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2# Gastric & intestinal motility
Q1. The muscularis externa of the gastrointestinal tract consists primarily of which two smooth muscle layers?
Inner longitudinal and outer circular
Inner circular and outer longitudinal
Inner oblique and outer circular
Inner longitudinal and outer oblique
Explanation:
The muscularis externa contains an inner circular layer and an outer longitudinal layer that function together to produce GI motility. :contentReference[oaicite:0]{index=0}
Q2. Sympathetic innervation of the gastrointestinal tract originates mainly from which spinal cord segments?
C1–C8
T1–T4
T5–L2
L4–S4
Explanation:
Sympathetic fibers supplying the GI tract originate from spinal cord segments T5–L2 and generally inhibit gastrointestinal motility.
Q3. The primary neurotransmitter released by sympathetic fibers affecting the GIT is:
Acetylcholine
Dopamine
Serotonin
Norepinephrine
Explanation:
Sympathetic fibers release norepinephrine which inhibits gastrointestinal smooth muscle activity and reduces motility.
Q4. Which component of the autonomic nervous system increases gastrointestinal motility and secretion?
Parasympathetic nervous system
Sympathetic nervous system
Somatic nervous system
Central nervous system
Explanation:
Parasympathetic stimulation increases gastrointestinal motility and secretions, mainly through acetylcholine release.
Q5. The enteric nervous system contains approximately how many neurons?
1 million
100 million
500 million
1 billion
Explanation:
The enteric nervous system contains about 100 million neurons and functions as a local nervous system within the GI tract.
Q6. Which enteric plexus primarily controls gastrointestinal motility?
Submucosal plexus
Celiac plexus
Myenteric plexus
Auerbach ganglion
Explanation:
The myenteric plexus primarily regulates GI motility including muscle tone, contraction intensity, and propagation of peristaltic waves.
Q7. Which neurotransmitter released by inhibitory neurons relaxes gastrointestinal sphincters?
Acetylcholine
Serotonin
Dopamine
VIP
Explanation:
Vasoactive intestinal peptide (VIP) is released by inhibitory neurons in the myenteric plexus and causes relaxation of GI sphincters.
Q8. The resting membrane potential of small intestinal smooth muscle is approximately:
-56 mV
-90 mV
-20 mV
0 mV
Explanation:
The resting membrane potential of intestinal smooth muscle is about -56 mV (range −50 to −60 mV).
Q9. Which condition makes intestinal smooth muscle less excitable?
Parasympathetic stimulation
Sympathetic stimulation
Stretching of the intestinal wall
Acetylcholine release
Explanation:
Sympathetic stimulation makes the resting potential more negative, reducing excitability of intestinal smooth muscle.
Q10. The pacemaker cells responsible for generating slow waves in the GIT are:
Goblet cells
Enterocytes
Interstitial cells of Cajal
Chief cells
Explanation:
Interstitial cells of Cajal act as pacemaker cells that generate slow waves (basic electrical rhythm) in GI smooth muscle.
Q11. The basic electrical rhythm (slow waves) in the stomach occurs at approximately:
12/min
8/min
6/min
3/min
Explanation:
Slow wave frequency varies by region; in the stomach it occurs about 3 times per minute.
Q12. Spike potentials in GI smooth muscle are primarily caused by influx of:
Potassium
Calcium and sodium
Chloride
Magnesium
Explanation:
Spike potentials are true action potentials produced mainly by calcium influx and some sodium influx.
Q13. Slow waves in GI smooth muscle primarily:
Determine rhythmicity of contractions
Directly cause contraction
Inhibit muscle activity
Control secretion only
Explanation:
Slow waves do not cause contraction directly but determine the rhythmic pattern that allows spike potentials to trigger contractions.
Q14. Propulsive movement of the gastrointestinal tract is called:
Segmentation
Haustration
Peristalsis
Tonic contraction
Explanation:
Peristalsis is the propulsive movement that pushes contents forward along the GI tract.
