Indirect acting cholinergic agonists

Question 1

toxic doses of cholinesterase inhibitors the NMJ

Answer 1

desensitization leads to neuromuscular blockage

Question 2

toxic doses of cholinesterase inhibitors in the brain (Nn)

Answer 2

convulsion, respiratory arrest

Question 3

effects of irreversible cholinesterase inhibitor toxicity

Answer 3

Salivation
Lacrimation
Urination
Defecation
Gastric distress
Emesis

Question 4

carbamates are reversed by

Answer 4

slow hydrolysis by AChE

Question 5

cholinesterase inhibitors are generally used to treat

Answer 5

myasthenia gravis

reverse neuromuscular blockage postop

Question 6

carbamates MOA

Answer 6

form a covalent bond with AChE lasting 30 mins-6 hours

Question 7

quarternary amines (2)

Answer 7

neostigmine, pyridostigmine

Not well absorbed orally

Question 8

enter the CNS

Answer 8

tertiary amines

Question 9

don’t enter the CNS

Answer 9

quarternary amines

Question 10

side effects of neostigmine/pyridostidmine and how to treat them in patients with MG

Answer 10

muscarinic side effects

patients become tolerant to them, or treat with muscarinic antagonists

Question 11

pyridostigmine uses

Answer 11

chronic therapy of MG

prophylaxis against irreversible cholinesterase inhibitors

Question 12

neostigmine uses

Answer 12

1. MG chronic therapy: also has some direct stimulatory NMJ effect
2. Reverse neuromuscular blockade postop
3. Increase bladder motility

Question 13

physostigmine is a

Answer 13

tertiary amine (enters CNS), well absorbed orally

Question 14

physostigmine systemic uses

Answer 14

muscarinic antagonist poisoning

otherwise has too many CNS side effects

Question 15

physostigmine topical uses

Answer 15

narrow angle glaucoma

Question 16

edrophonium is a _________ and is taken _______

Answer 16

quaternary ammonium
must be injected
short acting af

Question 17

edrophonium is used to

Answer 17

diagnose MG: will briefly improve symptoms

adjust dosing of AChE inhibitors:
too low a dose: will briefly improve symptoms
too high a dose: will briefly worsen symptoms (contributes to Nm desensitization)i

Question 18

how organophosphates get in your system

Answer 18

highly lipid soluble, easily absorbed through skin, lung, gut, eye

Question 19

organophosphate MOA

Answer 19

phosphorylate AChE –> very long lasting bond

bond undergoes aging –> irreversible until new AChE is synthesized

Question 20

aging means

Answer 20

breaking of phosphorus oxygen bonds

Question 21

organophosphate that isn’t lipid soluble and therefore not absorbed systemically

Answer 21

echothiophate

Question 22

echothiophate is used to treat __________ because _________

Answer 22

narrow angle glaucoma (topical)

very long lasting effects w/o systemic absorption

Question 23

thiophosphate pesticide

Answer 23

malathion

Question 24

malathion uses

Answer 24

insecticide (mosquitos) (not as well absorbed by animals)

Question 25

treatment of organophosphate poisoning seizures

Answer 25

diazepam

Question 26

treatment of organophosphate poisoning to block muscarinic receptors

Answer 26

atropine until pupils become dilated

Question 27

treatment of organophosphate poisoning to prevent enzyme aging

Answer 27

pralidoxime (within 3-4 hours)

Question 28

pralidoxime contraindications

Answer 28

carbamate poisoning (carbamates don’t undergo aging, will worsen)

Question 29

pralidoxime MOA

Answer 29

strong nucleophile that attracts and irreversibly binds organophosphates (preventing binding to or pulling off of AChE)

Question 30

pralidoxime side effects

Answer 30

htn

Question 31

pralidoxime side effects if an organophosphate is not present

Answer 31

binds to and inhibits AChE producing neuromuscular blockade

Question 32

pralidoxome has effects on

Answer 32

NMJ > ganglia, no CNS