L25, 26, 27 Parasympathetic, enteric nervous systems and snesory/motor pathways

Question 1

25

What are the major neurotransmitters in the autonomic nervous system (ANS)?

Answer 1

Acetylcholine (ACh): Used in both parasympathetic and sympathetic ganglia and at parasympathetic target organs.

Noradrenaline (NA): Used at most sympathetic postganglionic synapses.

Others: Dopamine (in renal vasculature), ATP, and nitric oxide (NO) in specific tissues.

Question 2

25

What receptors are associated with the parasympathetic nervous system?

Answer 2

Nicotinic receptors (nAChRs): Found at ganglia.

Muscarinic receptors (mAChRs): Found at target tissues (heart, glands, smooth muscle).

mAChR subtypes: M1–M5 (M1, M2, M3 most clinically relevant).

Question 3

25

What are the main receptor types for ACh in the ANS?

Answer 3

Nicotinic receptors: Ligand-gated ion channels in ganglia and adrenal medulla.

Muscarinic receptors: G-protein-coupled receptors at parasympathetic effector sites.

Question 4

25

How is acetylcholine (ACh) synthesised?

Answer 4

Choline + Acetyl-CoA → Acetylcholine + CoA
Catalyzed by Choline Acetyltransferase (ChAT) in nerve cytoplasm.

Question 5

25

How is choline taken up into the nerve terminal?

Answer 5

Via a Na⁺-dependent high-affinity carrier.
Drug: Hemicholinium inhibits this uptake, leading to ACh depletion (no clinical use).

Question 6

25

How is ACh stored in vesicles?

Answer 6

Stored via an ATP-dependent vesicular pump.
Drug: Vesamicol inhibits this pump → ACh depletion (experimental tool).

Question 7

25

How is ACh released?

Answer 7

By Ca²⁺-dependent exocytosis of vesicles.
Toxins:

Black widow venom (α-latrotoxin): massive release → depletion.

Botulinum toxin: blocks release → used to treat muscle spasms, sweating, cosmetic use.

Question 8

25

How is ACh inactivated after release?

Answer 8

Hydrolyzed by acetylcholinesterase (AChE) into choline and acetate.
Diffusion plays little role unless AChE is inhibited.

Question 9

25

What mechanisms regulate ACh release (feedback)?

Answer 9

Muscarinic autoreceptors (mAChRs): inhibit further ACh release.

ATP → Adenosine: inhibits release via A1 receptors.

Noradrenaline: inhibits ACh via α2-adrenoceptors (sympathetic cross-talk).

Opioids (e.g., morphine): inhibit ACh → constipation.

Question 10

25

Name 5 parasympathomimetic (muscarinic agonist) drugs.

Answer 10

Acetylcholine

Carbachol

Muscarine

Pilocarpine

Oxotremorine

Question 11

25

What are the effects of parasympathomimetics?

Answer 11

↓ Heart rate and cardiac output

Smooth muscle contraction (e.g., bronchoconstriction, bladder contraction)

Increased glandular secretions: sweat, tears, saliva, bronchial mucus

Question 12

25

What are clinical uses and dangers of parasympathomimetics?What are clinical uses and dangers of parasympathomimetics?

Answer 12

Use: Glaucoma (pilocarpine), Sjögren’s syndrome (dry mouth)

Misuse/Toxicity: Mushroom poisoning (muscarine in Inocybe species)

Question 13

25

Name common muscarinic antagonists and their uses.

Answer 13

Atropine: Bradycardia, pre-op to reduce secretions

Ipratropium: Asthma

Tropicamide: Dilate pupils

Oxybutynin: Overactive bladder

Hyoscine: Motion sickness

Pirenzepine: Reduce gastric acid secretion

Question 14

25

What are the general effects of muscarinic antagonists?

Answer 14

↑ Heart rate

↓ Secretions (dry mouth, dry eyes)

Relax smooth muscle (bronchodilation, urinary retention)

CNS effects: sedation, hallucination (especially with hyoscine)

Question 15

25

What are the main divisions of the autonomic nervous system?

Answer 15

Sympathetic – ‘Fight or flight’ response

Parasympathetic – ‘Rest and digest’ activities

Enteric – Controls gastrointestinal function (can act independently)

Question 16

25

Outline the six key steps in cholinergic neurotransmission.

Answer 16

1. Supply of choline (via Na⁺-dependent carrier from blood)
2. Synthesis of ACh (by choline acetyltransferase, ChAT)
3. Storage in vesicles (via ATP-dependent pump)
4. Release by Ca²⁺-dependent exocytosis
5. Inactivation by acetylcholinesterase
6. Feedback inhibition via presynaptic receptors

Question 17

25

Which drugs affect the supply of choline in cholinergic nerves?

Answer 17

Hemicholinium: Inhibits the high-affinity choline carrier → prevents choline uptake → ACh depletion

Not used clinically due to widespread action

Question 18

25

What is a ‘false transmitter’ in cholinergic nerves?

Answer 18

Triethylcholine is taken up and converted by ChAT to acetyltriethylcholine, a false transmitter

Stored and released like ACh but less effective at receptors → reduces physiological activity

Question 19

25

What drug blocks vesicular storage of ACh?

Answer 19

Vesamicol blocks ATP-dependent storage pump → depletes ACh vesicles

Used experimentally; not clinically

Question 20

25

How is ACh release modulated by toxins?

Answer 20

Black widow spider venom (α-latrotoxin): Causes massive ACh release → depletion

Botulinum toxin: Blocks ACh release

Clinical uses: blepharospasm, hyperhidrosis, achalasia, cosmetic purposes

Also a biological warfare agent

Question 21

25

How is acetylcholine inactivated?

