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

Pharmacology - Autonomics IV-V-VI Flashcards

(96 cards)

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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
Class: Ergotamine
Ergot alkaloid | alpha-adrenergic blocker BUT alpha-agonist??
26
Class: Ergonovine
Ergot alkaloid | alpha-adrenergic blocker BUT alpha-agonist??
27
Use: Ergonovine
to treat post-partum hemorrhage | "oxytocic"
28
Use: Ergotamine
to treat prodrome of migraines
29
Side Effects: Ergot alkaloids
Hallucinations (like LSD)
30
Use: Bromocriptine
Treat hyperprolactinemia; Treat Parkinsonianism DA2 agonist
31
Beta-1 selective agonist for cardiac stimulation
Dobutamine | also used during cardiac stress test
32
first generation beta blocker | non-selective
propranolol | non-seletive
33
second generation beta blocker | beta-1 selective
metoprolol | atenolol
34
third generation beta blocker | non-selective with additional actions
carvedilol | labetalol
35
third generation beta blocker | beta-1 selective with additional actions
betaxolol
36
plasma half life of metoprolol
about 4 hours | Metoprolo is a beta-1 selective 2nd generation beta blocker
37
plasma half life of atenolol
about 6-8 hours Atenolol is the least lipid soluble beta blocker, thus not in CNS; beta-1 selective second generation beta blocker
38
Use: Labetolol
to treat hypertension lowers TPR with little tachycardia 3rd generation - beta blocker with additional actions (ie some alpha-1 antagonism)
39
Use: Carvedilol
to treat HTN and CHF; | 3rd generation - beta blocker with additional actions (ie some alpha-1 antagonism)
40
Third generation beta blocker "additional actions" include:
``` NO production beta-2 agonism Ca entry blockade alpha-1 antagonism K channel opening antioxidant activity ```
41
Therapeutic uses of beta-blockers in general include:
``` Cardiac arrhythmias Angina Glaucoma Migraine Anxiety/stage fright Heart failure HTN ```
42
Use ONLY what kind of beta-blockers to treat heart failure?
2nd and 3rd generation
43
Too much stimulation of what receptor may precipitate an asthma attack?
Beta-2
44
Phentolamine Phenoxybenzamine Prazosin these drugs are all:
alpha receptor antagonists
45
What are the major side effects of alpha-reeptor antagonists?
tachycardia; | postural hypotension
46
Which alpha-receptor antagonist covalently binds to alpha-1 receptors?
Phenoxybenzamine | therefore, long-acting
47
Which alpha-receptor antagonists are nonselective, in that they affect alpha-1 and alpha-2?
Phentolamine Phenoxybenzamine **Prazosin is selective for alpha-1
48
Therapeutic use: Prazosin
HTN Peripheral vascular disease (including Raynaud's and frostbite and atherosclerosis) BPH
49
Therapeutic use: Phenoxybanzamine
Pheochromocytoma; | Peripheral vascular disease (including Raynaud's and frostbite);
50
Phentolamine and Phenoxybenzamine have what unfortunate sexual side effect?
Inhibit ejaculation
51
Therapeutic use: Phentolamine
Pheochromocytoma; | Peripheral vascular disease (including Raynaud's and frostbite);
52
Beta-2 blockers may not be appropriate for which patient population?
Diabetics | bc there can be a decrease in glycogenolysis and lipolysis in response to hypoglycemia
53
MOA: alpha-methyltyrosine
blocks synthesis of DA and NE by inhibiting tyrosine hydroxylase
54
Use: alpha-methyltyrosine
Mgmt of pheochromocytoma | Side effects are "many and serious"
55
MOA: Reserpine
Release of empty vesicles (NE is not taken into vesicles b/c it binds uptake transporter and stops it)
56
Class: alpha-methyltyrosine reserpine guanethidine
nerve ending blocker
57
MOA: guanethidine
``` False neurotransmitter (vesicles become full of guanethidine rather than NE) --CNS shooting blanks essentially ```
58
Use: guanethidine
HTN Side effects are "many and serious" not commonly used clinically
59
What is one major side effect of Reserpine and a reason it is not commonly used clinically?
depression/suicide
60
MOA: cocaine
prevents NE uptake
61
Use: cocaine
Local anesthetic, vasoconstrictor
62
Side effects: cocaine
insomnia anxiety arrhythmia
63
NE acts on what receptors?
alpha-1 alpha-2 beta-1
64
Therapeutic use: NE
treat hypotension NE vasoconstricts, increases BP and HR
65
Epinephrine acts on what receptors?
alpha-1 alpha-2 beta-1 beta-2
66
Therapeutic use: Epinephrine
anaphylactic shock; glaucoma Epinephrine increases HR and contractility, BP
67
Use: Isoproterenol
non-selective beta agonist: asthma shock heart block Isoproterenol decreases resistance, increases CO, increases HR and bronchodilates
68
Side effects: Isoproterenol
Palpitations tachyarrhymias headache
69
Therapeutic uses: dobutamine
cardiac decompensation shock heart block Dobutamine increases contractility, increases HR directly and indrectly
70
Side Effects: Dobutamine
Tachyarrhythmia | HTN
71
beta-2 selective agonists, name 2:
albuterol | terbutaline
72
Therapeutic uses: Albuterol Terbutaline
asthma COPD Albuterol and Terbutaline relax bronchial and uterine smooth muscle
73
Side Effects: Albuterol Terbutaline
Tachycardia | Muscle tremor
74
Uses: Phenylephrine
Nasal congestion Postural hypotension Phenylephrine is a vasoconstrictor
75
Side effects: Phenylephrine
Reflex bradycardia | HTN
76
Therapeutic use: Clonidine alpha-methyldopa (prodrug)
HTN shock withdrawal from drug dependence Actions: decrease sympathetic outflow from CNS, decrease resistance
77
Side effects: Clonidine alpha-methyldopa (prodrug)
Sedation
78
Side effects: Fenoldopam
Posturalhypotension
79
Uses: amphetamine
ADHD Narcolepsy recreational CNS stimulation, increase BP, increase HR
80
Side effects: amphetamine
Insomnia HTN anxiety arrhythmias
81
MOA: amphetamine
indirect acting release of NE
82
Uses: Dopamine
shock renal failure hypotention Actions: vasodilation, increase GFR, increase HR, increase BP
83
Side effects: dopamine
vasoconstriction at high doses
84
Give the agonist and antagonist for beta-1 receptor:
Agonist: Dobutamine Antagonist: Atenolol
85
Give the agonist and antagonist for non-selective beta-1 and 2 receptors:
Agonist: Isoproterenol Antagonist: Propranolol
86
An alternative to propranolol, that is also a non-selective beta antagonist, is:
Timolol
87
Uses: Propranolol Timolol
HTN Angina Arrythmias
88
Side effects: Propranolol Timolol
Bradycardia Bronchoconstriction sexual dysfunction
89
Give the agonist and antagonist for alpha-1 receptor:
Agonist: Phenylephrine Antagonist: Prazosin
90
Therapeutic use: Betaxolol
CHF HTN Side effects: bradycardia
91
MOA Terazosin
vasodilatory effect via block of a1 receptors, leading to a reflex tachycardia
92
MOA Atropine
Atropine would lead to block of cholinergic M3 receptors
93
BPH is often managed with:
BPH is often managed with alpha blockers ie Prazosin Terazosin
94
MOA alpha-methyltyrosine
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
Labetalol is:
a non-selective beta-blocker with additional α1 antagonist properties. "third generation"
96
Therapeutic Use: Ipratroprium
COPD, asthma | antimuscarinic

MS 2 - Unit 2 (26 decks)

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