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Pharmacology Test #3 > Pharmacology of Neuromuscular and Ganglionic Blockers > Flashcards

Pharmacology of Neuromuscular and Ganglionic Blockers Flashcards

1
Q

Nicotinic receptor antagonists are also known as

A

ganglionic blockers

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2
Q

Reflexes blocked by nicotinic receptor antagonists/ganglionic blockers

A

baroreceptor reflex and pupillary reflex

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3
Q

Two important ganglionic blocker drugs

A

Trimethaphan and mecamycalamine

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4
Q

Trimethaphan

A

hypotension for surgery

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5
Q

Mecamylamine

A

Tourette’s, smoking cessation, and severe hypertension

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6
Q

In general which is stronger, the PANS tone or the SANS tone

A

the PANS tone, except for regulating the smooth muscles of the vascular system

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7
Q

ganglionic blockade will result in

A

vasodilation and tachycardia

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8
Q

What do neuromuscular blockers do?

A

locally antagonize nicotinic receptors on skeletal muscle in the somatic nervous system

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9
Q

How do neuromuscular blockers block acetylcholine transmission pre-synaptically

A

decrease Ach formation/release, or increase metabolism

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10
Q

How do neuromuscular blockers block acetylcholine transmission post-synaptically

A

block cholinergic receptors (Nm)

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11
Q

Therapeutic use for neuromuscular blockers is primarily

A

to relax skeletal muscle: in surgery, orthopedic procedures, bronchoscopy and for artificial respiration/intubation

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12
Q

How do you monitor neuromuscular blockade with TOF impulses

A

procedures are usually performed when the patient responds with 1-2 twitches, as long as 1 twitch responses is observed the blockade can be quickly reversed, no additional dose of blocker should be given if no twitches are observable

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13
Q

Sequence of muscle paralysis by curare/neuromuscular blocker OD

A

muscles of the eye and those controlling speech are first to relax; fingers, toes then limbs become heavy; intercostals and diaphragm muscles are last; blockade of diaphragm muscles will lead to respiratory depression and eventual death

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14
Q

depolarizing neuromuscular blockers

A

agonist nicotinic acetylcholine receptors; persistent depolarization makes the muscle fiber resistant to further stimulation by ACh

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15
Q

Succinylcholine

A

depolarizing nicotinic acetylcholine receptor agonist - neuromuscular blocker

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16
Q

When is succinylcholine used

A

used in trauma care for intubation; also used for electro-convulsant therapy

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17
Q

What patients should you NOT give succinylcholine to?

A

patients with hyperkalemia as the additional release of potassium by the depolarizing agonist can cuase cardiac arrest

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18
Q

How does succinylcholine (suxamethonium) work?

A

agonist of the NAchR, causing a persistent opening of the channel, thereby preventing repolarization and thus preventing further action potentials from occuring

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19
Q

Non-depolarizing (curare-like) neuromuscular blockers

A

Pancuronium (Pavulon)
Vecuronium (Norcuron)
Atracurium (Tacrium)
Trimethaphan

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20
Q

How does the endogenous neurotransmitter acetylcholine bind

A

as an agonist to nicotine acetylcholinergic receptors; thereby opening the channels are causing an influx of sodium ions

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21
Q

Rocuronium

A

non depolarizing muscle relaxant and antagonist of the NAchR blocking acetylcholine induced activation and blocking nerve transmission

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22
Q

how can you reverse the actions of rocuronium

A

using an Ache inhibitor like neostigmine, which will increase the levels of acetylcholine that can compete with rocuronium or using sugammedex which directly binds and sequesters/scavenges rocuronium

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23
Q

Types of cholinesterases

A

Acetylcholinesterase (AChE) and Plasmacholinesterase (BuChE)

24
Q

Where is AChE and BuchE located?

