gastric physiology 2: Proteases, gastric motility and emptying

Question 1

what do chief cells produce?

Answer 1

pepsinogen (synthesised in inactive form (zymogen)

Question 2

how is pepsinogen mediated?

Answer 2

by input from enteric nervous system (ACh)

secretion parallels HCL secretion

Question 3

Protease activation

Answer 3

• Conversion of pepsinogen to pepsin is pH dependent
• Most efficient when pH <2
• Positive feedback loop (Pepsin also catalyses the reaction)
• Pepsin only active at low pH. Irreversible inactivation in small intestine by HCO3-

Question 4

role of pepsin in protein digestion

Answer 4

• Not essential (protein digestion can occur if the stomach is removed)
• Accelerates protein digestion
• Normally accounts for ~20% of total protein digestion
• Breaks down collagen in meat – helps shred meat into smaller pieces with greater surface area for digestion

Question 5

gastric motility - relax

Answer 5

• Empty stomach has volume of ~50mL
• When eating, can accommodate ~1.5L with little increase in luminal pressure
• Smooth muscle in body and fundus undergoes receptive relaxation

Question 6

gastric motility - receptive relaxation

Answer 6

• Mediated by parasympathetic nervous system acting on enteric nerve plexuses
• Coordination – afferent input via Vagus nerve
• Nitric oxide and serotonin released by enteric nerves mediate relaxation

Question 7

gastric motility - peristalsis

Answer 7

• Peristaltic waves begin in gastric body
• Weak contraction in body (little mixing)
• More powerful contraction in gastric antrum
• Pylorus closes as peristaltic wave reaches it
• Little chyme enters duodenum
• Antral contents forced back towards body (mixing)

Question 8

basic electrical rhythm

Answer 8

Frequency of peristaltic waves determined by pacemaker cells in muscularis propria (Interstitial cells of Cajal) and is constant (3/minute)
Pacemaker cells undergo slow depolarisation-repolarisation cycles
Depolarisation waves transmitted through gap junctions to adjacent smooth muscle cells
Do not cause significant contraction in empty stomach

Question 9

strength of peristaltic contractions

Answer 9

• Excitatory neurotransmitters and hormones further depolarise membranes
• Action potentials generated when threshold reached

Question 10

strength of peristaltic contractions increased by

Answer 10

• Gastrin

* Gastric distension (medicated by mechanoreceptors)

Question 11

strength of peristaltic contractions decreased by

Answer 11

Duodenal distension
increased Duodenal luminal fat
increased Duodenal osmolarity
decreased Duodenal luminal pH
increased Sympathetic NS action
decreased Parasympathetic NS action

Question 12

gastric emptying

Answer 12

Capacity of stomach > capacity of duodenum
Overfilling of duodenum by a hypertonic solution causes dumping syndrome:
Vomiting, bloating, cramps, diarrhoea, dizziness, fatigue
Weakness, sweating, dizziness

Question 13

gastroparesis

Answer 13

delayed gastric emptying
can be caused by: idiopathic, autonomic neuropathies, drugs, abdominal surgery, Parkinson’s disease, multiple sclerosis, scleroderma, amyloidosis, female gender

Question 14

delayed gastric emptying - drugs

Answer 14

Gastrointestinal agents:
		Aluminium hydroxide antacids
		H2 receptor antagonists
		Proton pump inhibitors
		Sucralfate
Anticholinergic medications
		Diphenhydramine (Benadryl)
		Opioid analgesics
		Tricyclic antidepressants
Miscellaneous
		Beta-adrenergic receptor agonists
		Calcium channel blockers
		Interferon alpha
		Levodopa

Question 15

consequences of delayed gastric emptying

Answer 15

Consequences:
•	Nausea
•	Early satiety
•	Vomiting undigested food
•	GORD
•	Abdo pain/bloating
•	Anorexia