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61 Cards in this Set

  • Front
  • Back
amphotericin B facts (MOA, bioavailability)
-produced by Streptomyces
-very effective, very toxic
-fungicidal: causes altered permeability in ion channels, cell becomes acidified.
-not orally available
amphotericin B spectrum, adverse events
everything except dermatophyte
-esp good for aspergillus

-reversible nephrotoxicity (80% patients, renal artery constriction and tubular permeability)
-anaphylactoid reaction
-thrombophlebitis (use catheter)
imidazole MOA, spectrum
-Inhibits sterol synthesis (lag time), channel permeability
-variable bioavailabilities (better with gastric acid - give w/ food)
-broad spectrum, no IV preps
imidazole adverse effects
gastrointestinal
-drug interactions (inhibits enzymes and competes for P-glycoprotein)
griseofulvin origin, MOA, spectrum
produced by Penicillium
-inhibits tubules for fungal mitosis
-treats dermatophyte
griseofulvin availability, distribution, adverse effects
ultra-microsize best for oral
-concentrates in keratin (lag time until growth)
-potent inducer of hepatic metabolizing enzymes
-teratogenic, allergic rxns in cats
allylamines
-Tolnafate
-inhibits fungal cell wall
-treats dermatophyte, aspergillus, sporothrix
iodides
-treatment of choice for sporothrix
2 antifungals that act synergistically
amphotericin B and imidazoles
3 methods of vasoconstriction during heart failure
adrenal releases catecholamines
-neuronal vasoconstriction
-juxtaglomerular cells release renin -- angiotensin II
aldosterone
-steroid that causes reabsorbtion of sodium and secretion of potassium in distal tubules
mechanism of increased after-load
vasoconstriction, increased peripheral resistance
mechanism of increased pre-load
aldosterone
mannitol uses
treatment of intra-cellular swelling
-emergency treatment of glaucoma, cerebro-spinal swelling
-contraindicated in ECF increases (pulmonary edema)
carbonic anhydrase inhibitors MOA, uses
inhibit CA in proximal tubule
-kidney cannot reabsorb bicarb
-causes loss of sodium and bicarb, retention of H+
-may cause metabolic acidosis
-used for glaucoma
acetazolamide
reversible carbonic anhydrase inhibitor
carbonic anhydrase adverse events
hepatic encephalopathy (increased urinary ammonia reabsorbed)
-hypothyroidism
sodium wasting drugs decrease pre/after load?
pre-load
loop diuretic MOA
blocks kidney from reabsorbing electrolytes in ascending loop
-most likely to cause dehydration
-some sodium (but not K+) reabsorbed in distal tubule
-need good renal blood flow (dont use with NSAIDs)
furosemide adverse effects, drug interactions, major use
dehydration, hypochloremic alkalosis
-don't use with digoxin, NSAIDs
-synergism with thiazides
-use for pulmonary edema, cardiac disease, renal disease, hypercalcemia
thiazide diuretic MOA, side effects
inhibits reabsorption of Na, Cl in distal tubule
-wide safety margin
-may need to supplement K+
thiazide use and contraindications
use for early CHF
-contraindicated in hypercalcemia, renal disease, diabetes mellitus
spironolactone (aldosterone antagonist) MOA
-competitive antagonist
-causes sodium loss, K+ retention
-active metabolite has longer half-life
-enterohepatic circulation
spironolactone use
CHF, liver disease
-use in combo with loop diuretic or thiazide
-cardio-protectant in early CHF
3 potassium-sparing diuretics
triamterene
-amiloride
-spironolactone
pre-load vs after-load
pre-load = venous return (emergency tmt)
after-load = arteries (long-term tmt)
cGMP causes contraction/relaxation?
cAMP?
cGMP causes contraction

