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IPE Pharmacology > CVS Drugs > Flashcards

CVS Drugs Flashcards

1
Q

Amiodarone mechanism of action

A

Primary mechanism of action: antiarrhythmic effect via blockage of voltage-gated potassium channels → prolonged repolarization of the cardiac action potential
Secondary mechanism of action: inhibits β-receptors and sodium and calcium channels → decreases conduction through the AV and sinus node
Only antiarrhythmic agent with (almost) no negative inotropic effect → use in patients with reduced EF

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2
Q

Amiodarone side effects

A 
Lungs	
-Pulmonary toxicity 
-Pulmonary fibrosis 
-Chronic interstitial pneumonitis
-Organizing pneumonia
-ARDS
-Solitary pulmonary mass 
Thyroid	
-May induce hypothyroidism and/or hyperthyroidism- prevents peripheral conversion of T4 to T3
-May aggravate pre-existing thyroid conditions 
Liver	
-AST/ALT > 2x normal - monitor at baseline and 6 months
-Hepatitis and cirrhosis 
Heart	
-Bradycardia and AV block 
-Proarrhythmia 
Eyes	
-Corneal micro-deposits  
-Optic neuritis 
GI tract	
-Nausea, anorexia, and constipation
Skin	
-Photosensitivity
-Blue discoloration
CNS	
-Various manifestations, esp. peripheral neuropathy (also ataxia, paresthesias, sleep disturbance, impaired memory, and tremor)
GU tract	
-Epididymitis and erectile dysfunction
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3
Q

Indications for amiodarone

A

Acute treatment (IV administration)
Second-line therapy for patients with ventricular tachycardia (VT) who are hemodynamically stable
Persistent VT after defibrillation
Pulseless ventricular fibrillation
Supraventricular tachycardia in patients with cardiac failure (LVEF < 40%)

Long-term treatment (oral administration)
Rhythm control in refractory symptomatic atrial fibrillation (supraventricular arrhythmia) and underlying heart disease → restoration and maintenance of sinus rhythm

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4
Q

Amiodarone contraindications

A

Severe sinus node dysfunction with marked sinus bradycardia
Second- and third-degree heart block (except in patients with a functioning pacemaker)
Hyperthyroidism and hypothyroidism
Known allergy to iodine
Pre-existing lung disease

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5
Q

Example of an irreversible COX inhibitor

A

Aspirin

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6
Q

Method of action of aspirin

A

COX-1 inhibition → irreversible inhibition of thromboxane (TXA2) synthesis in platelets → inhibition of platelet aggregation (antithrombotic effect)
Onset of antiplatelet action: within minutes
Duration of antiplatelet action: 7–10 days
COX-1 and COX-2 inhibition → inhibition of prostacyclin and prostaglandin synthesis → antipyretic, anti-inflammatory, and analgesic effect

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7
Q

Side effects of aspirin use

A 
Gastrointestinal (most common): dyspepsia, gastric ulceration, hemorrhage, perforation
Coagulopathy and bleeding
Reye’s syndrome
Aspirin exacerbated respiratory disease
Toxicity
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8
Q

Examples of P2Y12 receptor antagonists

A

Clopidogrel
Prasugrel
Ticagrelor

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9
Q

Mechanism of action of clopidogrel

A

Inhibition of P2Y12 receptor on platelets (ADP receptor) → inhibition of platelet aggregation

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10
Q

Side effects of clopidogrel

A 
Allergic reactions (rash, pruritus, anaphylaxis)
Hemorrhage 
Gastrointestinal complications
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11
Q

Examples of glycoproteins IIb/IIIa inhibitors

A

Abciximab
Eptifibatide
Tirofiban

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12
Q

Mechanism of action of abciximab

A

Gp IIb/IIIa inhibitors bind to and block glycoprotein IIb/IIIa receptors on the surface of the platelets → prevention of platelets binding to fibrinogen → inhibition of platelet aggregation and thrombus formation

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13
Q

Side effects of glycoprotein IIb/IIIa inhibitors

A

Acute profound thrombocytopenia

Hemorrhage

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14
Q

Contraindications to antiplatelet agents

A

Known allergy against an antiplatelet agent
Active/recent hemorrhage within the past 30 days (e.g., gastric ulcers or intracranial bleeding)
Major surgery/severe trauma within the past 30 days
Severe hypertension
Aortic dissection
Thrombocytopenia
Aspirin: children < 19 years of age with a febrile illness (risk of Reye syndrome)

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15
Q

Give examples of non-specific beta blockers

A

Propranolol

Sotalol

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16
Q

Effects of non-specific beta blockers

A

Block β1, β2, and β3 receptors
Cause bronchoconstriction: may exacerbate asthma/COPD
Cause vasoconstriction: avoid in patients with peripheral vascular disease (PVD)
Can cause hypo- and hyperglycemia

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17
Q

Give examples of some cardioselective beta blockers

A 
Atenolol
Metoprolol
Esmolol
Bisoprolol
Betaxolol
Bevantolol
Nebivolol
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18
Q

What are the effects of cardioselective beta blockers

A

Selectively bind to and block β1 receptors, which are primarily found in the heart
Do not cause bronchoconstriction or vasoconstriction
Do not interfere with glycogenolysis; safe in diabetics
Cardioselectivity is dose-dependent

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19
Q

What type of drug is labetolol? What’s it effect?

