Cholinergic Receptor Inhibiting Drugs Flashcards
Which of the classes of cholinergic receptor inhibiting drugs is most often used in practice and why?
Anti-muscarinic drugs; they are the most selective and have fewer unwanted side effects
What are the general effects of anti-muscarinic drugs?
SNS stimulation (PNS is blocked or dampened), except in CNS where the effect is sedating. Also reduction in sweating and salivation.
What is the use of atropine?
Induce mydriasis (dilation) or cycloplegia (loss of accommodation)
What is the use of scopolamine?
Prevent or reduce motion sickness
What is the use of dicyclomine?
Treatment of spastic colon (slows that shit down)
What is the use of tropicamide?
Induce mydriasis (dilation) or cycloplegia (loss of accommodation); shorter acting than atropine
What is the use of tolterodine?
Treatment of transient cystitis, postop bladder spasms, and incontinence
What is the use of benztropine?
Treatment of manifestations of Parkinson’s
What are the two anti muscarinic drugs used to induce bronchodilation in asthma or COPD, and which is longer acting?
Ipratropium, tiotropium (longer acting)
Which penetrates the CNS better, tertiary or quaternary amines?
Tertiary (atropine, scopolamine, dicyclomine, tropicamide, tolterodine, benztropine)
What are the general side effects of antimuscarinic drugs?
Hot as a JGL, dry as a bone, blind as a bat, red as a beet, mad as a hatter
What receptors do ganglionic blocker effect?
Nicotinic (Nn). Rarely used because both PNS and SNS ganglia are blocked
You’re in the middle of nowhere, and you stumble upon a guy who tripped and landed on a tree branch, which he proceeds to pull out. He learns that you’re a med student and begs you to do exploratory surgery to repair his wounds. What do you really wish you had in your bag with you?
A surgical attending and hexamethonium (to minimize bleeding). Hexamethonium would also be helpful in a hypertensive crisis.
Name two drugs that act at the NMJ to block Nm. Which is nondepolarizing, and which is depolarizing? What is their MOA?
NDP: tubocurarine (true antagonist)
DP: succinylcholine (super agonist)
You’re shadowing in the ED and a patient comes in with a compound tib-fib fracture. The attending asks you to help with the reduction, but they have to get the screaming patient to relax their muscles first; which drug will they most likely use and why?
Succinylcholine, which produces paralysis within one minute. The drug is rapidly cleared within 5-10 mins.
You’re on your psych rotation and your patient that has severe depression has just been recommended electroconvulsive therapy by the attending. You don’t want the patient to be struggling during the whole procedure, so you recommend a drug to relax the patient. What did you recommend?
Tubocurarine, producing motor weakness followed by flaccid paralysis (lasts 30-60 mins)
You’re on your PM&R peds elective and a patient with a history of cerebral palsy comes in to outpatient clinic. You notice severe spasticity in the adductor muscles of the legs, to the point where the legs are crossing and interfering with the child’s gait. What does the attending recommend for the severe localized spasticity and how does this treatment work?
Botulinum toxin A injection. Works at the NMJ to degrade SNAP25 and inhibit vesicle fusion and subsequent release of ACh. Overall effect: decreased ACh in the synapse.
