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MS 2 - Unit 2 > Pharmacology - Autonomics IV-V-VI > Flashcards

Pharmacology - Autonomics IV-V-VI Flashcards

1
Q

Effect of alpha-1 adrenergic receptor

A

increase in IP3, DAG

smooth muscle contraction

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2
Q

Effect of beta-1 adrenergic receptor

A

increase force and rate of contraction of heart
increase cAMP
increased renin secretion in kidney

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3
Q

Effect of beta-2 adrenergic receptor

A

increase cAMP

smooth muscle relaxation

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4
Q

Effect of beta-3 adrenergic receptor

A

increase cAMP

lipolysis

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5
Q

What is the primary mechanism for reducing/terminating the effects of NE?

A

re-uptake;

repackaged for future release

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6
Q

Monoamine oxidase (MAO) and Catechol-O-Methyltransferanse break down what?

A

NE, Epi, exogenous adrenergic drugs ie tyramine
major metabolic enzymes;
prominent in liver

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7
Q

Elevated levels of plasma metanephrine is an indicator of:

A

Pheochromocytoma

Metanephrine is a metabolite of NE/E

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8
Q

Non-selective beta-1 and 2 antagonist

A

Propranolol

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9
Q

Non-selective beta-1 and 2 agonist

A

Isoproterenol

**most potent agonist of beta-1 and 2

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10
Q

Beta-2 agonist

A

Albuterol

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11
Q

D1 agonist

A

Fenoldopam
dopamine receptor agonist
**does not cause NE release - just acts on D1

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12
Q

Alpha-2 selective agonist

A

Clonidine

**most potent agonist of alpha-2

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13
Q

Alpha-1 selective agonist

A

Phenylephrine

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14
Q

Alpha-1 antagonist

A

Prazosin

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15
Q

Beta-1 antagonist

A

Atenolol

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16
Q

Vasculature have both alpha-1 and beta-2 receptors. Which dominates?

A

Effects of alpha-1 (constriction) are dominant

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17
Q

Dopamine acts on what receptors?

A

DA
alpha-1
beta-1

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18
Q

What is the most potent stimulator of alpha-2?

A

Epinephrine

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19
Q

Tyramine and amphetamine are what kinds of adrenergic drugs?

A

Indirect agonists - cause release of NE

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20
Q

Ephedrine and Hydroxyamphetamine are what kinds of adrenergic agents?

A

Mixed (direct and indrect effects) agents

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21
Q

Uses: Fenoldopam

A

to treat a hypertensive emergency, anuria
to increase blood flow at renal, mesenteric and cerebral arteries;
to lower blood pressure (hypertensive emergencies)

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22
Q

Uses: Epinephrine

A

control hemorrhage;
vasoconstriction in dental procedures
alpha-1

anaphylactic shock alpha and beta activation - vasoconstriction, bronchodilation and decrease histamine release from mast cells (beta-2)

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23
Q

Uses: Ephedrine, Phenylephrine

A

Nasal decongestions

alpha-1

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24
Q

Uses: Dopamine

A

treat hypotension ie to replace adrenal catecholamines like with spinal anesthesia, following pheochromocytoma surgery

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25
Q

Class: Ergotamine

A

Ergot alkaloid

alpha-adrenergic blocker BUT alpha-agonist??

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26
Q

Class: Ergonovine

A

Ergot alkaloid

alpha-adrenergic blocker BUT alpha-agonist??

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27
Q

Use: Ergonovine

A

to treat post-partum hemorrhage

“oxytocic”

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28
Q

Use: Ergotamine

A

to treat prodrome of migraines

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29
Q

Side Effects: Ergot alkaloids

A

Hallucinations (like LSD)

