Pharmacology: Atropine Mechanism and Actions
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Questions and Answers

What is the primary mechanism of action of atropine on cholinergic receptors?

  • It activates N receptors directly.
  • It competes with ACh for binding sites on M receptors. (correct)
  • It irreversibly binds to M receptors.
  • It enhances ACh binding to receptors.

    • Which physiological effect results from atropine's action on the eye?

  • Enhanced near vision focus.
  • Persistent mydriasis and cycloplegia. (correct)
  • Increased sensitivity to light.
  • Contraction of the pupil.

    • What can overcome the blockade caused by atropine?

  • A decreased concentration of ACh.
  • Use of competitive antagonists for N receptors.
  • A larger concentration of ACh. (correct)
  • Inhibition of N receptors.

    • Which receptor subtype does atropine have the highest selectivity for?

    <p>M receptors.</p> Signup and view all the answers

    How long is the typical duration of action for atropine when administered systemically?

    <p>4 hours.</p> Signup and view all the answers

    What is a significant effect of atropine on the gastrointestinal tract?

    <p>It reduces smooth muscle activity.</p> Signup and view all the answers

    In patients with close-angle glaucoma, what is the concern regarding intraocular pressure?

    <p>It may rise dangerously high.</p> Signup and view all the answers

    Which drug is considered a selective M1-receptor antagonist for reducing gastric acid secretion?

    <p>Pirenzepine</p> Signup and view all the answers

    What effect does atropine have on the urinary system?

    <p>Relaxes smooth muscle in the bladder wall.</p> Signup and view all the answers

    What is a potential side effect of atropine related to salivary glands?

    <p>Drying of the oral mucous membranes.</p> Signup and view all the answers

    In which scenario is atropine less effective compared to other treatments for respiratory issues?

    <p>In chronic obstructive pulmonary disease (COPD).</p> Signup and view all the answers

    What cardiovascular effect does atropine produce at low doses?

    <p>Bradycardia from M1 receptor blockade.</p> Signup and view all the answers

    What condition might result from atropine use in infants and children?

    <p>Atropine fever.</p> Signup and view all the answers

    What potential outcome may occur with the use of short-acting agents in treatment related to intraocular pressure?

    <p>Reduced risk of significant pressure rise.</p> Signup and view all the answers

    Which medication type has largely replaced nonselective muscarinic antagonists as inhibitors of gastric acid secretion?

    <p>Histamine type-2 H2 receptor antagonists.</p> Signup and view all the answers

    What is a primary effect of ganglionic blockade on the cardiovascular system?

    <p>Decrease in arteriolar and venous tone</p> Signup and view all the answers

    Which mechanism is most likely responsible for urinary retention in men with prostatic hyperplasia when ganglionic blockers are used?

    <p>Reduced autonomic control</p> Signup and view all the answers

    Which drug is studied for possible use in reducing nicotine cravings?

    <p>Mecamylamine</p> Signup and view all the answers

    What condition is primarily treated with neuromuscular blocking drugs?

    <p>Complete muscle relaxation during surgery</p> Signup and view all the answers

    Which is a characteristic of nondepolarizing neuromuscular blockers?

    <p>They are structural analogs of acetylcholine</p> Signup and view all the answers

    What is a side effect of ganglionic blockade related to the gastrointestinal system?

    <p>Profound inhibition of motility and constipation</p> Signup and view all the answers

    Which neuromuscular blocking drug interferes with the release of Ca2+ from the sarcoplasmic reticulum?

    <p>Dantrolene</p> Signup and view all the answers

    Which of the following is NOT a clinical application of mecamylamine?

    <p>Muscle relaxation during surgery</p> Signup and view all the answers

    What effect does ganglionic blockade have on sexual functions?

    <p>Impedes both erection and ejaculation</p> Signup and view all the answers

    Which neuromuscular blocking agent was historically used by native hunters for paralyzing prey?

    <p>Curare</p> Signup and view all the answers

    What is a key characteristic of ingestion of A muscaria?

    <p>It may result in signs of atropine poisoning.</p> Signup and view all the answers

    What is the initial symptom of delayed-onset mushroom poisoning?

    <p>Nausea and vomiting</p> Signup and view all the answers

    Which of the following mushrooms is known for major toxicity involving hepatic and renal injury?

