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PHAR417 > Cholinesterase Inhibitors and Nicotinic Antagonists-T1 > Flashcards

Cholinesterase Inhibitors and Nicotinic Antagonists-T1 Flashcards

1
Q

the 11 cholinesterase inhibitors

A
  • ambenonium (mytelase)
  • demecarium (humorsol)
  • donepezil (aricept)
  • echothiophate (phospholine)
  • galantamine (reminyl)
  • neostigmine (prostigmin)
  • physostigmine (generic only)
  • pyridostigmine (mestinon)
  • rivastigmine (exelon)
  • tacrine (cognex)
  • edrophonium (tensilon)
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2
Q

cholinesterase regenerator

A

pralidoxime (protopam, 2-PAM)

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3
Q

cholinesterase inhibitors are generally

A

carbamate derivatives or organophosphates.

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4
Q

acetylcholinesterase (AchE) is a highly

A

active enzyme that rapidly metabolizes Ach to inactive products. found in high density in the synaptic cleft and nerve endings.

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5
Q

inhibiting AchE

A

potentiates the effects of Ach released from cholinergic nerves.

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6
Q

cholinesterase inhibitors have an indirect effect on

A

muscarinic receptors, parasympathetic mimetic

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7
Q

metabolism of Ach by cholinesterase

A
  • very rapid
  • example of base hydrolysis of an ester
  • Ach binds to enzyme active site via interactions with specific amino acid residues
  • the acetate group is hydrolyzed by the addition of water to regenerate the active enzyme.
  • during the intermediate state- the enzyme can’t bind another molecule of Ach
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8
Q

reversible cholinesterase inhibitors (3) and what they do

A
  • physostigmine, neostigmine lead to carbamoylation of cholinesterase which prevents binding and metabolism of Ach
  • edrophonium competes with Ach for binding and metabolism of Ach
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9
Q

inhibition of cholinesterase by carbamates

A
  • carbamate derivatives bind to same active site of the cholinesterase as Ach
  • cleavage of the carbamate yields amino alcohol and carbamoylated enzymes complex.
  • This the active site of the enzyme remains blocked for longer periods of time preventing Ach metabolism
  • intermediate remains carbamoylated for longer period of time- NOT hydrolyzed as quickly.
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10
Q

inhibition of AchE by organophosphates

A
  • phosphoester bond- very stable and not easy to break.
  • organophosphates bind with high affinity to serine residue resulting in phosphorylated enzyme complex.
  • complex can undergo aging where one of the ether bonds is broken and becomes even more resistant to hydrolysis.
  • result of inhibition leads to increased Ach and increased stimulation of muscarinic and nicotinic receptors.
  • 2-PAM able to regenerate active enzyme complex only if aging has not occurred. works by nucleophilic attack of phosphate group.
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11
Q

different rates of hydrolysis of the ether bond to determine extent of cholinesterase inhibition: Ach, neostigmine, and diisofluorophosphate

A

Ach: fast hydrolysis, low inhibition

neostigmine: slow hydrolysis; high, reversible inhibition
diisofluorophosphate: very slow hydrolysis; high, irreversible inhibition

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12
Q

pharmacological effects of cholinesterase inhibitors

A
  • cardio: decreased HR, force, small or no change in blood pressure
  • GI: increased motility, increased digestive secretions, gas, cramps, defecation
  • eyes: miosis, increased accommodation for near vision, increased then decreased intraocular pressure.
  • respiratory: increased bronchial tone
  • CNS: increased alertness, convulsions, seizures
  • neuromuscular junction: increased muscle strength, ataxia, tremors.
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13
Q

using cholinesterase inhibitor to treat glaucoma

A

physostigmine, echothiophate, DFP enhance cholinergic responses of the iris to increase aqueous flow and decrease intraocular pressure. cholinesterase inhibitors stimulate muscarinic receptors indirectly–> increased Ach, increased MR response –> increased constriction of ciliary muscles –> increased outflow of aqueous humor

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14
Q

cholinesterase inhibitor used to treat GI and urinary motility

A

neostigmine

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15
Q

cholinesterase inhibitors to treat atropine toxicity

A

reversed by giving physostigmine. want to increase [Ach] in synaptic space.
also can use echothiophate

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16
Q

cholinesterase inhibitors to improve neuromuscular transmission in myasthenia gravis

A

diagnostic: edrophonium.
therapeutic: pyridostigmine (mestinon)
- MG destroys receptors at NMJ
- want to build up Ach to get better stimulation of receptor- improve depolarization of motor end plate.

17
Q

toxicity related to cholinesterase inhibition

A

-usually due to insecticides

18
Q

SLUDGE

A 
symptoms of intoxication related to cholinesterase inhibition:
S- salivation
L- lacrimation
U- urination
D- defecation
G- gas
E- emesis
19
Q

8 nicotinic antagonists

A

mostly affect receptors in motor endplate:

  • atracurium (tacrium)
  • doxacurium (nuromax)
  • mivacurium (mivacron)
  • pancuronium
  • rocuronium
  • tubocurarine
  • succinylcholine
  • dantrolene (dantrium)
20
Q

nicotinic receptors are divided into___ and __

A

Nn: on nerve cells in ganglia
Nm: on skeletal muscle motor end plates

21
Q

nicotinic antagonists are divided into __ and __

A

depolorizing (succinylcholine)

nondepolarizing (pancuronium)

22
Q

4 non depolarizing nicotinic antagonists

A
  • D-tubocurarine
  • pancuronium
  • venocuronium
  • rocuronium
23
Q

2 depolarizing blockers of nicotinic antagonists

A
  • succinylcholine

- decamethonium

24
Q

depolarizing nicotinic antagonists bind to__

A

the nicotinic receptor of the neuromuscular junction and activate the receptor to cause partial depolarization and contraction of the muscle.

25
Q

flaccid paralysis occurs when

A

At released from the motor neuron activates the receptor further

26
Q

the partially depolarized motor end plates results in nicotinic receptor channels that are in the

A

inactive state

27
Q

nondepolarizing neuromuscular blockers compete with

A

Ach for binding to the nicotinic receptor at the neuromuscular junction

28
Q

nondepolarizing neuromuscular blockers bind to channel but

A

does not open channel

29
Q

activation of the nicotinic receptor requires

A

the binding of 2 molecules of Ach; binding of 1 molecule of the antagonist to the receptor decreases the activity.

30
Q

Administration of ___ can reverse paralysis from non depolarizing neuromuscular blocking

A

cholinesterase inhibitor

31
Q

adverse effects of nicotinic antagonists

A
  • histamine release
  • succinylcholine may release excessive K from muscle–> hyperkalemia
  • malignant hyperthermia
32
Q

nicotinic antagonist drug interactions (4)

A
  1. inhaled anesthetics: produce synergistic neuromuscular blockade
  2. aminoglycosides: decrease Ach release from cholinergic nerves to produce additive neuromuscular blockade
  3. calcium channel blockers: may decrease availability of Ca ions for contraction and enhance effects of neuromuscular blockers
  4. opiods, lidocaine, phenytoin

PHAR417 (10 decks)

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