A

Non-selective beta blocker, with alpha blocking action
Potent vasodilators
Can cause orthostatic hypotension

Labetalol
Carvedilol

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20
Q

Where are b1 receptors found?

A

Heart kidneys

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21
Q

What is the effect of blocking b1 receptors

A

Heart
Anti-ischemic effect
Antiarrhythmic effect
Kidneys: ↓ renin release→ ↓ BP

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22
Q

Where are b2 receptors found?

A 
Smooth muscle (bronchiolar and peripheral smooth muscle)
Ciliary body of the eye
Pancreatic beta cells
Skeletal muscle and liver
Lipoprotein lipase enzyme
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23
Q

What is the effect of blocking b2

A 
Vasculature: vasoconstriction 
Bronchioles: bronchoconstriction
Ciliary body: ↑ aqueous humor production → ↓ intraocular pressure
Hyperglycemia, new-onset diabetes
Hypoglycemia (esp. in diabetics) 
Hyperlipidemia
24
Q

Where are b3 receptors found

A

Adipose tissue

25
Q

What happens when b3 receptors are blocked?

A

↓ Lipolysis with weight gain

26
Q

Cardiac side effects of b1 and b2 receptor blockage

A

Bradycardia
Bradyarrhythmia
Ventricular tachyarrhythmia (torsades de pointes)
Orthostatic hypotension (esp. in the elderly)
Worsened heart failure (HF)

27
Q

CNS effects of b1 and b2 blockage

A

Drowsiness, sleep disorders, nightmares
Fatigue/lethargy
Depression, hallucinations

28
Q

Pulmonary effects of b2 blockage

A

Bronchoconstriction (esp. patients with asthma and reactive airway disease)

29
Q

Effect of b2 blockage on peripheral Vasculature

A

Peripheral vasoconstriction
Erectile dysfunction
Secondary Raynaud’s phenomenon
Cold extremities

30
Q

Metabolic effects of b2 blockage

A

Hyperglycemia and new-onset diabetes
Hypoglycemia
Weight gain

31
Q

What is beta blocker withdrawal

A

Caused by sudden termination of β blockers
Clinical features: tachycardia, tachyarrhythmia, hypertension, acute coronary syndrome, sudden cardiac death
Prevention: taper dose over 7–10 days before discontinuing

32
Q

Features of beta blocker overdose

A

bradycardia/bradyarrhythmia, cardiogenic shock (hypotension; cold, clammy extremities), hypoglycemia, hyperkalemia, wheezing (bronchoconstriction), neurological symptoms (seizure, delirium, coma)

33
Q

Treatment of beta blocker overdose

A

Secure airway
Correct hypotension: IV fluids and vasopressors (epinephrine)
Correct bradycardia: IV atropine
Treat cardiogenic shock: IV glucagon ; IV calcium salts (improves cardiac contractility)
Correct hypoglycemia: IV high-dose insulin with glucose
Prevent further absorption of β blocker: activated charcoal/gastric lavage ; IV lipid emulsions (esp. useful in lipophilic β blocker overdose)

34
Q

Absolute contraindications for beta blockers

A

Symptomatic bradycardia
Sick sinus syndrome (without a pacemaker); heart block greater than first-degree
Cardiogenic shock and hypotension
Pheochromocytoma
Decompensated heart failure
Asthma
Combination with calcium channel blockers (diltiazem or verapamil): can precipitate AV block

35
Q

Relative contraindications of beta blockers

A

Psoriasis
Raynaud’s phenomenon, peripheral artery occlusive disease
Pregnancy (atenolol is absolutely contraindicated in pregnancy)

36
Q

Classes of CCB

A

Dihydropyridines

Non-dihydropyridines: benzothiazepines, phenylalkylamines

37
Q

Dihydropyridine examples

A

Short-acting : nifedipine, clevidipine
Medium-acting : nitrendipine, nicardipine, lercanidipine
Long-acting : amlodipine

