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Pharmacology > From Jen: Cardio > Flashcards

From Jen: Cardio Flashcards

1
Q

Hydrochlorothiazide

A

Diuretic

Adverse:
↓K+
Mild ↑ lipids
↑ uric acid
lassitude (lethargy)
↑ Ca2+
hyperglycemia
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2
Q

Loop diuretics

A

Diuretic

Adverse: 
K+ wasting
hypotension
ototoxicity
metabolic alkalosis
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3
Q

Clonidine

A

α2 agonist

Adverse:
dry mouth
sedation
severe rebound HTN

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4
Q

Methyldopa

A

Adverse: sedation

Positive Coombs test

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5
Q

reserpine

A

Depletes central and peripheral catecholamines (inhibits VMAT-packaging catecholamines into vesicles)

Adverse:
sedation
depression
nasal stuffiness
diarrhea
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6
Q

Guanethidine

A

Reduces catecholamine release

Adverse: orthostatic and exercise hypotension
sexual dysfunction
diarrhea

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7
Q

Prazosin

A

α1 antagonist

Adverse:
orthostatic hypotension (1st dose)
dizziness
headache

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8
Q

beta blockers

A 
Adverse:
impotence
asthma exacerbation
bradycardia
CHF
AV block
CNS effects: sedation, sleep alterations
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9
Q

Hydralazine

A

Vasodilator

Adverse:
nausea
headache
lupus-like syndrome
reflex tachycardia (prevent with beta blocker)
angina
salt retention (prevent with diuretic)
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10
Q

Minoxidil

A

Vasodilator

Adverse: hypertrichosis
reflex tachycardia (prevent with beta blocker)
angina
salt retention (prevent with diuretic)

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11
Q

Nifedipine

Verapamil

A

Calcium channel blocker
vasodilator

Adverse:
flushing
constipation (verapamil)
AV block (verapamil)
nausea
edema
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12
Q

Nitroprusside

A

vasodilator

cyanide toxicity

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13
Q

Diazoxide

A

vasodilator

Adverse: hyperglycemia (reduces insulin release, hypotension)

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14
Q

ACE inhibitors

A

Captopril, enlapril, fosinopril

Adverse: cough
hyperkalemia
angioedema
taste changes
hypotension
fetal renal damage in pregnancy
rash increase renin
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15
Q

Angiotenin II receptor inhibitors

ARB

A

Losartan

Adverse: fetal renal toxicity, hyperkalemia

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16
Q

Hydralazine

MOA

A

MOA: increase cGMP; smooth muscle relaxation (arterioles > veins)

***afterload reduction

Use: severe HTN, CHF
First line in pregnancy with methyldopa

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17
Q

Hydralazine

Toxicity

A 
compensatory tachycardia (contraindicated in angina, CAD)
fluid retention
nausea
headache
angina
lupus-like syndrome
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18
Q

Minoxidil

A

K+ channel opener- hyperpolarized and relaxes vascular smooth muscle

Use: Severe HTN

toxicity: hypertrichosis
pericardial effusion
reflex tachycardia
angina
salt retention
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19
Q

Nifedipine
Diltiazem
Verapamil

A

Calcium channel blockers
-block voltage dependent L-type calcium channels of cardiac and smooth muscle; reduce muscle contractility

Use: HTN, angina, arrhythmias (not nifedipine), prinzmetal’s angina, Raynaud’s

Toxicity:
cardiac depression
peripheral edema
flushing
dizziness
constipation
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20
Q

Isosorbide dinitrate

nitroglycerin

A

Vasodilate by releasing NO in smooth muscle, causing increased cGMP and smooth muscle relaxation

Dilates veins» arteries
**decrease preload

Use: angina, pulmonary edema, erection enhancer

Toxicity: tachycardia, hypotension, flushing, headache
“Monday disease” in industrial exposure: loss of tolerance for vasodilating action during weekend result in in tachycardia, dizziness and headache on reexposure.

21
Q

Malignant HTN treatment

A

Nitroprusside- short acting, increase cGMP via direct release of NO

Fenoldopam- D1 receptor agonist: relaxes renal vascular smooth muscle

Diazoxide- K+ channel opener: hyperpolarizes and relaxes vascular smooth muscle

22
Q

Anti-anginal therapy

GOAL

A

Reduce myocardial O2 consumption by decreasing one or more of:

  • end diastolic volume
  • BP
  • HR
  • contractility
  • ejection time
23
Q

Nitrate use in angina:

EDV
BP
Contractility
HR
Ejection time
O2 consumption
A

*Decrease Preload

EDV: ↓
BP: ↓
Contractility: ↑ (reflex)
HR: ↑ (reflex)
Ejection Time: ↓
O2: ↓
24
Q

Beta blocker use in angina:

EDV
BP
Contractility
HR
Ejection time
O2 consumption
A 
EDV ↑
BP ↓
Contractility ↓
HR ↓
Ejection Time ↑ (slower)
O2: ↓
25
Q

Nitrates + beta blocker in angina

EDV
BP
Contractility
HR
Ejection time
O2 consumption
A 
EDV: no change
BP: ↓
Contractility: No change
HR: ↓
Ejection Time: No change
O2: ↓↓
26
Q

HMG CoA reductase inhibitors

A

Statins

MOA: inhibit cholesterol precursor, mevalonate
↓↓↓ LDL
↑HDL
↓Triglycerides

Adverse: reversible increase in LFTs, rhabdomyolysis

27
Q

Niacin

A

MOA: inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion
↓↓ LDL
↑↑ HDL
↓Triglycerides

