Mm Chapter 10. Cholinesterase Inhibitors

Front 1

The primary clinical use of cholinesterase inhibitors, also called anticholinesterases, is to

Back 1

reverse nondepolarizing muscle blockade.

Front 2

Acetylcholine is the neurotransmitter for

Back 2

1 entire parasympathetic nervous system (parasympathetic ganglions and effector cells),
2 parts of the sympathetic nervous system (sympathetic ganglions, adrenal medulla, and sweat glands),
3- some neurons in the central nervous system, and somatic nerves innervating skeletal muscle.

Front 3

Neuromuscular transmission is blocked when ...

Back 3

nondepolarizing muscle relaxants compete with acetylcholine to bind to nicotinic cholinergic receptors

Front 4

cholinesterase inhibitors work by .... (important)

Back 4

increase the amount of acetylcholine available to compete with the nondepolarizing agent, thereby reestablishing neuromuscular transmission.

Front 5

In excessive doses, acetylcholinesterase inhibitors can

Back 5

can paradoxically potentiate a nondepolarizing neuromuscular blockade. In addition, these drugs prolong the depolarization blockade of succinylcholine

Front 6

In monitoring a patient's recovery from neuromuscular blockade, the suggested end points are (2X)

Back 6

s in response to a 100-Hz stimulus in anesthetized patients or sustained head lift in awake patients. If neither of these end points is achieved, the patient should remain intubated and ventilation should be continued.

Front 7

The term cholinergic refers to

Back 7

effects of the neurotransmitter acetylcholine,

as opposed to the adrenergic effects of noradrenaline (norepinephrine)

Front 8

Acetylcholine is synthesized

Back 8

in the nerve terminal

Front 9

Acetylcholine is synthesized in the nerve terminal by

Back 9

enzyme choline acetyltransferase

Front 10

enzyme choline acetyltransferase, which catalyzes the reaction between

Back 10

acetylcoenzyme A and choline

Front 11

acetylcholine is rapidly hydrolyzed by

Back 11

acetylcholinesterase (true cholinesterase)

Front 12

After its release, acetylcholine is rapidly hydrolyzed by acetylcholinesterase (true cholinesterase)

Back 12

into acetate and choline.

Front 13

neurotransmitter for the entire parasympathetic nervous system

Back 13

Acetylcholine

Front 14

Cholinergic receptors have been subdivided into two major groups based on

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their reaction to the alkaloids muscarine and nicotine

Front 15

Nicotine stimulates the 2x

Back 15

autonomic ganglia and skeletal muscle receptors (nicotinic receptors),

Front 16

muscarine activates 3x

Back 16

end-organ effector cells in bronchial smooth muscle, salivary glands, and the sinoatrial node (muscarinic receptors)

Front 17

Nicotinic receptors are blocked by ....

Back 17

muscle relaxants (also called neuromuscular blockers,

Front 18

muscarinic receptors are blocked by

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anticholinergic drugs such as atropine

Front 19

Normal neuromuscular transmission critically depends on acetylcholine binding to

Back 19

to nicotinic cholinergic receptors on the motor end plate.

Front 20

Nondepolarizing muscle relaxants act by

Back 20

competing with acetylcholine for these binding sites, thereby blocking neuromuscular transmission.

Front 21

Reversal of blockade depends on 4x

Back 21

gradual diffusion, redistribution, metabolism, and excretion from the body of the nondepolarizing relaxant

Front 22

Cholinesterase inhibitors work by

Back 22

indirectly increase the amount of acetylcholine available to compete with the nondepolarizing agent, thereby reestablishing normal neuromuscular transmission.

Front 23

Cholinesterase inhibitors inactivate acetylcholinesterase by

Back 23

reversibly binding to the enzyme

The stability of the bond influences the duration of action: The electrostatic attraction and hydrogen bonding of edrophonium are short-lived; the covalent bonds of neostigmine and pyridostigmine are longer lasting.

Front 24

Organophosphates, a special class of cholinesterase inhibitors, form ....

Back 24

very stable, irreversible bonds to the enzyme. They are used in ophthalmology and more commonly as pesticides

Front 25

Muscarinic Side Effects of Cholinesterase Inhibitors.

Cardiovascular

Back 25

Decreased heart rate, bradyarrhythmias

Front 26

Muscarinic Side Effects of Cholinesterase Inhibitors.

Cerebral

Back 26

Diffuse excitation1

Front 27

Muscarinic Side Effects of Cholinesterase Inhibitors.


Pulmonary

Back 27

Bronchospasm, bronchial secretions

Front 28

Muscarinic Side Effects of Cholinesterase Inhibitors.