    <p>Amanita phalloides</p> Signup and view all the answers

    What treatment is NOT applicable for the type of mushroom poisoning caused by amatoxins?

    <p>Administration of atropine</p> Signup and view all the answers

    What must be used to treat both CNS and PNS effects of the organophosphate inhibitors?

    <p>Atropine</p> Signup and view all the answers

    Which of the following is true regarding pralidoxime (PAM)?

    <p>It regenerates cholinesterase associated with skeletal muscle.</p> Signup and view all the answers

    What duration may prolonged atropine treatment last for full control of muscarinic actions?

    <p>Up to 1 month</p> Signup and view all the answers

    What is the primary mechanism of action for reversible inhibitors of acetylcholinesterase (AChE)?

    <p>To competitively prevent binding of irreversible organophosphates</p> Signup and view all the answers

    What can be a life-threatening aspect of AChE inhibitors?

    <p>N and M effects of AChE inhibitors</p> Signup and view all the answers

    In what situation is prophylaxis with reversible AChE inhibitors recommended?

    <p>Anticipated lethal poisoning, such as in chemical warfare</p> Signup and view all the answers

    Which of the following muscles is most susceptible to blockade by competitive neuromuscular blockers?

    <p>Eye muscles</p> Signup and view all the answers

    At high doses, what effect do non-depolarizing muscle relaxants have on neuromuscular transmission?

    <p>They block the ion channels of the end plate.</p> Signup and view all the answers

    Which of the following drugs is NOT a non-depolarizing neuromuscular blocker derived from tubocurarine?

    <p>Succinylcholine</p> Signup and view all the answers

    What is the primary mechanism of action of non-depolarizing muscle relaxants at low doses?

    <p>Compete with ACh at the N cholinergic receptor.</p> Signup and view all the answers

    What is an expected side effect of tubocurarine due to histamine release?

    <p>Bronchospasms</p> Signup and view all the answers

    What is the correct sequence of paralysis caused by competitive blockers?

    <p>Face, jaw, larynx, limbs, and diaphragm</p> Signup and view all the answers

    Recovery from paralysis due to non-depolarizing muscle relaxants generally occurs in which order?

    <p>Diaphragm first, then intercostal, limbs, jaw, and face</p> Signup and view all the answers

    Which of the following represents a potential complication during the use of tubocurarine?

    <p>Histamine-like wheals</p> Signup and view all the answers

    Which muscarinic receptor effect is NOT caused by atropine?

    <p>Increased accommodation for near vision</p> Signup and view all the answers

    What is the primary reason atropine's effects can be countered by increasing ACh concentrations?

    <p>The binding of atropine is competitive in nature</p> Signup and view all the answers

    Which statement about the selectivity of atropine is accurate?

    <p>Atropine has higher selectivity for M receptors than N receptors</p> Signup and view all the answers

    What physiological action does atropine induce in the eye?

    <p>Dilated pupil with inability to focus</p> Signup and view all the answers

    What is a significant limitation of atropine's mechanism of action?

    <p>It cannot differentiate between M receptor subtypes</p> Signup and view all the answers

    What is the major metabolite of nicotine in the body?

    <p>Cotinine</p> Signup and view all the answers

    What is the typical half-life of nicotine after inhalation or intravenous administration?

    <p>2 hours</p> Signup and view all the answers

    Which symptom is NOT commonly associated with acute nicotine poisoning?

    <p>Fatigue</p> Signup and view all the answers

    What treatment may be employed in cases of acute nicotine poisoning?

    <p>Inducing vomiting</p> Signup and view all the answers

    How is nicotine primarily excreted from the body?

    <p>By the kidney</p> Signup and view all the answers

    What can happen if the urine is alkaline during nicotine excretion?

    <p>Reduced urinary excretion</p> Signup and view all the answers

    What is the acutely fatal dose of nicotine for an adult?

    <p>60 mg</p> Signup and view all the answers

    Which of the following signs may indicate respiratory failure due to acute nicotine poisoning?

    <p>Convulsions</p> Signup and view all the answers

    Which of the following best describes the primary therapeutic use of scopolamine?

    <p>To prevent motion sickness</p> Signup and view all the answers

    What is the role of ipratropium in treating respiratory conditions?

