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CVS Drugs Flashcards

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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

Study These Flashcards
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

Study These Flashcards
A

Adipose tissue

25
What happens when b3 receptors are blocked?
↓ Lipolysis with weight gain
26
Cardiac side effects of b1 and b2 receptor blockage
Bradycardia Bradyarrhythmia Ventricular tachyarrhythmia (torsades de pointes) Orthostatic hypotension (esp. in the elderly) Worsened heart failure (HF)
27
CNS effects of b1 and b2 blockage
Drowsiness, sleep disorders, nightmares Fatigue/lethargy Depression, hallucinations
28
Pulmonary effects of b2 blockage
Bronchoconstriction (esp. patients with asthma and reactive airway disease)
29
Effect of b2 blockage on peripheral Vasculature
Peripheral vasoconstriction Erectile dysfunction Secondary Raynaud's phenomenon Cold extremities
30
Metabolic effects of b2 blockage
Hyperglycemia and new-onset diabetes Hypoglycemia Weight gain
31
What is beta blocker withdrawal
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
Features of beta blocker overdose
bradycardia/bradyarrhythmia, cardiogenic shock (hypotension; cold, clammy extremities), hypoglycemia, hyperkalemia, wheezing (bronchoconstriction), neurological symptoms (seizure, delirium, coma)
33
Treatment of beta blocker overdose
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
Absolute contraindications for beta blockers
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
Relative contraindications of beta blockers
Psoriasis Raynaud's phenomenon, peripheral artery occlusive disease Pregnancy (atenolol is absolutely contraindicated in pregnancy)
36
Classes of CCB
Dihydropyridines | Non-dihydropyridines: benzothiazepines, phenylalkylamines
37
Dihydropyridine examples
Short-acting : nifedipine, clevidipine Medium-acting : nitrendipine, nicardipine, lercanidipine Long-acting : amlodipine
38
Effects of dyhydrpyridines
Potent vasodilator | Minimal myocardial depressant activity
39
Example of benzothiazepines
Diltiazem
40
Effect of diltiazem
Moderate vasodilator | Moderate myocardial depressant activity
41
Examples of phenylalkylamines
Verapamil | Gallopamil
42
Effects of phenylalkylamines
Less potent vasodilator than dihydropyridines | Potent myocardial depressant
43
Effects of calcium channel blockers
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
Side effects of dihydropyridines
``` 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
Side effects of benzothiazepines
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
Side effects of phenylalkylamines
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
Contraindications to all CCB classes
Allergy/hypersensitivity to CCBs Symptomatic hypotension Acute coronary syndrome
48
Contraindications to dihydropyridines
Hypertrophic obstructive cardiomyopathy (HOCM) | Severe stenotic heart valve defects
49
Contraindications to benzothiazepines and phenylalkylamines
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
Mechanism of action of cardiac glycosides
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
Contraindications to cardiac glycosides
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
Cardiac glycosides interactions
K+-depleting diuretics → hypokalemia → arrhythmias Verapamil, diltiazem, amiodarone, quinidine → possible overdose → reduce digoxin dose
53
Clinical features of glycoside overdose
Nausea/vomiting, diarrhea, gastrointestinal pain, and anorexia Blurry vision with a yellow tint and halos, disorientation, weakness
54
Diagnosis of cardiac glycosides toxicity
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
Treatment of digoxin toxicity
``` 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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