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Unit 4 > ANS drugs > Flashcards

ANS drugs Flashcards

1
Q

Where parts of spinal cord do symp and parasymp originate?

A

Symp—>thoracolumbar

Parasymp—>cranial sacral part

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2
Q

All ANS start with ___ neurotransmitter and the synapse at ___ receptor?

A

ACh/nicotinic receptor

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3
Q

Where do you find Nm receptor?

A

Skeletal muscle

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4
Q

What are the 2 exceptions for symp that do not use epi or norepi?

A 
Sweat gland (ACh)
Adrenal medulla--->recieve ACh--->produce epi
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5
Q

D1 receptor stimulation at the kidney causes?

A

Renal vasodilation

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6
Q

TPR or CO has a greater influence on BP?

A

TPR

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7
Q

Which 3 receptors control constriction or dilation of the blood vessels?

A

Alpha 1—>vasoconstrict
Beta 2—>vasodilate
M3—>vasodilate via NO

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8
Q

What if you give alpha 1 agonist with M antagonist?

A

Increase BP without reflex bradycardia

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9
Q

What if you give beta 2 agonist and a beta 1 antagonist?

A

Decrease BP without reflex tachycardia

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10
Q

What kind of drug block both reflex tachy and bradycardia?

A

Nn blocker—>hexamthonium/mecamylamine

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11
Q

What are the 2 receptor that cause brady or tachycardia?

A

Beta 1—>tachy

M2—>brady

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12
Q

What are parasymp/symp affect on the eye?

A

Parasymp—>sphincter (M)—>miosis
Parasymp—>ciliary muscle (M)—>accommodate to near sight
Symp—>radial muscle (alpha 1)—->mydriasis

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13
Q

How do you cause cycloplegia (paralysis of accommodation)?

A

anti M

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14
Q

How is ACh produced?

A

Choline uptake—>choline + acetyl CoA—(choline acetyl transferase)—>ACh

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15
Q

Which drug block the uptake of choline?

A

Hemicholinium

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16
Q

AChE inhibitor can only work on ___ organs?

A

innervated

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17
Q

Where are M1/2/3 located?

A

M1—>CNS
M2—>heart
M3—>peripheral

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18
Q

M stimulation at LES cause constriction or relaxation?

A

Constriction

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19
Q

Which M3 receptor is not innervated in your body?

A

M3 on blood vessel that does vasodilation through NO

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20
Q

Anti M would produce what kind of affect for M3 on blood vessel?

A

It would inhibit M3 on blood vessel but it would do nothing to the blood vessel since M3 is not innervated (thus no agonist to compete with)

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21
Q

M agonist and AChE inhibitor usually produce the same affect except for one place?

A

M3 on blood vessel—>AChE inhibitor has no effect there

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22
Q

What organs are only innervated by symp?

A

Sweat gland/blood vessels

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23
Q

AChE inhibitor activate both symp and parasymp, but why does it look like it’s mainly parasymp?

A

Parasymp is the dominate force

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24
Q

What are the 4 M agonist drugs?

A

Bethanechol/methocholine/cevimeline/pilocarpine

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25
Q

Which AChE inhibitor can cross the BBB?

A

Physostigmine (3rd ammine)

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26
Q

Neuromuscular blockade and myasthenia gravis have what in common?

A

They both work on Nm receptor

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27
Q

What’s the rationale behind treating Alzheimer’s with AChE inhibitor?

A

Alzheimer’s—>lost of cholinergic nerve in Meynert’s nucleus

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28
Q

Emesis is mediated by which M receptor?

A

M1

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29
Q

Why is organophosphate fatal?

A

Permanent depolarization of diaphragm—>inhibiting breathing

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30
Q

Why do we need to be careful on using antimuscarinic on elderly pt?

A

Precipitate elderly pt for glaucoma

31
Q

What are some other group of drugs that are antimuscarinic?

A

1st generation antihistamine/TCA/low potency typical antipsychotic/quinidine/amantadine (antiparkingson)/meperidine (opioid)

32
Q

List some antimuscarinic drugs

A

“trop” and “scop”

Atropine/Tropicamide/Ipratropium/Tiotropium/Scopolamine/

33
Q

What is Oxybutynin used for?

A

Antimuscarinic—>urge incontinence

34
Q

If a pt who is on pyridostigmine for myathenia gravis also takes atropine for side effect, would it interfere with pyridostigmine?

A

No—>Myathenia gravis has antibodies against Nm receptor—>atropine is M antagonist so it does not affect Nm

35
Q

How is norepi produced?

A

Tyrosine—(tyrosine hydroxylase)—>dopa—>[dopamine—>norepi]
Last step takes place in storage vesicle

36
Q

What are the rate limiting step for ACh and norepi production?

A

Uptake of choline/tyrosine hydroxylase

37
Q

How is norepi being taken out of the synaptic cleft once released?

A

COMT degrade norepi/norepi reuptake

38
Q

What does MAO-A do?

A

It degrades norepi when norepi is reuptaken into the presynaptic neuron

39
Q

What are the mechanism of amphetamine/TCA/cocaine

A

Amphetamine—>promote releasing of NE

TCA/cocaine—>prevent reuptake of NE

40
Q

What do AMPT/clonidine/alpha methyldopa/reserpine/guanethidine do?

