GI & Pancreas Flashcards
Reasons for anorexia for D2 post-op splenectomy:
- Lack of gastrocolic reflex
- Lack of motilin stimulation (by fat)
- Lack of CCK stimulation (by protein)
- Peritoneal inflammation -> decrease slow waves => NO production
- Opioids interrupting MMC
- Pain (?)
What are the 4 phases of MMCs?
I. Period of quiescence
II. ↑ AP and smooth muscle activity
III. Peak electrical activity and mechanical activity (lasts 5-10 minutes)
IV. Declining activity that leads back to phase I
Functions of the MMC are interrupted by:
Meals
Drugs: narcotics, atropine, alpha-2 agonist
Stress
Bacterial toxins e.g. Campy CdtB toxin
Main role of myenteric plexus:
Stimulation increases peristalsis
Main role of submucosal plexus:
Help with mixing: local segmental intestinal secretion, absorption and contraction of submucosal muscle
Gastrin
Stimuli for secretion
Site of secretion
Action
Stimuli for secretion:
- Protein
- Gastric distention
- (Acid inhibits release)
Site of secretion: G cells (located in: stomach, duodenum)
Actions:
Stimulates:
- Gastric acid secretion (parietal cells)
- Stimulates pepsinogen (chief cells)
- Mucosal growth/repair
Cholecystokinin
Stimuli for secretion
Site of secretion
Action
Stimuli for secretion:
Protein
Fat and its byproducts
Acid
Site of secretion: I cells (duodenum, jejunum, ileum)
Actions:
Stimulates:
- Pancreatic enzymes + bicarb secretion
- GB contraction to digest fat
- Relaxation of sphincter of Oddi
- Growth of exocrine pancreas
Inhibits:
- Appetite
- Gastric acid secretion
- Gastric emptying: gives time for digestion
Gastric Inhibitory Peptide (GIP)
Stimuli for secretion
Site of secretion
Action
Stimuli for secretion:
PROTEIN
Fat
Carbohydrate
Site of secretion: K cells (duodenum + jejunum)
Actions:
Stimulates: insulin release
Inhibits:
- Gastric acid secretion
- Gastric emptying
Vasoactive Intestinal Peptide (VIP)
Site of secretion
Main action
Site of secretion: enteric nerves
Main action
- increase water + electrolyte secretion from pancreas & gut
- relaxes smooth muscle (via NO)
Motilin
Stimuli for secretion
Site of secretion
Action
Stimuli for secretion: FAT
Acid
Nerve
Site of secretion: M cells & ECL cells (throughout)
Actions:
Stimulates:
- Gastric motility
- Intestinal motility
Secretin
Stimuli for secretion
Site of secretion
Action
Stimuli for secretion: Acid
Fat
Site of secretion: S cells (duodenum, jejunum)
Actions:
Stimulates:
- Pepsin secretion
- Pancreatic & biliary bicarb secretion
- Growth of exocrine pancreas
Inhibits: gastric acid secretion
Somatostatin
Stimuli for secretion
Site of secretion
Action
Stimuli for secretion: acid
Site of secretion: D cells (pancreatic islets, stomach, SI)
Actions: Inhibits:
- Secretion of: gastrin, VIP, GIP, secretin and motilin
- Pancreatic exocrine secretion
- Gastric acid secretion
- Gastric motility
- GB contraction
Absorption of aa and triglycerides
Ways to help improve motility:
- Drugs
- Early ambulation
- Early controlled enteral nutrition
- Multi-modal analgesia
- GIT decompression
- Judicious IVFT to limit bowel oedema
4 functions of the exocrine pancreas:
Acinar cells secrete:
1) zymogens (digestion)
2) antibacterial proteins (regulate SI flora)
Ductal cells secrete:
1) bicarb + water to neutralise duodenal pH
2) pancreatic intrinsic factor (aid with B12 handling in distal ileum)
What are the pathophysiologic mechanisms of diarrhoea? (4)
1) Osmotic diarrhoea -Excess luminal osmoles drawing fluid into the intestinal lumen
2) Secretory diarrhoea - Net increase in intestinal fluid secretion. either through ↑secretion or ↓absorption
3) altered permeability - Mircoscopic/macroscopic damage to epithelial cells or their junctions. Risk of translocation of bacteria
4) Deranged motility -
Either ↑ peristaltic contractions or ↓segmental contractions