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CCT > Medications > Flashcards

Medications Flashcards

1
Q

Calcium Channel Blockers

A

(Calcium channel antagonists) inhibit transport of Ca

  • dilation of vasculature
  • decrease in bp
  • increase of blood and oxygen delivery to hear
  • treats high bp
  • angina
  • some arrhythmias

class: dihydropyridines, non-dihydropryidines

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2
Q

dihydropyridines

A

(Ca channel blocker)
-decrease bp
-dilation of vasculature
nifedipine

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3
Q

Non-dihydropyridines

A

(Ca channel blocker)

  • decrease bp
  • dilation of vasculature
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4
Q

nitrates

A

-used to decrease heart’s oxygen demands
- relaxes coronary arteries, reducing workload of hear
relax muscles in blood vessels, vasodilation, decrease heart’s oxygen demands, decrease bp,
-isosobide mononitrate
-isosorbide dinitrate
-nitroglycerin
use: acute chest pain attacks, angina, prevent stress induced attacks of chest pain

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5
Q

Cardiac Glycosides

A 
-naturally occurring chemicals
bind to Na K ATP pump, 
increases intracellular Ca 
-increases force of contraction
- slows HR
-doesnt effect BP
-digoxin: in addition decreases conduction through AV node, prolonging refraction, reduces arrhythmias
-digitoxin
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6
Q

Beta Blockers

A

inhibits action of epinephrine or adrenaline or norepinephrone
- decreases HR
-decreases BP
-decreases force of contraction
-decreases oxygen demand
-hypertension, heart failure, arrhythmias, decrease risk of heart attacks with previous
WARNING: may increase bronchospasm, do not use for pre-exisiting pulmonary disorder, COPD, or diabetes

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7
Q

Digoxin

A

(cardiac glycoside) used for congestive heart failure, arrythmias, a-fib, a-flutter, supraventricular tachycardia
-may lead to cardiac toxicity

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8
Q

cardiac toxicity

A

(from digoxin) ventricular arrhythmias, AV block

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9
Q

Type 1 antiarrhythmics

A

sodium channel blockers, slows conduction velocity of electrical impulses and prolongs refraction

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10
Q

Type 1a antiarrhythmics

A

Na channel blocker

  • decreases automatic properties of some tissue, decreases generation of spontaneous impulses
  • slow conduction
  • prolong refractory period

use: ventricular and supraventricular arrhythmias
Quinidine, Procainamide, disopyramide

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11
Q

Type 1b antiarrhythmics

A 
Na channel blockers
lowest affinity for Na channels
-little effect on conduction, 
-shortens refractory period
more affective for ventricular arrhythmias than supraventricular arrhythmias
-Lidocaine, Mexiletine, Tocainide
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12
Q

Type 1c Antiarrhythmics

A

Na channel blocker
greatest affinity of Na channels
does not alter refractory period as much
can slow conduction to the point of non-conduction
affective for both ventricular and supraventricular arrhythmias
-not often used of ventricular arrhythmias because of proarrhythmias
-flecainide, propafenone, moricizine

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13
Q

Type III Antiarrhythmics

A

Potassium Channel Blockers

  • delay repolarization of heart muscle
  • increases refractory period, prolonging QT interval
  • most effective class for treating arrhythmia
  • all have different mechanism of action
  • amiodarone, bretylium, dofetilide, sotalol, ibutilide
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14
Q

ACE Inhibitors and ARB’s

A
  • dilation of blood vessels
  • lower blood pressure
  • decreases fluid retention
  • decreases aldosterone production

mechanism: angiotensin II increases all of the above
ACE inhibitors: inhibit angiotensin II formation
ARB’s: block action site of angiotensin II

use: hypertension
if first line diuretics don’t work

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15
Q

ACE inhibitors

A
  • dilation of blood vessels
  • lower blood pressure
  • decreases fluid retention
  • decreases aldosterone production

mechanism: angiotensin II increases all of the above
ACE inhibitors: inhibit angiotensin II formation

use: hypertension -if first line diuretics don’t work
benazepril, enalalpril, fosinpril, lisinopril, quinapril, ramipril

indicated: heart failure, previous MI, diabetes mellitus, chronic kidney disease

do not use during pregnancy due to risk of infant renal failure or death

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16
Q

ARB’s

A
  • dilation of blood vessels
  • lower blood pressure
  • decreases fluid retention
  • decreases aldosterone production

mechanism: angiotensin II increases all of the above
ARB’s: block action site of angiotensin II

use: hypertension -if first line diuretics don’t work
indication: second line therapy for heart failure, diabetes mellitus, chronic kidney disease, allergy to ACE inhibitors

do not use during pregnancy due to risk of infant renal failure or death

17
Q

Diuretics

A

first line drugs to treat hypertension
increase urine output (diuresis)

Three main types: thiazide diuretics, loop diuretic, potassium sparing diuretics

18
Q

Thiazide diuretics

A

hypertension medication
-preferred medication
-generally used to initiate therapy
if ineffective or patient has bp greater than 140 or 90, may be combined with another hypertensive medication

19
Q

Loop diuretics

A

more potent diuretic

use if patient has inadequate renal function

20
Q

potassium-sparing diuretics

A

not potent when used alone, effective when combined with thiazide or loop diuretics

aldosterone antagonist: subclass that could take up to 6 weeks to see benefits

21
Q

Central alpha-agonists

A

block alpha-2 receptors which are responsible for increasing HR and narrowing vessels

  • decrease in BP
  • decrease in HR

For patients who have failed first line bp lowering medication

  • use: panic disorders, hot flashes, drug withdrawal, migraine prevention
  • may cause water retention, add diuretic
  • clonidine, guanfacine, guanbenzene, methyldopa
22
Q

Type II Antiarrythmics

A 
-beta blockers
decrease conduction velocity
prolong refractory period
decrease automaticity in AV node
slow sinus rhythm
- decrease workload
-decrease oxygen demand
-used to treat atrial tachycardia and atrial fibrillation
-treat hypertension, bp, relieve angina
23
Q

Type IV antiarrhythmics

A

calcium channel blockers
-slows conduction
-prolongs refractory period
treats high bp, heart failure, coronary artery disease
-can be used to treat arrhythmias originating in SA or AV node

24
Q

Alpha blockers

A

antagonists at alpha-1 receptor in smooth muscle cell, inhibits norepinephrine, relaxation of veins and arterioles, do not act on alpha 2 therefore no increase in HR

25
Q

Atropine

A

blocks affects of vagus nerve: vagus nerve normally decreases HR,

  • blocks decrease of HR
  • accelerates conduction through heart
  • normally administered after epinephrine
  • administered if asystole to try to return HR

CCT (3 decks)

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