Answer 21

By acetylcholinesterase (AChE)

Rapidly hydrolyses ACh → acetate + choline

Inactivation is essential for short duration of ACh action

Diffusion plays minimal role unless AChE is inhibited

Question 22

25

How is ACh release regulated by feedback?

Answer 22

Muscarinic autoreceptors (mAChRs): Inhibit further ACh release (especially in enteric nerves)

Nicotinic autoreceptors: May enhance ACh release (less significant physiologically)

Adenosine (from ATP): Inhibits via A1 receptors

Noradrenaline (α2-adrenoceptors): Inhibits ACh release → sympathetic cross-inhibition

Opioids (µ-receptors): Inhibit ACh → contributes to constipation

Question 23

25

Describe muscarinic receptors.

Answer 23

G-protein coupled receptors (GPCRs) with 7 transmembrane domains

Subtypes: M1–M5

• M1: Gastric acid secretion, CNS
• M2: Heart (↓ rate)
• M3: Smooth muscle, glands (contraction, secretion)

Question 24

25

What are the physiological effects of parasympathomimetic drugs?

Answer 24

Cardiovascular: ↓ Heart rate, ↓ cardiac output

Smooth muscle: Contracts (e.g., GI tract, bladder), blood vessels dilate via NO (EDRF)

Glands: Increased secretion (saliva, tears, sweat, bronchial secretions)

Question 25

# 25 Which of the following best explains the mechanism of action of hemicholinium in cholinergic nerves? A. It inhibits choline acetyltransferase (ChAT), preventing ACh synthesis B. It irreversibly blocks muscarinic receptors at the effector site C. It competes with choline at the high-affinity transporter, reducing ACh synthesis D. It blocks vesicular storage of ACh, causing vesicle depletion E. It inhibits acetylcholinesterase, prolonging ACh activity

Answer 25

✅ Correct answer: C Explanation: Hemicholinium blocks the high-affinity, Na⁺-dependent choline uptake transporter → ↓ intracellular choline → ↓ ACh synthesis. A is incorrect (ChAT inhibition is not its mechanism); D refers to vesamicol; E refers to AChE inhibitors.

Question 26

# 25 A 65-year-old man is administered ipratropium inhaler for treatment of chronic obstructive pulmonary disease (COPD). What is the mechanism of this drug? A. β₂-adrenoceptor agonism B. Inhibition of phosphodiesterase C. Antagonism of nicotinic receptors D. Competitive antagonism of muscarinic receptors E. Inhibition of choline reuptake

Answer 26

✅ Correct answer: D Explanation: Ipratropium is a muscarinic antagonist that causes bronchodilation by blocking M3 receptors in bronchial smooth muscle. A = β-agonists (e.g. salbutamol); B = theophylline; C = neuromuscular blockers; E = hemicholinium.

Question 27

# 25 Which of the following clinical scenarios would most likely benefit from atropine administration? A. A patient with closed-angle glaucoma B. A patient with bradycardia after vagal stimulation during surgery C. A patient with urinary retention due to prostate enlargement D. A patient with uncontrolled hypertension E. A patient experiencing hallucinations from hyoscine overdose

Answer 27

✅ Correct answer: B Explanation: Atropine is used to treat bradycardia, especially vagally mediated. A = contraindicated (mydriasis increases intraocular pressure); C = worsens retention; E = would require atropine withdrawal, not administration.

Question 28

# 25 Which of the following statements about acetylcholine release is TRUE? A. Release is independent of calcium influx B. Vesamicol enhances vesicular packaging of ACh C. α-latrotoxin inhibits vesicle fusion D. Botulinum toxin prevents exocytosis of ACh vesicles E. Choline is synthesised de novo in the nerve terminal

Answer 28

✅ Correct answer: D Explanation: Botulinum toxin cleaves SNARE proteins, preventing vesicle fusion and ACh release. A = false (Ca²⁺ is essential); B = vesamicol inhibits vesicle loading; C = α-latrotoxin causes massive release; E = choline is taken up from plasma.

Question 29

# 25 A patient ingests a mushroom of the Inocybe species. Which of the following signs is MOST expected? A. Mydriasis and dry mouth B. Hyperthermia and tachycardia C. Bradycardia and excessive salivation D. Respiratory depression and miosis E. Flaccid paralysis and loss of tendon reflexes

Answer 29

✅ Correct answer: C Explanation: Inocybe mushrooms contain muscarine → muscarinic agonism → bradycardia, salivation, lacrimation, diarrhoea, bronchospasm. A = antimuscarinic effect; D = opioid toxicity; E = botulinum toxin poisoning.

Question 30

# 25 Which drug would be most appropriate to treat detrusor overactivity in a patient with urinary incontinence? A. Pilocarpine B. Atropine C. Oxybutynin D. Carbachol E. Neostigmine

Answer 30

✅ Correct answer: C Explanation: Oxybutynin is a muscarinic antagonist that reduces detrusor muscle overactivity, improving continence. A, D = muscarinic agonists (would worsen); E = enhances ACh (not suitable).

Question 31

# 25 In the enteric nervous system, which of the following substances inhibits the presynaptic release of acetylcholine? A. Nicotine B. Acetylcholine acting on nicotinic receptors C. Adenosine D. Dopamine E. Histamine

Answer 31

✅ Correct answer: C Explanation: ATP released alongside ACh can be metabolised to adenosine, which inhibits ACh release via A1 receptors. A = stimulant; B = may enhance release; D and E not involved in this context.

