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Medical Pharmacology Exam 1 > Adrenergics I > Flashcards

Adrenergics I Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the effect of epinephrine on bronchial smooth muscle, the heart and lastly, on vessels?

A

Bronchial muscle - vasodialation
Heart - Stimulation
Vessels - vasoconstriction

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2
Q

What is the receptor through which epinephrine is able to induce vasoconstriction?

A

Alpha 1 receptors

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3
Q

Epinephrine is used during what 2 emergency scenarios?

A

Elevated anterior eye chamber pressure (glaucoma)

Allegy / anaphylactic shock

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4
Q

How is epinephrine used during surgery?

A

It can be used to cause vasoconstriction, reducing drug diffusion from administration site

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5
Q

What is the effect of epinephrine on bleeding?

A

Causes vasoconstriction, reduces bleeding

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6
Q

What is the clinical indication for norepinephrine? How is it administered?

A

Used only for shock therapy

IV infusion

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7
Q

Norepinephrine is able to cause vasoconstriction and increase cardiac output via what two receptors, respectively?

A

Vasoconstriction - alpha 1

Cardiac output - beta 1

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8
Q

What is the clinical indication for dopamine? How is it administered?

A

Used only for shock therapy

IV infusion

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9
Q

Dopamine is able to cause vasoconstriction and increase cardiac output and dialate renal blood vessels via what three receptors, respectively?

A

Vasoconstriction - alpha 1
Cardiac output - beta 1
Renal blood vessels - DA 1

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10
Q

What is the major clinical use of isoproterenol, what receptor is targeted? When used for cardiac stimulation, what receptor is targeted then?

A

Relaxation of bronchial smooth muscle
Beta-2 adrenoreceptors
Beta 1 receptors

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11
Q

What are the 2 clinical uses of phenylephrine? What receptor is targeted?

A

Used as nasal decongestant (vasoconstriction)
Prevents shock
Alpha 1 adrenoreceptor

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12
Q

What is Metaraminol? What receptors does it target?

A

Long acting agonist

Alpha 1 and beta 1 receptor stimulant

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13
Q

What separates ephedrine from most of the other adrenergic agonists? What receptors does it target?

A

Orally effective

Targets most adrenoreceptors

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14
Q

True or false: The parasympathetic NS plays a major role in determining periperal vascular resistance, contractile force and venous tone.

A

False, these are all determined by sympathetic output

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15
Q

What are the 5 organ systems that receive sympathetic innervation alone?

A

Blood vessels, sweat glands, liver, spleen and adrenal gland

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16
Q

What are the six major adrenergic receptors? Which 2 are feedback mediators?

A

alpha 1,2
beta 1,2
DA 1,2
Feedback, alpha 2 and D2

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17
Q

Where are adrenergic receptors found, preganglionic, post ganglionic, both? Presynaptic or post-synaptic?

A

Found in post ganglionic locations

Found both pre and post-synaptically

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18
Q

What is the primary adrenergic neurotransmitter? What is the catecholamine released by the adrenal medulla?

A

NE

Epinephrine

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19
Q

The major adrenergic receptor controlling heart rate is

A

Muscarinic type 2

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20
Q

Where within the sympathetic NS is dopamine released from? What type of sweat glands receive adrenergic stimulation?

A

Splanchnic vascular smooth muscle and Renal vascular smooth muscle
Non-thermoregulatory sweat glands

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21
Q

What are the 5 components / steps of catecholamine biosynthesis? i.e. what is made in what order?

A

Tyrosine - dopa - dopamine - NE - Epi

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22
Q

What is the rate limiting enzyme in catecholamine synthesis? What is its substrate and product?

A

Tyrosine hydroxylase

Tyrosine - DOPA

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23
Q

What is the main determinant of catecholamine synthesis rate?

A

Increased neuronal firing frequency = increased rate of NT synthesis

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24
Q

Where is epinephrine synthesized?

A

In the adrenal medulla

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25
Q

What are the 2 enzymes involved in catecholamine metabolism? What are their main sites of action?

A 
catechol-o-methyltransferase (COMT) - Liver
Monoamine oxidase (MAO) - Adrenal nerve terminals, liver
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26
Q

What is the function of COMT? MAO? What is the net effect? What order do they work?

A

COMT - Methylation
MAO - Deamination
Reduce the biologic activity of the target catecholamines
No specific order of function

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27
Q

When NE or Epi are metabolized by COMT and or MAO, what are the two products that can be found in plasma or urine?

A

MHPG - methoxyhydroxyphenylglycol

VMA - vanillylmandelic acid

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28
Q

Among adrenergic receptor agonists, what is the effect of substituting the amino group? What are the examples (3)?

A

Increase beta-receptor activity

Isoproterenol, dobutamine, terbutaline

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29
Q

Among adrenergic receptor agonists, what is the effect of substituting the benzene ring? What are the examples (3)?