Adverse: flushing, decrease in by long term use or ASA

28
Q

Bile acid resin

A

Cholestyramine, colestipol, colesevelam

MOA: prevent reabsorption of bile acids
↓↓ LDL
Slightly ↑ HDL
Slightly ↑ Triglycerides

Adverse: GI side effects, fat soluble vitamin deficiency

29
Q

Ezetimibe

A

Competitively inhibit cholesterol absorption at brush border
↓↓ LDL
no effect on HDL or triglycerides

Adverse: Rare ↑ LFTs

30
Q

Fibrates

A

Gemfibrozil, clofibrate, bezafibrate, fenofibrate

MOA: upregulate lipoprotein lipase, increasing TG clearance
↓ LDL
↑ HDL
↓↓↓ Triglycerides

Adverse: myositis, increased LFTs

31
Q

Cardiac glycosides

A

Digoxin: 75% bioavailability
20-40% protein bound
half life: 40hrs
urinary excretion

32
Q

Digoxin

A

MOA: direct inhibition of Na/K ATPase leads to inhibition of Na/Ca exchanger; increased intracellular Ca with positive inotropy.
Also stimulates vagus nerve

Use: CHF (↑ contractility)
atrial fibrillation (↓ conduction at AV node and depression of SA node)
33
Q

Digoxin

Toxicity

A

↑ PR, ↓QT, scooping of ST segment, T wave inversion

↑ parasympathetic activity (SLUDGE)

arrhythmia

toxicity made worse by : renal failure (impaired excretion), hypokalemia (competitively binds K binding site on Na/K ATPase), quinidine (decrease clearance, displaces dig from tissue binding sites)

Antidote: Normalize K+
lidocaine, cardiac pacer, anti-digitoxin Fab fragments, Mg2+

34
Q

Class I antiarrhythmics

A

Na+ channel blockers

local anesthetics, slow or block conduction (slow upstroke)

Decrease slop of phase 4 depolarization in pacemaker cells (↑ threshold for firing)

State dependent-selectively depress tissue that is frequently depolarized

35
Q

Class IA

Drugs/MOA

A

Quinidine, Procainamide, Disopyramide

MOA: ↑ AP duration, ↑ effective refractory period, ↑ QT interval

Use: Affect atrial and ventricular arrhythmias **esp. rentrant and ectopic SVT, Vtach, WPW

36
Q

Class IA

Toxicity

A

Thrombocytopenia, Torsades de pointes (↑ QT interval)

Quinidine: cinchonism (headache/tinnitus)

Desopyramide: heart failure

Procainamide: reversible SLE-like syndrome

37
Q

Class IB

Drugs/MOA

A

Lidocaine, Mexiletine, Tocainide

MOA: ↓ AP duration, affect ischemic or depolarized Purkinje and ventricular tissue

Useful in acute ventricular arrhythmias **esp. post-MI or digitalis-induced arrhythmias

Class IB is BEST for post-MI

38
Q

Class IB

Toxicity

A

Lidocaine, Mexiletine, Tocainide

local anesthetic, CNS stimulation/depression, CV depression

39
Q

Class IC

Drugs/MOA

A

Flecainide, encainide, propafenone

MOA: prolongs refractory period in AV node, no effect on AP duration

Use: SVTs, afib, last resort in refractory VTach

40
Q

Class IC

Toxicity

A

Flecainide, encainide, propafenone

Pro-arrhythmic, especially post-MI (Class IC = Contraindicated)

Significantly prolongs the refractory period in AV node

41
Q

Class II
(beta blockers)

Drugs/MOA

A

Propranolol, esmolol, metoprolol, atenolol, timolol, carvedilol

MOA: Block beta receptor: ↓ cAMP and Ca2+ currents (↓ slope of phase 4)

Suppress abnormal pacemakers by ↓ slope of phase 4 (AV node particularly sensitive)- ↑ PR interval

Uses:
Vtach, SVT, to slow ventricular rate during atrial flutter/fibrillation

42
Q

Class II
(beta blockers)

Toxicity

A 
Impotence
asthma exacerbation
CHF
bradycardia
AV block
sedation/sleep alterations
mask hypoglycemia
metoprolol: dyslipidemia
43
Q 
Class III
(K+ channel blockers)

Drugs/MOA

A

Sotalol, ibutilide, amiodarone

MOA: ↑ AP duration, ↑ refractory period, ↑ QT interval

Use: when other antiarrhythmic fail

44
Q 
Class III
(K+ channel blockers)

Toxicity

A

Sotalol- torsades de pointes, excessive beta block

ibutilide- torsades

amiodarone- pulmonary fibrosis, hepatotoxicity, corneal deposits, skin deposits, neurologic effects, constipation, CV effects (bradycardia, CHF, heart block), hypo/hyperthyroidism

45
Q 
Class IV
(Calcium channel blockers)

Drugs/MOA

A

verapamil, diltiazem

MOA: primarily affect AV nodal cells, ↓ conduction velocity, ↑ refractory period and PR interval

Use: prevention of nodal arrhythmias

46
Q 
Class IV
(Calcium channel blockers)

Toxicity

A

Verapamil, diltiazem

Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

47
Q

Adenosine

A

↑ K+ out of cells, hyperpolarizing the cell and decreasing intracellular Ca
very short acting

Use: drug of choice when abolishing AV nodal arrhythmias

Toxicity: flushing, hypotension, chest pain

48
Q

K+

A

Depresses ectopic pacemakers in hypokalemia (digoxin toxicity)

49
Q

Mg2+

A

Effective in torsades de pointes and digoxin toxicity

Pharmacology (18 decks)

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