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38 Cards in this Set
- Front
- Back
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What are the non-depolarizing agents (isoquinoline derivatives)? |
Atracurium Cisatracuium |
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What are the non-depolarizing agents (steroid derivatives)? |
Pancuronium Rocuronium Vecuronium |
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What is the depolarizing agent? |
Succinlycholine |
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What are the reversal agents? |
Edrophonium Pyridostigmine Neostigmine
Sugammedex (steroidal only) |
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When are the reversal agents given and why? |
Given post-procedurally to reverse the residual effects of the paralytic agents and restore normal neuromuscular activity and tone. |
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Draw the pathway of cholinergic signaling: |
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What are the two types of nicotinic receptors? Where is each found? Which receptor is the site of a cation of paralytic agents? |
Nicotinic N = autonomic ganglia
Nicotinic M = skeletal muscle (site of action of paralytic agents) |
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What type of receptor is the nicotinic acetylcholine receptor? How many molecules needed to bind to activate? |
Multimeric ligan-gated ion channel => gates for sodium influx into cell => depolarization
Two molecules of Ach |
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What is the difference between a non-depolarizing blocker (rocuronium) and a depolarizing blocker (succinylcholine) in terms of action on the channel? |
Non-depolarizing prevents opening, depolarizing occupies receptor and blocks the channel (normal closure prevented) => flaccid paralysis |
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How does strength/contraction change with addition of non-depolarizer or depolarizing block? |
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Patients given a depolarizing blocker show brief __________ before paralysis. |
Twitching |
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True or false: The durability of effect closely correlates with drug half-life, indicating that the binding kinetics to the nicotinic receptor are short lived and effects are dependent upon local tissue concentration. |
True |
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Non-depolarizing:
Rapid or slow distribution, rapid or slow elimination How are they eliminated? Are they highly ionized? Do they bind protein? |
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How is atracrium metabolized and eliminated? What product is produced related to seizures?
Which drug replaced it? |
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Succinylcholine:
Short or long duration of action What is it rapidly hydrolyzed by? Where? Broken down into what?
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Of the three isoquinolones, which has the longest duration? |
Tubucurarine |
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Which drug has the shortest duration? Which drugs have the highest potency? |
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Which drugs cause block of ganglia block and histamine release?
Which drug causes cardiac M receptor block?
Which drug causes ganglia stimulation, cardiac M receptor stimulation, and slight histamine release? |
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Which drug exhibits significantly expanded series of adverse effects when compared to the non-depolarizing agents? What are some of these AEs? |
Succinylcholine:
Hemodynamic changes Hyperkalemia Prolonged neuromuscular blockade Increase in pressures Malignant hyperthermia |
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How is malignant hyperthermia produced? |
Drugs cause an uncontrolled release of calcium from the SR => symptoms indicated in image |
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What drug is commonly associated with malignant hyperthermia? Other drugs?
What is the treatment (4 things)? |
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What drug interactions can occur with volatine anesthetics? (Isoflurane, sevoflurane, desflurane, and halothane, N20) |
Malignant hyperthermia = Ca2+ release from SR, administer dantrolene |
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What drug interactions can occur with antibiotics (amino glycosides)? |
Enhancement of blockade (pre-junctional P-type Ca2+ channels), depressed Ach release similar to that caused by magnesium |
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What drug interactions with local anesthetics? |
Can depress via pre-junctional neural effect Block in large doses |
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What drug interactions with other neuromuscular blocking drugs? (succinylcholine) |
Depolarizing effect of succinyl choline => antagonized by administering a small dose of a non-depolarizing blocker |
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What are two ways to reverse blockade and restore muscle tone and function? |
1. Increase levels of Ach by prevention metabolism of endogenous ligand by AchE, AchE => outcompete paralytic and restore activity
2. The future... |
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What are the three AchE inhibitors? Do they cross the BB? Which has the longest duration? Shortest? Anticholinergic of each? |
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Atropine, Scopolamine, Glycopyrrolate
Which causes tachycardia, which causes bronchodilation, sedation, antisialogogue |
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What are some of the off target actions of AchE inhibitors? (think about increase parasympathetic activity). |
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What is the alternative approach to reverse NMB?
Which drug used in Europe does this? What drugs is it active against? |
Remove the blocking drug from the equation
Steroidals |
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What is the mechanism of sugammadex? |
Pore structure into which NMB inserts, preventing blocker from being capable of accessing the binding site on the Ach nicotinic receptor |
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What are some therapeutic uses of NMBs? How are they administered? |
Surgical anesthesia Short orthopedic procedures Endotrachel intubation
Administed IV |
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