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30
Q

Use: Bromocriptine

A

Treat hyperprolactinemia;
Treat Parkinsonianism
DA2 agonist

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31
Q

Beta-1 selective agonist for cardiac stimulation

A

Dobutamine

also used during cardiac stress test

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32
Q

first generation beta blocker

non-selective

A

propranolol

non-seletive

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33
Q

second generation beta blocker

beta-1 selective

A

metoprolol

atenolol

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34
Q

third generation beta blocker

non-selective with additional actions

A

carvedilol

labetalol

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35
Q

third generation beta blocker

beta-1 selective with additional actions

A

betaxolol

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36
Q

plasma half life of metoprolol

A

about 4 hours

Metoprolo is a beta-1 selective 2nd generation beta blocker

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37
Q

plasma half life of atenolol

A

about 6-8 hours
Atenolol is the least lipid soluble beta blocker, thus not in CNS;
beta-1 selective second generation beta blocker

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38
Q

Use: Labetolol

A

to treat hypertension
lowers TPR with little tachycardia
3rd generation - beta blocker with additional actions (ie some alpha-1 antagonism)

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39
Q

Use: Carvedilol

A

to treat HTN and CHF;

3rd generation - beta blocker with additional actions (ie some alpha-1 antagonism)

40
Q

Third generation beta blocker “additional actions” include:

A 
NO production
beta-2 agonism
Ca entry blockade
alpha-1 antagonism
K channel opening
antioxidant activity
41
Q

Therapeutic uses of beta-blockers in general include:

A 
Cardiac arrhythmias
Angina
Glaucoma
Migraine
Anxiety/stage fright
Heart failure
HTN
42
Q

Use ONLY what kind of beta-blockers to treat heart failure?

A

2nd and 3rd generation

43
Q

Too much stimulation of what receptor may precipitate an asthma attack?

A

Beta-2

44
Q

Phentolamine
Phenoxybenzamine
Prazosin
these drugs are all:

A

alpha receptor antagonists

45
Q

What are the major side effects of alpha-reeptor antagonists?

A

tachycardia;

postural hypotension

46
Q

Which alpha-receptor antagonist covalently binds to alpha-1 receptors?

A

Phenoxybenzamine

therefore, long-acting

47
Q

Which alpha-receptor antagonists are nonselective, in that they affect alpha-1 and alpha-2?

A

Phentolamine
Phenoxybenzamine

**Prazosin is selective for alpha-1

48
Q

Therapeutic use: Prazosin

A

HTN
Peripheral vascular disease (including Raynaud’s and frostbite and atherosclerosis)
BPH

49
Q

Therapeutic use: Phenoxybanzamine

A

Pheochromocytoma;

Peripheral vascular disease (including Raynaud’s and frostbite);

50
Q

Phentolamine and Phenoxybenzamine have what unfortunate sexual side effect?

A

Inhibit ejaculation

51
Q

Therapeutic use: Phentolamine

A

Pheochromocytoma;

Peripheral vascular disease (including Raynaud’s and frostbite);

52
Q

Beta-2 blockers may not be appropriate for which patient population?

A

Diabetics

bc there can be a decrease in glycogenolysis and lipolysis in response to hypoglycemia

53
Q

MOA: alpha-methyltyrosine

A

blocks synthesis of DA and NE by inhibiting tyrosine hydroxylase

54
Q

Use: alpha-methyltyrosine

A

Mgmt of pheochromocytoma

Side effects are “many and serious”

55
Q

MOA: Reserpine

A

Release of empty vesicles (NE is not taken into vesicles b/c it binds uptake transporter and stops it)

56
Q

Class:
alpha-methyltyrosine
reserpine
guanethidine

A

nerve ending blocker

57
Q

MOA: guanethidine

A 
False neurotransmitter (vesicles become full of guanethidine rather than NE)
--CNS shooting blanks essentially
58
Q

Use: guanethidine

A

HTN
Side effects are “many and serious”
not commonly used clinically

59
Q

What is one major side effect of Reserpine and a reason it is not commonly used clinically?

A

depression/suicide

60
Q

MOA: cocaine

A

prevents NE uptake

61
Q

Use: cocaine

A

Local anesthetic, vasoconstrictor

62
Q

Side effects: cocaine

A

insomnia
anxiety
arrhythmia

63
Q

NE acts on what receptors?

A

alpha-1
alpha-2
beta-1

64
Q

Therapeutic use: NE

A

treat hypotension

NE vasoconstricts, increases BP and HR

65
Q

Epinephrine acts on what receptors?

