Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MWU Pharmacology I > BETA ADRENERGIC RECEPTOR ANTAGONISTS > Flashcards

BETA ADRENERGIC RECEPTOR ANTAGONISTS Flashcards

1
Q

What are the 4 Non-selective (first generation) beta adrenergic receptor antagonists?

A

Nadolol
Propranolol
Timolol
Sotalol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

4 B-1 selective Antagonists (Second Gen)

A

Atenolol
Bisoprolol
Esmolol
Metroprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

2 Non-selective 3rd generation Beta antagonists

A

Carvedilol
Labetalol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name 1 B1-selective (3rd gen.) antagonist

A

Nebivolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

B1-receptor locations and what they affect

2 organs of interest

A

Heart
* Rate
* Contractility
* Automaticity
* Conduction velocity

Kidney (juxtaglomerular cells)
* Renin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

B-2 receptor locations and functions

3 organs of interest

A

Lung
* Bronchorelaxation

Skeletal muscle
* Vasodilation
* Glycogenolysis

Liver
* Glycogenolysis
* Gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Identify some pharmacological properties of Beta receptor antagonists

Absorption (exceptions) / Distribution / Metabolism (exception)

A

Well absorbed after oral administration

Bioavailability is limited to varying degrees due to first-pass
metabolism
* Except for sotalol

Rapidly distributed and have large volumes of distribution

Most β antagonists have half-lives in the range of 3-10
hours
* Esmolol is a major exception, 10 min half-life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Primary mechanisms of action of B-antagonists

A

Specifically block β adrenergic receptors

Differ in their relative affinities for β1 and β2 receptors

None are absolutely specific for β1 receptors
* Selectivity is dose-related

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Identify some secondary (variable) mechanisms of action. (when do they inhibit activation of B receptors, and when do they activate them).

Agonist / ISA / what can they help prevent

A

Secondary mechanisms (variable)
* Partial agonists as well
- Also referred as intrinsic sympathomimetic activity (ISA)
- Inhibit the activation of β receptors in the presence of high catecholamine concentrations
– but moderately activate the receptors in absence of endogenous agonists
* May help prevent profound bradycardia or negative inotropy
* Clinical significance is unclear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Identify additional secondary mechanisms of action

anesthetic / what do they block / CV effects

A

Local anesthetic or membrane-stabilizing activity

Block α1 receptors (labetalol, carvedilol)

Additional cardiovascular effects (third generation β blockers)
* Vasodilator (nebivolol, carteolol)
* Antioxidant (carvedilol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

B-adrenergic antagonists effects on the cardiovascular system. (HR, contractility, automaticity and conduction)

When are effects most evident?

A

Decreases most sympatheticallysupported cardiac functions
* Heart rate, contractility, automaticity and conduction

Depends on activity of sympathetic nervous system
* Modest effect when tonic stimulation is low
* Cardiovascular effects are most evident with exercise
- Attenuates expected rise in heart rate and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

B antagnoist effects on BP, Cardiac Output, short term / long term effect on total peripheral resistance (TPR).

effect on presynaptic norepinephrine release / renin

A

Lowers blood pressure in patients with hypertension
* Generally do not lower blood pressure in normotensive patients

Mechanisms not fully understood
* Decreased CO
- Acute compensatory increase in TPR
- Reduction in TPR with long-term use

Block presynaptic β2 receptors that enhance NE release

Reduced β1-stimulation of renin release from juxtaglomerular cells

Additional vascular effects (e.g. vasodilation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

B antagonist effects on the eye

A
  • Reduce intraocular pressure
  • Decreased aqueous humor
  • Useful for patients with chronic open-angle glaucoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Adverse effects on the CV-system

heart failure / Heart rhythm / Vascular / discontinuation / exercise

A

May cause or exacerbate heart failure
* Yet, extensive clinical evidence demonstrates that β blockers prolong the lives of heart failure patients

Bradyarrhythmias
* Particularly in patients taking other drugs that impair sinus or AV node function

