Autonomic Nervous System Effects Quiz

Podcast

Play an AI-generated podcast conversation about this lesson

Questions and Answers

Which of the following is the primary mechanism of action of atropine on the eye?

Causes mydriasis (pupil dilation) and cycloplegia (inability to focus for near vision) (correct)

Increases intraocular pressure (IOP)

Causes miosis (pupil constriction)

Decreases lacrimal gland secretion

What is the rationale for using a short-acting agent like tropicamide or phenylphrine for ophthalmic examination, instead of atropine?

Tropicamide and phenylphrine do not cause persistent mydriasis

Tropicamide and phenylphrine do not cause unresponsiveness to light

Tropicamide and phenylphrine do not cause cycloplegia

Tropicamide and phenylphrine do not cause dangerous elevation of intraocular pressure (IOP) (correct)

Why is atropine used as an antispasmodic in the gastrointestinal tract (GIT)?

Atropine reduces gastric acid production

Atropine reduces gastrointestinal motility (correct)

Atropine increases gastrointestinal motility

Atropine has no effect on the gastrointestinal tract

What is the cardiovascular effect of atropine at low and high doses?

Low dose: Bradycardia, High dose: Tachycardia Signup and view all the answers

Which of the following is a common side effect of atropine overdose?

Respiratory depression Signup and view all the answers

How does the central nervous system (CNS) effects of scopolamine differ from atropine?

Scopolamine has higher CNS activity than atropine Signup and view all the answers

Which of the following is NOT a direct effect of acetylcholine?

Increase in blood pressure via vasoconstriction Signup and view all the answers

What is the mechanism by which acetylcholine regulates heart rate and cardiac output?

Release of acetylcholine at the sinoatrial node Signup and view all the answers

Which of the following statements about bethanechol is FALSE?

It is hydrolyzed by acetylcholinesterase Signup and view all the answers

What is the mechanism of action of bethanechol on the gastrointestinal tract and bladder?

Increasing gastrointestinal motility and tone, and stimulating the detrusor muscle Signup and view all the answers

Which of the following is a side effect of carbachol?

Nausea and abdominal pain Signup and view all the answers

What is the duration of action of carbachol?

1 hour Signup and view all the answers

What is the mechanism of action of pralidoxime in reactivating acetylcholinesterase?

Displacing the alkyl group from organophosphate Signup and view all the answers

Which type of agents selectively bind to muscarinic receptors and block their activity?

Anti-muscarinic agents Signup and view all the answers

What is the primary action of neuromuscular blocker agents?

Interfere with impulse transmission to skeletal muscle Signup and view all the answers

Which characteristic best describes the mechanism of action of atropine?

Competes with acetylcholine for muscarinic receptors Signup and view all the answers

What is the most significant limitation in the chronic treatment of open-angle glaucoma?

Risk of developing cataracts Signup and view all the answers

What distinguishes ganglionic blockers from other anticholinergic agents?

Show preference for nicotinic receptors at neuromuscular junctions Signup and view all the answers

Which of the following statements accurately describes the effects of pilocarpine on the cardiovascular system (CVS) and central nervous system (CNS)?

It initially stimulates the CVS and CNS, followed by depression of these systems. Signup and view all the answers

Why is pilocarpine rarely used systemically and primarily limited to ophthalmic applications?

It has a long duration of action and high potency, making systemic use impractical. Signup and view all the answers

What is the primary use of pilocarpine in ophthalmic applications?

To cause miosis and lower intraocular pressure in glaucoma. Signup and view all the answers

Which of the following statements accurately describes the mechanism of action of reversible acetylcholinesterase inhibitors?

They prolong the lifetime of acetylcholine by inhibiting its breakdown by acetylcholinesterase. Signup and view all the answers

Which of the following statements accurately describes D-pilocarpine?

It is a tertiary amine and is stable to hydrolysis by acetylcholinesterase. Signup and view all the answers

What is the primary use of cevimeline, a non-specific cholinergic agent similar to pilocarpine?

To promote salivation in conditions like xerostomia and Sjögren's syndrome. Signup and view all the answers

Which of the following statements about succinylcholine is NOT true?

It is metabolized by plasma cholinesterase within the synaptic cleft. Signup and view all the answers

What is the mechanism of action of non-depolarizing neuromuscular blockers?

They act as acetylcholine antagonists and block the nicotinic receptors. Signup and view all the answers

Which of the following is NOT a use of neuromuscular blocker agents?

Treating spasticity in patients with cerebral palsy. Signup and view all the answers

What is the mechanism of action of dantrolene, a central muscle relaxant?

It interferes with calcium release from the sarcoplasmic reticulum. Signup and view all the answers

Which of the following is a characteristic of the depolarizing phase (Phase I) of succinylcholine's action?

It results in transient muscle fasciculations. Signup and view all the answers

Which of the following agents acts by binding to GABA receptors in the central nervous system?