Gastrointestinal

Back 28

Intestinal spasm, increased salivation

Front 29

Muscarinic Side Effects of Cholinesterase Inhibitors.
Ophthalmological

Back 29

Pupillary constriction

Front 30

Muscarinic Side Effects of Cholinesterase Inhibitors.

Genitourinary

Back 30

Increased bladder tone

Front 31

Unwanted muscarinic side effects are minimized by prior

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concomitant administration of anticholinergic medications such as atropine sulfate or glycopyrrolate

Front 32

For intermediate-acting agents such as atracurium and vecuronium, a palpable posttetanic twitch appears about ____ min before spontaneous recovery of the first twitch of the TOF.

Back 32

10

Front 33

Neostigmine

renders the molecule lipid insoluble, so that it cannot pass through the blood–brain barrier.

Back 33

a quaternary ammonium group

Front 34

The effects of neostigmine (0.04 mg/kg) are usually apparent in ..

last more than ...

Back 34

5–10 min, peak at 10 min, and last more than 1 h

Front 35

Muscarinic side effects are minimized by

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prior or concomitant administration of an anticholinergic agent.

Front 36

most rapid onset of action (1–2 min) and the shortest duration of effect of any of the cholinesterase inhibitors

Back 36

Edrophonium

Front 37

1. ACh is synthesized in the nerve terminal by:
a. Acetylcholinesterase
b. Acetyl methytransferase
c. Choline acetyltransferase
d. Choline acetylmoveerase

Back 37

C

Front 38

2. What are the end products of Acetylcholinesterase hydrolysis?
a. Acetate and Choline
b. Acetyl and Choline
c. Acetate and Chlorine
d. Acetyl and Chlorine

Back 38

A

Front 39

3. How do edrophonium and neostigmine attach to Acetylcholinesterase?
a. Both by H bonds
b. Both by covalent bonds
c. Edrophonium by H bonds and neostigmine by covalent bonds
d. Edrophonium by covalent bonds and neostigmine by H bonds

Back 39

C

Front 40

4. With regards to organophosphates, what must happen to have active Acetylcholinesterase?
a. The organophosphate must diffuse away from the enzyme and then be metabolized in the liver before the enzyme is active again
b. The organophosphate must diffuse away from the enzyme and then be metabolized in the blood before the enzyme is active again
c. There will never be active enzyme again
d. New enzyme must be synthesized

Back 40

D

Front 41

5. You have a patient who is chronically treated for her glaucoma with ecothiophate. What may you expect to happen when giving her six?
a. She is enzyme induced and will have a decreased sensitivity to the drug
b. She will have significant prolongation of blockade because the ecothiophate is inhibiting the true cholinesterase needed to metabolize the sux.
c. She will have significant prolongation of blockade because the ecothiophate is inhibiting the plasmacholinesterase needed to metabolize the sux
d. There will be no change because ecothiophate affects acetylcholinesterase and not plasmacholinesterase

Back 41

C

Front 42

6. Neostigmine, in excessive doses, can potentiate a blockade caused by sux by:
a. Increasing acetylcholine
b. Inhibiting pseudocholinesterase activity
c. None of the above
d. All of the above

Back 42

D

Front 43

7. Which of the following are suggested end points of recovery from muscle relaxants
a. Sustained tetanus for 5 seconds in response to a 100 Hz stimulus
b. Sustained head lift in awake patients
c. TV of 7ml/kg
d. A and B
e. All of the Above

Back 43

D

Front 44

8. Structurally, how does edrophonium differ from neostigmine?
a. Edrophonium is a tertiary amine whereas neostigmine is a quaternary ammonium
b. Edrophonium is a quaternary ammonium whereas neostigmine is a tertiary amine
c. Edrophonium has a carbamate group that neostigmine does not
d. Edrophonium does not have the carbamate group that neostigmine has

Back 44

D

Front 45

9. You are going to reverse your pregnant patient’s NDMR. Which would be the best combination to reverse her?
a. Edrophonium and atropine
b. Neostigmine and atropine
c. Neostigmine and robinol
d. Edrophonium and robinol

Back 45

B

Front 46

10. Structurally, how does physostigmine differ from neostigmine?
a. Physostigmine is a tertiary amine whereas neostigmine is a quaternary ammonium
b. Neostigmine is a tertiary amine whereas physostigmine is a quaternary ammonium
c. Physostigmine has a carbamate group whereas neostigmine does not
d. Physostigmine does not have the carbamate group the neostigmine has

Back 46

A

Front 47

11. Which of the following anticholinesterase drugs would be the best to treat an overdose of atropine?
a. Neostigmine
b. Pyridostigmine
c. Physostigmine
d. Edrophonium

Back 47

C