Exacerbate peripheral vascular disease
* Raynaud’s phenomenon

Abrupt discontinuation
* Exacerbates angina
* Increased risk of sudden death

Exercise intolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Adverse effects on pulmonary system

receptor / asthma / COPD / less likely / ischemic heart disease

A

Block β2 receptors in bronchial smooth muscle
* Little effect in normal individuals
* In patients with asthma or COPD, can cause life-threatening bronchoconstriction

Less likely with β1-selective antagonists or β antagonists with Intrinsic sympathomimetic activity
* Should still be used with great caution in patients with bronchospastic diseases
* Patients with COPD may tolerate β1- selective blockers
- Benefits for patients with concomitant ischemic heart disease may outweigh the risks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Adverse effects on CNS

A
  • Fatigue
  • Sleep disturbances (insomnia, nightmares)
  • Depression
  • No clear correlation with the incidence of CNS effects and
    lipophilicity
17
Q

Adverse Metabolic Effects

which ones less likely to affect metabolism?

A

Delays recovery from hypoglycemia
* β2-mediated effects of catecholamine on gluconeogenesis and glycogenolysis
* β1-selective antagonists are less likely to delay recovery from hypoglycemia

Blunts the perception of symptoms of hypoglycemia
* Tremor, tachycardia, nervousness

18
Q

Propranolol (first gen. non-selective prototype) mechanism of action.

receptors / onset / bioavailability

A
  • Competitive, reversible antagonist of β1 and β2 receptors
  • Rapid and completely absorbed
  • Substantial first pass metabolism causes variable bioavailability
19
Q

PROPRANOLOL clinical uses

BP / heart /

A

Hypertension

Angina pectoris

Cardiac arrhythmias

Myocardial infarction

Pheochromocytoma
-As an adjunct to alpha-adrenergic blockade to control blood pressure and reduce symptoms of catecholamine- secreting tumors

Migraine prophylaxis

Essential tremor

20
Q

PROPRANOLOL Adverse effects

A

Cardiovascular:
* Bradycardia
* Hypotension
* Acute heart failure

Other:
* Bronchospasm
* Blunt recognition of hypoglycemia
* Fatigue

Abrupt withdrawal symptoms

21
Q

TIMOLOL (non-selective 1st Gen) mechanism of action / therapeutic use

A

Competitive, reversible antagonist of β1 and β2 receptors

Major therapeutic use
* Glaucoma
- Decreases aqueous humor formation

  • Also available orally and used similarly as propranolol
22
Q

METOPROLOL (B1 2nd gen) mechanism of action

A

Competitive, reversible antagonist of β1 receptors
* Cardioselective

At low doses, is more selective for β1 receptor (10 fold)

23
Q

METOPROLOL Clinical Uses

A
  • Hypertension
  • Angina
  • Acute myocardial infarction
  • Congestive heart failure
24
Q

METOPROLOL: Adverse Effects

A

Some overlap with propranolol, especially with cardiovascular effects:
* Bradycardia
* Hypotension
* Acute heart failure
* Fatigue

Less risk of bronchoconstriction or metabolic effects
* Mediated by β2 receptors

25
Q

ESMOLOL: Mechanism of action / half-life / metabolism / route / and clinical uses

A

Moderately selective β1 receptor antagonist

Ultra-short acting
* t1/2 = ~8 min

Cleaved by esterases in the plasma

Administered intravenously and is used when β blockade of
short duration is desired
* Intraoperative and postoperative tachycardia and/or hypertension
* Sinus tachycardia
* Supraventricular tachycardia and atrial fibrillation/flutter

26
Q

Labetalol: Mechanism of action / clinical uses

A

Competitive, reversible antagonist of α1 and both β receptors

Used to treat:
* Hypertension
* Hypertensive emergencies (IV administration)

27
Q

Nebivolol: Mechanism of action / vascular effects / clinical uses

A

Highly selective β1 receptor antagonist

Also stimulates NO-mediated vasodilation

Used to treat:
* Hypertension

28
Q

Carvedilol: Mechanism of action / inflammation / clinical uses

A

Competitive, reversible antagonist of α1 and both β receptors

Also has antioxidant and anti- inflammatory properties

Blocks L-type calcium channels at higher doses

Used to treat:
* Heart failure with reduced ejection fraction
* Hypertension
* Reduces mortality in patients after myocardial infarction

