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Clinical Therapeutics > Alpha, Beta and Calcium Channel Blockers > Flashcards

Alpha, Beta and Calcium Channel Blockers Flashcards

1
Q

Arterial blood pressure directly proportional to the product of what?

A

Cardiac output (CO) and Peripheral vascular resistance (PVR)

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2
Q

What regulates blood pressure?

A

Sympathetic nervous system, the kidneys and vasoactive motors on the endothelium

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3
Q

What is cardiac output and how is it increased?

A

Stroke volume x Heart rate, increased by sympathetic Beta 1 receptor stimulation in the heart

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4
Q

What is peripheral vascular resistance (PVR)?

A

Resistance to blood flow through the arteries

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5
Q

How does the sympathetic nervous system regulate blood pressure?

A
  • Short term control though baroreceptor reflex
  • Modules sympathetic stimulation of CO and PVR
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6
Q

How do the kidneys regulate blood pressure?

A
  • Long Term Control through Modulation of the renin-angiotensin-aldosterone system
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7
Q

What classes of drugs are diuretics?

A
  • Thiazides
  • Loop diuretics
  • Potassium-sparing diuretics
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8
Q

What classes of drugs are sympathoplegic agents?

A
  • Non-specific adrenoreceptor antagonists
  • alpha blockers
  • beta blockers
  • CNS acting agents
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9
Q

What classes of drugs are direct vasodilators?

A
  • CCBs
  • Organic nitrates
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10
Q

What classes of drugs act on the renin-angiotensin-aldosterone system?

A
  • ACE inhibitors
  • ARBs
  • Direct renin inhibitors
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11
Q

What compensatory mechanisms can antihypertensives be susceptible to?

A
  • Reflex tachycardia
  • Fluid retention by kidneys
  • Activation of the renin-angiotensin-aldosterone system
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12
Q

What are examples of centrally acting sympathoplegic agents?

A

Clonidine and Methyldopa

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13
Q

What is the mechanism of action and clinical effects of sympathoplegic agents?

A

Increases baroreceptor influence on vasomotors
Leads to reduced SNS activation and increased parasympathetic nervous system activation

Reduces PVR, blood pressure and tachycardia

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14
Q

What are the adverse drug reactions of centrally acting sympathoplegic agents?

A
  • Severe rebound hypertension if discontinued abruptly
  • nightmares, sedation, diminished mental acuity
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15
Q

What are examples of alpha blockers?

A

Doxazosin, prazosin, terazosin (all alpha-1 selective)

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16
Q

Why are non selective and alpha-2 selective antagonists not clinically useful?

A

Lead to a continued release of norepinephrine which causes beta-1 stimulation in heart = tachycardia

17
Q

What is the mechanism of action and clinical effects of alpha blockers?

A

Prevents SNS stimulation of arteriolar smooth muscle contraction.

Vasodilation, decreased PVR

18
Q

What are is the general mechanism of action and side effects of beta blockers?

A

Lowers blood pressure by blocking Beta-1 receptors in heart.

Fatigue, depression, vivid dreams, reduced exercise capacity.

19
Q

Name a non-selective beta blocker and give their mechanism of action

A

Propranolol

Blocks beta-1 and 2 receptors, causing a reduction in HR and contractility, reducing cardiac output and arterial pressure.

20
Q

What are the adverse drug reactions of non selective beta blockers?

A
  • Cardiac bronchospasm risk to asthmatics and COPD patients
  • can reduce hypoglycaemia response in diabetics
  • Nightmares, fatigue, cold extremities
21
Q

What is the mechanism of action of beta-1 blockers?

A

Block beta-1 receptors selectively, reduces HR and contractility = reduces cardiac output and arterial pressure, and inhibits renin secretion

22
Q

What are lipid soluble variants of beta-1 blockers (Metoprolol, nebivolol and bisoprolol) more likely to cause?

A

CNS effects (nightmares, etc) due to BBB passage

23
Q

What are the clinical effects of alpha/beta receptor blockers? (Labetalol, carvedilol)

A

Block alpha-1 and beta-1 receptors, reduce renin release, decrease CO and BP, lowers PVR

24
Q

What are the adverse effects of non-selective alpha/beta receptor blockers? (Labetalol)

A

Orthostatic hypertension, Sleep disturbances, fatigue, reduced exercise capacity.

25
Q

How does calcium affect cardiac muscle contraction?

A
  1. Ca2+ enters cell and binds to troponin C
  2. transforms myosin from a low-actin-binding state to a strongly actin-bound state
  3. Force of contraction depends on influx of Ca2+ into cell during an action potential
26
Q

How does calcium channel blockers affect cardiac action potential?

A
  1. CCBs block L-type calcium channels (Phase 2 of action potential) and so slow Ca2+ influx into cell
  2. Shortens AP depolarisation -> reduces amount of intracellular calcium available for contraction
  3. Decreases force generated during contraction -> reduced HR
27
Q

How does the effects of CCBs on cardiac tissue differ between Dihydropyridines (Amlodipine, Felodipine, Nicardipine and Nifedipine) and Non-dihydropyridines?

A

Dihydropyridines - MORE effect on vasodilation, LESS effect on heart function
Non-Dihydropyridines - LESS effect on vasodilation, MORE effect on heart function

28
Q

Why is caution needed in giving Non-Dihydropyridines (Such as Diltiazem and Verapamil) to patients with heart failure?

A

They both significantly reduce cardiac output

Clinical Therapeutics (27 decks)

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