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48 Cards in this Set

  • Front
  • Back
2 Hypertensive drugs used in pregnancy
Methyldopa
Hydralazine
Methyldopa major toxicity
hemolytic anemia
(positive Coombs test, direct)
Methyldopa MOA
work on alpha-2 receptors in CNS to decrease sympathetic nervous system output
Hydralazine major toxicity
Lupus-like syndrome
(anti-histone antibodies)

Also: reflex tachy (CONTRAINDICATED in agina/CAD), salt retention, nausea, headache
nitroglycerine/ isosorbide dinitrate decrease what?
preload
Hydralazine decreases what?
Afterload
Minoxidil MOA
K-channel opener. Hyperpolarizes to relax smooth muscle.

Use in severe hypertension
Minoxidil toxicity
Similar to hydralazine. Reflex tachy, salt retention, angina, PERICARDIAL EFFUSION
Rx co-prescribed with Minoxidil and Hydralazine? (2)
Beta-blocker to prevent reflex tachy

Diuretic to prevent salt retention
Rx interaction when diuretics are used in hypertension?
Digoxin (via hypokalemia)
Nitroprusside toxicity?
release cyanide

(direct inhibitor of electron transport. decreases proton gradient causing decreased ATP production)

Used in Hypertension
Tx of Cyanide poisoning?
hydroxocobalamin, nitrite, thiosulfate
Diazoxide toxicity
hyperglycemia. (reduces insulin release, hypotension)

used in HT
Calcium channel blocker that works mainly on the heart?
Verapamil

(do not use w/ beta blockers, due to effect on dec. contractility)

Note: can accelerate heart failure due to depression of myocardial contractility
Calcium channel blocker that works mainly in the vascular smooth muscle?
Nifedipine

(not useful in exertional angina b/c it allows for reflex tachycardia)
Verapamil MOA
block voltage-dependent L-type Ca channels, thereby reducing muscle contractility. (no Ca released from the sarcoplasmic reticulum)
Rx given during stress test when patient is incapable of exercise
Dobutamine (synthetic catecholamine)
Partial beta-antagonists that are contraindicated in angina? (2)
Pindolol and acebutolol
Statin MOA
HMG-CoA reductase inhibitors
(rate-limiting step in cholesterol synthesis. HMG-CoA --> mevalonic acid)
Reduction of flushing in niacin use
by long-term aspirin use
Niacin MOA
inhibits lipolysis in adipose tissue, reduces VLDL secretion into circulation
Bile acid resin contraindications?
(ie, cholestyramine, colestipol, colesevelam)
contraindicated in pts. with gallstones

(also, can dec. fat soluble vitamin uptake or bind oral Rx's (ie, digoxin))
Lipid-lowering agent that works strongly on triglycerates?
Fibrates (-fibrate and gemfibrozil)

(PPAR-alpha receptor agonist. Upregulates LPL --> inc. triglyceride clearance.
Results in:
Increased β-oxidation in the liver
Decreased hepatic triglyceride secretion
Increased lipoprotein lipase activity, and thus increased VLDL clearance
Increased HDL
Increased clearance of remnant particles
Firates toxicity?
Myositis, increase LFT
Ryanodine receptors are coupled with what?
L-type calcium channels in cell membrane. They are located in the sarcoplasmic reticulum.
action of protein kinase A in cardiac cells
Activated through Beta-1 and G(s).

phosphorylates L-type and Ca channels and phospholamban, both of which increase intracellular Ca during contraction
Class 1A antiarrhythmics
Quinidine, Procainamide, Disopyramide

(The QUeen PROClaims DISO's PYRAMID)
Prolongation of QT interval by which drugs?
Class IA and III. Risk of Torsades de Pointes.

Familial Long QT syndrome is from mutation in K-channel.
Class I antiarrhythmics decrease what?
Slope of Phase 0 upstroke and amplitude of action potential

*Also: decrease slope in phase 4.
--> increase time between depolarization.
Effect on phase 3 by Class IA, IB, and IC antiarrhythmics?
IA: elongate (inc AP duration)
IB: shorten (dec AP duration)
IC: no change
Indication for IA drugs?
atrial and ventricular arrhythmias, esp:
reentry
ectopic supravenricular
ventricular
Indication for IB drugs?
acute ventricular arrhythmias
(especially post MI)
digitalis-induced arrhythmias
Indication for IC drugs?
Last resort for refractory tachyarrhythmias
For patients without structural abnormalities
Class IB drugs?
Lidocaine, Mexiletine, Tocainide
(I'd Buy LIDy's MEXIcan Tacos)

Can also include phenytoin
Class IC drugs?
Flecaninide, encainide, propafenone
Toxicity of IC?
Pro-arrhythmic, esp. post MI
significantly prolongs refractory in AV node
Class II antiarrhythmics?
Beta-blockers
Propanolol (non-selective)
Esmolol and Metaprolol (cardio selective)
Atenolol
Timolol
Actions of Class II?
decrease cAMP, decrease Ca currents
Suppress abnormal pacemakers by dec phase 4 (AV node very sensitive)
Increase PR interval
Toxicities of Class II
Impotence, exacerbation of asthma/allergic rxns, bradycardia, AV block, CHF, exercise intolerance (inability to inc HR), mask hypoglycemia in diabetics, CNS sleep alterations
Metaprolol Toxicity?
dyslipidemia
Class III antiarrhythmics?
Soltalol, ibutilide, amiodarone
Amiodarone Toxicity
Pulmonary fibrosis, corneal deposits, hepatotoxicity, skin deposits resulting in blue skin (photodermatitis), hypo/hyperthyroidism

Remember to check PFTs LFTs and TFTs when using amiodarone

Note: takes 1-3 weeks to work, not suitable for acute managment
Tx of Nodal arrhythmias?
#1: Adenosine (very short acting)
#2 Class IV: verapamil, diltiazem

(avoid use with class II due to synergistic dec in contractility)
Action of class IV?
on nodal cells. dec amplitude and extends length of AP
(ERP is increased, also inc in IA)
Causes of AV block?
Lyme disease, tertiary syphilis, OD of beta-blocker or ca-channel blockers
Adenosine MOA
increase K out of cells --> hyperpolarization and decreased calcium influx

Drug of choice in dx/abolishing AV nodal arrhythmias.
Epinephrine reversal with what drugs?
With alpha-blockers.
ie, phenoxybenzamine or phentolamine (fyi: irrev, rev)

Normally, non-selective beta and alpha agonist would increase BP. When alpha antagonist is administered, the beta-activation causes a dec in BP due to vasodilatation.
Alpha-1 blockers and use
Prazosin, terazosin, doxazosin

for HT and urinary retention due to BPH