[PCOL] 2.7 Parasympathetic Nervous System (Parasympathoplegics)

Which natural Anti-Muscarinic drug is considered the prototype for the class, derived from sources like Atropa belladona (deadly nightshade)?

A. Scopolamine (hyoscyine)

B. Ipratropium

C. Atropine (hyoscyamine)

D. Pirenzipine

C. Atropine (hyoscyamine)

Explanation: Atropine is the prototype natural Anti-Muscarinic agent, primarily an alkaloid from the Solanaceae family of plants.

What is the effect of Atropine on the M2 receptor in the heart, and what is this effect clinically termed?

A. M2 Block:Decreased acid secretion

B. M2 Block:Bronchodilation

C. M2 Block:Positive ino/chrono/dromotropism; vagolytic

D. M2 Block:Miosis

C. M2 Block:Positive ino/chrono/dromotropism; vagolytic

Explanation: Atropine blocks M2 receptors on the heart, removing parasympathetic (vagal) inhibition. This vagolytic effect results in increased heart rate (chronotropism) and conduction (dromotropism), leading to tachycardia.

What is the DOC (Drug of Choice) clinical use for Atropine related to cardiac function?

A. Management of hypertension

B. Management of stable angina

C. Management of symptomatic bradycardia

D. Management of tachyarrhythmia

C. Management of symptomatic bradycardia

Explanation: Atropine is the DOC for symptomatic bradycardia because its M2 blockade removes vagal tone, which directly increases heart rate.

M3 receptor blockade by Atropine causes loss of near vision. What is this effect called, and how long can it potentially last?

A. Miosis; lasts 5 minutes

B. Mydriasis; lasts 1 hour

C. Cycloplegia; can last up to 72 hours

D. Accommodation; is reversible immediately

C. Cycloplegia; can last up to 72 hours

Explanation: M3 blockade causes cycloplegia (paralysis of the ciliary muscle and loss of accommodation) which can be prolonged, lasting up to 72 hours.

The Anti-Muscarinic side effect "Blind as a bat" implies which ocular contraindication for Atropine?

A. Glaucoma

B. Conjunctivitis

C. Retinal detachment

D. Cataracts

A. Glaucoma

Explanation: Blind as a bat refers to Mydriasis and increased intraocular pressure due to reduced aqueous humor drainage. This makes Atropine Contraindicated in Narrow-angle glaucoma.

Which natural Anti-Muscarinic alkaloid is a potent CNS-acting agent used to treat motion sickness and as a sedative hypnotic?

A. Atropine

B. Tropicamide

C. Scopolamine (hyoscyine)

D. Benztropine

C. Scopolamine (hyoscyine)

Explanation: Scopolamine is known for its CNS effects, including sedative and anti-motion sickness properties, and is derived from Hyoscyamus niger.

Which 3o Ammonium Anti-Muscarinic drug is used in ophthalmology to cause Mydriasis and Cycloplegia?

A. Pirenzipine

B. Benztropine

C. Tropicamide

D. Ipratropium

C. Tropicamide

Explanation: Tropicamide is a 3o Ammonium compound listed in the Mydriatic/Cycloplegic group (ATCH) for eye exams (Mydriatic) and injury (Cycloplegic).

Which 4o Ammonium Anti-Muscarinic drug is the DOC for the management of Parkinsonism and EPS (Extrapyramidal Symptoms)?

A. Ipratropium

B. Tiotropium

C. Benztropine (Cogentin)

D. Oxitropium

C. Benztropine (Cogentin)

Explanation: Benztropine is a CNS-acting anticholinergic used as the DOC for Parkinson's disease and drug-induced EPS like pseudoparkinsonism.

Which 4o Ammonium Anti-Muscarinic drugs are classified as SAMA (Short Acting Muscarinic Antagonists) and LAMA (Long Acting Muscarinic Antagonists) and are the DOC for COPD?

A. Benztropine and Trihexyphenidyl

B. Atropine and Scopolamine

C. Ipratropium and Tiotropium

D. Pirenzipine and Tropicamide

C. Ipratropium and Tiotropium

Explanation: Ipratropium (SAMA) and Tiotropium (LAMA) are inhaled anticholinergics that cause bronchodilation and are the 1st line relievers/DOC for COPD and alternatives for BA.

