Beta Blockers

Question 1

Where are beta receptors common?

Answer 1

-heart -skeletal muscle vasculature

Question 2

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

Answer 2

an inhibitory action, preventing the entry of calcium that is critical to the contraction of vascular smooth muscleActivation of beta-2 receptors in skeletal muscle leads to relaxation andincreased perfusion of this muscle group, which is of critical importance in the fight-flight-fright response which characterizes the activity of the sympathetic nervoussystem.

Question 3

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

Answer 3

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

Question 4

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

Answer 4

leads to the release of renin, which converts angiotensinogen to angiotensin I andangiotensin II, a potent vasoconstrictor agentIn this manner, beta-blockers candiminish hypertension due to excessive renin release.

Question 5

What effect can NSAIDs have on renin release?

Answer 5

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

Question 6

What is intrinsicsympathomimetic activity?

Answer 6

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

Question 7

What are third-generation b-blockers?

Answer 7

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

Question 8

How does reflexive vasoconstriction occur?

Answer 8

Recall, baroreceptors will sense the decline in blood pressure produced by beta blockade and will activate alpha-1 mediatedvasoconstriction.A drug with an extended action will prevent this occurrence

Question 9

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

Answer 9

T, although these events are alsoreported, on occasion, with the less lipid soluble agents.

Question 10

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

Answer 10

-Nadolol-Pindolol-Proprandolol-Timolol

Question 11

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

Answer 11

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

Question 12

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

Answer 12

propranolol (high lipid soluble) and pindolol weakly

Question 13

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

Answer 13

-acebutolol-atenolol-esmolol-metoprolol

Question 14

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

Answer 14

carvedilollabetalol

Question 15

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

Answer 15

-betaxolol-nebivolol

Question 16

Naming convention for b-blockers

Answer 16

Drugs from A to M are beta-1 selective; those from N to T are non-selective, exceptnebivolol. Those with an unusual spelling “ILOL” or “ALOL” have extended actions inpreventing alpha-mediated reflex vasoconstriction.

Question 17

Which b-blockers have membrane stabilizing activity?

Answer 17

-propranolol-acebutolol-carvedilolothers with higher doses-pindolol, betaxolol, metoprolol, labetalol

Question 18

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

Answer 18

Antiarrhythmicagents (class II)

Question 19

How do the selective b-blockers stabilize membranes?

Answer 19

bind to and block fast sodium channels that are essential to theinitial depolarizing event in the cardiac cycle decreasing the action potential. This is separate from their other effectsmediated via beta-1 adrenergic receptors

Question 20

Which drugs have intrinsic sympathomimetic activity?

Answer 20

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)

Question 21

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

Answer 21

Nebivolol-NO production, antioxidant activity Carvedilol- a-1 antagonist, Ca2+ entry blockade, antioxidant activity Labetaolol- a-1 antagonistBetaxolol- Ca2+ entry blockade

Question 22

What are some indications for b-blockers?

Answer 22

-HTN-IHD-supraventricular and ventricular arrhythmias-CHF

Question 23

T or F. B-blockers are most effective inpatients with high plasma renin activity

Answer 23

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, todepression of the renin-angiotensin-aldosterone system

Question 24

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

Answer 24

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 nerveactivity.

Question 25

How do b-blockers prevent IHD?

Answer 25

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

Question 26

How do b-blockers prevent supraventricular and ventricular arrhythmias?

Answer 26

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

Question 27

Which b-blockers are indicated for CHF prevention?

Answer 27

-Metoprolol, bisoprolol, and carvedilol

Question 28

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

Answer 28

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

Question 29

What are the symptoms of overdose of b-blockers?

Answer 29

Bradycardia and bradyarrhythmia are typical symptoms

Question 30

What happens in b-blocker overdose?

Answer 30

beta receptors lose specificity

Question 31

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

Answer 31

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

Question 32

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

Answer 32

seizures and coma

Question 33

What happens in overdose of b-blockers with ISA?

Answer 33

tachycardia and HTN

Question 34

What is Sotalol?

Answer 34

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

Question 35

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

Answer 35

direct vasodilation contributes to hypotension

Question 36

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

Answer 36

glucagon or high-dose insulin/glucose

Question 37

Why could a beta blocker induce bronchospasm?

Answer 37

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

Question 38

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

Answer 38

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

Question 39

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

Answer 39

-B1 selective drugs or those with ISA

Question 40

Other side effects of B-blockers?

Answer 40

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

Question 41

Other side effects of B-blockers?

Answer 41

-hypoglycemia-diabetic masking

Question 42

How can b-blockers cause hypoglycemia?

Answer 42

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

Question 43

How can b-blockers cause diabetic masking?

Answer 43

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

Question 44

How do beta-blockers affect lipids?

Answer 44

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

Question 45

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

Answer 45

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

Question 46

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

Answer 46

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

Question 47

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

Answer 47

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