A

alpha-1
alpha-2
beta-1
beta-2

66
Q

Therapeutic use: Epinephrine

A

anaphylactic shock;
glaucoma

Epinephrine increases HR and contractility, BP

67
Q

Use: Isoproterenol

A

non-selective beta agonist:
asthma
shock
heart block

Isoproterenol decreases resistance, increases CO, increases HR and bronchodilates

68
Q

Side effects: Isoproterenol

A

Palpitations
tachyarrhymias
headache

69
Q

Therapeutic uses: dobutamine

A

cardiac decompensation
shock
heart block

Dobutamine increases contractility, increases HR directly and indrectly

70
Q

Side Effects: Dobutamine

A

Tachyarrhythmia

HTN

71
Q

beta-2 selective agonists, name 2:

A

albuterol

terbutaline

72
Q

Therapeutic uses:
Albuterol
Terbutaline

A

asthma
COPD

Albuterol and Terbutaline relax bronchial and uterine smooth muscle

73
Q

Side Effects:
Albuterol
Terbutaline

A

Tachycardia

Muscle tremor

74
Q

Uses: Phenylephrine

A

Nasal congestion
Postural hypotension

Phenylephrine is a vasoconstrictor

75
Q

Side effects: Phenylephrine

A

Reflex bradycardia

HTN

76
Q

Therapeutic use:
Clonidine
alpha-methyldopa (prodrug)

A

HTN
shock
withdrawal from drug dependence

Actions: decrease sympathetic outflow from CNS, decrease resistance

77
Q

Side effects:
Clonidine
alpha-methyldopa (prodrug)

A

Sedation

78
Q

Side effects: Fenoldopam

A

Posturalhypotension

79
Q

Uses: amphetamine

A

ADHD
Narcolepsy
recreational

CNS stimulation, increase BP, increase HR

80
Q

Side effects: amphetamine

A

Insomnia
HTN
anxiety
arrhythmias

81
Q

MOA: amphetamine

A

indirect acting release of NE

82
Q

Uses: Dopamine

A

shock
renal failure
hypotention

Actions:
vasodilation, increase GFR, increase HR, increase BP

83
Q

Side effects: dopamine

A

vasoconstriction at high doses

84
Q

Give the agonist and antagonist for beta-1 receptor:

A

Agonist: Dobutamine
Antagonist: Atenolol

85
Q

Give the agonist and antagonist for non-selective beta-1 and 2 receptors:

A

Agonist: Isoproterenol
Antagonist: Propranolol

86
Q

An alternative to propranolol, that is also a non-selective beta antagonist, is:

A

Timolol

87
Q

Uses:
Propranolol
Timolol

A

HTN
Angina
Arrythmias

88
Q

Side effects:
Propranolol
Timolol

A

Bradycardia
Bronchoconstriction
sexual dysfunction

89
Q

Give the agonist and antagonist for alpha-1 receptor:

A

Agonist: Phenylephrine
Antagonist: Prazosin

90
Q

Therapeutic use: Betaxolol

A

CHF
HTN

Side effects: bradycardia

91
Q

MOA Terazosin

A

vasodilatory effect via block of a1 receptors, leading to a reflex tachycardia

92
Q

MOA Atropine

A

Atropine would lead to block of cholinergic M3 receptors

93
Q

BPH is often managed with:

A

BPH is often managed with alpha blockers
ie Prazosin
Terazosin

94
Q

MOA alpha-methyltyrosine

A

Alpha-methyltyrosine blocks tyrosine hydroxylase and would cause a depletion of norepinephrine (and dopamine and epinephrine) stores. This effectively produces a chemical sympathectomy, resulting in post-synaptic receptor up-regulation; thus, producing a
denervation supersensitivity.

95
Q

Labetalol is:

A

a non-selective beta-blocker with additional α1 antagonist properties.
“third generation”

96
Q

Therapeutic Use: Ipratroprium

A

COPD, asthma

antimuscarinic

MS 2 - Unit 2 (26 decks)

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