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Anes. Pharm I Test 1
Anticholinesterases and Anticholinergics
| Question | Answer |
|---|---|
| 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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