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Cardio Week 1 > Beta blockers > Flashcards

Beta blockers Flashcards

1
Q

Where are beta receptors common?

A
  • heart

- skeletal muscle vasculature

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2
Q

What does stimulation of beta receptors in skeletal muscle vasculature cause?

A

an inhibitory action, preventing the entry of calcium that is critical to the contraction of vascular smooth muscle

Activation of beta-2 receptors in skeletal muscle leads to relaxation and
increased perfusion of this muscle group, which is of critical importance in the fight-flight-fright response which characterizes the activity of the sympathetic nervous
system.

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3
Q

What does stimulation of beta-1 receptors in the heart cause?

A

leads to an acceleration in heart rate and an increase in the force of cardiac
contraction.

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4
Q

What does stimulation of beta-1 receptors on juxtaglomerular cells cause?

A

leads to the release of renin, which converts angiotensinogen to angiotensin I and
angiotensin II, a potent vasoconstrictor agent

In this manner, beta-blockers can
diminish hypertension due to excessive renin release.

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5
Q

What effect can NSAIDs have on renin release?

A

Chronic use of
nonsteroidal anti-inflammatory drugs will diminish the production of prostaglandins
and can have an adverse effect upon renal perfusion, especially in the elderly, by
preventing the vasoconstrictor actions instigated through renin release via beta-1-agonism.

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6
Q

What is intrinsic

sympathomimetic activity?

A

This means that the drugs are actually weak partial
agonists that will provide some cardio stimulation but prevent excessive stimulation via the endogenous neurotransmitters epinephrine and norepinephrine

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7
Q

What are third-generation b-blockers?

A

These drugs have effects upon alpha receptors or activate other signaling systems to prevent reflexive vasoconstriction from reducing the
clinical effectiveness of beta blockade.

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8
Q

How does reflexive vasoconstriction occur?

A

Recall, baroreceptors will sense the decline in blood pressure produced by beta blockade and will activate alpha-1 mediated
vasoconstriction.

A drug with an extended action will prevent this occurrence

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9
Q

T or F. Highly lipid soluble b-blockers tend to produce more adverse CNS effects such as bad dreams

A

T, although these events are also

reported, on occasion, with the less lipid soluble agents.

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10
Q

What are the classic non-selective 1st gen b-blockers?

A
  • Nadolol
  • Pindolol
  • Proprandolol
  • Timolol
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11
Q

Some b-blockers have membrane-depressant (quinidine-like) effects. What does this result in?

A

Further depression of myocardial contractility and conduction, over and above activity in
the SA and AV nodes, and may be associated with ventricular tachyarrhythmias

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12
Q

Which 1st gen b-blockers have membrane stabilizing activity?

A

propranolol (high lipid soluble) and pindolol weakly

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13
Q

What are the 2nd gen B-1 selective blockers?

A
  • acebutolol
  • atenolol
  • esmolol
  • metoprolol
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14
Q

What are the 3nd gen non-selective beta blockers with additional actions?

A

carvedilol

labetalol

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15
Q

What are the 3nd gen B1-selective beta blockers with additional actions?

A
  • betaxolol

- nebivolol

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16
Q

Naming convention for b-blockers

A

Drugs from A to M are beta-1 selective; those from N to T are non-selective, except
nebivolol.

Those with an unusual spelling “ILOL” or “ALOL” have extended actions in
preventing alpha-mediated reflex vasoconstriction.

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17
Q

Which b-blockers have membrane stabilizing activity?

A
  • propranolol
  • acebutolol
  • carvedilol

others with higher doses-pindolol, betaxolol, metoprolol, labetalol

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18
Q

Beta-blocking drugs with membrane stabilizing activity are used as what?

A 
Antiarrhythmic
agents (class II)
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19
Q

How do the selective b-blockers stabilize membranes?

A

bind to and block fast sodium channels that are essential to the
initial depolarizing event in the cardiac cycle decreasing the action potential.

This is separate from their other effects
mediated via beta-1 adrenergic receptors

20
Q

Which drugs have intrinsic sympathomimetic activity?

A

pindolol and acebutolol have this ability which allows them to slightly reverse the bradycardia and negative inotropy caused by b-bockade by partially mimicking catecholamine function (bad for prevention of secondary MI)

21
Q

Some b-blockers have extended actions to further prevent reflexive vasoconstriction. Name them and what they do.

A

Nebivolol-NO production, antioxidant activity

Carvedilol- a-1 antagonist, Ca2+ entry blockade, antioxidant activity

Labetaolol- a-1 antagonist

Betaxolol- Ca2+ entry blockade

22
Q

What are some indications for b-blockers?

