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Heart Drugs Flashcards

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1
Q

Calcium Channel blockers tissue selectivity vascular smooth muscle

A

Vascular smooth muscle: alodipine= nifedipine > diltiazem > verapamil

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2
Q

Ca channel blocker tissues selectivity for heart

A

Verapamil> diltiazem > amlodipine = nifedipine

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3
Q

Ca channel blocker toxicity

A

Av block, peripheral edema, dizziness, constipation, cardiac depression

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4
Q

Hydralazine mechanism

A

Increase cGMP to relax smooth muscle which vasodilation of arteries more than veins so after load is lower

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5
Q

Co administered with hydralazine and why

A

Beta blocker for reflex tachycardia

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6
Q

Treatment for pregnancy hypertension

A

Hydralazine plus methyldopa

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7
Q

Hydralazine sides

A

Compensatory tachycardia (so no in angina or cad) , fluid retention, nausea, lupus like, angina

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8
Q

Nitroprusside mechanism

A

Short acting increase cGMP via NO release

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9
Q

Nitroprusside tox

A

Has cyanide so cyanide toxicity

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10
Q

Fenoldopam

A

Dopamine d1 receptor agonist, vasodilation including coronary renal and splanchnic, decrease bp and increase naturesis

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11
Q

Calcium Channel blockers drugs

A

Nifedipine, verapamil , diltiazem, amlodipine

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12
Q

Nitroglycerin/ isosorbide dinitrate: mechanism and clincial use

A

vasodialation (veins) by NO release -> cGMP increase

used for angina and pulmonary edema

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13
Q

nitroglyerin/ isosorbide dinitrate toxicity

A

reflex tachycardia, hyoptension, flushing, headache, monday’s disease in industry exposure

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14
Q

what do statins stop HMG-CoA from becoming?

A

mevalonate

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15
Q

side effects of statins

A

hepatotoxicity, rhabdomyolysis

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16
Q

statins effect on : LDL, HDL, Triglycerides

A

way down, up, down

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17
Q

niacin effect on LDL HDL Triglycerides

A

down, up, down

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18
Q

bile acid resin effect on LDL HDL Triglyceries

A

down, slightly up, slightly up

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19
Q

niacin: other name and mech

A

vitamin b3, inhibits lipolysis in adipose, reduces hepatic VLDL secretion

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20
Q

niacin sides

A

red flushed face (fix with aspirin), hyperglycemia (causing acanthosis nigricans), hyperuricemia (exacerbates gout)

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21
Q

bile acid resins and effects

A

cholestyramine, colestipol, colesevelam. prevents reabsorption of bile so liver must use cholesterol to make more

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22
Q

bile acid resins sides

A

tastes bad, gi discomfort, cholesterol gallstones, cant absorb fat soluble vitamins

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23
Q

ezetimibe

A

Cholestrol absorption blockers. rarely causes high LFTs and diarrhea

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24
Q

Fibrates

A

drives down triglycerides a lot, activates lipoprotein lipase. tox: myositis, hepatotox, cholestrol gallstones

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25
Class I Antiarrhythmics are what?
Na channel blockers
26
Class IA drugs
Quinidine, Procainamide, Disopyramide
27
Class IA actions
increase AP duration, increase effective refractory period, increase QT interval.
28
Class IA uses
atrial and ventricular arrythmias. especially reentrant currents and ectopic supraventricular or ventricular tachycardia
29
Quinidine tox and class
Class IA. cinchonism = headache and tinnitus
30
Procainamide tox and class
Class IA. reversible SLE-like syndrome
31
disopyramide tox and class
heart failure
32
Class IA shared toxicities
thrombocytopenia, torsades de pointes due to high QT interval
33
Class IB drugs
Lidocaine, Mexilentine, Tocainide
34
Class IB actions
decrease AP duration. preferentially targets ischemic or depolarized purkinje and ventricular tissue
35
Class IB uses
acute ventricular arrhythmias especially post MI and digitalis arrhythmias
36
Digoxin availability and action
75% available, 1/2 life is 40 hrs. directly inhibits Na/K ATPase, thus indirectly inhibits Na/Ca
37
Digoxin effects
increases intracellular Ca -> positive inotropy. stimulates vagus nerve -> lower heart rate. improves contractility. slows down the AV node and depresses SA node
38
Digoxin use
CHF (contractility), atrial fib (slowed AV node conduction and SA depression)
39
Digoxin tox
Cholinergic effects: nausea, comiting, diarrhea, blurry yellow vision (van Gogh) ECG: increase PR, down QT, ST scooping, T-wave inversion, arrhythmia, av block hyperkalemia - bad sign
40
Digoxin tox predisposing factors
renal failure, hypokalemia, quinidine
41
Antidote to digoxin poisoning
slowly normalize K, lidocain, cardiac pacer, anti-digoxin Fab fragments, Mg.
42
Class IC drugs
Flecainide, propafenone
43
Class IC uses
last resort for refractory tachyarrhythmias without structural anomaly
44
Class IC effects
no effect on AP duration
45
Class IC tox
proarrhythmic (post MI, so contraindicated). prolongs refractory period of AV node a lot
46
class two anti arrythmics: drugs and type of drug
beta blockers: metoprolol, propranolol, esmolol, atenolol, timolol
47
shortest acting betablocker?
esmolol
48
beta blocker actions on the heart
Decreases SA and AV node actiity by decrease cAMP and Ca currents. Makes phase 4 have a shallower long slope. AV node hit more
49
class II uses
v tach, svt, slowing ventricle during a fib/flutter
50
beta blocker toxicity
impotence, asthma attack, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations), mask signs of hyperglycemia
51
special sides of metoprolol
dyslipidemia. treat with high dose glucagon
52
special sides of propranolol
can exacerbate vasospasm of Prinzmetals (cyclical) angina
53
Class III drugs and type
Potassium Channel Blocker. Amiodarone, Ibutilide, Dofetilide, Sotalol
54
Class III effects and use
increase AP duration, increase ERP, used when other antiarrythmics fail (like IC), increase QT
55
Sotalol tox
torsades de pointes, excessive beta block
56
ibutilide tox
torsades
57
amiodarone tox
pulmanary fibrosis, hepatotox, hypo/hyperthyroid (amiodorone is 40% iodine), corneal deposits, blue/grey skin deposits, neurological effects, constipation, CV (bradycardia, heart block, CHF)
58
Amiodarone special precautions
check PFTs, LFT, and TFTs
59
what makes amiodarone unique
has class I, II, III, and IV effects (plus iodine effects) cause it disrupts membrane
60
Class IV drugs and type
Ca channel blockers, Verapmil and diltiazen
61
Class IV effects
decrease conduction velocity, increase: ERP, PR
62
Class IV use
prevent nodal arrhytmias
63
Adenosine mech
increase K out of cells -> hyperpolarize
64
Adenosine use
best drug for diagnose and treat supraventricular tachy. very short acting (15 secs)
65
Adenosine tox
flushing, hypotension, chest pain. Fix with: theophyllin or caffeine
66
Mg use
torsades de pointes and digoxin toxicty

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