38
Q

Effects of dyhydrpyridines

A

Potent vasodilator

Minimal myocardial depressant activity

39
Q

Example of benzothiazepines

A

Diltiazem

40
Q

Effect of diltiazem

A

Moderate vasodilator

Moderate myocardial depressant activity

41
Q

Examples of phenylalkylamines

A

Verapamil

Gallopamil

42
Q

Effects of phenylalkylamines

A

Less potent vasodilator than dihydropyridines

Potent myocardial depressant

43
Q

Effects of calcium channel blockers

A

CCBs bind to and block L-type calcium channels → failure of calcium channels to open in response to depolarization of the cell membrane → decreased transmembrane calcium current
→ Vascular smooth muscle relaxation → vasodilation → ↓ peripheral vascular resistance →↓ blood pressure
→ ↓ Cardiac muscle contractility (negative inotropic action) → ↓ cardiac output → ↓ blood pressure
→ ↓ SAN rate (negative chronotropic action) → ↓ heart rate (bradycardia) → ↓ cardiac output → ↓ blood pressure
→ ↓ AVN conduction (negative dromotropic action) → termination of supraventricular arrhythmias

44
Q

Side effects of dihydropyridines

A 
Effects due to vasodilation
Peripheral edema (esp. amlodipine) 
Headaches, dizziness
Facial flushing, feeling feverish
Reflex tachycardia (esp. nifedipine) 
May worsen symptoms of angina 
Gingival hyperplasia
45
Q

Side effects of benzothiazepines

A

Side effects similar to the other classes of CCBs, but milder

Except for reflex tachycardia, which is a side effect seen only with short-acting and intermediate-acting dihydropyridines

46
Q

Side effects of phenylalkylamines

A

Reduced contractility/bradyarrhythmia and drug-induced atrioventricular block
Constipation

Phenylalkylamines (verapamil) primarily affect the calcium channels of the heart and are contraindicated in cases of heart failure because of their negative effect on myocardial contractility!

47
Q

Contraindications to all CCB classes

A

Allergy/hypersensitivity to CCBs
Symptomatic hypotension
Acute coronary syndrome

48
Q

Contraindications to dihydropyridines

A

Hypertrophic obstructive cardiomyopathy (HOCM)

Severe stenotic heart valve defects

49
Q

Contraindications to benzothiazepines and phenylalkylamines

A

Pre-existing cardiac conduction disorders
Wolff-Parkinson-White syndrome
Sick sinus syndrome
Systolic dysfunction (in congestive heart failure)
Bradycardia
Second or third-degree atrioventricular block

Combination with beta blockers → risk of AV block

50
Q

Mechanism of action of cardiac glycosides

A

Inhibition of Na+/K+-ATPases → higher intracellular Na+ concentration → reduced efficacy of Na+/Ca2+ exchangers → higher intracellular Ca2+ concentration

Cardiac glycosides inhibit Na+/K+-ATPase, increasing cardiac contractility and decreasing AV conduction and heart rate!

51
Q

Contraindications to cardiac glycosides

A

Ventricular fibrillation
Use with caution in pregnant women and in patients with:
Electrolyte and fluid disorders (e.g., volume depletion, hypokalemia, hypomagnesemia, and/or hypercalcemia )
Cardiovascular disorders (e.g., acute coronary syndrome, AV blocks, Wolff-Parkinson-White syndrome, hypertrophic obstructive cardiomyopathy, sick sinus syndrome)
Renal failure (can lead to digoxin overdose and, vice versa, digoxin can also cause/worsen renal failure)
Certain medications → See “Interactions” below.

52
Q

Cardiac glycosides interactions

A

K+-depleting diuretics → hypokalemia → arrhythmias

Verapamil, diltiazem, amiodarone, quinidine → possible overdose → reduce digoxin dose

53
Q

Clinical features of glycoside overdose

A

Nausea/vomiting, diarrhea, gastrointestinal pain, and anorexia
Blurry vision with a yellow tint and halos, disorientation, weakness

54
Q

Diagnosis of cardiac glycosides toxicity

A

ECG: potentially severe cardiac arrhythmias
Premature ventricular beats
T-wave inversion or flattening
Downsloping ST segment depression (“scooped” ST segments)
↓ QT interval
↑ PR interval
Atrial tachycardia with AV block
Laboratory studies
Serum digoxin concentration (ideally, measure 6 hours after ingestion)
Serum electrolyte levels: hyperkalemia
Creatinine and blood urea nitrogen to evaluate renal function

55
Q

Treatment of digoxin toxicity

A 
Antibodies - Fab fragments of IgG binds to digoxin
Slowly normalize serum K+ levels
Mg2+
Class IB antiarrhythmics
Temporary cardiac pacing

IPE Pharmacology (3 decks)

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