cAMP causes relaxation
hydralazine
arterial vasodilator
-positive inotrope
-effect is longer than half-life
-use for CHF (decreases after-load)
calcium-channel blocker
arterial vasodilator
amlodipinde used for feline hypertension, 2nd choice in dogs
2 types of calcium channels
T (transient) - phase 4
L (long) - phase 0
ACE inhibitors
impacts aldosterone, angiotensin, bradykinin, ADH (vasopressin)
-decreases pre/after-load, positive inotrope
-most are prodrugs
-tissue ACE must be saturated
Enalapril, Benazepril
ACE inhibitors
Enalapril for dogs, Benazepril for cats
ACE inhibitors contra-indications
severe cardiac disease (kidneys can't constrict efferents, heart can't keep up, so GFR decreases - positive inotropes may help)
ACE inhibitor use
CHF, hypertension (helps kidneys), proteinuria
organic nitrates MOA
nitric oxide -- cGMP -- venous dilation
nitroglycerin effects
low dose - venous
high dose - also arteries
-emergency venodilation
phases that calcium effects
pace-maker: 0 and 4
non-pacemaker: 0 and 2
Class I (Na+ blockers)
block sodium channels
-phase 0: decreased upswing, velocity, prolonged RP, increased threshold
Class I (K+ blockers)
-prolonged refractory period (RP)
-decrease of slope of phase 4
quinidine effects and uses
class I sodium blocker
-addition anti-vagal effect (paradoxical increased heart rate)
-used for atrial arrhythmias (A-fib)
quinidine adverse effects/drug interactions
-Don't use with digoxin (competition)
-paradoxical acceleration
-GI upset
-alpha-adrenergic blockade
procainamide MOA
class IA
-targets open sodium channels (some K+ block by metabolite)
-no anti-vagal effect
-better for ventricular arrhythmias
-less K+ block in dogs b/c acetylation deficiency (use higher dose)
procainamide uses and side effects
GI upset, hypotension
-use for ventricular arrhythmias
-can use IV, switch to oral
Lidocaine MOA
Class IB
-targets open and inactive sodium channels (more prevalent in diseased, rapidly beating tissues)
-causes prolonged RP
-great for ventricular tachycardia
lidocaine preps, interactions
-mexiletine is oral prep
-IV bolus is dangerous
-direct chemical interaction with other drugs
lidocaine side effects
-myocardial depression (cats more)
-contraindicated with heart block
-IV bolus can cause seizures (dogs)
beta-blockers MOA, effects
blocks calcium and K+
-negative chronotrope, inotrope
-cardioprotection in early to middle CHF (outweighs neg. inotrope)
atenolol
beta blocker used for hypertrophic cardiomyopathy
Carvedilol
beta-blocker
-also has some alpha blockade (reduces after-load)
beta blocker metabolism, clearance, side effects
"flow limted" hepatic metabolism
-many different metabolites, isomers, affinities
-difficult to predict response
-bradycardia, decompensation in patients with low cardiac reserve
beta blocker uses
negative chronotrope - atrial arrhythmias
-hyperthyroidism in cats
-cardioprotective
Class IV - calcium channel blockers MOA
negative chrono, inotrope
-targets slow calcium channels
Diltiazem metabolism, availability, side effects
class IV (Calcium channel blocker)
-hepatic metabolism (acetylation)
-variable availabilities
-side effects same as B-blocker (hypotension, bradycardia)
-inhibits metabolizing enzymes
digoxin effects
negative chronotrope
-increases vagal tone (risk for A-fib), decreases symp. tone
-hyperpolarize, increase RP
atropine effects
-positive chronotrope
-short term tmt of bradycardias
digoxin targets
-inhibits Na+/K+ pumps - direct (positive inotrope)
-vago-mimetic, sympatho-lytic - indirect (negative chronotrope)
digoxin use, preps, interactions
-narrow therapeutic range
-renally excreted
-other drugs cause increased conc.
-treats A-fib
phosphodiesterase inhibitor effects
Pimobendan
-increase myocardial calcium (positive inotrope)
-cardioprotectant
-peripheral vasodilation (decreases pre and afterload)
-hepatic metabolite more active
-use for CHF
dopamine
used for diuresis (increases CO and dilate renal ateries) - low doses to prevent NE release
dobutamine
no release of NE, but also no renal dilation
-more effective inotrope
-less arrhythmogenic
-short term tmt for CHF
epinephrine
most potent vesopressor
-positive inotrope, chronotrope
-increase in cardiac oxygen demand