45 Questions
Which drug produces mydriasis for 24 hours?
Cyclopentolate
What is the primary action of antimuscarinic agents like oxybutynin in the bladder?
Competitively blocking M3 receptors
Which antimuscarinic agent is relatively more selective for M3 muscarinic receptors?
Darifenacin
What are benztropine and trihexyphenidyl primarily used for?
Adjuncts with other antiparkinson agents
Which type of receptor do antimuscarinic agents mainly block to cause adverse effects?
M3 receptors
What is the mechanism of action of antimuscarinic agents like darifenacin and solifenacin in the bladder?
Selective antagonism of M3 receptors
Which antimuscarinic agent is thought to undergo ester hydrolysis?
Trospium
Which antimuscarinic agent is a preferred choice in treating overactive bladder in patients with dementia due to its minimal CNS effects?
Trospium
Which formulation of oxybutynin has a lower incidence of adverse effects compared to the immediate-release form?
Transdermal patch
Which cytochrome P450 enzyme is primarily responsible for the hepatic metabolism of antimuscarinic agents?
CYP 3A4
Which antimuscarinic agent is available in an extended-release formulation allowing for once-daily dosing?
Tolterodine
Which antimuscarinic agent is contraindicated in patients with angle-closure glaucoma?
Trospium
What is the primary effect of atropine on the eye?
Dilation of the pupil
Why is atropine not effective for the treatment of ulcers?
It reduces hydrochloric acid production
What is the most potent antispasmodic property of atropine and scopolamine?
Reduced gastric motility
In patients with angle-closure glaucoma, what dangerous effect can atropine cause in the eye?
Increased intraocular pressure
Which neuroeffector organs exhibit the greatest inhibitory effects to atropine?
Salivary and sweat glands
What is the mechanism of action of nondepolarizing (competitive) neuromuscular blocking agents at low doses?
Overcome by administration of cholinesterase inhibitors
At low doses, what is the predominant effect of atropine on the heart?
Decrease in heart rate
What happens to the ability of cholinesterase inhibitors to reverse the actions of nondepolarizing blockers at high doses?
Weakened
How do nondepolarizing blockers affect the muscle's response to direct electrical stimulation at high doses?
Completely block response
What is the primary action of cholinesterase inhibitors like neostigmine in the context of neuromuscular blockade?
Increase ACh concentration at the NMJ
What is the specific effect of nondepolarizing blockers at high doses on neuromuscular transmission?
Reduce transmission strength
What is a key difference in the muscle's response to electrical stimulation between low and high doses of nondepolarizing agents?
Muscle does not respond at all to direct stimulation at high doses
What is the mechanism of action of depolarizing neuromuscular blocking agents like succinylcholine?
Depolarizes the plasma membrane by acting like ACh
Why does succinylcholine persist for a longer time compared to ACh at the neuromuscular junction?
It is resistant to degradation by plasma cholinesterase
What is unique about succinylcholine among muscle relaxants?
It is resistant to plasma cholinesterase degradation
How does succinylcholine differ from acetylcholine in terms of degradation?
Succinylcholine remains attached longer at the receptor sites
How do genetic variants affecting plasma cholinesterase levels impact neuromuscular paralysis?
They can prolong the duration of neuromuscular paralysis
What role does succinylcholine play at the neuromuscular junction?
It depolarizes the muscle cell by attaching to nicotinic receptors
What is the main reason for the brief duration of action of succinylcholine?
Hydrolysis by plasma cholinesterase
Why should succinylcholine be used cautiously or avoided in patients with electrolyte imbalances who are receiving digoxin or diuretics?
It may increase potassium release
Which adverse effect is most concerning in burn patients or those with massive tissue damage when administered succinylcholine?
Hyperkalemia
What is the potential consequence of succinylcholine administration in patients deficient in plasma cholinesterase?
Prolonged apnea
Why should succinylcholine be used cautiously in patients with renal failure?
Potential for hyperkalemia
What is the primary cause of apnea following succinylcholine administration in patients with electrolyte imbalances?
Potassium release
Which process contributes significantly to the rapid disappearance of drug effects upon discontinuation of succinylcholine?
Redistribution in the body
Which muscle group is typically paralyzed first when neuromuscular blocking agents are administered?
Fingers
What is the organ-independent elimination pathway for cisatracurium mentioned in the text?
Hofmann elimination
How do nondepolarizing neuromuscular blocking agents mainly terminate their drug action?
Quaternary amines in bulky ring structures
What is the primary pharmacokinetic characteristic of neuromuscular blocking agents that prevents their absorption from the gut?
Quaternary amines
Which neuromuscular blocking agent is excreted unchanged in urine according to the text?
Pancuronium
What is the main effect of neuromuscular blocking agents on intercostal muscles?
Paralysis
Sugammadex acts as a selective relaxant-binding agent for which two specific neuromuscular blocking drugs?
Rocuronium and cisatracurium
What is the role of plasma cholinesterase in metabolizing which neuromuscular blocking agent?
Succinylcholine
Explore the pharmacokinetics of drugs available in oral dosage forms with a focus on once-daily administration and extended-release formulations. Learn about drugs metabolized by the cytochrome P450 system, such as CYP 3A4 and 2D6.
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