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Anes. Pharm I Test 1

Anticholinesterases and Anticholinergics

Acetylcholine binds to ____________ and _____________ receptors nicotinic muscarinic
The goal of reversing a NMB is to maximize _____________ receptor transmission by ACh and minimize ______________ receptor transmission nicotinic muscarinic
How does anticholinesterase inactivate acetylcholine? by binding to it
Neostigmine, Pyridostigmine and Physostigmine are ________ by AChE & cause it to become carbamylated so they can _________ inhibit AChE's ability to hydrolyze ACh hydrolyzed reversibly
Which reversal drug is thought to have presynaptic effects which cause an increase in the availability of acetylcholine? edrophonium
How it is possible for a reversal drug to actually enhance a neuromuscular blockade? When the NMJ is flooded with ACh, it can becomes desensitized to ACh preventing ACh from competing with the NMB on the receptor and actually allowing the blockade to continue
Edrophonium forms _________ bonds with AChE. These bonds are ________ lived, requiring a _________ dose and producing a _________ onset. hydrostatic short higher quick
Neostigmine & Pyridostigmine form _________ bonds with AChE. These bonds last __________ than the bonds formed between Edrophonium and AChE covalent longer
What is the dose of Edrophonium? 0.5 - 1 mg/kg
What is the onset and duration of Edrophonium? onset: 30 - 60 seconds duration: 30 - 60 minutes
What is the dose of Neostigmine? 0.06 mg/kg
What is the maximum dose of Neostigmine? 0.07 mg/kg 5 mg is MAXIMUM dose despite weight
What is the onset and duration of Neostigmine? onset: 7 - 11 minutes duration: 45 - 90 minutes
What is the dose of Pyridostigmine? 0.3 mg/kg
What is the onset of Pyridostigmine? 10 - 20 minutes
What is the dose of Physostigmine (Antilirium)? 0.5 - 2 mg (0.01 - 0.03 mg/kg)
Why do you have to give Physostigmine (Antilirium) slowly? because it will cause projective vomiting if given quickly
What is the onset of Physostigmine (Antilirium)? 5 minutes
Why is Physostigmine (Antilirium) typically given? to treat Central Anticholinergic Syndrome (post op delirium)
What is the mechanism of action of organophosphate anticholinesterase agents? they form irreversible bonds with AChE, causing massive amounts of ACh to bind with muscarinic and nicotinic receptors
What are some examples of organophosphate anticholinesterase agents? echothiophate eye gtts, insecticides, nerve gas
What does stimulation of cardiac muscarinic receptors by ACh cause? bradycardia, junctional rhythms, PVCs, ventricular rhythms, asystole, and slowing of AV conduction
What does stimulation of GI/GU muscarinic receptors by ACh cause? increased secretions, increased GI motility, PONV
What does stimulation of pulmonary muscarinic receptors by ACh cause? bronchoconstriction and increased secretions
What does stimulation of opthalmic muscarinic receptors by ACh cause? miosis (pupillary constriction), farsightedness, decreased intraocular pressure
What is an unlikely side effect of stimulation of muscarinic receptors that one should be mindful of in patients with myotonia, muscular dystrophies, spinal cord transection or burns? contractions and fasiculations
When does cholinergic crisis occur? when there is an overstimulation of both nicotinic and muscarinic receptors due to increased amounts of ACh at the NMJ
What are the muscarinic symptoms associated with cholinergic crisis? miosis, inability to focus vision, salivation, bronchoconstriction, bradycardia, abdominal cramps, loss of control of bowel and bladder
What are the nicotinic symptoms associated with cholinergic crisis? weakness ranging to paralysis
What are the CNS symptoms associated with cholinergic crisis? confusion, ataxia, coma, respiratory depression
What is the usual cause of cholinergic crisis? overdose of anticholinesterase drugs, nerve gas exposure, organophosphate insecticide exposure
What are the treatments for cholinergic crisis? atropine, Pralidoxime (2-PAM, used in military settings), ventilatory support, control of seizures and other symptoms
What is the rational for pretreating patients with anticholinergic drugs prior to administration of anticholinesterase drugs? The effects of anticholinesterase are not limited to the NMJ. Anticholinergic drugs block the undesirable muscarinic effects without having an effect on the nicotinic effects in the NMJ.
What is the chemical structure of atropine and what implications does it have? tertiary ammonium, so its lipid soluble = crosses the blood brain barrier and can make patients crazy
What is the dose of atropine? 0.03 mg/kg
What is the onset of atropine? 1 minute
You want to see an increase in __________ after giving atropine and before you give anticholinesterase (reversal agent) heart rate
Why is atropine the best choice for prevention of vagal response? blocks the effect of ACh on the SA node, which shortens the PR interval
Atropine and Glycopyrrolate cause relaxation of _______ ________ which could cause an increased risk of aspiration esophageal sphincter
What is the dose of Glycopyrrolate (Robinul)? 0.015 mg/kg
What is the onset of Glycopyrrolate (Robinul)? 2 - 3 minutes
What is the chemical structure of Glycopyrrolate (Robinul) and what implications does this have? quaternary ammonium; lipid insoluble so cannot cross blood brain barrier = no CNS effects
What is the dose of Scopolamine? 0.4 mg IV/IM
What is the onset of Scopolamine? 10 minutes (IV) and 30 - 60 minutes (IM)
What is the chemical structure of Scopolamine and how does this affect its clinical use? tertiary amine; crosses blood brain barrier so sedative and amnestic effects, also treats PONV and has antisialagogue effects
Rank the three anticholinergic agents in terms of usefulness for antisialagogue effects scopolamine > glycopyrrolate > atropine
Rank the anticholinergic agents in terms of usefulness for treatment of bradycardia atropine > glycopyrrolate > scopolamine
Rank the anticholinergic agents in terms of usefulness for treatment of sedative/CNS effects scopolamine > atropine
What determines the choice of which anticholinergic to administer with which anticholinesterase? the speed of onset
Which anticholinergic is used as pretreatment for Edrophonium? Atropine
Which anticholinergic is used as pretreatment for Neostigmine? Glycopyrrolate (Robinul)
What are the symptoms of Central Anticholinergic Syndrome? restlessness and hallucinations>>>somnolence and unconsciousness, dry mouth, blurred vision, tachycardia, dilation of cutaneous vessels, increased temperature, sensitivity to light
What is the treatment for Central Anticholinergic Syndrome (post op delirium)? Physostigmine (Antilirium) 0.015 - 0.06 mg/kg
What is the mechanism of action of Sugammadex (Org 25969)? encapsulates steroidal NMB and forms a stable complex, preventing the action of the NMB on the NMJ
Sugammadex is NOT an _____________ and therefore does NOT require an _____________ for pretreatment. anticholinesterase anticholinergic
Sugammadex was produced specifically for the NMB __________ and makes this drug a __________ duration NMB for difficult airway cases. Rocuronium short
Why is the FDA still approving the use of Sugammadex in the US, despite its widespread use in the UK? it is thought to have a inhibitory effect on the immune system
Created by: Mary Beth



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