Drugs Cholinoceptor blockers Flashcards

1
Q

Cholinoceptor blockers also called

A

Parasympatholytics/plegics

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2
Q

Two type of Parasympatholytics

A

Antimuscarinic

Antinicotinics

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3
Q

Name drugs that are antimuscarinic

A

Atropine
Scopolamine
Tropicamide
Ipratromine

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4
Q

name Depolarizing antinicotinic muscle relaxers

A

Succinylcholine and acetylcholine

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5
Q

name Non-depolarizing antinicotinic muscle relaxers

A

Derivatives of curare

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6
Q

cholineceptor blockers are agonist or antagonists

A

antagonists

antimuscarinic or antinicotinic

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7
Q

what are the 2 types of nicotinic antagonist (antinicotinic)

A

1) ganglion blockers

2) NMJ blockers(muscle relaxers)

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8
Q

what do ganglion blockers do and what category are they. why arent they used much?

A

category–> antinicotinic; nicotinic antagonist

not used much bc affect both SNS and PNS bc target all nicotinic receptors–> nicotinic neuronal and nicotinic muscular

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9
Q

difference between nicotinic neuronal and nicotinic muscular receptors

A

NN–> found in the CNS so both SNS and CNS; involved in communication btw post and preganglionic neurons
-have beta and alpha receptors
-THINK NEURAL SIGNALING WITH ANS AND CNS

NM–> located in the NMJ of skeletal muscle so communication btw neurons and muscle fibers
-Ach binding to these leads to muscle contraction
-THINK SKELETAL MUSCLE CONTRACTION

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10
Q

how do NMJ blockers work

A

also called muscle relaxers; block n-Ach at neuromuscular endplate so block Ach from binding and blocks muscle contraction

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11
Q

name the 2 different types of muscle relaxants

A

also called NMJ blockers

depolarizing(agonist) and non depolarizing(antagonist)

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12
Q

how do depolarizing muscle relaxants work

A

antinicotinic receptors so depolarizes muscle endplate so cell not able to receive the Ach and contract then relax(tetanus)–> instead just get one contraction then not able to repolarize to contract again

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13
Q

describe how succinylcholine works and what it is

A

depolarization acetylcholine muscarinic receptor AGONIST because bind to mAch

really good agonist bc does not get broken down at the NMJ; instead gets broken down in the plasma very fast(10 minutes)

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14
Q

describe the difference between succinylcholine phase 1 and phase 2 block

A

Phase 1 block- bind to receptor and causes continuous depolarization which causes relaxation. Lack of repolarization

Phase 2 Block(deeper block)- give drug for extended amount of time then muscle not reacting well to it and you will get repolarization

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15
Q

how do nondepolarization muscle relaxants work

A

competitive antagonist bc block Ach from binding so no signal

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16
Q

excessive concentration of nondepolarizing NMJ blockers cause what

A

a channel blockade so get a paralyzed patient

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17
Q

what is the reversal of nondepolarization NMJ blockers

A

sugammadex–> surrounds drug so cannot interact with receptor

neostigmine–> make more acetylcholine available

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18
Q

use of depolarizing NMJ blockers

A

intubation and used to use it for electroconvulsion therapy

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19
Q

where and when was curare found

A

frogs in the rainforest in 1930s

20
Q

signs and symptoms of depolarization NMJ blockers

A

fasciculation (1st twitch then relaxation), muscle pain, HYPERKALEMIA, malignant hyperthermia, and apnea

21
Q

how long do nondepolarizing NMJ last

A

there is short acting, intermediate acting, and long acting

22
Q

hypo or hyper kalemia is a s/s of deporalizing muscle relaxants

A

hyperkalemia

23
Q

why is malignant hyperthermia a s/s from depolarizing muscle relaxants

A

from the excess amounts of muscle activity

24
Q

antimuscarinic prototype

A

atropine–> blocking acetylcholine at the mAch receptor so we are inhibiting muscarinic response aka antimuscarinic

25
Q

what kind of antagonist are atropine and scopolamine

A

competitive antagonist so can be outcompeted if more acetylcholine

26
Q

where does atropine come from

A

plant based alkaline–> belladona plant–> means beautiful italian bc women would crush these berries and put them on their eyelids to block constriction so would make them dilate

27
Q

atropine is given as a ___

A

Racemic Isomer;

L is from the plant and is more potent than D isomer

28
Q

why and when would you give atropine

A

ONLY given for muscarinic overdose/excess

ppl in army took atropine during gas attacks

29
Q

when do you not give atropine and why

A

closed angle glaucoma bc no drainage in the canal of schlemm and if you give atropine we are dilating the eye and this puts pressure on the ocular nerve and person can go blind

30
Q

describe scopolamine

A

antimuscarinic similar to atropine but safer and lipid soluble so can go into CNS and affect our vomiting centers

31
Q

what is scopolamine used for

A

motion sickness

32
Q

indications for scopolamine

A

anytime we have an overproducting PNS and want to block it–> not activating sympathetic response just blocking it

GI/GU motion sickness, ophthalmic, respiratory disorders, bradycardia, parkinsons

33
Q

do antimuscarinic stimulate a SNS response

A

no; we are just blocking the PNS response

34
Q

describe atrovent

A

antimuscarinic

atrovent for bronchodilation during bronchospasm(usually during COPD)

35
Q

how does atropine increase HR

A

by blocking the vagus nerve

36
Q

describe why you see small dip in HR before you see increase in HR with atropine

A

with small doses of atropine you see a small dip first and the theory is that more mAch receptors at the presynaptic than at the target postsynaptic

37
Q

why do you see increase salivation first before you see decreased secretions with antimuscarinics like atropine

A

same theory for the heart–> more mAch receptors at the presynaptic than postsynaptic

38
Q

atropine/antimuscarinic response in respiratory secretions and GI activity

A

reduce respiratory secretions and block GI activity

39
Q

atropine effects in the eye

A

block SNS effect so see dilation

40
Q

describe what happens when we dilate the eye with atropine

A

when we dilate the eye we get cycloplegia–> paralyzing the ciliary muscle so we are not able to accommodate by switching from near and far vision

also get decreased watering bc decreased secretions

41
Q

what is the ciliary muscle

A

it holds the lens in place so we are able to switch from near to far vision

42
Q

with atropine eye accommodation increases or decreases

A

decreases so sensitive to sun light

43
Q

tropicamide is what type of atropine

A

short acting atropine so dilate the eye for 4 hours

also get decreased watering bc decreased secretions

44
Q

describe overall atropine effects

A

decreased–> salivation, micturition speed(urination) and accommodation

increased HR

45
Q

describe atropine contraindication with elderly men

A

elderly men with known prostatic hyperplasia and given atropine then worsening of prostate gland swelling so even more decreased urination which can lead to urinary retention