Question 32

# 25 A 45-year-old woman develops symptoms of dry mouth, dilated pupils, and tachycardia after taking a motion sickness medication. Which agent is most likely responsible? A. Pilocarpine B. Scopolamine (hyoscine) C. Bethanechol D. Neostigmine E. Tropicamide

Answer 32

✅ Correct answer: B Explanation: Hyoscine (scopolamine) is a centrally acting muscarinic antagonist used for motion sickness → causes anticholinergic side effects. A = agonist; C = agonist; D = AChE inhibitor; E = used ophthalmically, not systemic.

Question 33

# 25 What is the most likely effect of vesamicol administration on a functioning cholinergic nerve terminal? A. Increased choline synthesis B. Inhibition of ACh degradation C. Disruption of vesicular ACh storage D. Inhibition of choline reuptake E. Increased receptor sensitivity to ACh

Answer 33

✅ Correct answer: C Explanation: Vesamicol blocks the vesicular ACh transporter → prevents ACh from being packaged into synaptic vesicles. A, D = choline-related; B = AChE inhibitors; E = receptor-level change.

Question 34

# 25 A 70-year-old man treated for overactive bladder develops blurred vision and confusion. What is the most likely mechanism of this adverse effect? A. β-adrenoceptor activation in the CNS B. Muscarinic receptor overstimulation C. Inhibition of nicotinic ganglia D. Central antimuscarinic effect of oxybutynin E. Excess stimulation of α₁-adrenoceptors in the brainstem

Answer 34

✅ Correct answer: D Explanation: Oxybutynin has CNS penetration and causes central anticholinergic effects: confusion, blurred vision, dry mouth. B = effects would be opposite; C, E = incorrect receptor types.

Question 35

# 26 What is the enteric nervous system (ENS)?

Answer 35

The ENS is the intrinsic nervous system of the gastrointestinal (GI) tract. It can function independently of the CNS, although it is modulated by autonomic input. It is often referred to as the "second brain."

Question 36

# 26 What are the roles of extrinsic autonomic control of the gut?

Answer 36

Preparing for food (cephalic phase of digestion) Defaecation Coordinating gut function with systemic metabolic needs (e.g., during stress or rest)

Question 37

# 26 What are the primary roles of the intrinsic ENS?

Answer 37

Gut motility (e.g., peristalsis) Regulation of water and electrolyte secretion Control of blood flow Control of acid and mucus secretion Secretion of some gut hormones

Question 38

# 26 What are the two main plexuses of the ENS and their locations?

Answer 38

1. Myenteric plexus (Auerbach’s plexus): Between the longitudinal and circular muscle layers — regulates motility. 2. Submucosal plexus (Meissner’s plexus): In the submucosa — regulates secretion, blood flow, and local reflexes.

Question 39

# 26 What are the Interstitial Cells of Cajal (ICCs)?

Answer 39

A: Pacemaker-like cells within the GI tract Mediate between nerves and smooth muscle Found in: - Myenteric plexus (ICC-MY) - Within the circular muscle (ICC-IM) - At the inner surface of circular muscle (ICC-SM) Express c-Kit (CD117) and are connected to muscle via gap junctions

Question 40

# 26 What is the function of ICCs in gut motility?

Answer 40

ICCs generate rhythmic electrical slow waves that help coordinate smooth muscle contraction and peristalsis.

Question 41

# 26 What are the primary neurotransmitters of the ENS?

Answer 41

- Acetylcholine (ACh): excitatory - Nitric oxide (NO): inhibitory - ATP, serotonin (5-HT), and substance P also play key roles - Modulation by enkephalins (endogenous opioids)

Question 42

# 26 Name three classes of drugs used to reduce gastric acid secretion and give examples.

Answer 42

Proton pump inhibitors (PPIs): Omeprazole H₂-receptor antagonists: Ranitidine Prostaglandin analogues: Misoprostol (Note: muscarinic antagonists and vagotomy are obsolete approaches.)

Question 43

# 26 Name key anti-emetics and their mechanisms.

Answer 43

- H₁ antagonists: Cyclizine - Muscarinic antagonists: Hyoscine (scopolamine) - D₂ antagonists (neuroleptics): Chlorpromazine - Peripheral and central D₂ antagonists: Metoclopramide, Domperidone - 5-HT₃ antagonists: Ondansetron

Question 44

# 26 What is cisapride and why is it no longer used?

Answer 44

5-HT₄ receptor agonist that increases ACh release → prokinetic Used for gastro-oesophageal reflux Withdrawn due to cardiac arrhythmias (QT prolongation)

Question 45

# 26 What is octreotide and its clinical relevance?

Answer 45

A somatostatin analogue Used in portal hypertension Also inhibits: - - Gut hormone secretion - GI secretions - Gut motility

Question 46

# 26 How do opiates affect the gut, and give an example drug.

Answer 46

Reduce ACh release via µ-opioid receptors → ↓ motility Can cause constipation Example: Loperamide (Imodium) — peripherally acting; doesn't cross BBB due to first-pass metabolism

Question 47

# 26 What are the GI effects of antimuscarinic drugs (e.g., atropine, hyoscine)?

Answer 47

↓ Gut motility May be used to treat cramping or as premedication for surgery Also cause constipation as a side effect when used for other indications

Question 48

# 26 What is Hirschsprung’s disease?

Answer 48

Congenital absence of enteric neurons (aganglionosis), especially in the rectum or colon Causes chronic constipation and bowel obstruction Treated surgically by removing the non-functional segment

Question 49

# 26 Name two degenerative/inflammatory enteric neuropathies.

Answer 49

1.Paraneoplastic enteric neuropathy: Autoimmune (antibodies against enteric neurons) 2. Chagas disease: Caused by Trypanosoma cruzi (common in Central and South America) → leads to megacolon and megaoesophagus

