M2 L3: parasympathetic NS Flashcards

1
Q

parasympathomimetic agents

A

=cholinergics, cholinomimetics, cholinoceptor activating drugs
stim PSNS

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2
Q

parasympatholytic agents

A

= anticholinergics, anti parasympathomimetics
inhibit PSNS

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3
Q

what does indirect acting drugs do to AChE enzyme activity

A

decrease

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4
Q

what are parasympathomimetics agents therapeutic indications that it would help w

A

treatment of: glaucoma, myasthenia gravis (MG), poor muscle tone in the bladder, ileus
diagnosis of asthma

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5
Q

glaucoma
1. pathology
2. treatment

A
  1. increased intraocular pressure (IOP), due to obstruction of aqueous humor drainage, may compress the optic nerve leading to blindness
  2. muscarinic receptor stimulants, carbonic anhydrase inhibitors, α receptor agonists, β receptor antagonists
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6
Q

drug treatment of glaucoma

A

Beta blocks - reduce secretion
Cholinomimetics- increases out flow
Alpha agonists -does both
Beta blockers - reduces secretions
Carbonic anhydrase inhibitors - increases out flow
Prostaglandins - increases secretions

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7
Q

diagnostic test of asthma

A

Methacholine challenge test
- Muscarinic agonist
- Inhalation -> bronchoconstriction
- Positive test = 20% drop of pulmonary function = asthma
- Safe test but may precipitate asthma

Bronchial - constriction
Stim parasympathetic drug = constriction
Induce bronchoconstriction - induced asthma
Causes reduction of air flow which is equivalent to the asthma effect

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8
Q

parasympatholytic agents

A

decreased PSNS -> reverse its effect

classes:
- antinicotinic agents: block N receptors (aka ganglion blockers)
- antimuscarinic agents: block M receptors

Where are the nicotinic agents: both ganglia, and the neuromuscular junction, and the sympathetic and parasympathetic.

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9
Q

ganglion blockers

A

Block all autonomic ganglia - decrease both SNS and PSNS
Limited therapeutic use due to wide range of adverse effects
E.g. hexamethonium

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10
Q

muscarinic receptor blockers

A

Prototype drug is atropine
- Competitive antagonist of all M receptors
- Strong long lasting anticholinergic effect

Main effects: dilated pupils, tachycardia, bronchodilation, dry all secretions

Blocks all 5 types of receptors
Reversal of the standard parasympathetic actions
Secretions - sweat, saliva, vomiting, GI fluids
Atropine will make everything low secretion and will make everything dry
Everything opposite to parasympathetic nervous system

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11
Q

therapeutic indications of M blockers

A
  • pupil dilation for fundus examination
  • asthma
  • intestinal cramps and diarrhea
  • urinary disorders
  • organophosphate poisoning
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12
Q

organophosphate compounds

A

Irreversibly inhibit AChE enzyme
Mechanism:
- Phosphorylate serine residue on the active site of the AChE -> irreversible enzyme inhibition
Ex: nerve gases (sarin), insecticides (malathion)

Some people use this to attempt suicide
Farmers who use this can get this through the skin: big amounts are bad and poisonous

Compounds compete with the acetocolyne compounds.

Link between enzyme and organophosphate is permanent and irreversible. You likely won’t be able to save the patient.

Severe contraction and muscle spasms.

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13
Q

organophosphate poisoning

A

DUMMBBLESS
D- diarrhea
U- urination
M- miosis
M- muscle spasm
B- bradycardia
B- bronchoconstriction
L- lacrimation
E- emesis
S- salivation
S- sweating

treatment: atropine, oximes (antidote - reactivate AChE)

Lots of secretions is the key here
Lots of vomiting, sweating, tears, GI fluids, etc.
Muscle spams and severe miosis
Bronchoconstriction.
Basically made to kill the patient.

Atropine is the fix here for the patient. Every 5 minutes until the patient is better or is on too much of it (either is better than death) - will improve the situation
Oximes - are the antidotes to reactivate the enzyme

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