Which M3 Blockade side effect leads to Anhidrosis (decreased sweating), which in turn causes Hyperthermia (Hot as a hare)?

A. CNS effects

B. Exocrine gland drying

C. Ileus and constipation

D. Cutaneous vasodilation

B. Exocrine gland drying

Explanation: M3 Blockade causes exocrine gland drying, including anhidrosis. The inability to sweat prevents body cooling, leading to hyperthermia. Cutaneous vasodilation (Red as a beet) is a compensatory mechanism for the fever.

The selective M1 Antagonists are primarily used as adjuncts in the management of what gastrointestinal condition?

A. Urinary incontinence

B. Bronchospastic disorders

C. Acid peptic disease (hyperacidity)

D. Motion sickness

C. Acid peptic disease (hyperacidity)

Explanation: M1 receptors in the gastric glands promote HCl secretion. Selective M1 blockers like Pirenzepine and Telenzepine are used as adjuncts to reduce acid secretion in acid peptic disease.

Which two drugs are classified as selective M1 Antagonists?

A. Dicycloverine and Clidinium

B. Pirenzepine and Telenzepine

C. Ipratropium and Tiotropium

D. Benztropine and Oxybutinin

B. Pirenzepine and Telenzepine

Explanation: Pirenzepine and Telenzepine are the selective M1 blockers listed for use in the GIT.

Selective M3 Antagonists primarily act on which two body systems to produce their clinical effects?

A. Heart and CNS

B. CNS and Lungs

C. Gastrointestinal tract and Urinary bladder

D. Skeletal muscles and Eyes

C. Gastrointestinal tract and Urinary bladder

Explanation: M3 receptors mediate smooth muscle contraction in both the GIT and the Urinary bladder (Detrusor muscle), making these the primary targets for M3 blockade.

Selective M3 Antagonists are used to manage which two hypermotility states?

A. Hypertension and Glaucoma

B. Hypermotility states (cramps) and Urinary incontinence

C. Bradycardia and Bronchospasm

D. Myasthenia Gravis and Parkinsonism

B. Hypermotility states (cramps) and Urinary incontinence

Explanation: M3 blockade relaxes smooth muscle. In the GIT, this treats hypermotility cramps. In the bladder, it relaxes the Detrusor, treating urinary incontinence (overactive bladder).

Which specific M3 Antagonist has an off-label use for cervical dilation?

A. Dicycloverine

B. Glycopyrrolate

C. Clidinium

D. Hyoscine−N−butylbromide

D. Hyoscine−N−butylbromide

Explanation: Hyoscine-N-butylbromide is listed as a selective M3 blocker used for hypermotility states with an off-label use for cervical dilation.

M3 Antagonists are clinically used as Spasmolytics for the pain associated with renal and biliary colic due to what primary mechanism?

A. Decreased acid secretion

B. Smooth muscle relaxation

C. CNS sedation

D. Increased heart rate

B. Smooth muscle relaxation

Explanation: Colic is caused by painful smooth muscle spasms. M3 Antagonists block M3-mediated contraction, resulting in smooth muscle relaxation (spasmolysis).

Which M3 Antagonist is often used as a component in combination products to manage hypermotility disorders?

A. Telenzepine

B. Glycopyrrolate

C. Dicycloverine

D. Pirenzepine

C. Dicycloverine

Explanation: Dicycloverine is listed as an M3 Antagonist used to manage hypermotility states (cramps), a common use for this class of antispasmodic agents.

Which subtype of Nicotinic receptor is targeted by Ganglionic Blockers (Hexamethonium, Trimetophan, Mecamylamine)?

A. Nm (Muscular)

B. M1 (Muscarinic)

C. Nn (Neuronal)

D. N Presynaptic

C. Nn (Neuronal)

Explanation: Ganglionic blockers inhibit the Nn receptor found in the autonomic ganglia, thereby blocking signal transmission in both the sympathetic and parasympathetic systems.

Why are Ganglionic Blockers now considered obsolete for treating hypertensive crisis?