Question 50

# 26 What are functional gastrointestinal disorders (FGIDs), and give one example.

Answer 50

GI disorders without identifiable structural cause Example: Irritable Bowel Syndrome (IBS) — abdominal pain with altered bowel habit (constipation or diarrhoea) Affects 10–20% of people; difficult to treat, may follow a viral illness

Question 51

# 26 What distinguishes the ENS from other parts of the autonomic nervous system?

Answer 51

The ENS can function autonomously without direct input from the brain or spinal cord It contains as many neurons as the spinal cord and includes sensory neurons, interneurons, and motor neurons Sometimes called the "brain of the gut"

Question 52

# 26 What is the significance of the ENS in coordinating peristalsis?

Answer 52

ENS integrates local reflexes using sensory input from the gut wall It coordinates circular and longitudinal muscle contraction in a highly synchronised wave Excitatory neurotransmitters (e.g., ACh) stimulate contraction behind the bolus, while inhibitory transmitters (e.g., NO) promote relaxation ahead of it

Question 53

# 26 How do enteric sensory neurons contribute to gut function?

Answer 53

Sense stretch, chemical changes, pH, and osmolarity Relay signals to interneurons and motor neurons within the ENS Initiate local reflexes (e.g., peristalsis, secretion)

Question 54

# 26 What does immunoreactivity for c-Kit (CD117) indicate in GI tissue?

Answer 54

Identifies Interstitial Cells of Cajal (ICCs) Used clinically in diagnosis of GI stromal tumours (GISTs) which are also c-Kit positive

Question 55

# 26 Why are muscarinic antagonists now largely obsolete for acid suppression?

Answer 55

Muscarinic blockade reduces acid by blocking M3 receptors, but has systemic anticholinergic side effects More selective and effective drugs now exist, such as PPIs and H₂ antagonists

Question 56

# 26 How do 5-HT₄ receptor agonists (e.g., cisapride) increase motility?

Answer 56

Enhance ACh release from enteric neurons Promote peristalsis and sphincter tone, especially in the oesophagus and stomach Withdrawn due to risk of QT interval prolongation and arrhythmias

Question 57

# 26 Why is loperamide preferred for diarrhoea over systemic opioids?

Answer 57

Acts on µ-opioid receptors in the gut wall Does not cross the blood–brain barrier due to high first-pass hepatic metabolism Minimises risk of CNS opioid effects (e.g., sedation, dependence)

Question 58

# 26 How does Chagas disease cause GI dysfunction?

Answer 58

Caused by Trypanosoma cruzi infection Leads to destruction of enteric neurons Results in achalasia, megaoesophagus, or megacolon due to failure of coordinated motility

Question 59

# 26 What are the proposed mechanisms of Irritable Bowel Syndrome (IBS)?

Answer 59

Thought to involve ENS hypersensitivity, altered gut-brain axis, and sometimes post-infectious inflammation No structural lesions on investigation Symptoms include abdominal pain, bloating, and altered bowel habits (diarrhoea or constipation)

Question 60

# 26 What is the rationale for combining atropine with neostigmine during anaesthetic reversal?

Answer 60

Neostigmine increases ACh to reverse neuromuscular blockade Atropine is given concurrently to block muscarinic side effects (e.g., bradycardia, bronchoconstriction)

Question 61

# 26 Which structure within the enteric nervous system primarily regulates gut motility? A. Submucosal plexus (Meissner's) B. Vagus nerve C. Myenteric plexus (Auerbach's) D. Dorsal motor nucleus E. Pelvic splanchnic nerves

Answer 61

✅ Correct answer: C Explanation: The myenteric plexus lies between the circular and longitudinal muscle layers and is responsible for coordinating smooth muscle contraction (i.e., motility). A = controls secretion; B, D, E = extrinsic pathways.

Question 62

# 26 Which of the following cells act as pacemakers of the gut and are positive for c-Kit (CD117)? A. Enterochromaffin cells B. Paneth cells C. Interstitial Cells of Cajal D. Goblet cells E. Submucosal neurons

Answer 62

✅ Correct answer: C Explanation: ICCs generate rhythmic slow waves for peristalsis and are c-Kit positive, which is also a marker for GI stromal tumours. A = release serotonin; B = antimicrobial; D = mucus-secreting.

Question 63

# 26 What is the main mechanism of action of loperamide in treating diarrhoea? A. Blocks serotonin receptors in the CNS B. Stimulates chloride secretion to absorb water C. Acts on µ-opioid receptors in the gut wall to reduce ACh release D. Antagonises muscarinic receptors in the colon E. Enhances 5-HT₄ receptor activity to increase motility

Answer 63

✅ Correct answer: C Explanation: Loperamide is a peripherally acting µ-opioid receptor agonist that reduces excitatory neurotransmitter (ACh) release, thereby slowing motility.

Question 64

# 26 A 32-year-old man with IBS is found to have increased visceral sensitivity without structural abnormalities. Which term best describes this condition? A. Functional gastrointestinal disorder B. Inflammatory bowel disease C. Neuropathic megacolon D. Paraneoplastic enteric syndrome E. Pseudo-obstruction

Answer 64

✅ Correct answer: A Explanation: IBS is a functional GI disorder (FGID) — symptoms without clear pathology. It often involves ENS hypersensitivity and altered gut-brain interaction.

Question 65

# 26 Which drug class is now considered obsolete for acid suppression due to poor specificity and anticholinergic side effects? A. Proton pump inhibitors B. H₂-receptor antagonists C. Muscarinic antagonists D. Prostaglandin analogues E. Dopamine antagonists

Answer 65

✅ Correct answer: C Explanation: Muscarinic antagonists (e.g., atropine) were once used to reduce acid secretion but are now obsolete due to their systemic side effects and lack of selectivity.

