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11 Cards in this Set
- Front
- Back
Osmotics
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Mannitol
a sugar alcohol given IV, it increases the oncotic pressure thus trapping the water. It inhibits water reabsorption throughout the tubule. uses: - decreases intraocular pressure in glaucoma - decreases intracranial pressure - reopen kidney function: tex in rhabdomyolysis myoglobin will be released and trapped in tubules and damages it. mannitol increases the clearance side effect: hypovolemia |
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carbonic acid inhibitors
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Acetazolamide, Dorzolamide
We need CA in the proximal tubule so that H is made. Without the protons, Na cant enter. With CA inhibitors Na will build up in the lumen, water will follow, you will excrete it. also bicarbonate will be lost - metabolic acidosis. uses: glaucoma, metabolic alkalosis, acute mountain sickness. what is special: hypokalemia and acidosis together. (hypokalemia: when you get hypovolemia aldosterone will increase pga RAS, aldosterone cause Na reabsorption in expense of H and K) side effects: - bicarbonaturia, acidosis, hypokalemia, hyperchloremia, renal stones, sulfonamide hypersensitivity |
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Loooooop diuretics
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Furosemide, Ethacrynic acid (no sulphur), Torsemide
inhibits Na/K/2Cl transporter: so you will get hypo-all ions. måla upp bilden är lättast, för normalt kommer K leak back out to cause positive charge in lumen, which is why Mg and Ca gets reabsorbed into blood. uses: - DOC in acute pulmonary edema (heart failure) - Acute renal failure - Edema - HTN (they cause VD by increasing prostaglandins: so NSAIDs can cancel HTN effect of furosemide) - anion overdose Side effects: Sulfonamide hypersensitivity, hypo all ions, alkalosis, hyperuricemia (forusemide is a weak acid so it competes with urate to be secreted in proximal tubule), ototoxicity drug interaction: aminoglycosides (it also causes ototoxicity: additive), Lithium, Digoxin (hypokalemia enhances digoxin toxicity: digoxin competes with K) |
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Thiazides
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Hydrochlorothiazide, Indapamide, Metolazone
Inhibits Na/Cl symport in distal tubule. Here is where Ca enters via PTH. (PTH R: Gs: cAMP, PKA: phosphorylates the Ca channel). You get low Na inside the cell which helps getting the Ca into the blood causing hypercalcemia. Uses: - Nephrolithiasis (calcium stones) - HTN - Nephrogenic diabetes insipidus side effects: Sulfonamide hypersensitivity, hypokalemia and alkalosis, hypercalcemia, hyperuricemia, hyperglycemia, hyperlipidemia Drug interactions: Digoxin, also avoid this drug in DM patients (thiazides are also ATP-dependent K channel openers) |
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K sparing agents
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Spironolactone, Eplerenone (blocks aldosterone R)
Amiloride, Triamferene (blocks Na channel) Uses of spironolactone: - hyperaldosterone states - CHF: aldosterone is elevated in CHF pga RAS - adjunct to K wasting agents: to correct the hypokalemia (it is itself K sparing) - Antiandrogenic use: spironolactone is not very selective as a steroid receptor antagonist (gynecomastia in men, females may treat acne and hirsutism) side effects: hyperkalemia and acidosis, antiandrogen Amiloride and Triamferene uses: adjunct to K wasting diuretics, lithium induced nephrogenic diabetes insipidus side effects: hyperkalemia and acidosis Note: Eplerenone is a selective aldosterone receptor blocker |
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ADH agonists
ADH antagonists |
ADH agonists:
activates V2 receptors: Gs: insertion of aquaporin H2O channels into luminal membrane: this reduces urine volume. H2O gets reabsorbed into blood. - Desmopressin ADH antagonists used in SIADH. - Conivaptan: inhibits V2 receptor - Lithium: inhibits ADH |
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Summary af all Diuretics
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all increase urinary Na
All increase K except K sparing agents only CA inhibitors increases HCO3 Loops increase Ca, Thiazide decrease Ca |
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CA inhibitors: urine
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Na, K, HCO3
blood pH: acidosis |
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Loops: urine
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Na, K, Ca, Mg, Cl
blood pH: alkalosis |
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Thiazide: urine
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Na, K, Cl, (mindre Ca)
blood pH: alkalosis |
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K sparing agents
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Na, K
blood pH: acidosis |