Diazepam Signup and view all the answers

Study Notes

Cholinergic Agents

Decrease in heart rate and cardiac output, similar to vagal stimulation, by releasing acetylcholine at the sinus node (SA node)
Decrease in blood pressure via vasodilation, despite no parasympathetic innervation, but cholinergic receptors are found; increase intracellular Ca++ (atropine blocks these receptors)

Muscarinic Agents

Bethanechol: structurally related to acetylcholine, but acetate is replaced by carbamate, and choline is methylated; not hydrolyzed by acetylcholinesterase, but by other esterases; strong muscarinic effect, little or no nicotinic action; 1-hour duration of action; acts on smooth muscle of GIT and bladder
Increases GIT motility and tone, stimulates detrusor muscle of bladder, and relaxes trigone and sphincter → urine expulsion; used to treat atonic bladder (postpartum and postoperative non-obstructive retention)

Side Effects of Muscarinic Agents

Sweating, salivation, flushing, decreased blood pressure, nausea, abdominal pain, diarrhea, bronchospasm

Carbachol (Carbamylcholine)

Both muscarinic and nicotinic action; ester of carbamic acid; poor substrate for acetylcholinesterase; 1-hour duration of action; effects on both GIT and CVS due to ganglion-stimulating activity (stimulates then depresses these systems); on local eye application, causes miosis like acetylcholine; releases epinephrine from adrenal medulla by its nicotinic action; rarely used (long duration and high potency), so used in the eye only to cause constriction of pupils and decrease intraocular pressure (IOP)

Pilocarpine

Tertiary amine, stable to hydrolyze by acetylcholinesterase; less potent than acetylcholine; used for eye application only (muscarinic action); causes rapid miosis, but not able to focus (spasm of accommodation); potent stimulant of secretion of sweat, tears, and saliva, but not used for this purpose (non-selective agents); used to treat:
- Emergency lowering of IOP in both open and closed-angle glaucoma (effect lasts for 1 day)
- Promoting salivation in xerostomia (resulting from head-neck irradiation) and Sjogren's syndrome (treated by oral tablet of pilocarpine)

Side Effects of Pilocarpine

Enters CNS, causing disturbance; causes severe sweating and salivation

Cevimeline

Other non-specific cholinergic agent like pilocarpine

Anticholinesterase (Reversible)

Acetylcholinesterase enzyme that cleaves acetylcholine to acetate and choline; located in pre- and post-synaptic nerve terminals; inhibition of acetylcholinesterase → prolongs lifetime of acetylcholine and accumulates in synaptic space, introducing a response at muscarinic and nicotinic receptors (NMJ and Autonomic NS)

Neuro-Muscular Blocker Agents

Block transmission of cholinergic between motor nerve ending and the nicotinic receptor on the neuromuscular end plate of skeletal muscle; structurally analogs of acetylcholine; divided into depolarizing (acetylcholine agonist) and non-depolarizing (acetylcholine antagonists) agents; useful for:
- During surgery to produce complete muscle relaxation
- Facilitating intubation

Depolarizing Agents

Succinylcholine: used as IV, but of short duration of action, so used as continuous infusion; unlike acetylcholine, it persists for a long time in the synaptic cleft (time dependent on diffusion from motor end plate and hydrolysis by plasma cholinesterase) within synaptic cleft, not metabolized by cholinesterase until diffused to circulation; mode of action:
- Attach to nicotinic receptor and depolarize the junction
- 1st open Na channel → depolarize of the receptor (phase I) → transient muscle fasciculation
- Then, within a few minutes, on continuous attachment to receptor, make receptor incapable of transmitting further impulses; continuous depolarizing gives way to gradual repolarization as Na channel closed or blocked, causing resistance to depolarization (phase II) and flaccid paralysis

Uses of Succinylcholine

Endotracheal intubation (anesthesia induction)
Electroconvulsive shock treatment

Action of Succinylcholine

On eye: persistent mydriasis (dilate pupil), unresponsiveness to light, and cycloplegia (unable to focus for near vision); dangerous elevation of IOP, so short-acting agents like tropicamide or alpha adrenergic like phenylphrine are used for ophthalmic examination
GIT: as antispasmolytic to reduce GIT activity, not affecting HCl production
GUT: reduce hypermotility of urinary bladder (rare use in enuresis instead)
CVS: at low dose, causes bradycardia (central activation of vagal efferent outflow block M1), at high dose, causes tachycardia (block M2 in SA node)
Secretion: decrease salivation, sweat, and lacrimal glands
Uses: for eye to measure refractive errors (induce mydriasis and cycloplegia), relax both GIT and bladder, antidote for cholinergic agonist poisoning, and as an antisecretary to reduce block secretion from upper and lower RS prior to surgery

Side Effects of Succinylcholine

Dry mouth, blurred vision, tachycardia, constipation, on CNS: delirium, hallucination, and depression, collapse of respiratory system, and death; increase body temperature, especially in children; overdose treated by physostigmine

Scopolamine

Tertiary amine, belladonna-derived, peripheral effects like atropine, high action on CNS than atropine; most effective anti-motion sickness agent, sedation, but at high dose, excitement, and induce euphoria (subject to abuse); used for motion sickness and amnesic action, so used in anesthesia; used for chronic treatment of open-angle glaucoma as a solution (effect lasts for 1 week after single use); side effects and causing cataracts limit its use

Reactivation of Acetylcholinesterase (Pralidoxime)

Able to reactivate the enzyme if used at a time before aging of acetylcholinesterase (before losing its alkyl group); does not cross into CNS; acts by displacing the phosphate group from organophosphate and regenerating the enzyme; side effects like acetylcholinesterase inhibitors at high doses

Studying That Suits You

Use AI to generate personalized quizzes and flashcards to suit your learning preferences.

Description

Test your knowledge on the effects of the autonomic nervous system on heart rate, blood pressure, gastrointestinal system, and other physiological functions. Explore topics like vagal stimulation, cholinergic receptors, and intracellular calcium regulation.