    <p>It enhances the effects of β2-AR agonists.</p> Signup and view all the answers

    What physiological condition arises from an imbalance of cholinergic and dopaminergic activity in Parkinson's disease?

    <p>Excessive cholinergic activity</p> Signup and view all the answers

    Which antimuscarinic drug is primarily used to treat gastrointestinal spasms?

    <p>Hyoscine-N-butylbromide</p> Signup and view all the answers

    Why is scopolamine considered more effective prophylactically for motion sickness?

    <p>It alters balance and vestibular function prior to onset.</p> Signup and view all the answers

    What distinguishes ipratropium's pharmacokinetics from atropine?

    <p>Ipratropium is poorly absorbed orally.</p> Signup and view all the answers

    What is a common adverse effect shared by scopolamine and atropine?

    <p>Dry mouth</p> Signup and view all the answers

    Which medication is primarily indicated for the management of chronic obstructive pulmonary disease (COPD)?

    <p>Ipratropium</p> Signup and view all the answers

    Which of the following is true regarding the pharmacological effects of methscopolamine?

    <p>It is used mainly for GIT diseases.</p> Signup and view all the answers

    What is a known benefit of combining an antimuscarinic agent with a dopamine precursor drug?

    <p>Enhances the effectiveness of treatment for Parkinson's symptoms.</p> Signup and view all the answers

    What is a potential cardiovascular effect of ganglionic blockade?

    <p>Decreased venous tone</p> Signup and view all the answers

    Which of the following is a common effect of ganglionic blockade on the gastrointestinal tract?

    <p>Profound inhibition of motility</p> Signup and view all the answers

    What side effect related to sexual function can occur due to ganglionic blockade?

    <p>Erection failure</p> Signup and view all the answers

    Which drug is known for its potential to treat hypertensive crises?

    <p>Trimethaphan</p> Signup and view all the answers

    What is a characteristic of neuromuscular blocking drugs?

    <p>They block cholinergic transmission at motor nerve endings</p> Signup and view all the answers

    What is a serious complication associated with ganglionic blockade in men with prostatic hyperplasia?

    <p>Urinary retention</p> Signup and view all the answers

    Which neuromuscular blocker was historically utilized by South American hunters?

    <p>Tubocurarine</p> Signup and view all the answers

    What is the primary mechanism of action of competitive neuromuscular blockers?

    <p>They bind to nicotinic receptors and block the action of acetylcholine</p> Signup and view all the answers

    What can occur as a result of excessive release of histamine due to non-depolarizing muscle relaxants?

    <p>Hypotension</p> Signup and view all the answers

    Which agent is known for profoundly inhibiting muscle relaxation and is used during surgery?

    <p>Curare</p> Signup and view all the answers

    What symptoms typically manifest 6-12 hours after ingesting certain types of mushrooms?

    <p>Hepatic and renal cellular injury</p> Signup and view all the answers

    What is the primary treatment recommended for the muscarinic effects of organophosphate inhibitors?

    <p>Atropine</p> Signup and view all the answers

    Which of the following is NOT a recommended treatment for mushroom poisoning from amatoxins?

    <p>Intravenous atropine</p> Signup and view all the answers

    What mechanism prevents the binding of irreversible organophosphate inhibitors?

    <p>Pretreatment with reversible AChE inhibitors</p> Signup and view all the answers

    How often may atropine sulfate be administered intravenously for effective treatment?

    <p>Every 5-15 minutes</p> Signup and view all the answers

    Which of the following agents is used to regenerate cholinesterase after exposure to organophosphate compounds?

    <p>Pralidoxime (PAM)</p> Signup and view all the answers

    Which effect can result from both N and M effects of AChE inhibitors?

    <p>Life-threatening symptoms</p> Signup and view all the answers

    What is a notable pharmacological characteristic of pralidoxime?

    <p>It does not enter the CNS</p> Signup and view all the answers

    What type of mushrooms typically causes major toxicity through hepatotoxicity?

    <p>Amanita phalloides</p> Signup and view all the answers

    Where are muscarinic effects primarily exerted during poisoning treatment?