A

Increases duration of action (reduced COMT binding) but reduced potency.
Metaraminol, ephedrine, phenylephrine

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30
Q

Among adrenergic receptor agonists, what is the effect of substituting the alpha carbon? What are the examples (2)?

A

Increased duration of action (blocks MAO metabolism), displaces NE in storage vesicles
Metaraminol, Ephedrine

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31
Q

Alpha 1 receptor stimulation generally [contracts / constricts] muscles. What is the exception?

A

Relaxes intestinal smooth muscle

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32
Q

Arterial and venoconstriction, ejaculation, piloerection are all regulated by _ receptor activation

A

Alpha 1

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33
Q

Iris radial muscle contraction and glycogenolysis are all regulated by _ receptor activation

A

Alpha 1

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34
Q

What are the 2 alpha 1 selective agonists drugs provided as examples?

A

Phenylephrine

Methoxamine

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35
Q

What are the 2 alpha 2 selective (relatively) drugs provided as examples?

A

Clonidine

Methyl-NE

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36
Q

What are the 2 mixed alpha and beta receptor agonists provided as examples?

A

NE

Epi

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37
Q

What is the pharmacological difference between NE and Epi?

A

Epi is able to bind beta1 and beta2 equally, while NE binds beta1 alot better than beta2

38
Q

What are the 3 beta 2 selective agonist provided as examples?

A

Albuterol, Terbutaline, metaproterenol

39
Q

Isoproterenol is a beta selective agonist. How does its binding of the 2 main beta receptors compare?

A

It binds both of the receptors equally

40
Q

What is the single example if a beta 1 selective agonist provided?

A

Dobutamine

41
Q

Where are alpha 2 receptors found? What is their g-protein? What is their function

A

Presynaptically located
Gi
Negative feedback, reduce NE release

42
Q

Activation of what receptor will increase heart rate, contractile force, CO and lypolysis?

A

Beta 1

43
Q

Mydriasis, contraction of the iris muscle, is mediated by which adrenergic receptor?

A

Alpha 1

44
Q

Where are beta 1 receptors found? What is the assoc. g protein? Generally, what is the net effect of stimulation?

A

Heart
Gs
Increase heart function, including lipolysis

45
Q

What is the major effect of beta 2 stimulation?

A

Counters alpha 1 (mostly)

  • skeletal muscle vasodilation
  • bronchodialation, myometrial replaxation,
  • decreased intraoccular pressure
  • intestinal relaxation (exception)
46
Q

What is the effect of beta 3 stimulation?

A

Increased glycogenolysis in liver and skeletal muscle

47
Q

How does dopamine binding to DA1 and DA2 compare? What is the example of a DA1 selective agonist provided?

A

Equivalent binding

Fenoldopam

48
Q

What is the G-protein assoc. with DA1? DA2?

A

Gs and Gi, respectively

49
Q

What is the effect of DA1 stimulation? DA2?

A

DA1 - vasodialation of renal and mesenteric vessels

DA2 - Presynaptic, reduce neurotransmitter release

50
Q

What is the Amine 1 transporter? What is the effect of its inhibition?

A

It is the reuptake system for norepinephrine

If inhibited, NE levels increase in the synapse

51
Q

What are the specific inhibitors of the Amine 1 transporter mentioned?

A

Cocaine

Desmethylimipramine (DMI), a tricyclic antidepressant

52
Q

What are they 2 presynaptically located adrenergic receptors? What are their functions? What is the effect of antagonists?

A

Alpha 2 and DA 2
They are feedback regulators, decrease release
Antagonists will block feedback, increase synaptic NT levels

53
Q

How are amine 1 transporter inhibitors (cocaine, DMI) related to antagonists of presynaptic adrrenergic receptors?

A

Their net effect is the same (increased synaptic NT), the mechanism of action is different

54
Q

What are the 2 DA2 specific antagonists provided as examples? What are they used for?

A

Haloperidol
Chlorpromazine
Antipsychotics

55
Q

There are 4 drugs that are provided as examples of releasing agent (Increase NE release). What are they?

A

Dopamine
Ephedrine
Tyramine
Amphetamine

56
Q

Why is tyramine (found in certain cheeses) dangerous for patients on MAO inhibitors?

A

Tyramine blocks MAO activity as well as increases NE release, can lead to increased arterial pressure

57
Q

What are they 2 ways amphetamines increase synaptic NE?

A

Block NE reuptake

Reverse NE transport (release NE already within the nerve terminals)

58
Q

What are the effects of ephedrine (2)?

A

Acts as releasing agent

Directly stimulates alpha 1 and beta 1 receptors

59
Q

Where are beta 1 receptors located? What is the effect of stimulation?

A

Heart and adipose tissue

Increased cardiac function, lipolysis

60
Q

As a rule, alpha 1 receptor stimulation leads to smooth muscle constriction. What organ system is the exception?