A

They all decrease NE release
AMPT—>tyrosine hydroxylase inhibitor
Clonidine/alpha methyldopa—>alpha 2 agonist
Reserpine—>destroy storage vesicle
Guanethidine—>replace NE in the vesicle (release wrong things)

41
Q

Where do alpha 1 receptor found in your body?

A

Radial muscle of the eye/blood vessels/bladder (stimulate—>contract—>urinary retention)/kidney (decrease renin release)

42
Q

Where do alpha 2 receptor found in your body and what happens if you stimulate them?

A

Presynaptic nerve terminal/platelets (aggregation)/pancreas (decrease insulin secretion)

43
Q

Stimulate what receptor cause increase renin release?

44
Q

What are the effect of increase cAMP on skeletal and smooth muscle?

A

Skeletal muscle—>contract

Smooth muscle—>relax

45
Q

What is special about beta 2 receptors and where are they found?

A 
They are mostly not innervated (thus activated by epi)
Blood vessel (vasodilate)/uterus (relax)/branchioles (dilation)/skeletal muscle (contract)
46
Q

What would happen to skeletal muscle if you take too much beta 2 agonist for asthma?

A

Muscle tremor (skeletal muscle has beta 2)

47
Q

What are the metabolic affects of beta 2 receptor?

A

If stimulated—>increase glycogenolysis—>increase blood glucose
increase insulin secretion

48
Q

What happens when you stimulate D1 receptor?

A

Increase renal perfusion—>increase GFR and Na secretion

49
Q

What is dose dependent character of dopamine?

A

Low dose stimulate D1—>medium dose beta 1—>high dose alpha 1

50
Q

What is fenoldopam used for?

A

D1 agonist for severe HTN

51
Q

Between beta and alpha receptor, which one would be activated first in terms of doses?

A

Beta (low)—>alpha (high)

52
Q

Which drug is a alpha 1 agonist? what does it used for?

A

Phenylephrine

Nasal decongestant/eye exam (dilate pupil)

53
Q

Stimulation of what receptor increase pulse pressure?

A

Beta 1 (decrease diastolic pressure)

54
Q

What are the nonselective beta agonist/beta 1 agonist/beta 2 agonist?

A 
Nonselective--->isoproterenol (iso=same)
Beta 1--->dobutamine--->HF
Beta 2: bronchodilator 
Albuterol
Terbutaline--->also used to relax uterus during labor (prevent preterm labor)
55
Q

What receptors do NE work on? what is its affect on the heart?

A

Alpha 1/alpha 2/beta 1 only (Beta 2 is not innervated)

Increase HR but then decrease (due to reflex bradycardia responding to increase BP caused by alpha 1)

56
Q

What receptors do epi work on?

A

Alpha1/2 beta1/2

57
Q

What are the affect of low and high dose epi?

A

Low dose—>same as isoproterenol (only beta1/2)

High dose—>same as norepi (mainly alpha1/beta1)

58
Q

How to distinguish between norepi and high dose epi?

A

Give alpha 1 blocker
Norepi—>BP goes back to normal
Epi—>BP goes below normal because of beta 2 affect

59
Q

Which one (epi or norepi) is used for anaphylaxis shock?

60
Q

What does tyramine (cheese and wine) do?

A

Degraded by MAO-A

If taken MAOi—>tyramine increase NE release like amphetamine—>HTN crisis

61
Q

What do MAO-A/B metabolize and where are they found?

A

MAO-A—>metabolize NE/5-HT/tyramine (found Anywhere)

MAO-B—>dopamine (Brain)

62
Q

Indirect adreoceptor agnoist (e.g. amphetamine/cocaine) can only work on what kind of tissue?

A

Innervated

63
Q

Why is reflex tachycardia worse with nonselective alpha blocker?

A

Blocking alpha 2 as well—>block an inhibitor—>increase NE activity—>worsen reflex tachycardia

64
Q

What are the 2 non selective alpha blockers and which one is the competitive and which one is the noncompetitive inhibitor? and what are they used for?

A

Phentolamine—>competitive
Phenoxybenzamine—>noncompetitive (longer name)
They are used for pheochromocytoma

65
Q

What are the alpha 1 blockers and what do they do?

A

“zosin” —>HTN and BPH

Tamsulosin—>alpha 1a receptor blocker—>BPH only

66
Q

What is the alpha 2 blocker?

A

Mirtazapine—>antidepressant

67
Q

What are some affects of beta 2 blockade?

A

Bronchospasm/decrease aqueous humor production/decrease glucose/increase LDLs and TGs (prevent breakdown)

68
Q

How to distinguish beta 1 or non selective beta blockers?

A

start with A-M—>beta 1 blocker only

N-Z—>non selective

69
Q

What are 2 beta blockers that are also partial agonists?

A

Acebutolol and pindolol/they do not increase LDL and TG

70
Q

What should we be cautious about pt who is on chronic beta blocker?

A

Don’t abruptly stop the beta blocker

71
Q

What can you give with beta blocker overdose?

A

Glucagon (increase cAMP to oppose beta blocker)

72
Q

What are selective and nonselective beta blocker most commonly used for?

A

Selective–>HTN/angina/anti arrhythmia

Nonselective—>glaucoma/migraine prevention/thryotoxicosis/performance anxiety/essential tremor

73
Q

What is special about carvedilol and labetalol?

A

Nonselective beta blocker and alpha 1 blocker

Treat HTN and CHF

74
Q

What is sotalol?

A

Nonselective beta block + K+ channel blocker (class III anti arrhythmia)

Unit 4 (28 decks)

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