    <p>Both CNS and PNS</p> Signup and view all the answers

    Study Notes

    Atropine

    • Atropine and related compounds have a higher affinity for muscarinic receptors (M) than for nicotinic (N) receptors
    • Atropine competitively binds to cholinergic receptors, blocking acetylcholine (ACh) and other cholinergic agonists from stimulating these receptors
    • Atropine can be overcome by increasing the concentration of ACh at the receptor sites or by using equivalent muscarinic agonists (bethanechol)
    • Atropine is highly selective for M receptors, but it does not discriminate between the M1, M2, and M3 subgroups

    ### Physiological Actions of Atropine

    • Eye: Atropine blocks cholinergic activity in the pupillary sphincter muscles and ciliary muscles of the eye, resulting in mydriasis (dilated pupils), cycloplegia (paralysis of ciliary muscles), and inability to focus for near vision.
    • Gastrointestinal Tract (GIT): Atropine has antispasmodic actions, reducing GIT activity. It does not significantly reduce HCl production, making it ineffective in promoting peptic ulcer healing.
    • Urinary system: Atropine relaxes smooth muscle of the ureter and bladder wall, slowing voiding.
    • Secretions: Atropine blocks salivary glands, causing xerostomia (dry mouth). It also affects sweat glands, suppressing thermoregulatory sweating.
    • Respiratory system: Atropine has limited effectiveness in treating chronic obstructive pulmonary disease (COPD) because it blocks both inhibitory and stimulatory M receptors.
    • Cardiovascular: Atropine can affect the cardiovascular system depending on the dose. Low doses may decrease cardiac rate, while higher doses may increase cardiac rate.

    ### Neuromuscular Blocking Drugs

    • These drugs block cholinergic transmission between motor nerve endings and nicotinic receptors on the neuromuscular end plate of skeletal muscle.
    • They can be classified as either nondepolarizing (competitive) blockers or depolarizing blockers.
    • Clinical applications include producing muscle relaxation during surgery.

    Nondepolarizing (Competitive) Blockers

    • Examples: tubocurarine, atracurium, cisatracurium, doxacurium, metocurine, mivacurium, pancuronium, rocuronium, pipecurium, and vecuronium.
    • These blockers bind to the N cholinergic receptor, competitively blocking ACh and preventing depolarization of the muscle cell membrane.
    • Their action can be overcome by increasing ACh concentration in the synaptic gap.

    Pharmacological Actions of Nondepolarizing Muscle Relaxants

    • Sequence and characteristics of paralysis: Muscles of the face and eye are most susceptible to paralysis, followed by the jaw, larynx, limbs, neck, trunk, intercostal muscles, and lastly the diaphragm. Recovery occurs in reverse order.
    • Histamine release: Tubocurarine can produce histamine-like effects, including wheals, bronchospasms, hypotension, and excessive secretions.

    Treatment of Cholinergic Poisoning

    • Antimuscarinic agents: Treat both the N and M effects of AChE inhibitors. Atropine is used to treat both CNS and PNS effects of organophosphate inhibitors.
    • Reversible inhibitors of the enzyme: Pretreatment with reversible inhibitors of AChE can competitively prevent binding of irreversible organophosphate inhibitors.
    • Cholinesterase regenerator compounds: Oxime agents like pralidoxime (PAM) and diacetylmonoxime (DAM) can hydrolyze the phosphorylated enzyme, if the complex has not "aged."
    • Mechanism of action: Oximes have high affinity for the phosphorus atom and can regenerate cholinesterase.
    • Pralidoxime: Most effective in regenerating cholinesterase associated with skeletal muscle neuromuscular junctions. It does not enter the CNS and is ineffective in reversing central effects of organophosphate poisoning.

    Atropine

    • Atropine blocks the action of acetylcholine (ACh) by competitively binding to muscarinic (M) receptors
    • Atropine’s action can be overcome with a sufficiently high concentration of ACh or muscarinic agonists
    • Atropine is highly selective for M receptors, with low potency at nicotinic (N) receptors
    • Atropine does not discriminate between M1, M2, and M3 subtypes of muscarinic receptors

    Atropine - Physiological Actions

    • Atropine blocks cholinergic activity in the pupillary sphincter muscles of the iris and ciliary muscles of the eye
    • This results in dilated pupils (mydriasis), unresponsiveness to light, paralysis of ciliary muscles (cycloplegia), and inability to focus for near vision

