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45 Cards in this Set

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Carbonic Anhydrase Inhibitor MOA
Inhibition of CA leads to decrease in symport Bicarb and Na transport on Basolateral surface
Carbonic Anhydrase inhibitor Drugs
Acetazolamide and Methazolamide
Adverse reactions of CAI
Marrow Suppression, rash, Bicarbonaturia/Metabolic acidosis. May worsen acidosis so avoid in pt's with COPD and renal failure
Loop Diuretic MOA
Inhibition of Na/K/Cl symport on luminal surface
Adverse effects of Loop
Wasting of Ca, Mg and Na
Acute (uricosuria) Chronic (hyperuricemia)
Why do loops cause hypo Mg and Ca ?
Loss of charge gradient btw lumen and basolateral surface (no Cl- transport=no Mg or Ca via paracellular)
Why hyperuricemia in Loops?
Uric acid and loops compete for the same Organic acid secretory pathway
List Loop Drugs and rank by potency
Bumetanide> Toresemide >Furosemide > Ethacrynic acid

Sulfa Drugs= rash rxn
How does dosage change for Loops when pt's with renal insufficiency ?
Larger doses, b/c Organic Acid Secretory to lumen side is compromised.
Loops Adverse reactions
Hypokalemia (arrhythmias)
Hypocalcemia (tetany)
Hypomagnesiemia (arrhythmia)
metabolic alkalosis
Ototoxicity (high doses of ethacrynic acid)
Atypical thiazides
Chlorthalidone
Indapamide
Metolazone
Loops and thiazides affect on Ca and Mg
Loops lose Ca and Mg
Thiazides lose only Mg
Thiazides Adverse reactions
ED, Metabolic Alkalosis
Impaired Glucose Tolerance
Sulfonamide allergy
Therapeutic Uses of Thiazides
HTN (1st line)
Edema
Ca Nephorlithiasis
Nephrogenic Diabetes Insipidus!
2 subtypes of Potassium Sparing Diuretics
KSD
ARA(Aldosterone receptor antagonist)
MOA of KSDs
Block Na Channel on Luminal side at Collecting Duct. Without Na influx K efflux less favorable
MOA of ARAs
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!)
Endogenous levels of Aldosterone effects the amount of natriuresis of which diuretic?
ARAs
Spironolactone & Eplerenone
Amiloride & Triamterene
KSDs
Spironolactone & Eplerenone
ARAs
Which KSDs can you not give in patients with Liver failure
Triamterene, b/c it must be converted in the liver to active form 4-hydroxytriamterene (which is renally excreted!
Adverse Effects of KSDs
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
Adverse Effects of ARAs
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
Therapeutic uses of KSDs
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!
Therapeutic uses of ARAs
Decreases mortality in CHF
primary and secondary hyperaldosteronism (cirrhosis /w ascities)
Not used in Pregnancy!
Arginine Vasopressin (ADH) amount release is associated with what?
Increases with Osmolality and hypotension (20% vol. loss).
ADH MOA
V2 Stimulation Increases H20 permeability via insertion of AQP2 at medullary CD, up-regulates Na/K/2Cl symporter of TAL
Promoters of ADH release
Ang II/III
Nicotine, EPI, SSRI, TCAs
Inhibitors of ADH release
ETOH, phenytoin, Glucocorticoids, haloperidol,
ADH preps
Pitressin (IV, IM, SC)
Desmopressin (IC, SC, nasal)
Central Diabetes Insipidus
Lack of ADH, give ADH preps
Nephrogenic Diabetes Insipidus
Rx's can cause (Li, Foscarnet, cloazapine, demeclocycline)
Tx: Amiloride for lithium induced, or Thiazides
Adverse Affects of exogenous ADH
V1 mediated: vasoconstiction,
GI (N/belching/Cramping/Urge to deficate),
Coronary vasocontriction (CAD!)
V2 mediated: H20 intox (hyponatremia)
Tolvaptan
V2 antagonist, (dec H20 reabsorption)
Tx: hyponatremia (must start in Hospital, CYP3a substrate=many interactions)
Inotropic action MOA
Inactivate Na/K pump so Na/Ca pump takes over, thereby increasing intra-cellular Ca2+ to increase force and velocity of contraction (inc EF)
EKG Changes with Inotropic drug
T wave diminished amplitude
J point Depression
PR Interval: prolong
QT Interval: Shortened
Digitalis effect on sympathetic tone for CHF and normal heart
CHF: reduced tone
Normal Heart: Increased tone
Effects of digitalis
Slow AV conduction
Prolonged ERP of AV Node
Factors increasing the AV depressive effects of Digitalis
hypokalemia
CCB
BB
Effects of Digitalis on Area Postrema
Dec seizure threshold
N/V, arrhythmias
IV administration of Digitalis
can cause vasoconstriction (but only transiently)
Dopamine effects by dose levels
Low dose- Vasodilation
Moderate dose- Inc PP (inc SBP with no change in DBP)
High dose- Vasoconstriction
Dobutamine site of action
Beta 1 agonist (+ isomer)
Increase PP, with inc HR
Uses of Epi
Relieve bronchospasm, hypersensitivity reactions, cardiac arrest, NOT CHF
Uses of Norepi
Cardiogenic Shock
NOT CHF