A

The intestines

61
Q

While epinephrine is able to stimulate both alpha and beta receptors, which of the 2 is more sensitive to epi i.e. which receptors will be affected first by low doses of epinephrine?

A

Beta receptors, 10X more sensitive

62
Q

Under what conditions will dopamine affect receptors other than DA1 and DA2? What receptors will now be affected?

A

High doses of dopamine stimulate alpha 1 and beta 1. No effect on beta 2 and alpha 2

63
Q

Where is NE made? What protein is responsible for its packaging into vessicles?

A

In the nerve terminal

vesicular monoamine transporter (VMAT)

64
Q

NE release is dependent on which cation? What is the protein that recycles NE back into the synapse?

A

Calcium dependent exocytosis

The Amine 1 Transporter

65
Q

Upon stimulation, what is released from the adrenal medulla? Where is “X” released into?

A

Epinephrine (80%) and NE (20%)

Directly into venous circulation

66
Q

What is a pheochromocytoma?

A

A tumor of the adrenal medulla, causes increased catecholamine release.

67
Q

What are the 4 major symptoms associated with pheochromocytoma?

A

Severe tachycardia
Hypertension
Headaches
Increased sweating

68
Q

What is the function of dopamine in the PNS? What is the clinical use of dopamine? Why?

A

PNS - Stimulates alpha 1 and beta 1 receptor at higher doses

Used in treatment of shock because it can stimulate alpha 1 and beta 1 receptors

69
Q

Both alpha 1 and beta 2 receptors are activated by several drugs. However, which one dominants regarding peripheral effects (constriction vs relaxation)?

A

Alpha 1 will usually dominate, i.e. you will see constriction of peripheral blood vessels

70
Q

Epinephrine is considered a potent vasoconstrictor and a cardiac stimulant. What receptors mediate each of these characterizations?

A

Potent vasoconstrictor - Because of alpha 1 stimulation

Cardiac stimulant - Because of beta 1 stimulation

71
Q

Epinephrine can decrease total peripheral resistance. What receptor subtype mediates this action and what is the mechanism?

A

Stimulation of beta 2 receptors in skeletal muscle blood vessels leads to vasodilation

72
Q

What is the effect of NE administration? What receptor subtype won’t be activated?

A

Increases both peripheral resistance and blood pressure. No effect on beta 2 receptors

73
Q

Isoproterenol is considered a potent vasodialator. Why?

A

It will selectively affect the beta receptors, but no vasoconstriction because no alpha 1 activity

74
Q

How will infusion of low dose epinephrine affect HR and MAP, compared to high dose? What receptors mediate its low dose effects?

A

Either dose will increase HR
Low dose will decrease MAP (beta 2), high dose will increase MAP (alpha 1)
Only affects beta receptors

75
Q

Bolus injection of epinephrine can result in a paradoxical immediate drop in MAP. Why?

A

This is a vagal reflex, increasing parasymp. activity

76
Q

Why does NE infusion consistently lead to increased MAP?

A

No stimulation of the beta 2 receptors

77
Q

Clinically used beta agonists for the treatment of hypotensive crisis are _ (3)

A

NE
Phenylephrine
Methoxamine

78
Q

Clinically used beta agonists for the treatment of chronic orthostatic hypotension are _ (2)

A

Midodrine

Ephedrine

79
Q

Clinically used adrenergic agonists for the treatment of shock (1)

A

Dopamine

80
Q

Clinically used adrenergic agonists for the treatment of cardiogenic shock following MI (2)

A

Dopamine, dobutamine

81
Q

Clinically used beta agonists for reducing blood flood during surgery (2)

A

epinephrine, cocaine

82
Q

Clinically used beta agonists for reducing diffusion of local anesthetics (3)

A

Epi, NE, phenylephrine

83
Q

Clinically used beta agonists for the treatment of congested mucus membranes (3)

A

Phenylephrine
Ephedrine
Pseudoephedrine

84
Q

Clinically used beta agonists for the treatment of heart block or cardiac arrest

A

Epinephrine

85
Q

Clinically used beta agonists for the treatment of heart failure

A

Dobutamine

86
Q

Clinically used beta agonists for the treatment of bronchial symptoms (beta 2 selective, (3))

A

MEtaproterenol
Terbutaline
Albuterol

87
Q

Clinically used beta agonists for the treatment of anaphylaxis

A

Epinephrine

88
Q

Clinically used beta agonists for achieving mydriasis

A

Phenylephrine

89
Q

Clinically used beta agonists for relaxing a pregnant uterus

A

Terbutaline

90
Q

Clinically used beta agonists for the treatment of stress incontinence

A

Ephedrine

91
Q

Generally, Alpha 1 and Beta 2 receptors [complement / counteract] each other. What is the exception?

A

Counter act

Intestinal smooth muscle, both cause relaxation

Medical Pharmacology Exam 1 (15 decks)

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