Lecture 14 Flashcards
What does gastric motility result from?
Contraction/relaxation of layers of muscle in stomach (myenteric plexus)
How does gastric motility occur?
Myenteric plexus receives input from ANS: parasympathetic stimulation increases motility, sympathetic input decreases motility
Zymogen?
Inactive form of enzyme
Role of pepsin?
Hydrolyses proteins to polypeptide/amino acids which stimulates acid production
When is pepsin inactivated?
At pH higher than 6 (can be reactivated upon re-acidification)
Role of salivary amylase?
acts on carbohydrate if pH~6 (mouth) so far less active in stomach (acidic)
What increases antral contraction?
Distension (swelling from pressure inside) of stomach + increased gastrin levels
What does stomach emptying involve?
Constriction of lower oesophageal sphincter, contraction of gastric muscularis, relaxation of pyloric sphincter
What inhibits gastric emptying (entry to duodenum)?
Distension of duodenum, presence of fat, increased HCl concentration
Role of enterogastric reflex?
Prevents too much chyme entering duodenum all at once/aids digestion
What occurs when there’s fat in duodenum?
Fundus relaxes lowering intragastric pressure (high fat meal = full for longer)
Absorption in stomach?
Limited (some water/electrolytes/alcohol/drug, stomach wall impermeable to most materials
When does absorption properly start?
When contents reach small intestine, food acted upon by products of pancreas/liver/gallbladder
Gastric ulcer?
Erosion of mucosal layer causing inflammation/damage to underlying tissue (acid not necessarily the main damaging feature)
Causes of gastric ulcers?
Associated with H. Pylori infection, NSAID uses, smoking, alcohol…