A. They only cause bronchospasm.

B. They are poorly absorbed.

C. Their effects are unpredictable (anticholinergic and vasodilation).

D. They cause diaphragmatic paralysis.

C. Their effects are unpredictable (anticholinergic and vasodilation).

Explanation: The simultaneous blockade of both ANS branches makes their clinical effects (anticholinergic and vasodilation) highly unpredictable, leading to their obsolescence.

Which specific serious side effect is common to Nm (Neuromuscular Blockers) and requires treatment via mechanical ventilation or AChE inhibitors?

A. Hyperacidity

B. Hypertensive crisis

C. Respiratory / diaphragmatic paralysis

D. Urinary retention

C. Respiratory / diaphragmatic paralysis

Explanation: Since Nm receptors are responsible for skeletal muscle contraction, their blockade paralyzes the diaphragm, leading to respiratory / diaphragmatic paralysis, which is a major concern during surgical anesthesia.

The Depolarizing Neuromuscular Blocker Succinylcholine (Suxamethonium) causes initial Irreversible stimulation of the Nm receptors. What is the characteristic feature of its Phase 1: Depolarization?

A. Desensitization and muscle paralysis

B. Hyperkalemia

C. Tetanic muscle contraction / tremors

D. Acute kidney failure

C. Tetanic muscle contraction / tremors

Explanation: Succinylcholine acts like an ACh overdose, initially causing sustained depolarization that manifests as muscle contraction / tremors before paralysis sets in.

What is the final effect and cause of Succinylcholine's Phase 2: Desensitizing block?

A. Initial depolarization due to Na

+

inflow

B. Depolarization blockade due to Ca

2+

depletion / fatigue, resulting in paralysis

C. Increased Nm receptor sensitivity

D. Competitive inhibition of ACh

B. Depolarization blockade due to Ca

2+

depletion / fatigue, resulting in paralysis

Explanation: After initial depolarization, the receptor becomes desensitized and inactive, and Ca

2+

is depleted from the muscle cell, leading to the final muscle paralysis.

What life-threatening adverse effect is associated with Succinylcholine use, especially with inhalational anesthetics, and what is its specific antidote?

A. Rhabdomyolysis; Antidote:Neostigmine

B. Malignant hyperthermia; Antidote:Dantrolene or Bromocriptine

C. Hyperkalemia; Antidote:Edrophonium

D. Acute tubular necrosis; Antidote:Atropine

B. Malignant hyperthermia; Antidote:Dantrolene or Bromocriptine

Explanation: Malignant hyperthermia is a severe complication characterized by massive hypersecretion of Ca ions / muscle rigidity. The antidote Dantrolene acts as a ryanodine receptor antagonist to block this Ca

2+

release.

What serious electrolyte imbalance is caused by the widespread muscle breakdown (Rhabdomyolysis) induced by Succinylcholine, and what is the potential terminal consequence?

A. Hypokalemia; Terminal:Tachyarrhythmia

B. Hypernatremia; Terminal:Dehydration

C. Hyperkalemia; Terminal:Acute kidney failure

D. Hypoglycemia; Terminal:Coma

C. Hyperkalemia; Terminal:Acute kidney failure

Explanation: Muscle cell breakdown releases potassium into the blood (Hyperkalemia), which can lead to cardiac arrest. Rhabdomyolysis also releases myoglobin, which is toxic to the renal tubules, causing acute kidney failure.

What is the overall mechanism of action (MOA) for Non-Depolarizing Neuromuscular Blockers (NMBs), such as Tubocurarine?

A. Irreversibly stimulates Nm receptors

B. Inhibits AChE

C. Reversibly blocks Nm receptors

D. Stimulates ACh release

C. Reversibly blocks Nm receptors

Explanation: Non−Depolarizing NMBs (Curare derivatives) are competitive antagonists that reversibly block Nicotinic Muscular (Nm) receptors, leading to immediate skeletal muscle relaxation.

What is the major adverse effect (AE) associated with Tubocurarine (prototype) that can lead to an anaphylactoid reaction, and what is the DOC for its management?

A. Bronchodilation; DOC:Atropine

B. Hyperkalemia; DOC:Insulin

C. Histamine release; DOC:Epinephrine

D. Tachycardia; DOC:Lidocaine

C. Histamine release; DOC:Epinephrine

Explanation: Tubocurarine often causes Histamine release from mast cells, resulting in bronchospasm and hypotension (anaphylactoid reaction), which requires Epinephrine for management.