Question 66

# 26 Which of the following combinations is used to reverse non-depolarising neuromuscular blockade after surgery? A. Atropine and omeprazole B. Neostigmine and hyoscine C. Neostigmine and atropine D. Domperidone and metoclopramide E. Cyclizine and cisapride

Answer 66

✅ Correct answer: C Explanation: Neostigmine increases ACh to reverse blockade; atropine prevents muscarinic side effects (e.g., bradycardia). B = hyoscine is less specific and more sedating.

Question 67

# 26 Which best describes the action of cisapride on gastrointestinal motility? A. H₂ antagonist that reduces acid B. 5-HT₄ agonist that enhances ACh release C. µ-opioid agonist that slows motility D. Dopamine antagonist that increases tone E. 5-HT₃ antagonist that prevents vomiting

Answer 67

✅ Correct answer: B Explanation: Cisapride is a 5-HT₄ receptor agonist, increasing ACh release from enteric neurons → prokinetic. Withdrawn due to cardiac toxicity.

Question 68

# 26 A patient presents with chronic constipation since birth. Barium enema reveals a narrowed rectum and dilated colon. Which is the most likely diagnosis? A. Chagas disease B. Megacolon due to opioid use C. Hirschsprung’s disease D. IBS with constipation E. Crohn’s disease

Answer 68

✅ Correct answer: C Explanation: Hirschsprung’s involves congenital absence of enteric neurons, especially in the rectum → functional obstruction and upstream dilation.

Question 69

# 26 Which of the following anti-emetics acts both centrally and peripherally as a 5-HT₃ receptor antagonist? A. Metoclopramide B. Ondansetron C. Cyclizine D. Hyoscine E. Ranitidine

Answer 69

✅ Correct answer: B Explanation: Ondansetron blocks 5-HT₃ receptors in the gut and brainstem, effective for chemotherapy-induced and postoperative nausea. A = D₂ and 5-HT₄; C = H₁; D = muscarinic.

Question 70

# 26 Which drug is a somatostatin analogue used in portal hypertension and also inhibits gut hormone secretion and motility? A. Misoprostol B. Domperidone C. Cisapride D. Octreotide E. Loperamide

Answer 70

✅ Correct answer: D Explanation: Octreotide mimics somatostatin → used in variceal bleeding, also reduces GI secretions, hormones, and motility.

Question 71

# 26 Which neurotransmitter is primarily responsible for excitatory signalling in the enteric nervous system? A. Dopamine B. Nitric oxide C. Acetylcholine D. Adenosine E. GABA

Answer 71

✅ Correct answer: C Explanation: ACh is the main excitatory neurotransmitter in the ENS → promotes muscle contraction and secretion. B = inhibitory; A, D, E play modulatory roles.

Question 72

# 26 Which pathology results from autoimmune destruction of enteric neurons and is often paraneoplastic? A. Megacolon from opioid use B. Hirschsprung’s disease C. Functional bowel disorder D. Degenerative enteric neuropathy E. Achalasia

Answer 72

✅ Correct answer: D Explanation: Paraneoplastic enteric neuropathy involves autoimmune damage to enteric neurons. Chagas also causes similar neuronal destruction but is infectious.

Question 73

# 26 Which neurotransmitter is primarily responsible for inhibitory motor signals in the ENS, promoting relaxation of smooth muscle? A. Acetylcholine B. Substance P C. Serotonin D. Nitric oxide E. Histamine

Answer 73

✅ Correct answer: D Explanation: Nitric oxide (NO) is a key inhibitory neurotransmitter in the ENS, mediating smooth muscle relaxation, particularly during peristalsis.

Question 74

# 26 A patient undergoing chemotherapy develops severe vomiting. Which anti-emetic is most effective due to its action on 5-HT₃ receptors both centrally and peripherally? A. Hyoscine B. Ondansetron C. Domperidone D. Metoclopramide E. Cyclizine

Answer 74

✅ Correct answer: B Explanation: Ondansetron is a selective 5-HT₃ antagonist that works in both gut and chemoreceptor trigger zone (CTZ), making it first-line for chemo-induced emesis.

Question 75

# 26 Which statement best explains why loperamide has minimal central nervous system (CNS) effects? A. It is metabolised to a CNS-inactive form B. It selectively activates δ-opioid receptors C. It is a weak µ-opioid receptor agonist D. It has low oral bioavailability E. It undergoes high first-pass metabolism and does not cross the blood–brain barrier

Answer 75

✅ Correct answer: E Explanation: Loperamide is extensively metabolised by the liver and does not penetrate the CNS, avoiding opioid-related sedation or dependence.

Question 76

# 26 Which part of the ENS is most closely associated with controlling intestinal fluid secretion and blood flow? A. Myenteric plexus B. Submucosal plexus C. Circular smooth muscle layer D. Longitudinal muscle layer E. Vagal afferents

Answer 76

✅ Correct answer: B Explanation: The submucosal (Meissner’s) plexus regulates secretion and vasodilation within the intestinal wall.

Question 77

# 26 Which of the following drug combinations might impair GI motility as a side effect of reversing neuromuscular blockade? A. Metoclopramide and cyclizine B. Omeprazole and misoprostol C. Neostigmine and atropine D. Ranitidine and hyoscine E. Ondansetron and domperidone

Answer 77

✅ Correct answer: C Explanation: Neostigmine increases ACh, which may enhance GI motility; however, atropine counteracts this, and its antimuscarinic effect can reduce gut motility.

