GI Flashcards
what are the derivatives of the foregut?
- oesophagus
- stomach
- first half of duodenum (parts 1 + 2)
- pancreas
- liver & biliary system
- dorsal & ventral mesentery (omentum)
what are the three developmental parts to the gut?
- foregut: starting at lower end of hypopharnyx
- midgut: starting at third part of duodenum
- hindgut: starting 2/3 of way along transverse colon & finishing at anal canal
what is the arterial & nerve supply of the foregut?
-coeliac trunk & greater splanchnic nerve (T6-T9)
what is the arterial & nerve supply of the midgut?
-superior mesenteric artery & lesser splanchnic nerve (T10-T11)
what is the arterial & nerve supply of the hind-gut?
-inferior mesenteric artery & least splanchnic nerve (T12, sometimes L1)
what does the endoderm give rise to in the gut?
-bowel epithelium, liver hepatocytes and end/exocrine cells of the pancreas
what does the visceral mesoderm give rise to in the gut?
-muscle wall, connective tissues for wall, liver, pancreas and visceral peritoneum
what are the parts of the pancreas?
- head: the part which sits right next to the duodenum
- neck: the part directly anterior to the hepatic portal vein and superior mesenteric vein
- body:main part of pancreas extending to the left side
- tail: most lateral part of the pancreas
what are the five stages for development of gut tube?
1) elongation
2) physiological herniation
3) rotation
4) retraction
5) fixation
what are the fixed/mobile parts of the gut?
fixed: -duodenum (except 1st cm) -ascending colon -descending colon -rectum mobile: -stomach -jejunum & ileum -appendix (caecum) -transverse colon -sigmoid colon
what are the functions of the stomach?
- store & mix food
- dissolve & continue digestion
- regulate emptying into duodenum
- kill microbes
- secrete proteases
- secrete intrinsic factor
- activate proteases
- lubrication
- mucosal protection
what are the key cell types in the stomach & their functions?
- mucous cells - bicarb rich mucus to protect against attack by HCl
- parietal cells - secrete HCl & intrinsic factor
- chief cells - pepsinogen
- enteroendocrine - hormones
summarise how H+ and Cl- ions are secreted into stomach lumen
- H+ ions exchanged against conc. gradient - H+/K+ ATPase pump on luminal surface (neutral charge must be maintained)
- K+ & Cl- can be lost passively via ion channels
- H+ & Cl- combine in stomach to form HCl
- bicarb pumped out at capillary end, Cl- pumped in replenishing those lost at luminal end
summarise turning gastric acid secretion on during cephalic phase
- parasympathetic nervous system (CNX)
- sight, smell, taste, chewing
- Ach release from nerve fibres
- Ach acts directly on parietal cells, turns gastric cells on
- Ach triggers release of gastrin & histamine
- net effect- increased HCl production
summarise turning gastric acid secretion on during gastric phase
- gastric distension, presence of peptides & amino acids
- gastrin release
- gastrin (by g cells) directly acts on parietal cells
- gastrin triggers histamine release
- histamine acts directly on parietal cells
- net effect - increased acid production
summarise turning gastric acid secretion off during gastric phase
- low luminal pH
- directly inhibits gastrin secretion
- indirectly inhibits histamine release
- stimulates somatostatin release, inhibiting parietal cell activity
summarise turning gastric acid secretion off during intestinal phase
- in duodenum:
- -duodenal distension
- -low luminal pH
- -hypertonic luminal contents
- -presence of amino acids & fatty acids
- trigger release of enterogastrones:
- secretin (inhibits gastrin, promotes somatostatin)
- cholecystokinin (CCK)
summarise factors affecting digestion
- controlled by brain, stomach & duodenum
- 1 (parasympathetic) neurotransmitter (ACh +)
- 1 hormone (gastrin +)
- 2 paracrine factors (histamine +, somatostatin -)
- 2 key enterogastrones (secretin -, CCK -)
what are the main causes of peptic ulcers?
- helicobacter pylori (majority)
- drugs (NSAIDs)
- chemical irritants (alcohol, bile salts, diet)
- gastrinoma
- increased acid production
- reduced mucosal defence
how does gastric mucosa defend itself?
- alkaline mucus
- tight junctions b/t epithelial cells in gastric epithelium
- rapid replacement of damaged cells
- feedback loops (-ve)
how does helicobacter pylori cause peptic ulcers?
-lives in alkaline environment
-secretes urease, splitting urea -> CO2 + ammonia
-ammonia + H+ = ammonium
-ammonium, secreted proteases, phospholipase & vacuolating cytotoxin A damage gastric epithelium
-inflammatory response
reduced mucosal defence of stomach
(requires triple therapy- 1PPI, 2 antibiotics)
how do NSAIDs cause peptic ulcers?
-mucus secretion stimulated by prostaglandins
-cyclo-oxygenase 1 (target of NSAIDs) needed for prostaglandin synthesis
NSAIDs inhibit cyclo-oxygenase 1
-reduced mucosal defence
(treatment: prostaglandin analogues
how do bile salts cause peptic ulcers
- duodeno-gastric reflex
- regurgitated bile strips away mucus layer
- reduced mucosal surface
how is protease secreted and mediated?
- chief cells produce pepsinogen
- synthesised in inactive form (zymogen)
- pepsinogen mediated by input from enteric nervous system (ACh)
- secretion parallels HCl secretion
- luminal activation
