parasthesia, GI problems, erectile dysfunction *NSAIDS decrease effectiveness ** Amphotericin B and corticosteroids increase risk of hypokalemia and carrythmias |
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THIAZIDE Use: hypertension, edema with CHF, daily dosing, treat calcium nephrolithiasis and osteoporosis, nephrogenic diabetes insipidus by decreasing urine volume Mechanism: block Na/Cl symport but not K+ and act on distal collecting tubule **K+ wasting and common, safe Effects: increae Na, K, H, Mg, Cl, HCO3, H2PO4, uric acid; DECREASE CA Other: good for people in danger of dehydration because its not too strong, increase plasma Ca with chronic use, medullary concentration not affected so water retention preserved Side Effecs: small risk of sudden death and renal cell carcinoma, hypovolemia, hypotension, hypokalemia, hyponatremia, metbaolic acidosis, hypercalcemia, hyperuremia, decrease glucose tolerance, allergies to sulfonamides, interact with probenecid, increase anesthesia, vertigo, headache, parasthesia, GI problems, erectile dysfunction *NSAIDS decrease effectiveness ** Amphotericin B and corticosteroids increase risk of hypokalemia and carrythmias |
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HYDROFLUMETHIAZIDE (SALURON) |
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THIAZIDE Use: hypertension, edema with CHF, daily dosing, treat calcium nephrolithiasis and osteoporosis, nephrogenic diabetes insipidus by decreasing urine volume Mechanism: block Na/Cl symport but not K+ and act on distal collecting tubule **K+ wasting and common, safe Effects: increae Na, K, H, Mg, Cl, HCO3, H2PO4, uric acid; DECREASE CA Other: good for people in danger of dehydration because its not too strong, increase plasma Ca with chronic use, medullary concentration not affected so water retention preserved Side Effecs: small risk of sudden death and renal cell carcinoma, hypovolemia, hypotension, hypokalemia, hyponatremia, metbaolic acidosis, hypercalcemia, hyperuremia, decrease glucose tolerance, allergies to sulfonamides, interact with probenecid, increase anesthesia, vertigo, headache, parasthesia, GI problems, erectile dysfunction *NSAIDS decrease effectiveness ** Amphotericin B and corticosteroids increase risk of hypokalemia and carrythmias |
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HYDROCHLOROTHIAZIDE (HYDRODIURIL) |
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THIAZIDE Use: hypertension, EDEMA with CHF, daily dosing, treat calcium nephrolithiasis and osteoporosis, nephrogenic diabetes insipidus by decreasing urine volume Mechanism: block Na/Cl symport but not K+ and act on distal collecting tubule **K+ wasting and common, safe Effects: increae Na, K, H, Mg, Cl, HCO3, H2PO4, uric acid; DECREASE CA Other: good for people in danger of dehydration because its not too strong, increase plasma Ca with chronic use, medullary concentration not affected so water retention preserved Side Effecs: small risk of sudden death and renal cell carcinoma, hypovolemia, hypotension, hypokalemia, hyponatremia, metbaolic acidosis, hypercalcemia, hyperuremia, decrease glucose tolerance, allergies to sulfonamides, interact with probenecid, increase anesthesia, vertigo, headache, parasthesia, GI problems, erectile dysfunction *NSAIDS decrease effectiveness ** Amphotericin B and corticosteroids increase risk of hypokalemia and carrythmias |
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Definition
THIAZIDE Use: hypertension, edema with CHF, daily dosing, treat calcium nephrolithiasis and osteoporosis, nephrogenic diabetes insipidus by decreasing urine volume Mechanism: block Na/Cl symport but not K+ and act on distal collecting tubule **K+ wasting and common, safe Effects: increae Na, K, H, Mg, Cl, HCO3, H2PO4, uric acid; DECREASE CA Other: good for people in danger of dehydration because its not too strong, increase plasma Ca with chronic use, medullary concentration not affected so water retention preserved Side Effecs: small risk of sudden death and renal cell carcinoma, hypovolemia, hypotension, hypokalemia, hyponatremia, metbaolic acidosis, hypercalcemia, hyperuremia, decrease glucose tolerance, allergies to sulfonamides, interact with probenecid, increase anesthesia, vertigo, headache, parasthesia, GI problems, erectile dysfunction *NSAIDS decrease effectiveness ** Amphotericin B and corticosteroids increase risk of hypokalemia and carrythmias |
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DICHLORPHENAMIDE (DURAMIDE) |
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CARBONIC ANHYDRASE INHIBITOR Use: open angle glaucoma, pre-surgery relief of glaucoma pressure, altitude sickness by alkinalating the urine, counteract diuretic induced metabolic acidosis Mechanism: acts on carbonic anhydrase in the lumen cells of the proximal tubule and distal collecting duct - keeps Na Bicarbonate in the urine Effects: increase K+, Na+, HCO3, and H2PO4 in the urine **K+ wasting diuretic (high Na delivery to distal nephron) Other: based on sulfanilamide chemo drugs Side Effects: allergy, metabolic acidosis, divert renal ammonia into circulation increasing hepatic encephelopathy, kidney stones from alkaline urine, bone marrow depresison, parasthesias and tingling |