Question 78

# 26 Which condition is caused by the loss of inhibitory ganglion cells in the distal colon, leading to tonic contraction and proximal dilation? A. Crohn’s disease B. Megacolon from opioid use C. Hirschsprung’s disease D. Functional bowel obstruction E. Paraneoplastic neuropathy

Answer 78

✅ Correct answer: C Explanation: Hirschsprung’s disease results in the absence of ganglion cells, typically in the rectum, causing functional obstruction and colonic dilation.

Question 79

# 26 In the context of ENS pathology, which infectious disease may result in both megacolon and megaoesophagus due to destruction of enteric neurons? A. E. coli enteritis B. Rotavirus gastroenteritis C. Trypanosoma cruzi (Chagas disease) D. Norovirus E. Entamoeba histolytica infection

Answer 79

✅ Correct answer: C Explanation: Chagas disease, caused by Trypanosoma cruzi, damages ENS neurons and may lead to achalasia, megacolon, and megaoesophagus.

Question 80

# 26 Which of the following would most likely increase gut motility by enhancing ACh release from enteric neurons? A. Loperamide B. Atropine C. Cisapride D. Hyoscine E. Cyclizine

Answer 80

✅ Correct answer: C Explanation: Cisapride is a 5-HT₄ receptor agonist → stimulates ACh release → increases gut motility. Now withdrawn due to cardiac side effects.

Question 81

# 26 What is the mechanism of action of octreotide in the GI tract? A. Dopamine D₂ receptor antagonist B. H₂ receptor antagonist C. Enhances 5-HT₄ receptor activity D. Inhibits gut hormone secretion and motility via somatostatin receptor activation E. Blocks µ-opioid receptors in the gut

Answer 81

✅ Correct answer: D Explanation: Octreotide mimics somatostatin, inhibiting gut hormones, secretion, and motility; used in variceal bleeding and some diarrhoeal syndromes.

Question 82

# 26 Which of the following drugs can reduce GI motility and cause constipation as a side effect when used for motion sickness? A. Ondansetron B. Metoclopramide C. Hyoscine D. Cisapride E. Octreotide

Answer 82

✅ Correct answer: C Explanation: Hyoscine is a muscarinic antagonist that can reduce GI motility, leading to dry mouth and constipation.

Question 83

# 27 What does the term “somatic nervous system” refer to in this lecture context?

Answer 83

The somatic nervous system (SNS) involves voluntary control of skeletal muscles and sensory input from skin, joints, and muscles. This lecture focuses on SNS components associated with spinal nerves and the spinal cord.

Question 84

# 27 What is the difference between sensory and motor pathways in the somatic nervous system?

Answer 84

Sensory (afferent): Carries signals from receptors (e.g., skin, muscles, joints) to the CNS. Motor (efferent): Carries signals from the CNS to skeletal muscles to initiate movement.

Question 85

# 27 What does tract naming convention in neuroanatomy typically reflect?

Answer 85

It reflects the origin and destination of the neural pathway. E.g.: - Spinothalamic = spinal cord → thalamus - Corticospinal = cortex → spinal cord

Question 86

# 27 What is the difference between “sensory reception” and “perception”?

Answer 86

- Reception: The detection of sensory stimuli by receptors - Perception: The interpretation of that sensory information by the brain, often involving memory and decision-making

Question 87

# 27 What are the three main somatosensory tracts in the spinal cord?

Answer 87

1. Dorsal Column–Medial Lemniscus (DCML): Fine touch, vibration, proprioception 2. Spinothalamic tract: Pain, temperature, crude touch 3. Spinocerebellar tracts: Unconscious proprioception to cerebellum

Question 88

# 27 How many neurons are typically involved in sensory pathways to the cortex?

Answer 88

Three neurons: 1. First-order: From sensory receptor to spinal cord or medulla 2. Second-order: From spinal cord/brainstem to thalamus 3. Third-order: From thalamus to primary somatosensory cortex

Question 89

# 27 Where is sensory information ultimately processed in the brain?

Answer 89

In the primary somatosensory cortex of the parietal lobe. This region is somatotopically mapped, meaning different body regions correspond to specific cortical areas.

Question 90

# 27 What are the two main types of motor tracts?

Answer 90

1. Lateral motor tracts (e.g., corticospinal): Responsible for conscious, fine movement 2. Ventromedial motor tracts: Involved in unconscious functions, such as posture and balance

Question 91

# 27 How many neurons are typically involved in motor pathways to skeletal muscles?

Answer 91

Two neurons: 1. Upper motor neuron (UMN): From motor cortex to spinal cord 2. Lower motor neuron (LMN): From spinal cord to muscle

Question 92

# 27 Where do upper motor neurons primarily originate in the brain?

Answer 92

From the primary motor cortex, brainstem, and cerebellum.

Question 93

# 27 What determines the clinical outcome of a spinal cord injury?

Answer 93

The level of injury (e.g., cervical vs lumbar) Whether sensory, motor, or both pathways are affected Whether the lesion is unilateral or bilateral Whether it occurs before or after decussation (crossing over) of the tract

Question 94

# 27 What happens to reflex control as organisms evolve more complex nervous systems?

Answer 94

In simpler organisms, responses are mainly reflexive In humans, higher brain centres modulate reflexes and allow for decision-based motor activity, such as voluntary movement

Question 95

# 27 What are the key differences between sensory and motor pathways in the somatic nervous system?

Answer 95

Sensory pathways : - Afferent, meaning they carry information towards the CNS. - Typically involve three neurons: a first-order neuron (from receptor to CNS), a second-order neuron (to the thalamus), and a third-order neuron (to the somatosensory cortex). - These pathways are responsible for detecting sensations like touch, pain, temperature, vibration, and proprioception. Motor pathways: - Efferent, carrying signals from the CNS to skeletal muscles. - Involve two neurons: an upper motor neuron (from the brain to spinal cord) and a lower motor neuron (from spinal cord to muscle). - Motor pathways control voluntary movements (via lateral tracts) and involuntary posture/balance (via ventromedial tracts).

