Autonomic - Acetylcholinesterase Inhibitors (Indirect Cholinonmimetics)

Question 1

How do acetycholinesterase inhibitors (indirect cholinomimetics) raise acetylcholine levels?

Answer 1

Prevent aetycholinesterase from degrading acetylcholine to raise or increase length of time of acetylcholine.

Question 2

What is the suffix of most acetycholinesterase inhibitors?

Answer 2

“-stigmine” (STIGMA graffiti)

Question 3

Where does acetylcholinesterase inhibit acetylcholine?

Answer 3

At the neuromuscular junctions (plug box). Increase activity of nicotinic acetylcholine receptors.

Question 4

Acetycholinesterase inhibitors increases or decreases strength of contraction?

Answer 4

Increases by increasing activity of nictoinc Ach receptors

Question 5

What are the symptoms of myasthenia Gravis? How does it cause these symptoms?

Answer 5

Progressive muscle weakness, ptosis, diplopia by creating antibodies against nicotinic Ach receptors at motor end plates, inactivating them.

Question 6

What does pyridostigmine treat? How?

Answer 6

Pyridostigmine (girl wearing community pride jacket) treats myasthenia gravis by increasing Ach to outcompete MG antibodies.

Question 7

What does neostigmine treat?

Answer 7

Neostigmine (Neon STIGMA sign) also treats myasthenia gravis. But it is not as common

Question 8

What does edrophonium treat?

Answer 8

Transiently reverses symptoms of myasthenia gravis.

Question 9

What are the quaternary amines. What is special about them?

Answer 9

Pyridostigmine, neostigmine, edrophonium. They do not penetrate into the CNS

Question 10

How is edrophonium used int he Tensilon test?

Answer 10

Because it only relieves muscle weakness for 5-15 minutes it is used as a diagnostic tool. If it is positive tensilon test then the patient is being under treated and needs more medication (phonebooth with person talking on phone and tense phone line). The negative tensilon test means that it failed to reverse muscle weakness and patient needs to reduce amount of medication taking (phone boooth with cut off phone line).

Question 11

What are non-depolarizing neuromuscular blocking agents? What do they do?

Answer 11

Tubucurarine, pancuronium, cisatracurium (“curare” crayons). Inhibit nicotinic Ach receptors at NMJ endplate.

Question 12

What drug reverses the non-depolarizing neuromuscular blockade?

Answer 12

Neostigmine (Neon sign store owner kicking out Curare crayon kid).

Question 13

What is a depolarizing neuromuscular blocking agent? What does it do to do?

Answer 13

Succinylcholine (“SUCKS” graffiti). Overstimulates NMJ causing muscles to remain depolarized and unable to respond to stimulus.

Question 14

Is the initial Phase-1 of the depolarizing blockade of succinylcholine reversible or irreversible? How does acetycholinesterase inhibitors affect this?

Answer 14

Irreversible. It potentiates the blockade.

Question 15

What type of drug is succinylcholine?

Answer 15

Nictonic Ach receptor agonist

Question 16

What can acetylcholinesterase inhibitors be used to treat other than myasthenia gravis?

Answer 16

Urinary retention (bladder hose)

Question 17

Which drug is an acetycholinesterase inhibitors with central effects?

Answer 17

Physostigmine (PHYS Ed center)

Question 18

What does physostigmine reverse?

Answer 18

Atropine overdose

Question 19

Where is atropine naturally occurring?

Answer 19

Belladonna flowers and jimson weed

Question 20

What are the symptoms of acetycholinesterase inhibitor toxicity (side effects of acetycholinesterase inhibitors)?

Answer 20

DUMBBELS (diarrhea, urination, miosis, bronchospasm, bradycardia, lacrimation, salivation, sweating)

(Dumbbellls in PHYS ED gym)

Question 21

What other side effect does acetycholinesterase inhibitors cause?

Answer 21

Flaccid paralysis (NMJ nictonic Ach receptor over-activation)

(Weak nicotine kid in PHYS ED building)

Question 22

What are types of acetycholinesterase inhibitors?

Answer 22

Insecticides (organophosphates): parathion, malthion, echotiophate

(Thiol spray)

Question 23

What are organophosphates a major cause of?

Answer 23

Acute cholinergic toxicity

Question 24

What reverses organophosphate toxicity?

Answer 24

Pralidoxime (Closing lid of of garbage dump on toxicity)

Question 25

What drug reverses cholinergic toxicity including flaccid paralysis? How?

Answer 25

Pralidoxime. Regenerates acetycholinesterase at muscarinic and nicotinic receptors (new toxic waste dumpsters)

Question 26

What reverses both peripheral and central muscarinic toxicity from organophosphate poisoning?

Answer 26

Atropine

Question 27

What reverses only peripheral muscarinic toxicity?

Answer 27

Pralidoxime

Question 28

What does aging of organophosphate lead to?

Answer 28

Irreversible binding (old pest control man that is spraying a hole in the garbage can cuasing acety cola bottles to spill out)

Question 29

When is pralidoxime ineffective?

Answer 29

Once aging of organophosphate cholinesterase complex has occurred

Question 30

What is used to treat Alzheimer’s disease?

Answer 30

Gala time (Alzheimer’s Gala), Rivastigmine (Reverse the Stigma), Donepezil (Done with the puzzle)

Question 31

T/F: Galantine, Rivastigmine, and Donepezil do not penetrate the CNS

Answer 31

F, they do.