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47 Cards in this Set

  • Front
  • Back
Digoxin
Cardiac glycoside; long term use

Inhibits Na/K ATPase; increases intracellular Ca++

Results in (+) inotropy
Digitoxin
Cardiac glycoside; long term use

Inhibits Na/K ATPase; increases intracellular Ca++

Results in (+) inotropy

Can be used as digoxin substitute in patients with renal disease because it is metabolized by liver
Ouabin
Cardiac glycoside; long term use

Inhibits Na/K ATPase; increases intracellular Ca++

Results in (+) inotropy
Dobutamine
Beta1 agonist; short term use

Results in PKA activation

+ inotrope, chronotrope, lusitrope
Milrinone
PDE3 inhibitor; short term use only

Inhibit metabolism of cAMP by PDE3

Inodilator
Inamrinone
PDE3 inhibitor; short term use only

Inhibit metabolism of cAMP by PDE3

Inodilator
Levosimendan
Stabilizes Ca++ bound conformation of TnC

Not approved for use in US

For short term use only
Carvedilol
Mixed beta and alpha-1 antagonist; long term use

Normalize receptor expression
Metoprolol
Beta antagonist; long term use

Normalize receptor expression
Bisoprolol
Beta 1 antagonist; long term use

Normalize receptor expression
Amiloride
K sparing diuretic

Competitive inhibition of ENaC

Results in decreased Na reabsorption and increased K reabsorption
Spironolactone
K sparing diuretic

Competitive inhibition of MR

Results in decreased Na reabsorption and increased K reabsorption
Mannitol
Osmotic agent

Increases osmolarity of tubular fluid
Acetazolamide
Primary site of action: PCT

Noncompetitive/reversible inhibition of PCT cell carbonic anhydrases

Results in decreased bicarbonate reabsorption and subsequent decreased Na reabsorption

AE: Metabolic acidosis

Has sulfa moiety
Furosemide
Primary site of action: TAL

Competitive inhibition of TAL cell NKCC2 (Na/K/2Cl) transporter

Results in decreased Na reabsorption and loss of positive transepithelial potential (decrease Mg/Ca reabsorption)

Has sulfa moiety
Thiazides
Primary site of action: DCT

Competitive inhibition of DCT cell NCC1 (Na/Cl) transporter

Results in modest decrease in Na reabsorption and increased Ca reabsorption

Has sulfa moiety
Conivaptan
Competitive inhibition of V1R and V2R

Results in decreased aquaporin insertion into apical membrane which increases water excretion
Tolvaptan
Competitive inhibition of V2R

Results in decreased aquaporin insertion into apical membrane which increases water excretion
Lixivaptan
Competitive inhibition of V2R

Results in decreased aquaporin insertion into apical membrane which increases water excretion
Quinidine
Class IA Na and K ch blocker

AE: Anticholinergic effect

DDI w/digoxin for CYP metabolism (pharmacokinetic)
Procainamide
Class IA Na and K ch blocker

AE: Hypotension and lupus like symptoms

If acetylated in liver, metabolite only has K ch activity
Lidocaine
Class IB Na ch blocker

AE: Na ch blocking in CNS can cause seizure, dizziness

DDI potential bc of metabolism via liver
Flecainide
Class IC Na ch blocker

TX of emergency supraventricular and ventricular arrthymias

AE: Can be pro-arrthymic in some patients

Not useful if problem is repol
Bisoprolol
Beta 1 blocker selective (Class II)

SA node: Decr slope of phase 4 and depol

AV node: Prolongs repol

Effect: Decr automaticity (SA) and incr refractory period (AV, therefore decr re-entry)
Atenolol
Beta 1 blocker selective

Class II
Carvedilol
Non selective beta blocker and alpha 1 blocker

Class II
Metoprolol
Beta 1 blocker selective

Class II
Dofetilide
Class III K ch blocker

Prolongs repolarization and increases APD

AE: Torsades de pointes and early afterdepolarizations

Extensive renal clearance
Sotalol
Mixed class II (b-blocker)/III (K channel blocker) activity
Racemic mixture

Decreased automaticity, decreased AV conduction and increased AV refractoriness

AE: Usually with overdose, bradycardia and torsades de pointes

Extensive renal clearance
Amiodarone
Mixed class I-IV activity

Decr automaticity, conduction velocity and incr refractoriness

Low incidence of torsades de pointes

AE: Hypo- or hyperthyroidism due to similarity on structure to thyroxine (iodine moieties); heart block; hypotension; pulmonary fibrosis; elevated liver enzymes
Dronedarone
Related to amiodarone; mixed class I-IV activity

Less toxic bc lacks iodine moieties and decr lipophilicity
Verapamil
Cardiac CCB

Tx of supraventricular arrthymias

AE: AV block and hypotension with high doses

DDI with beta blocker which results in HF

CCB can incr digoxin levels via competition for renal excretion
Diltiazem
Cardiac CCB

Tx of supraventricular arrthymias

AE: AV block and hypotension with high doses

DDI with beta blocker which results in HF

CCB can incr digoxin levels via competition for renal excretion
Adenosine
Promotes increased K channel opening and decreased Ca channel opening in SA and AV nodes

Leads to increased refractoriness, decreased APD and slowed automaticity

Given IV only for supraventricular arrhythmias (extremely short ½ life)
K and dialysis
Restore K+ levels for proper AP generation

Hypokalemia: early and delayed depolarizations

Hyperkalemia: decreased conduction velocity
Nifedipine
VSMC arterial vasoD

MOA: Block LTCC

AE: Causes reflex tachycardia which aggrevates MI, flushing

Beneficial DDI: Beta blocker to prevent reflex tachycardia
Amlodipine
VSMC arterial vasoD

MOA: Block LTCC

Slower metabolism exhibits less reflex tachycardia
Minoxidil
K ch opener in VSMC

AE: HA and flushing; reflex tachycardia if use as monotherapy

Off target: Reduces male pattern baldness
Sitaxsentan
Competetive antagonism of ETAR

AE: HA, flushing, teratogenic
Bosentan
Competitive antagonism of ETAR and ETBR

AE: HA, flushing, teratogenic, liver toxicity
Hydralazine
MOA: Membrane hyperpol or Ca release from SR

Predominantly vasoD arteries

Used w/other antihypertensives for HTN and w/nitrates for HF

Acetylation in liver causes low oral bioavail

AE: Rapid reflex tachycardia
Prazosin
Antagonize VSMC alpha1 receptor thereby decr Ca mobilization

AE: Hypotension with reflex tachycardia, Na and H2O retention
Use with beta blockers and diuretics to prevent AEs
Losartan
ARB

Antagonism of AT1R, blocks downstream effects of AT1R stimulation, allows AngII stimulation of AT2R
Valsartan
ARB


Antagonism of AT1R, blocks downstream effects of AT1R stimulation, allows AngII stimulation of AT2R


AE: HyperK, precipitate renal failure in patients with bilateral renal artery stenosis, teratogenicity, incr renin secretion
Candesartan
ARB


Antagonism of AT1R, blocks downstream effects of AT1R stimulation, allows AngII stimulation of AT2R


AE: HyperK, precipitate renal failure in patients with bilateral renal artery stenosis, teratogenicity, incr renin secretion
Aliskiren
DRI

Decr renin activity, blocks downstream effects of angiotensinogen, no impact on bradykinin

AE: Possible hyperK in conjunction with ACE inhibitors/ARBs/K sparing diuretics, teratogenicity
Nesiritide
B type natriuretic peptide

Tx of HF, short term

IV only because it is a peptide

AE: Hypotension from vasorelaxation effects