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Pharmacology > Adrenergic Agonists > Flashcards

Adrenergic Agonists Flashcards

1
Q

What are some of the effects of a1 activation?

A

-Vasoconstriction
-Pupil dilation

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2
Q

What are some of the effects of a2 activation?

A

-Inhibits NT release
-Vasoconstriciton

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3
Q

What are some of the effects of b1 activation?

A

-Stimulates increase in inotropy and chronotropy of the heart

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4
Q

What are some of the effects of b2 activation?

A

-Vasodilation
-Bronchodilation

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5
Q

What is the mechanism for a2?

A

Negative coupling of adenylyl cyclase

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6
Q

What is the mechanism for b1?

A

Positive coupling of adenylyl cyclase

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7
Q

What is the mechanism for b2?

A

Positive coupling of adenylyl cyclase

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8
Q

What is the most effective agonist on the beta receptors?

A

Isoproterenol

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9
Q

What has the greatest effect on diastolic pressure?

A

TPR

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10
Q

What has the greatest effect on systolic pressure?

A

CO

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11
Q

What does EPI stimulate?

A

Stimulates α1, α2, β1 and β2 receptors

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12
Q

What are the effects of EPI at low doses?

A

β2 receptor activation causes peripheral vasodilation, thereby decreasing diastolic BP; β1 receptor activation has positive inotropic and chronotropic effects thereby increasing CO and systolic BP

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13
Q

What are the effects of EPI at high doses?

A

At higher doses (>0.2 μg/kg/min, solid lines) effects of α1 receptor activation predominate:

Producing peripheral vasoconstriction, elevated systolic pressure and elevated diastolic pressure due to increased TPR and increased CO.

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14
Q

What are the effects of EPI on the lung?

A

β2 receptor - bronchodilation
α1 receptor - decrease in bronchial secretions

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15
Q

EPI indication

A

-Anaphylaxis
-Cardiac arrest
-Bronchospasm

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16
Q

EPI Toxicity

A

Arrhythmia

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17
Q

EPI Contraindications

A

Late term pregnancy

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18
Q

What does NE stimulate?

A

α1, α2 and β1 receptors

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19
Q

What are the effects of NE?

A

β1: Increase CO
α1, α2: Increase TPR

Decrease in heart rate due to baroreceptor reflex
Increase in MAP

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20
Q

NE indication

A

Vasodilatory shock

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21
Q

What is the effect of NE on the lung?

A

NE has limited affinity for β2 receptors and so has limited effects on bronchiole smooth muscle.

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22
Q

NE Toxicity

A

Ischemia due to the increase in TPR

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23
Q

NE Contraindications

A

Pre-existing excessive vasoconstriction and ischemia

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24
Q

What does DOPA stimulate?

A

Stimulates D1,D2, β1, α1 and α2

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25
Q

What are the effects of DOPA at low dose?

A

D1: Decreased TPR
β1: Increased CO

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26
Q

What are the effects of DOPA at high dose?

A

Increased MAP
Increased TPR

β1, α1 and α2 are all activated too and lead to the increased BP

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27
Q

DOPA indication

A

Cardiogenic shock

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28
Q

What is an advantage of DOPA?

A

It has a vasodilatory effect in renal and mesenteric vascular beds

29
Q

DOPA Toxicity at Low and High Doses

A

Low infusion rates – hypotension
High infusion rates – ischemia

30
Q

DOPA Contraindications

A

Tachyarrhythmias and ventricular fibrillation

31
Q

What does isoproterenol stimulate?

A

Stimulates β1 and β2

32
Q

What are the effects of isoproterenol?

A

Decreased TPR
Increased CO

Small decrease in MAP

33
Q

Isoproterenol indication

A

Bradycardia
Heart Block with high TPR

34
Q

Isoproterenol Contraindications

A

Angina, particularly with arrhythmias

35
Q

Isoproterenol Toxicity

A

Tachyarrhythmias

36
Q

What happens to the baroreflex with isoproterenol?

A

It can lead to greatly increased HR due to the decreased MAP

37
Q

What does dobutamine stimulate?

A

β1 > β2 > α

(selective beta-1 agonist)

38
Q

What are the effects of dobutamine?

A

Increased CO

39
Q

Dobutamine indication

A

Short-term treatment of cardiac insufficiency in CHF
Cardiogenic shock
Excess β-blockade

40
Q

Dobutamine Toxicity

A

Hypotension

41
Q

What is special about the β1 effects of dobutamine?

