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47 Cards in this Set
- Front
- Back
The primary clinical use of cholinesterase inhibitors, also called anticholinesterases, is to
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reverse nondepolarizing muscle blockade.
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Acetylcholine is the neurotransmitter for
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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. |
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Neuromuscular transmission is blocked when ...
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nondepolarizing muscle relaxants compete with acetylcholine to bind to nicotinic cholinergic receptors
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cholinesterase inhibitors work by .... (important)
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increase the amount of acetylcholine available to compete with the nondepolarizing agent, thereby reestablishing neuromuscular transmission.
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In excessive doses, acetylcholinesterase inhibitors can
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can paradoxically potentiate a nondepolarizing neuromuscular blockade. In addition, these drugs prolong the depolarization blockade of succinylcholine
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In monitoring a patient's recovery from neuromuscular blockade, the suggested end points are (2X)
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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.
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The term cholinergic refers to
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effects of the neurotransmitter acetylcholine,
as opposed to the adrenergic effects of noradrenaline (norepinephrine) |
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Acetylcholine is synthesized
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in the nerve terminal
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Acetylcholine is synthesized in the nerve terminal by
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enzyme choline acetyltransferase
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enzyme choline acetyltransferase, which catalyzes the reaction between
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acetylcoenzyme A and choline
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acetylcholine is rapidly hydrolyzed by
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acetylcholinesterase (true cholinesterase)
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After its release, acetylcholine is rapidly hydrolyzed by acetylcholinesterase (true cholinesterase)
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into acetate and choline.
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neurotransmitter for the entire parasympathetic nervous system
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Acetylcholine
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Cholinergic receptors have been subdivided into two major groups based on
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their reaction to the alkaloids muscarine and nicotine
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Nicotine stimulates the 2x
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autonomic ganglia and skeletal muscle receptors (nicotinic receptors),
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muscarine activates 3x
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end-organ effector cells in bronchial smooth muscle, salivary glands, and the sinoatrial node (muscarinic receptors)
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Nicotinic receptors are blocked by ....
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muscle relaxants (also called neuromuscular blockers,
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muscarinic receptors are blocked by
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anticholinergic drugs such as atropine
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Normal neuromuscular transmission critically depends on acetylcholine binding to
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to nicotinic cholinergic receptors on the motor end plate.
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Nondepolarizing muscle relaxants act by
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competing with acetylcholine for these binding sites, thereby blocking neuromuscular transmission.
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Reversal of blockade depends on 4x
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gradual diffusion, redistribution, metabolism, and excretion from the body of the nondepolarizing relaxant
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Cholinesterase inhibitors work by
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indirectly increase the amount of acetylcholine available to compete with the nondepolarizing agent, thereby reestablishing normal neuromuscular transmission.
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Cholinesterase inhibitors inactivate acetylcholinesterase by
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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. |
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Organophosphates, a special class of cholinesterase inhibitors, form ....
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very stable, irreversible bonds to the enzyme. They are used in ophthalmology and more commonly as pesticides
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Muscarinic Side Effects of Cholinesterase Inhibitors.
Cardiovascular |
Decreased heart rate, bradyarrhythmias
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Muscarinic Side Effects of Cholinesterase Inhibitors.
Cerebral |
Diffuse excitation1
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Muscarinic Side Effects of Cholinesterase Inhibitors.
Pulmonary |
Bronchospasm, bronchial secretions
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Muscarinic Side Effects of Cholinesterase Inhibitors.
Gastrointestinal |
Intestinal spasm, increased salivation
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Muscarinic Side Effects of Cholinesterase Inhibitors.
Ophthalmological |
Pupillary constriction
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Muscarinic Side Effects of Cholinesterase Inhibitors.
Genitourinary |
Increased bladder tone
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Unwanted muscarinic side effects are minimized by prior
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concomitant administration of anticholinergic medications such as atropine sulfate or glycopyrrolate
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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.
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10
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Neostigmine
renders the molecule lipid insoluble, so that it cannot pass through the blood–brain barrier. |
a quaternary ammonium group
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The effects of neostigmine (0.04 mg/kg) are usually apparent in ..
last more than ... |
5–10 min, peak at 10 min, and last more than 1 h
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Muscarinic side effects are minimized by
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prior or concomitant administration of an anticholinergic agent.
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most rapid onset of action (1–2 min) and the shortest duration of effect of any of the cholinesterase inhibitors
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Edrophonium
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1. ACh is synthesized in the nerve terminal by:
a. Acetylcholinesterase b. Acetyl methytransferase c. Choline acetyltransferase d. Choline acetylmoveerase |
C
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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 |
A
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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 |
C
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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 |
D
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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 |
C
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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 |
D
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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 |
D
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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 |
D
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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 |
B
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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 |
A
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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 |
C
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