Question 96

# 27 What is the role of the dorsal column–medial lemniscus pathway?

Answer 96

It carries information about fine touch, vibration, and proprioception (body position sense). This pathway decussates (crosses over) in the medulla before ascending to the thalamus and somatosensory cortex.

Question 97

# 27 What sensations are carried by the spinothalamic tract?

Answer 97

- Lateral spinothalamic tract: carries pain and temperature - Anterior spinothalamic tract: carries crude touch and pressure It decussates in the spinal cord shortly after entering.

Question 98

# 27 What does the spinocerebellar tract do?

Answer 98

It transmits unconscious proprioceptive information to the cerebellum, helping coordinate posture and movement without conscious awareness.

Question 99

# 27 What is meant by “decussation,” and why is it clinically important?

Answer 99

Decussation is the crossing of nerve fibres from one side of the CNS to the other. It's important because damage before or after decussation determines whether the symptoms appear ipsilateral (same side) or contralateral (opposite side) to the lesion.

Question 101

# 27 How does the brain integrate sensory input after it reaches the somatosensory cortex?

Answer 101

The cortex interprets and integrates the input with other sensory modalities and with stored memories, forming a perception. This integration can inform conscious decisions or reflexive responses.

Question 102

# 27 What is the function of the ventromedial motor tracts?

Answer 102

These tracts mediate subconscious control of posture, balance, and gross motor movements. They originate mainly from the brainstem, not the cerebral cortex.

Question 103

# 27 What is the role of the cerebellum in motor control?

Answer 103

The cerebellum coordinates movement by processing unconscious proprioceptive input and adjusting motor output, ensuring smooth, accurate movements and maintaining balance and posture.

Question 104

# 27 How does the complexity of motor control evolve in higher organisms like h\umans?

Answer 104

In simpler organisms, movements are mainly reflex-based. In humans, the brain modulates spinal reflexes, allowing for voluntary, goal-directed movement. Reflexes remain, but they are under cortical influence.

Question 105

# 27 Which of the following spinal tracts is responsible for transmitting fine touch, vibration, and proprioception? A. Spinothalamic tract B. Spinocerebellar tract C. Corticospinal tract D. Dorsal column–medial lemniscus pathway E. Reticulospinal tract

Answer 105

✅ Correct answer: D Explanation: The dorsal column–medial lemniscus (DCML) system conveys fine touch, vibration, and conscious proprioception. It decussates in the medulla.

Question 106

# 27 What is the correct sequence of neurons involved in a typical sensory pathway to the cortex? A. Motor neuron → interneuron → cortex B. Receptor → lower motor neuron → cortex C. First-order → second-order → third-order neurons D. Dorsal horn → upper motor neuron → thalamus E. Posterior root → anterior horn → cerebellum

Answer 106

✅ Correct answer: C Explanation: A standard sensory pathway involves: First-order neuron: receptor to spinal cord/medulla Second-order neuron: to thalamus Third-order neuron: to somatosensory cortex

Question 107

# 27 Which tract primarily transmits pain and temperature sensations? A. Corticospinal tract B. Dorsal column C. Spinocerebellar tract D. Spinothalamic tract E. Vestibulospinal tract

Answer 107

✅ Correct answer: D Explanation: The spinothalamic tract, particularly its lateral portion, carries pain and temperature from the spinal cord to the thalamus and cortex.

Question 108

# 27 What distinguishes the corticospinal (pyramidal) tract from ventromedial motor tracts? A. It controls balance and posture subconsciously B. It originates in the cerebellum C. It regulates conscious, voluntary movement D. It carries sensory information E. It has no decussation

Answer 108

✅ Correct answer: C Explanation: The corticospinal tract originates from the motor cortex and controls voluntary, conscious movements, especially fine control of distal limbs.

Question 109

# 27 Where do the majority of corticospinal tract fibres decussate? A. Midbrain B. Thalamus C. Medulla oblongata (pyramids) D. Pons E. Cerebellum

Answer 109

✅ Correct answer: C Explanation: Approximately 80–90% of corticospinal fibres cross at the pyramidal decussation in the medulla, forming the lateral corticospinal tract.

Question 110

# 27 Which pathway conveys unconscious proprioceptive information to the cerebellum? A. Corticospinal tract B. Spinothalamic tract C. Dorsal column D. Spinocerebellar tract E. Tectospinal tract

Answer 110

✅ Correct answer: D Explanation: The spinocerebellar tracts carry unconscious proprioception to the cerebellum for coordination of movement and balance.

Question 111

# 27 A lesion affecting the anterior white commissure of the spinal cord would most likely impair which function? A. Conscious proprioception B. Motor control of distal limbs C. Reflex arcs D. Pain and temperature from both sides at the lesion level E. Cerebellar coordination

Answer 111

✅ Correct answer: D Explanation: Pain and temperature fibres from both sides decussate in the anterior white commissure, so a central lesion there causes bilateral loss of these modalities at that spinal level.

Question 112

# 27 Which region of the brain is primarily responsible for interpreting somatosensory input? A. Temporal lobe B. Primary motor cortex C. Cerebellum D. Primary somatosensory cortex E. Brainstem nuclei

Answer 112

✅ Correct answer: D Explanation: The primary somatosensory cortex (postcentral gyrus, parietal lobe) processes touch, pain, temperature, and proprioception from the body.