A

It has greater inotropy than chronotropy due to lack of β2 activation at low doses

42
Q

What are the Direct Acting Sympathomimetics?

A

EPI
NE
DOPA

43
Q

What is a Non-selective β-adrenergic Agonist?

A

Isoproterenol

44
Q

What is a Selective β1-adrenergic receptor Agonist?

A

Dobutamine

45
Q

What are Selective β2 adrenergic Agonists?

A

Terbutaline
Albuterol

46
Q

What is a Selective α1-adrenergic Agonist?

A

Phenylephrine

47
Q

What is a Selective α2-adrenergic Agonist?

A

Clonidine

48
Q

What does terbutaline/albuterol stimulate?

A

Selectively activate β2 receptors

49
Q

What are the effects of terbutaline/albuterol?

A

Bronchodilation
Uterine relaxation

Both via β2 receptor activation

50
Q

Terbutaline and Albuterol indication

A

Bronchospasm
Obstructive Airway Disease

51
Q

Terbutaline and Albuterol Toxicity

A

Tachycardia b􏰃1
Muscle Tremor b􏰃2
Tolerance 􏰃b2

52
Q

How can terbutaline and albuterol lead to muscle tremors?

A

Activation of β2- receptors expressed on pre-synaptic nerve terminals of cholinergic somatomotor neurons increases release of neurotransmitter. This can lead to muscle tremor, a side effect of β-agonist therapy.

53
Q

What does phenylephrine stimulate?

A

Selective 􏰀a1 receptor agonist

54
Q

What are the effects of phenylephrine?

A

Increase TPR and MAP
Decrease HR (baroreflex)
Pupillary dilation
Decrease bronchiole and sinus secretions

All via a1 agonist

55
Q

Phenylephrine indication

A

Paroxysmal supraventricular tachycardia
Mydriatic agent (dilation of eyes)
Nasal decongestant

Used for hypotension seen in anesthesia

56
Q

Phenylephrine Toxicity

A

Hypertension

57
Q

Phenylephrine Contraindications

A

Pre-existing hypertension
Ventricular tachycardia

58
Q

What is the duration of phenylephrine action?

A

Phenylephrine is not a catecholamine and therefore is not subject to rapid degradation by COMT. It is metabolized more slowly; therefore it has a much longer duration of action than endogenous catecholamines.

59
Q

What does clonidine stimulate?

A

Selective 􏰀a2 adrenergic receptor agonist

60
Q

What are the effects of clonidine?

A

Acute increase in BP (peripheral effect)
Reduced BP (central effect)

Peripherally, clonidine causes mild vasoconstriction and slight increase in BP, also crosses BBB to cause reduced sympathetic outflow thereby reducing vasoconstriction and BP. The loss of sympathetic activity predominates over the direct vasoconstrictor effects of the drug leading to overall reduction in blood pressure.

61
Q

Clonidine indication

A

Hypertension when cause is due to excess sympathetic drive

62
Q

Clonidine Toxicity

A

Dry mouth
Hypertensive crisis (after acute withdrawal)

63
Q

How do indirectly acting sympathomimetics work?

A

Indirect acting sympathomimetic agents increase the concentration of endogenous catecholamines in the synapse and circulation leading to activation of adrenergic receptors. This occurs via either:

1) release of cytoplasmic catecholamines or
2) blockade of re-uptake transporters

64
Q

What do the following stimulate: Amphetamine Methamphetamine Methylphenidate Ephedrine Pseduoephedrine Tyramine?

A

They stimulate the release of endogenous catecholamines. Amphetamine-like drugs are taken up
by re-uptake proteins and subsequently cause reversal of the re-uptake mechanism resulting in release of neurotransmitter in a calcium-independent manner.

65
Q

What are the effects of the indirectly acting sympathomimetics?

A

Increased TPR and diastolic BP

Positive inotropic and chronotropic effects leading to an increased systolic pressure

CNS stimulant Probably increased NE
Anorexia Possibly increased DA

66
Q

Indirectly acting sympathomimetics indication

A

Attention Deficit Disorder
Narcolepsy
Nasal congestion

67
Q

Indirectly acting sympathomimetics Toxicity

A

Tachycardia

68
Q

Indirectly acting sympathomimetics Contraindications

A

Rx with MAO inhibitors within previous 2 weeks
-This can cause exaggeration of the effect in cases like with tyramine

Pharmacology (5 decks)

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