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45 Cards in this Set
- Front
- Back
Carbonic Anhydrase Inhibitor MOA
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Inhibition of CA leads to decrease in symport Bicarb and Na transport on Basolateral surface
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Carbonic Anhydrase inhibitor Drugs
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Acetazolamide and Methazolamide
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Adverse reactions of CAI
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Marrow Suppression, rash, Bicarbonaturia/Metabolic acidosis. May worsen acidosis so avoid in pt's with COPD and renal failure
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Loop Diuretic MOA
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Inhibition of Na/K/Cl symport on luminal surface
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Adverse effects of Loop
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Wasting of Ca, Mg and Na
Acute (uricosuria) Chronic (hyperuricemia) |
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Why do loops cause hypo Mg and Ca ?
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Loss of charge gradient btw lumen and basolateral surface (no Cl- transport=no Mg or Ca via paracellular)
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Why hyperuricemia in Loops?
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Uric acid and loops compete for the same Organic acid secretory pathway
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List Loop Drugs and rank by potency
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Bumetanide> Toresemide >Furosemide > Ethacrynic acid
Sulfa Drugs= rash rxn |
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How does dosage change for Loops when pt's with renal insufficiency ?
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Larger doses, b/c Organic Acid Secretory to lumen side is compromised.
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Loops Adverse reactions
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Hypokalemia (arrhythmias)
Hypocalcemia (tetany) Hypomagnesiemia (arrhythmia) metabolic alkalosis Ototoxicity (high doses of ethacrynic acid) |
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Atypical thiazides
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Chlorthalidone
Indapamide Metolazone |
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Loops and thiazides affect on Ca and Mg
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Loops lose Ca and Mg
Thiazides lose only Mg |
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Thiazides Adverse reactions
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ED, Metabolic Alkalosis
Impaired Glucose Tolerance Sulfonamide allergy |
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Therapeutic Uses of Thiazides
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HTN (1st line)
Edema Ca Nephorlithiasis Nephrogenic Diabetes Insipidus! |
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2 subtypes of Potassium Sparing Diuretics
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KSD
ARA(Aldosterone receptor antagonist) |
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MOA of KSDs
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Block Na Channel on Luminal side at Collecting Duct. Without Na influx K efflux less favorable
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MOA of ARAs
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Bind cytoplasmic MRs, which is the site where Aldosterone binds to exert its effect on the cellular transcription of mRNA associated with Na reabsorption (slow onset of Action!)
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Endogenous levels of Aldosterone effects the amount of natriuresis of which diuretic?
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ARAs
Spironolactone & Eplerenone |
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Amiloride & Triamterene
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KSDs
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Spironolactone & Eplerenone
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ARAs
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Which KSDs can you not give in patients with Liver failure
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Triamterene, b/c it must be converted in the liver to active form 4-hydroxytriamterene (which is renally excreted!
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Adverse Effects of KSDs
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Hyperkalemia, metab acidosis (Dec H secretion via intercalated Cell depolarization)
N/V, Triamterene inhibits folic acid pathway(megaloblastic anemia) as well as causing hyperglycemia, interstitial nephritis, renal stones and photosensitivity |
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Adverse Effects of ARAs
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Hyperkalemia (caution rx causing inc K ~NSAIDS, ACEI) and metabolic acidosis, D/Gastritis (caution in PUD)
Steroid structure: gynecomastia, impotence, decreased libido. Maybe not so much in Eplerenone |
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Therapeutic uses of KSDs
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Used in combo more potent diuretics to dec hypokalemia
Aerosolized Amiloride- CF patients (limit Na/H20 reabsorption for lung clearance) Diabetes Insipidus 2ndary to Li Toxicity... blocks lithium transport into tubule Not used in Pregnancy! |
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Therapeutic uses of ARAs
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Decreases mortality in CHF
primary and secondary hyperaldosteronism (cirrhosis /w ascities) Not used in Pregnancy! |
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Arginine Vasopressin (ADH) amount release is associated with what?
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Increases with Osmolality and hypotension (20% vol. loss).
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ADH MOA
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V2 Stimulation Increases H20 permeability via insertion of AQP2 at medullary CD, up-regulates Na/K/2Cl symporter of TAL
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Promoters of ADH release
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Ang II/III
Nicotine, EPI, SSRI, TCAs |
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Inhibitors of ADH release
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ETOH, phenytoin, Glucocorticoids, haloperidol,
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ADH preps
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Pitressin (IV, IM, SC)
Desmopressin (IC, SC, nasal) |
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Central Diabetes Insipidus
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Lack of ADH, give ADH preps
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Nephrogenic Diabetes Insipidus
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Rx's can cause (Li, Foscarnet, cloazapine, demeclocycline)
Tx: Amiloride for lithium induced, or Thiazides |
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Adverse Affects of exogenous ADH
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V1 mediated: vasoconstiction,
GI (N/belching/Cramping/Urge to deficate), Coronary vasocontriction (CAD!) V2 mediated: H20 intox (hyponatremia) |
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Tolvaptan
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V2 antagonist, (dec H20 reabsorption)
Tx: hyponatremia (must start in Hospital, CYP3a substrate=many interactions) |
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Inotropic action MOA
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Inactivate Na/K pump so Na/Ca pump takes over, thereby increasing intra-cellular Ca2+ to increase force and velocity of contraction (inc EF)
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EKG Changes with Inotropic drug
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T wave diminished amplitude
J point Depression PR Interval: prolong QT Interval: Shortened |
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Digitalis effect on sympathetic tone for CHF and normal heart
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CHF: reduced tone
Normal Heart: Increased tone |
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Effects of digitalis
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Slow AV conduction
Prolonged ERP of AV Node |
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Factors increasing the AV depressive effects of Digitalis
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hypokalemia
CCB BB |
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Effects of Digitalis on Area Postrema
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Dec seizure threshold
N/V, arrhythmias |
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IV administration of Digitalis
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can cause vasoconstriction (but only transiently)
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Dopamine effects by dose levels
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Low dose- Vasodilation
Moderate dose- Inc PP (inc SBP with no change in DBP) High dose- Vasoconstriction |
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Dobutamine site of action
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Beta 1 agonist (+ isomer)
Increase PP, with inc HR |
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Uses of Epi
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Relieve bronchospasm, hypersensitivity reactions, cardiac arrest, NOT CHF
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Uses of Norepi
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Cardiogenic Shock
NOT CHF |