Question 113

# 27 Which best describes the role of the ventromedial motor system? A. Fine voluntary movement of hands B. Eye tracking movements C. Balance and postural control via subconscious pathways D. Facial muscle control E. Coordination of reflex arcs

Answer 113

Explanation: The ventromedial motor tracts (e.g., vestibulospinal, reticulospinal) control subconscious movements, especially posture and balance.

Question 114

# 27 In an upper motor neuron lesion, which of the following signs is most likely to be observed? A. Flaccid paralysis B. Fasciculations C. Hyporeflexia D. Hypertonia and hyperreflexia E. Muscle atrophy without spasticity

Answer 114

✅ Correct answer: D Explanation: Upper motor neuron (UMN) lesions lead to spasticity, hyperreflexia, and increased tone, due to loss of inhibitory cortical input.

Question 115

# 27 A 68-year-old man presents with right-sided loss of proprioception and left-sided loss of pain and temperature sensation below the waist. Where is the most likely site of the lesion? A. Left spinothalamic tract in the brainstem B. Right dorsal column in the spinal cord C. Left dorsal column in the spinal cord D. Right hemisection of the spinal cord E. Central lesion in cervical spinal cord

Answer 115

✅ Correct answer: D Explanation: This is a classic Brown-Séquard syndrome (spinal cord hemisection). - Ipsilateral loss of proprioception (dorsal columns don’t decussate until medulla) - Contralateral loss of pain and temperature (spinothalamic tract decussates in spinal cord)

Question 116

# 27 A patient has difficulty initiating voluntary movement and shows weakness in fine finger control. Which tract is most likely affected? A. Vestibulospinal B. Spinothalamic C. Corticospinal (lateral) D. Reticulospinal E. Spinocerebellar

Answer 116

✅ Correct answer: C Explanation: The lateral corticospinal tract controls voluntary, fine motor function, especially of distal limbs and digits.

Question 117

# 27 A 24-year-old rugby player suffers a hyperextension neck injury. He now has a cape-like loss of pain and temperature over his shoulders and upper arms, but light touch is preserved. What is the most likely diagnosis? A. Central cord syndrome B. Anterior cord syndrome C. Posterior cord syndrome D. Brown-Séquard syndrome E. Complete spinal transection

Answer 117

Answer: A Explanation: Central cord syndrome typically affects the decussating spinothalamic fibres near the central canal, sparing dorsal columns (touch, vibration).

Question 118

# 27 A 54-year-old woman with multiple sclerosis presents with spasticity and increased reflexes in both legs. Which part of the CNS is likely affected? A. Lower motor neurons in the anterior horn B. Corticospinal tracts C. Cerebellum D. Spinothalamic tracts E. Dorsal columns

Answer 118

✅ Correct answer: B Explanation: Spasticity and hyperreflexia indicate upper motor neuron (UMN) involvement, particularly of the corticospinal tracts.

Question 119

# 27 A lesion in the right primary motor cortex would most likely cause which of the following? A. Left-sided spastic paralysis B. Right-sided flaccid paralysis C. Bilateral loss of sensation D. Left-sided proprioception loss E. Right-sided cerebellar ataxia

Answer 119

✅ Correct answer: A Explanation: The corticospinal tract decussates in the medulla, so a lesion in the right motor cortex affects left-side voluntary movement (UMN signs).

Question 120

# 27 Which of the following best describes the spinocerebellar tract's functional role? A. Initiating reflex arcs in the spinal cord B. Providing conscious proprioceptive input to cortex C. Controlling fine hand movements D. Transmitting unconscious proprioceptive signals for coordination E. Regulating emotional response to pain

Answer 120

✅ Correct answer: D Explanation: The spinocerebellar tracts transmit unconscious proprioceptive information to the cerebellum, helping with coordination and balance.

Question 121

# 27 A lower motor neuron lesion affecting the femoral nerve would most likely result in which of the following signs? A. Spastic paralysis and increased muscle tone B. Flaccid paralysis and loss of reflexes in the quadriceps C. Contralateral loss of proprioception D. Bilateral pain and temperature loss in the thigh E. Uncoordinated hip rotation

Answer 121

✅ Correct answer: B Explanation: Lower motor neuron lesions cause flaccid paralysis, muscle wasting, and areflexia in the affected region (here, the quadriceps).

Question 122

# 27 In a neurological exam, a patient demonstrates loss of vibration sense in the lower limbs but preserved pain and temperature sensation. Which tract is most likely damaged? A. Spinothalamic B. Dorsal column C. Corticospinal D. Spinocerebellar E. Ventral horn

Answer 122

✅ Correct answer: B Explanation: Vibration and proprioception are carried by the dorsal columns, which ascend ipsilaterally until the medulla.

Question 123

# 27 Which statement best describes the function of the ventromedial (extrapyramidal) motor tracts? A. Facilitate fine motor control of the fingers B. Transmit pain from the periphery C. Modulate unconscious posture and axial control D. Provide proprioception to the cerebral cortex E. Inhibit voluntary movement during sleep

Answer 123

✅ Correct answer: C Explanation: Ventromedial tracts (e.g., vestibulospinal, reticulospinal) regulate posture, balance, and gross trunk movements, unconsciously.

Question 124

# 27 Which of the following is true regarding sensory perception in the cortex? A. It occurs in the anterior horn of the spinal cord B. It is mediated entirely by first-order neurons C. It involves integration with memory and other senses D. It is a reflex action that bypasses the brain E. It occurs in the cerebellum

Answer 124

✅ Correct answer: C Explanation: Perception involves the primary somatosensory cortex, where sensory input is interpreted, often with input from memory and other modalities.