Lectures 10, 11, 12: Adrenergic System 1, 2 and 3 (Adrenergic Agonists & Antagonists) Flashcards Preview

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Flashcards in Lectures 10, 11, 12: Adrenergic System 1, 2 and 3 (Adrenergic Agonists & Antagonists) Deck (36)
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1
Q
  • Blocks transport of NA into the vesicles, thus depleting noradrenaline stores.
  • Not used clinically.
A

Reserpine

2
Q

Bronchoconstriction (due to the blockade of β2-adrenergic receptors on bronchial smooth muscle)

A

Propranolol

3
Q
  • Non-catecholamine (First, they lack the catechol group, therefore they are not substrates for COMT and are metabolized slowly by MAO.
  • As a result, the half-lives of non-catecholamines are much longer than those of catecholamines.
  • Second, because they do not undergo rapid degradation by MAO and COMT, non- catecholamines can be given Orally.
  • Third, non-catecholamines are considerably less polar than catecholamines, and hence are more able to cross the blood-brain barrier.)
A

Phenylephrine

4
Q

Direct-acting agonists act directly on adrenoceptors (α and/or β) by activating them, and are said to be sympathomimetic (Drugs that produce an effect similar to the effect that is produced by stimulation of the sympathetic nervous system).

A

Noradrenaline (Norepinephrine), Phenylephrine, Clonidine, Isoprenaline (Isoproterenol), Dobutamine, Salbutamol

5
Q

-Promotion of NA Release. By acting on terminals of sympathetic nerves to cause NA release.
-These agents don’t act directly on postsynaptic receptors.
-They cause NA release from the nerve terminals by displacing NA from vesicles.
-Found in fermented foods such as cheese and is metabolized by MAO.
-The effect of indirect acting adrenergic agonists is much enhanced by
monoamine oxidase (MAO) inhibition, which can lead to severe hypertension following ingestion of tyramine-rich foods by patients treated with MAO inhibitors.
-The patient is taking MAO inhibitors, tyramine- containing diet can
cause serious vasopressor effects (hypertensive crisis).
-Promotion of NA release

A

Amphetamine and Tyramine

6
Q

β-Blockers (Propranolol, and Atenolol)

A
  • β-Blockers are used to treat multiple diseases of the heart. They interfere with the effects of endogenous catecholamines.
  • When β-blocking drugs are given, they block the access of catecholamines to their receptors, so that the heart will pump with less intensity.
  • Therefore, beta-blockers cause: a decrease in heart rate (-ve chronotropic effect) & decreased contractility (-ve inotropic effect).
7
Q

Therapeutic uses of: Propranolol & Atenolol (β- Antagonist)

A

Therapeutic Uses of β- Antagonists:
-Reduction of blood pressure in hypertension:
● Can be used alone or in combination with other blood pressure-lowering drugs to maximize effect.
● Mechanism of action: Lower blood pressure by decreasing cardiac output & inhibiting the release of renin.
-Angina: Chest pain due to an inadequate supply of oxygen to the heart muscle.
● Blockade of β1-receptors in the myocardium reduces the influence of endogenous catecholamines.
● Result in decreased cardiac output & decreased blood pressure.
-Myocardial infarction:
● β-blockers have protective effect on the myocardium.
● Patients who have had one myocardial infarction appear to be protected against a second attack by prophylactic use of β blockers.
-Hyperthyroidism: There is increased sympathetic activity.
● Some of the symptoms of hyperthyroidism (such as tachycardia and anxiety) can be improved by beta-blockers.

8
Q

What does Isoprenaline (Isoproterenol) cause?

A

Causes: bronchodilation, peripheral vasodilation, and increased cardiac output.

9
Q

Used as nasal decongestants.

A

Phenylephrine

10
Q

Adverse effects of α-adrenergic blockers are:

  • Orthostatic hypotension (the change in the BP due to changing posture)
  • Nasal congestion (due to dilation of nasal mucosal arterioles)
  • Reflex tachycardia
A

Phentolamine, Prazosin, and Yohimbine (adverse effects of α-adrenergic blockers are for both selective and non selective α blockers)

11
Q

Stimulates adrenergic receptors directly and also causes the release of noradrenaline from the adrenergic neuron.

A

Ephedrine

12
Q

_____ acts on adrenergic receptors: α and β adrenergic receptors

A

Noradrenaline (Norepinephrine)

13
Q

Selective α1-adrenoceptor agonists (vasoconstrictors)

A

Phenylephrine

14
Q

Block the release of NA into the synaptic space.

A

Guanethidine

15
Q

Selective β1 agonists (produce increased cardiac contractility, clinically useful to increase cardiac output in congestive heart failure.

A

Dobutamine

16
Q

Selective α2 agonists (centrally-acting)

A

Clonidine

17
Q

Mixed-action adrenergic agonists

A

Ephedrine

18
Q

Selective α1 antagonists

A

Prazosin

19
Q

Adverse effects of: Propranolol & Atenolol (β- Antagonist)

A

adverse effects:

  • Bronchoconstriction can occur, especially when non-selective beta-blockers are administered to asthmatic patients.
  • Cardio-selective beta-1 blockers should be used for asthmatic patients.
  • Non-selective beta-blockers are contraindicated in patients with asthma.
20
Q

Selective β1 antagonist

A

Atenolol

21
Q

Non selective α blockers (block both α1 & α2 receptors)

A

Phentolamine

22
Q

Tyrosine, is the substrate for the syntheses of _____

A

Noradrenaline (Norepinephrine)

23
Q

________, an indirect acting adrenergic agonist, is found in fermented foods such as cheese. It is metabolized by MAO.

A

Tyramine

24
Q

Non selective β receptor antagonist (blocks both β1 & β2)

A

Propranolol

25
Q
  • By blocking neuronal NA reuptake (uptake 1), drugs can cause NA to accumulate within the synaptic gap, and can thereby increase receptor activation.
  • Inhibition of NA reuptake
A

Cocaine, Tricyclic antidepressants

26
Q

Selective α2 antagonist

A

Yohimbine

27
Q

Indirect acting adrenergic agonists

A

Amphetamine

28
Q

Treatment of hypertension

A

Clonidine, Prazosin

29
Q

Selective β2 agonists used mainly for their bronchodilator action in asthma and in the treatment of premature labor.

A

Salbutamol

30
Q

_____ is released at the postganglionic sympathetic nerve terminals (e.g. Cardiac muscle, smooth muscle, glands) & also at the adrenal medulla where the hormone adrenaline is formed.

A

Noradrenaline (Norepinephrine)

31
Q

Treatment of shock.

A

Noradrenaline (Norepinephrine)

32
Q

If the patient is taking MAO inhibitors, _______- containing diet can cause serious vasopressor effects (hypertensive crisis).

A

tyramine

33
Q

The effect of indirect acting adrenergic agonists is much enhanced by monoamine oxidase (MAO) inhibition, which can lead to severe hypertension following ingestion of __________ foods by patients treated with MAO inhibitors.

A

tyramine-rich

34
Q

Neurotransmitter

A

Noradrenaline (Norepinephrine)

35
Q

Treatment of hypertensive emergencies caused by pheochromocytoma

A

Phentolamine

36
Q

Non selective β-agonist, it stimulates both β-1 and β-2 adrenergic receptors.

A

Isoprenaline (Isoproterenol)