    Scopolamine

    • Scopolamine is similar to atropine but has limited therapeutic use, primarily for preventing motion sickness and blocking short-term memory
    • Scopolamine is more effective prophylactically for motion sickness than as a treatment
    • Scopolamine can be absorbed through the skin and has similar adverse effects to atropine

    Ipratropium

    • Ipratropium is a quaternary derivative of atropine that is poorly absorbed orally and has minimal CNS effects
    • Inhaled ipratropium is useful for treating asthma in patients who cannot tolerate β2-adrenergic receptor (β2-AR) agonists or as a combination therapy with β2-AR agonists
    • Inhaled ipratropium is also used for managing chronic obstructive pulmonary disease (COPD)

    Hyoscine-N-butylbromide

    • Hyoscine-N-butylbromide is a structural analog of hyoscine used to treat GI spasms

    Other Anti-Muscarinic Drugs

    • Methscopolamine, a quaternary ammonium derivative of scopolamine, lacks CNS effects and is used for treating gastrointestinal (GIT) diseases
    • Homatropine methylbromide, a quaternary derivative of homatropine, is less potent than atropine but has ganglionic blocking properties

    Nicotine

    • Nicotine is a potent stimulant that acts primarily on nicotinic receptors in the CNS and PNS
    • Nicotine increases the release of dopamine in the brain, leading to feelings of pleasure and reward
    • Nicotine has a short half-life of approximately 2 hours
    • Nicotine is metabolized primarily in the liver and excreted by the kidneys
    • Acute nicotine poisoning can be fatal and manifests with symptoms like nausea, vomiting, headache, dizziness, and respiratory distress

    Non-Depolarizing Ganglionic Blockers

    • These agents block the action of acetylcholine at autonomic ganglia
    • Examples include trimethaphan, mecamylamine, hexamethonium, and tetraethylammonium
    • These drugs are rarely used due to their nonselective nature and the availability of more selective autonomic blockers

    Ganglionic Blockers - Organ System Effects

    • Cardiovascular system: Blood vessels receive vasoconstrictor fibers from the sympathetic nervous system, leading to decreased vascular tone and possible hypotension
    • Gastrointestinal (GIT): Reduced secretions and impaired motility, potentially leading to constipation
    • Genitourinary: Impaired function, particularly in men with prostatic hyperplasia, leading to potential urinary retention
    • Sexual functions: Impairment of both erection and ejaculation

    Neuromuscular Blocking Drugs

    • These drugs block cholinergic transmission at the neuromuscular junction, causing muscle relaxation
    • They are classified as either non-depolarizing (competitive) or depolarizing blockers
    • These drugs are used clinically to induce muscle relaxation during surgery

    Non-Depolarizing (Competitive) Blockers

    • These drugs competitively block the binding of acetylcholine to nicotinic receptors at the neuromuscular junction
    • Examples include curare, tubocurarine, and pancuronium

    Treatment of Cholinergic Poisoning

    • Antimuscarinic agents: Used to block the muscarinic effects of cholinesterase inhibitors, such as atropine
    • Cholinesterase regenerator compounds: Used to reverse the effects of irreversible cholinesterase inhibitors, such as pralidoxime (PAM)
    • Symptomatic treatment: Additional interventions like supportive care and management of respiratory symptoms

    Mushroom Poisoning

    • Symptoms: Nausea, vomiting, and delayed-onset hepatic and renal injury
    • Atropine is ineffective for this form of mushroom poisoning
    • Amatoxins in some mushrooms inhibit RNA polymerase

    Chemical Warfare Nerve Gases

    • These agents are highly potent cholinesterase inhibitors that can cause severe and potentially fatal poisoning
    • Treatment involves large doses of atropine to block the muscarinic effects
    • Pralidoxime (PAM) can be used to reactivate the cholinesterase enzyme if the poisoning is not too advanced
    • Prophylactic treatment with reversible cholinesterase inhibitors, like pyridostigmine, is reserved for situations where exposure to nerve gases is likely

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    Description

    This quiz covers the pharmacological properties of Atropine, focusing on its affinity for muscarinic and nicotinic receptors. It will also explore the physiological actions of Atropine in the eye and gastrointestinal tract. Test your understanding of how Atropine affects cholinergic activity and its clinical applications.

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