A
  • HTN
  • IHD
  • supraventricular and ventricular arrhythmias
  • CHF
23
Q

T or F. B-blockers are most effective in

patients with high plasma renin activity

A

T, Beta-blockers inhibit the stimulation of renin production by catecholamines
(mediated by β1 receptors). It is likely, therefore, that drug effect is due, in part, to
depression of the renin-angiotensin-aldosterone system

24
Q

Do b-blockers help HTN in those with low renin activity?

A

Yes, Undoubtedly some of the clinical effect might arise from the inhibition of presynaptic β-adrenoceptors
(stimulation of these receptors by epinephrine helps to augment release of NE from the pre-synaptic terminal), this would reduce sympathetic vasoconstrictor nerve
activity.

25
Q

How do b-blockers prevent IHD?

A

They reduce cardiac work, reduce O2 demands, and slow and regularize HR

26
Q

How do b-blockers prevent supraventricular and ventricular arrhythmias?

A

by increasing AV nodal refractory period, B-blockers slow ventricular response rates in atrial flutter and fibrillation

27
Q

Which b-blockers are indicated for CHF prevention?

A

-Metoprolol, bisoprolol, and carvedilol

28
Q

T or F. Note that abrupt discontinuation of beta-blocker treatment is ill advised

A

T, doses should be tapered over time. Upregulation in beta-receptor expression can lead to rebound and life-threatening cardiotoxic effects.

29
Q

What are the symptoms of overdose of b-blockers?

A

Bradycardia and bradyarrhythmia are typical symptoms

30
Q

What happens in b-blocker overdose?

A

beta receptors lose specificity

31
Q

What happens in overdose of b-blockers with membrane stabilizing activity?

A

further depression of myocardial contractility and conduction and may cause ventricular tachyarrhythmias

32
Q

What is a side effect of Propranolol (lipid-soluble) overdose?

A

seizures and coma

33
Q

What happens in overdose of b-blockers with ISA?

A

tachycardia and HTN

34
Q

What is Sotalol?

A

an antiarrhythmic agent that also has type III activity and when overdosed can prolong QT interval and may cause tornado de points and ventricular fibrillation

35
Q

What is a common result of OD on third gen b-blockers with additional activity?

A

direct vasodilation contributes to hypotension

36
Q

What is the typical treatment for OD of a b-blocker?

A

glucagon or high-dose insulin/glucose

37
Q

Why could a beta blocker induce bronchospasm?

A

beta-2 adrenergic receptors have an important role in the
treatment of bronchospasm of asthma or COPD. Given that, non-specific beta
blockers and indeed beta-1 specific blockers (to a lesser extent) have the capacity to induce bronchospasm in such patients by removing endogenous bronchodilatory
signaling.

38
Q

Non-specific beta-blockers are CONTRAINDICATED in asthmatics and their use is cautioned against in patients with COPD

A

Likewise, beta1-adrenergic selective
beta-blockers, such as atenolol, should be used with caution in these patients,
particularly with high-dose therapy. Remember, receptor specificity is dose-related.

39
Q

What kinds of b-blockers are less likely to induce bronchospasm?

A

-B1 selective drugs or those with ISA

40
Q

Other side effects of B-blockers?

A

-CNS depression, resulting in mental disorders, fatigue, vivid dreams (less common with hydrophilic beta-blockers)

41
Q

Other side effects of B-blockers?

A
  • hypoglycemia

- diabetic masking

42
Q

How can b-blockers cause hypoglycemia?

A

B-2 receptors normally stimulate hepatic glycogen breakdown and precreatic glycogen release

43
Q

How can b-blockers cause diabetic masking?

A

B-1 blockers mask the tachycardia which serves as a warning sign for insulin-induced hypoglycemia

use cautiously here

44
Q

How do beta-blockers affect lipids?

A

Beta-blockers have been shown to increase TAG levels and decrease
plasma HDL, but they have little effect on total cholesterol and
LDL.

45
Q

Since b-blockers increase TAG levels, what patients are they contraindicated in?

A

CHD patients

The question at hand is to what degree the benefits of treatment
of hypertensive patients-with respect to CHD–are reduced by these lipid changes.

46
Q

T or F. Cardioselective agents or those with ISA tend to have less of an effect on plasma
lipids

A

T. Those with both characteristics tend to reduce total cholesterol and LDL

47
Q

What are some non-CV uses of b-blockers?

A
  • essential tremor
  • thyrotoxicosis
  • anxiety
  • prophylaxis of migraine
  • treatment of glaucoma
  • secondary prophylaxis of bleeding associated with esophageal varicies (non-specific b-blockers preferred)

Cardio Week 1 (22 decks)

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