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METHAZOLAMIDE (GLAUCTABSo |
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CARBONIC ANHYDRASE INHIBITOR Use: open angle glaucoma, pre-surgery relief of glaucoma pressure, altitude sickness by alkinalating the urine, counteract diuretic induced metabolic acidosis Mechanism: acts on carbonic anhydrase in the lumen cells of the proximal tubule and distal collecting duct - keeps Na Bicarbonate in the urine Effects: increase K+, Na+, HCO3, and H2PO4 in the urine **K+ wasting diuretic (high Na delivery to distal nephron) Other: based on sulfanilamide chemo drugs Side Effects: allergy, metabolic acidosis, divert renal ammonia into circulation increasing hepatic encephelopathy, kidney stones from alkaline urine, bone marrow depresison, parasthesias and tingling |
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CARBONIC ANHYDRASE INHIBITOR Use: open angle glaucoma, pre-surgery relief of glaucoma pressure, EPILEPSY, altitude sickness by alkinalating the urine, counteract diuretic induced metabolic acidosis Mechanism: acts on carbonic anhydrase in the lumen cells of the proximal tubule and distal collecting duct - keeps Na Bicarbonate in the urine Effects: increase K+, Na+, HCO3, and H2PO4 in the urine **K+ wasting diuretic (high Na delivery to distal nephron) Other: based on sulfanilamide chemo drugs Side Effects: allergy, metabolic acidosis, divert renal ammonia into circulation increasing hepatic encephelopathy, kidney stones from alkaline urine, bone marrow depresison, parasthesias and tingling |
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Increase rate of urine flow, increase Na and Cl exrection, may increase K+ excretion, used for hypertension, heart failure, renal failure, and cirrhosis and nephrotic syndrome, to decrease edema **INcrease solute exretion to increase volume of urine |
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Loop of henle includes (4) parts |
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proximal straight tubule descending thin limb ascending thin limb ascending thick limb post macular segment |
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mechanical filter of fludis from proteins and lipids by size, about 120ml/min and 1 ml/min of urine made, 99% resorbed in kidney |
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Single nephrone glomerular filtration rate |
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Proximal convoluted tubule |
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65% of H2O is resorbed back into blood, most K+ and 65% of NaCl resorbed ***Resorption site 65% of bicarb taken out of urine Driving force is Na/K+ ATPase on Basolateral surface urine is iso-osmotic with blood secrete organic acids and bases into urine |
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H2O goes out do to NaCl gradient in ascending limb and leads to a high NaCL concentration - no NaCl or urea is resorbed |
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diluting segment with NaCl being resorbed but no H2O and no Urea leaves the urine |
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feedback sensor for the neprhone sensing osmolality of the urine - if NaCl is high it sends a signal to the afferent arteriole too cut down the flow of blood and give less filtration tubuloglomerular feedback |
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K+ uptake and dilutes urine **diluting segment - transports out of the urine NaCl but keeps H2O in the urine - fluid here is hypotonic urine even when dehydrated - no urea resorbed either |
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Resorbs H2O from urine if ADH is present |
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Urea is resrobed and adds to medullary salt gradient to draw water out - especially with ADH |
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increases excretion of water but not of solutes - dilutes urine |
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incfreases excretion of Na+ and produces natriuresis - also gets rid of H2O |
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increases excretion of Na and chloride ions (saluresis) |
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increases excretion of potassium |
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secreted by adrenal glands and cause retention of salt and water and excertion of K_+ and protons - primary receptor sites in DCT and collecting ducts |
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