29
Q

Efficacy of BETA
ADRENERGIC RECEPTOR
ANTAGONISTS treating hypertension

first line therapy? /

A

Effective and well-tolerated

No longer a first-line therapy, particularly in patients over
age 60 years
* May be associated with inferior protection against stroke risk (particularly among smokers)

Beta blockers without ISA are preferred in patients with
angina or a history of myocardial infarction

30
Q

How do BETA ADRENERGIC RECEPTOR ANTAGONISTS help treat Ischemic Heart Disease?

cardiac work / O2 / angina / exercise / MI / indicated during…

A

Blockade of cardiac β receptors results in:
* Decreased cardiac work
* Reduction in oxygen demand

Reduces the frequency of angina episodes

Improves exercise tolerance in many patients with angina

Prolongs survival of patients who have had a myocardial infarction
* Timolol, propranolol, metoprolol

Strongly indicated in the acute phase of myocardial infarction
* To reduce cardiovascular mortality in patients who have survived the acute phase of myocardial infarction and are clinically stable
* Should use a β antagonist without ISA (Intrinsic sympathomimetic activity)

31
Q

CLINICAL USE OF BETA ADRENERGIC RECEPTOR ANTAGONISTS for Cardiac arrhythmias

AFIB / AV-node / ectopic beats / esmolol / sotalol

A

Effective in the treatment of both supraventricular and ventricular arrhythmias

Slows ventricular response rates to atrial flutter and fibrillation
* Increases atrioventricular nodal refractory period

Can also reduce ventricular ectopic beats, especially if precipitated by catecholamines

Esmolol is useful against acute perioperative arrhythmias
* Short duration of action

Sotalol has antiarrhythmic effects involving ion channel blockade

32
Q

CLINICAL USE OF BETA ADRENERGIC RECEPTOR ANTAGONISTS in Heart failure

A

Effective in reducing mortality in patients with chronic
heart failure
* Metoprolol, bisoprolol, carvedilol

Mechanisms are uncertain
* Beneficial effects on myocardial remodeling
* Decreases the risk of sudden death

33
Q

CLINICAL USE OF BETA
ADRENERGIC RECEPTOR
ANTAGONISTS in Glaucoma

pressure / topical administration / adverse effects

A

Reduces intraocular pressure
* Reduced production of aqueous humor by the ciliary body

Open-angle glaucoma
* Comparable efficacy to epinephrine or pilocarpine
* Better tolerated

Beta blockers that lack local anesthetic properties are suitable for local use in the eye

Topical administration:
* Timolol
* Local daily dose applied is small compared to common systemic doses
* Still, may be absorbed from the eye and cause serious adverse effects in the heart and airways

34
Q

CLINICAL USE OF BETA
ADRENERGIC RECEPTOR
ANTAGONISTS in Hyperthyroidism

A

Beta blockers ameliorate the symptoms of hyperthyroidism
that are caused by increased beta-adrenergic tone
* These include palpitations, tachycardia, tremulousness, anxiety, and heat intolerance

Should be given to most hyperthyroid patients who do not
have a contraindication to their use

35
Q

CLINICAL USE OF BETA
ADRENERGIC RECEPTOR
ANTAGONISTS for Migraines

preventative / effective / maybe effective

A

Preventative treatment
* Reduces the frequency and intensity

  • Established as effective
  • Propranolol, metoprolol, timolol

Probably effective
* Atenolol, nadolol

36
Q

CLINICAL USE OF BETA ADRENERGIC RECEPTOR ANTAGONISTS for Essential Tremors

A

Sympathetic activity may
enhance skeletal muscle tremor
* Propranolol

37
Q

CLINICAL USE OF BETA
ADRENERGIC RECEPTOR
ANTAGONISTS for performance anxiety

A
  • Reduction of the somatic
    manifestations of anxiety
  • Propranolol
38
Q

B1-selective antagonists are preferable in patients with:

A
  • Bronchospasm
  • Diabetes
  • Peripheral vascular disease
  • Raynaud’s phenomenon
  • Third generation β antagonists may offer therapeutic advantages

MWU Pharmacology I (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions