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Cardiovascular Pharmacology > Cardiovascular Pharmacology Summary Part 1 > Flashcards

Cardiovascular Pharmacology Summary Part 1 Flashcards

1
Q

Which beta-blocker is non-selective?

A

Propranolol

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2
Q

What are the pharmacokinetics of propranolol?

A

Short half life, needs to be taken 3-4 times per day

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3
Q

What is the mechanism of action of propranolol (cellular)?

A
  1. Blocks the effect of NA & adrenaline on beta-1 receptors n heart and beta-2 receptors in lungs, skeletal blood vessels and liver.
  2. Acts on JG cells of kidney to reduce renin release
  3. Also blocks beta cells in the brain
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4
Q

What is the mechanism of action of propranolol (physiological)?

A
  1. Slows conduction through the AV node
  2. Reduced rate of depolarization in SA node leading to bradycardia
  3. Decreases contractility of the heart
  4. Decreases O2 demand by reducing heart rate.
  5. Lowers exercise maximal heart rate
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5
Q

What are the therapeutic uses of propranolol?

A

Used in many aspects of CVD but superseded by drugs with greater beta-selectivity and longer half lives.

  • effective in the treatment of enhanced SNS activity
  • used in somatic anxiety
  • used in stable coronary artery disease angina pectoris (decreases myocardial O2 consumption)
  • supraventricular tachycardia: AV node conduction blocker used in atrial fibrillation / flutter to reduce ventricular rate
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6
Q

What are the adverse effects and contraindications of propranolol?

A
  • Type I DM: blocks SNS response to hypoglycemia
  • Heart block
  • Heart failure
  • Worsens COPD, asthma and PVD by blocking beta-2 receptors
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7
Q

What are the two cardio-selective beta blockers?

A

Atenolol

Bisoprolol

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8
Q

What are the pharmacokinetics of the cardio-selective beta blockers?

A

Long half life, needs to be taken 1-2 times / day

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9
Q

What is the mechanism of action of Atenolol and Bisoprolol (cellular)?

A
  1. Blocks the effect of NA & adrenaline on beta-1 receptors in the heart and JG.
  2. Little blocking potential on beta-2 in the lungs, skeletal blood vessels and liver. At high doses loses selectiveness for beta-1 and blocks beta-2 receptor.
  3. Acts on JG cells of kidney to reduce renin release.
  4. Blocks beta cells in brain
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10
Q

What is the mechanism of action of Atenolol and Bisoprolol (physiological)?

A
  1. Slows conduction through the AV node
  2. Reduces the rate of depolarization through the SA node leading to bradycardia and partial AV block
  3. Decreases contractility
  4. Decreases O2 demand by reducing heart rate
  5. Reduced maximal heart rate in exercise
  6. Action in hypertension not clearly understood but could be a result of drop in cardiac output
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11
Q

What are the therapeutic uses of Atenolol and Bispoprolol?

A

Previously extensively used in hypertension but efficacy is under scrutiny. Not used as an add-on agent.

  1. Reduces BP in combination with Thiazide diuretics
  2. Effective in the treatment of enhanced SNS activity
  3. Used in somatic anxiety and migraine
  4. Supraventricular tachycardia: AV node conduction blocker used in atrial fibrillation / flutter to reduce ventricular rate. Used in many types of supraventricular arrhythmia.
  5. Reduces HR and SV
  6. Used in stable coronary artery disease angina pectoris (decreases myocardial O2 consumption)
  7. Used post MI to protect against negative remodeling
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12
Q

What is a specific therapeutic use of Bisoprolol?

A

Used in heart failure (same as Carvedilol)

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13
Q

What are the adverse effects and contraindications of Atenolol and Bisoprolol?

A
  • Type I DM: blocks SNS response to hypoglycemia
  • Heart block
  • Heart failure
  • Worsens COPD, asthma and PVD by blocking beta-2 receptors
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14
Q

Which drugs are beta-1, beta-2 and alpha-1 blockers?

A

Cavedilol and Labetalol

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15
Q

What are the pharmacokinetics of Carvedilol?

A

Longer half life, needs to be taken 2 times a day

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16
Q

What is the mechanism of action of Carvedilol (cellular)?

A
  1. Blocks the effect of NA & adrenaline on beta-1 in the heart and JG cells.
  2. Blocks beta-2 in the lungs, skeletal blood vessels and liver
  3. Blocks alpha-1 adrenoceptors on vascular smooth muscle in arterioles
  4. Acts on JG cells of the kidney to reduce renin release
  5. Also blocks beta cells in the brain
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17
Q

What is the mechanism of action of Carvedilol (physiological)?