What treatment can be used to reverse the blockade caused by Non-Depolarizing NMBs like Atracurium?

A. Tetanic stimulation or Cholinesterase inhibitors (Neostigmine)

B. Sugammadex

C. Dantrolene

D. Atropine

A. Tetanic stimulation or Cholinesterase inhibitors (Neostigmine)

Explanation: Since the blockade is competitive, increasing the concentration of ACh (via Cholinesterase inhibitors) or Tetanic stimulation can overcome the blockade. Neostigmine is the chemical antidote.

Which specific Steroidal NMB can block Muscarinic receptors in the heart, leading to tachycardia as a side effect?

A. Atracurium

B. Rocuronium

C. Pancuronium

D. Vecuronium

C. Pancuronium

Explanation: Pancuronium is a Steroidal NMB that has vagolytic effects (M2 blockade in the heart) in addition to Nm blockade, often resulting in tachycardia.

Which Steroidal NMBs (Rocuronium, Vecuronium) have the antidote Sugammadex?

A. Pancuronium

B. Tubocurarine

C. Isoquinolines

D. Steroidals

D. Steroidals

Explanation: Sugammadex is a specific Antidote for Steroidal NMBs (-curonium drugs) Rocuronium and Vecuronium. It works by encapsulating the drug and inactivating it.

Which Nm Antagonist class (-curonium drugs) is characterized by No initial muscle contraction and Direct / immediately cause paralysis?

A. Depolarizing NMBs (Succinylcholine)

B. Steroidal NMBs

C. Isoquinoline NMBs

D. Ganglionic Blockers

B. Steroidal NMBs

Explanation: Non−Depolarizing NMBs (Steroidals) immediately cause paralysis by blocking the receptor without the initial depolarizing phase of Succinylcholine (muscle contraction/tremors).

Ganglionic Blockers (Hexamethonium, Trimetophan, Mecamylamine) were historically used to treat Hypertensive crisis. What specific severe condition can Trimetophan be used to manage?

A. Urinary retention

B. Diaphragmatic paralysis

C. Pulmonary edema and dissecting aortic aneurysm

D. Symptomatic bradycardia

C. Pulmonary edema and dissecting aortic aneurysm

Explanation: Trimetophan's ability to cause controlled hypotension (vasodilation) made it useful in managing severe conditions like pulmonary edema and dissecting aortic aneurysm.

Botulinum Toxin and β-Bungarotoxin are Neurotoxins that inhibit exocytosis of ACh. What are the active components and MOAs of these two toxins?

A. Botulinum:Phospholipase; β-Bungarotoxin:Peptidase

B. Botulinum:Peptidase; β-Bungarotoxin:Phospholipase

C. Both:Competitive Nm blockers

D. Both:Inhibit AChE

B. Botulinum:Peptidase; β-Bungarotoxin:Phospholipase

Explanation: Botulinum Toxin is a peptidase that cleaves fusion proteins. β-Bungarotoxin is a phospholipase that degrades the nerve terminal membrane, and both result in reduced ACh release.

Laudanosine is a metabolite of which Isoquinoline Non−Depolarizing Neuromuscular Blocker (NMB)?

A. Tubocurarine

B. Pancuronium

C. Atracurium

D. Succinylcholine

C. Atracurium

Explanation: Laudanosine is produced during the Hofmann elimination (spontaneous non-enzymatic breakdown) of Atracurium.

What is the major adverse effect associated with the Atracurium metabolite Laudanosine?

A. Malignant hyperthermia

B. Diaphragmatic paralysis

C. Histamine release

D. Induction of seizures (CNS stimulation)

D. Induction of seizures (CNS stimulation)

Explanation: Laudanosine is a lipophilic, CNS-penetrant metabolite that can induce seizures at high concentrations, particularly in patients with renal failure or when high doses are used.

Laudanosine is typically eliminated via the kidneys and liver. Its potential to induce seizures is increased in patients with what concurrent condition?

A. Cardiac failure

B. Renal impairment

C. COPD

D. Glaucoma

B. Renal impairment

Explanation: Since Laudanosine is eliminated via the kidneys, renal impairment can lead to its accumulation, increasing the risk of CNS toxicity (seizures).