Q15. Migrating motor complexes occur primarily during:
Immediately after meals
Digestion
Intestinal absorption
Fasting periods
Explanation:
Migrating motor complexes occur during fasting to clear residual food from the stomach and small intestine.
Q16. The hormone that regulates migrating motor complexes is:
Motilin
Gastrin
Secretin
CCK
Explanation:
Motilin stimulates migrating motor complexes during fasting.
Q17. Rush peristalsis is most commonly associated with:
Constipation
Normal digestion
Infectious diarrhea
Peptic ulcer
Explanation:
Rush peristalsis occurs in severe intestinal irritation such as infectious diarrhea to rapidly clear the intestine.
Q18. Which hormone slows gastric emptying by inhibiting stomach contraction?
Gastrin
CCK
Motilin
VIP
Explanation:
Cholecystokinin (CCK) inhibits gastric contractions and slows gastric emptying.
Q19. Which factor most strongly accelerates gastric emptying?
Fat-rich meal
Protein-rich meal
Acidic chyme
Carbohydrate-rich meal
Explanation:
Carbohydrates empty from the stomach faster than proteins, which empty faster than fats.
Q20. Distension of the duodenum causes what effect on gastric emptying?
Delays gastric emptying
Accelerates gastric emptying
No effect
Stimulates gastric secretion
Explanation:
Duodenal distension activates the enterogastric reflex, which slows gastric emptying.
Q21. Segmentation contractions in the small intestine primarily function to:
Propel chyme rapidly
Move contents backward
Mix intestinal contents
Prevent reflux
Explanation:
Segmentation contractions mix chyme and enhance contact with intestinal mucosa.
Q22. Peristalsis requires the presence of which plexus?
Submucosal plexus
Myenteric plexus
Celiac plexus
Cardiac plexus
Explanation:
The myenteric plexus is essential for coordinating peristaltic movements in the gastrointestinal tract.
Q23. Which hormone enhances intestinal peristalsis?
Secretin
Somatostatin
GIP
Gastrin
Explanation:
Gastrin enhances intestinal peristalsis along with CCK and motilin.
Q24. The ileocecal valve primarily functions to:
Prevent backflow from cecum to ileum
Mix colonic contents
Absorb electrolytes
Control bile secretion
Explanation:
The ileocecal valve prevents backflow of colonic contents into the small intestine.
Q25. Distension of the cecum causes:
Relaxation of ileocecal valve
Increased tone of ileocecal valve
Increased ileal peristalsis
Gastric emptying
Explanation:
Distension of the cecum increases the tone of the ileocecal valve and decreases ileal peristalsis.
Q26. Paralytic ileus is most commonly caused by:
Mechanical obstruction
Hyperactivity of ENS
Inhibition of intestinal smooth muscle
Excess gastrin secretion
Explanation:
Paralytic ileus occurs when intestinal smooth muscle activity is inhibited, often after abdominal surgery or peritoneal irritation.
Q27. Mass movements of the colon typically occur:
Every 5 minutes
Once per week
Continuously
1–3 times per day
Explanation:
Mass movements occur 1–3 times daily and move fecal matter toward the rectum.
Q28. The urge to defecate typically occurs when rectal pressure reaches approximately:
18 mmHg
5 mmHg
40 mmHg
80 mmHg
Explanation:
The urge to defecate occurs when rectal pressure rises to about 18 mmHg.
Q29. The parasympathetic defecation reflex originates primarily in which spinal segments?
T5–T10
S2–S4
L1–L3
C5–C8
Explanation:
The parasympathetic defecation reflex originates from sacral spinal segments S2–S4.
Q30. Which component of feces contributes most to stool composition?
Protein
Fat
Dead bacteria
Inorganic salts
Explanation:
Approximately 30% of feces consists of dead bacteria, making it the largest component.