A
  1. Slows rate of depolarization through AV node and reduces rate of depolarization in SA node (= bradycardia and partial AV block) BUT not used for arrhythmia control because of alpha-1 effects and unique dosing of very low, go slow.
  2. Decreases contractility and O2 demand
  3. Reducing heart rate improves diastolic filling time and increases time for coronary blood flow.
  4. Reduces maximal heart rate in exercise
  5. Especially useful in HEART FAILURE because of peripheral vasodilation and reducing afterload
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18
Q

What are the therapeutic uses of Carvedilol?

A
  1. Effective in the treatment of enhanced SNS activity
  2. NOT used for supraventricular tachycardia
  3. Reduces HR and SV
  4. Used in stable coronary artery disease angina pectoris (decreases myocardial O2 consumption)
  5. Used post MI to protect against negative remodeling caused by catecholamines
  6. Main use is in HEART FAILURE: slows heart rate, improves diastolic filling, reduces arrhythmic potential, prevents remodeling and also reduces ischemic damage.
    - Vasodilation by blocking alpha-1 adrenoceptors reduces afterload in heart failure and may improve blood flow to many organs
  7. Can be used for treating hypertension
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19
Q

What are the adverse effects and contraindications of Carvedilol?

A
  • Type I DM: blocks SNS response to hypoglycemia
  • Heart block
  • Heart failure
  • Worsens COPD, asthma and PVD by blocking beta-2 receptors
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20
Q

What are the pharmacokinetics of Labetalol?

A

Used as a sublingual and IV formulation

21
Q

What is the mechanism of action of Labetalol (cellular)?

A
  1. Blocks the effect of NA & adrenaline on beta-1 in the heart and JG cells.
  2. Blocks beta-2 in the lungs, skeletal blood vessels and liver
  3. Blocks alpha-1 adrenoceptors on vascular smooth muscle in arterioles
  4. Acts on JG cells of the kidney to reduce renin release
22
Q

What is the mechanism of action of Labetalol (physiological)?

A
  1. Slows rate of depolarization through AV node and reduces rate of depolarization in SA node (= bradycardia and partial AV block) BUT not used for arrhythmia control because of alpha-1 effect.
  2. Decreases contractility and O2 demand
  3. Reducing heart rate improves diastolic filling time and increases time for coronary blood flow.
  4. Reduces maximal heart rate in exercise
  5. Especially useful in HEART FAILURE because of peripheral vasodilation and reducing afterload
23
Q

What are the therapeutic uses of Labetalol?

A
  1. NOT used for supraventricular tachycardia.
  2. Reduces HR and SV
  3. Used in hypertensive emergencies to reduce diastolic and systolic blood pressure. Main use = HYPERTENSIVE EMERGENCY with history of DISSECTING AORTIC ANEURYSM.
  4. Decreases myocardial O2 consumption to protect against negative remodeling caused by catecholamines.
  5. Improves diastolic filling, reduces arrhythmic potential and prevents ischemic and catecholamine damage.
  6. Vasodilation by blocking alpha-1 adrenoceptors, reduces afterload, improves blood flow to many organs.
  7. Can also be used for treating hypertension.
24
Q

What are the adverse effects and contraindications of Labetalol?

A
  • Type I DM: blocks SNS response to hypoglycemia
  • Heart block
  • Heart failure
  • Worsens COPD, asthma and PVD by blocking beta-2 receptors
25
Q

Which two calcium channel blockers are both cardiac and vascular?

A

Verapamil, Diltiazem

26
Q

What are the pharmacokinetics of Verapamil & Diltiazem?

A

Short acting but used as a slow release formulation, metabolized in the liver.

27
Q

What is the mechanism of action of Verapamil and Diltiazem (cellular)?

A

Blocks the entry of calcium into the vascular smooth muscle cells, arterioles, and the myocardium - both the contractile tissue and the conducting activity.

28
Q

What is the mechanism of action of Verapamil and Diltiazem (physiological)?

A
  1. Blocks conduction through the AV node.
  2. Blocks conduction in SA node.
  3. Decreases contractility.
  4. Decreases O2 demand by the heart.
  5. Decreases TPR.
29
Q

What are the therapeutic uses of Verapamil and Diltiazem?