A

AchE is located in synapses

BuchE is located in the plasma

25
Q

Classes of AchE inhibitors

A

carbamates, organophosphates, quarternary ammonium alcohols

26
Q

Describe carbamates

A

quaternary or teritary amine groups, temporary covalent modification to AChE, reversible and rapid

27
Q

Three important carbamate class AchE inhibitors

A

physostigmine, neostigmine, and pyridostigmine

28
Q

Describe physostigmine

A

tertiary amine and can enter the CNS

29
Q

What is physostigmine used for?

A

used for atropine OD, glaucoma and Alzheimer’s disease

30
Q

What are neostigmine and pyridostygmine used to treat?

A

myasthenia graviis, reversal of neuromuscular blockers and post-operative ileus

31
Q

Why is pyridostygmine better than neostigmine?

A

pyridostygmine is orally available and has a longer duration of action and fewer side effects compared to neostigmine

32
Q

How do organophosphates bind

A

covalently but irreversibly to AchE

33
Q

How has the irreversible nature of organophosphates been exploited?

A

in their use as insecticides and as nerve gas (ex. sarin gas)

34
Q

How can insecticides cause problems in mammals?

A

although they are rapidly inactivated in mammals, high concentrations will still lead to paraysympathomimetic symptoms

35
Q

Primary antidote for organophosphate poisoning?

A

parlidoximine (2-PAM) in combination with atropine

36
Q

Explain why you have to use 2-PAM within a couple of hours after exposure to an organophosphate?

A

after an organophosphate has covalently bonding with AchE it will be further hydrolysed, once this has occured the bond is permanent and cannot be rescued anymore by 2-PAM, this hydrolysis process is known as aging

37
Q

Signs of AchE inhibitor overdose or poisoning

A

DUMBBELSS
diarrhea, urination, miosis, branchospasms, bradycardia, excitation of skeletal muscle and CNS, lacrimation, sweating, salivation

38
Q

Describe edrophonium

A

AchE inhibitor

39
Q

How is edrophonium used?

A

used for the diagnosis of myasthenia gravis

40
Q

Myasthenia gravis

A

autoimmune disease in which antibodies attack nicotinic acetylcholine receptors at the postsynaptic neuromuscular junction

41
Q

Lambert Eaton induced myasthenia gravis

A

antibodies against vg calcium channels

42
Q

What happens when you exercise with myasthenia gravis?

A

exercise worsens muscle strength

43
Q

What happens when you exercise with Lambert Eaton induced myasthenia gravis?

A

exercise improves muscle strength

44
Q

What happens when you give a mysasthenia gravis patient edrophonium?

A

edrophonium improves muscle strength

45
Q

What happens when you give a lambert eaton MG patient edrophonium?

A

edrophonium has no effect/small increase in muscle strength

46
Q

What happens when you give edrophonium in a patient experiencing a cholinergic crisis?

A

edrophonium has no effect/small decrease in muscle strength

47
Q

What is a cholinergic crisis?

A

ex) overdose of Ache inhibitor

overstimulation -> paralysis -> weak muscles

48
Q

Contraindications to the use of parasympathomimetic drugs?

A

asthma/COPD; coronary deficiency; peptic ulcer; obstruction of the urinary or GI tract; epilepsy

49
Q

Cholinergic (Ach) centers in the CNS

A

nucleus basalis of meynert; medial septal nuclei; mesopontine tegmentum (brainstem)

50
Q

Adrenergic (NE) centers in the CNS

A

locus ceruleus (pons-brainstem)

51
Q

Degernation of the cholinergic cells in the nucleus basalis occurs in what?

A

dementia and PD (identified by Lewy bodies)

52
Q

Alzheimer’s disease

A

most common cause of dementia after age 50; atrophy of the brain, widening of sulci and thinning of gyri; senile plaques, neurofibrillary tangles

53
Q

Reversible AchE inhibitors that are used in managing symptoms of Alzheimer’s

A

donepezil, rivastigmine, galanthamine

54
Q

Rivastigmine

A

reversible carbamate AChE inhibitor, enhances cognitive ability in AD by increasing cholinergic function

55
Q

Galanthamine

A

reversible competitive AChE inhibitor; extract from daffodil bulbs; loses effectiveness as AD progresses

Pharmacology Test #3 (13 decks)

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