A
  1. Hypertension (primarily on decreasing vascular resistance)
  2. Angina pectoris (decreases O2 consumption by direct effect on heart and reducing TPR)
  3. Supraventricular arrhythmia: slows AV conduction through acting on calcium channels
30
Q

What are the adverse effects and contraindications of Verapamil and Diltiazem?

A
  1. SA or AV nodal problems
  2. AV nodal block and bradycardia
  3. Headache
  4. Ankle oedema (not true oedema, due to vasodilation)
31
Q

What are the two vascular selective dihydropyridines (calcium channel blockers)?

A
  1. Nifedipine

2. Amlodipine

32
Q

What is the difference in pharmacokinetics between Nifedipine and Amlodopine?

A
  1. Nifedipine = short acting, used only as slow release formulation
  2. Amlodipine = long acting, only needs to be used once daily
33
Q

What is the mechanism of action of Nifedipine and Amlodipine (cellular)?

A

Blocks the entry of calcium into the vascular smooth muscle cells and decreases TPR. Causes VSM relaxation.

34
Q

What is the mechanism of action of Nifedipine and Amlodipine (physiological)?

A

Potent peripheral vasodilator. Can cause an increased heart rate.

35
Q

What are the therapeutic uses of Nifedipine and Amlodipine?

A
  1. Hypertension (primarily on vascular resistance)

2. Angina pectoris (decreases O2 consumption by decreasing afterload

36
Q

What are the adverse effects and contraindications of Nifedipine and Amlodipine?

A
  1. Headache
  2. Ankle oedema (not true oedema but due to vasodilation, cannot be mobilized)
  3. Some reflex tachycardia but generally cardiac effects on heart rate and contractility are minimal.
37
Q

Which drug is a short acting organic nitrate?

A

Glycerol Trinitrate

38
Q

What are the pharmacokinetics of Glycerol Trinitrate?

A

Short acting.

Cannot be taken orally, bioavailability <5% (high first pass metabolism). Taken SL. IV form also available for MI.

39
Q

What is the mechanism of action of Glycerol Trinitrate (cellular)?

A

Increases cGMP levels by nitric oxide effect. Mainly acts to increase venous capacitance. More blood is stored, less blood returns to heart, EDP and EDD drops, wall stress decreases and oxygen consumption goes down.

40
Q

What is the mechanism of action of Glycerol Trinitrate (physiological)?

A

Decreases in wall stress decrease O2 demand and angina is relieved. Also shunts blood to ischemic areas of the heart. Causes vasodilation and venodilation, but more effect in veins. Drops in TPR, increases in HR.

41
Q

What are the therapeutic uses of Glycerol Trinitrate?

A
  1. Angina pectoris (decrease O2 consumption by decreasing preload and after load.
    - used to abort exercise induced angina with short acting SL tablets.
42
Q

What are the adverse effects and contraindications of Glycerol Trinitrate?

A
  1. Headache
  2. Tolerance to effect
  3. Hypotension
  4. Tachycardia
    DI: Do NOT use with Sildenafil - drug interaction causes drop in venous return and BP that can be fatal.
43
Q

Which drug is a long acting organic nitrate?

A

Isosorbide Mononitrate

44
Q

What are the pharmacokinetics of Isosorbide Mononitrate?

A

Long acting, taken orally
Bioavailability = 100%
No first pass metabolism

45
Q

What is the mechanism of action of Isosorbide Mononitrate (cellular)?

A

Nitric oxide donor, increases cGMP through guanylate cyclase.
- Mainly acts to increase venous capacitance. More blood is stored, less blood returns to the heart, EDP drops, wall stress decreases.

46
Q

What is the mechanism of action of Isosorbide Mononitrate (physiological)?

A

Decreases in wall stress decrease in O2 demand and angina is relieved. Also shunts blood to ischemic areas of the heart.
Causes vasodilation and venodilation. Drop in TPR. Increases HR.
Nocturnal nitrate free period recommended.

47
Q

What are the therapeutic uses of Isosorbide Mononitrate?

A
  1. Angina pectoris (decreases O2 consumption) by decreasing preload and afterload (less effect). Used as a long term prophylactic.
  2. Used in combination with hydralazine in heart failure in patients with CI to ACE/ARBs
48
Q

What are the adverse effects and contraindications of Isosorbide Mononitrate?

A
  1. Headache
  2. Tolerance to effect
  3. Hypotension
  4. Tachycardia
    DI: Do NOT use with Sildenafil - drug interaction causes drop in venous return and BP that can be fatal.

Cardiovascular Pharmacology (5 decks)

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