Stomach Physiology Flashcards
Incisura
Inflection point of the stomach
Lesser Curve Stomach left/right
Right
Saliva Stimulation
Sight, smell, taste of food
Acid in the oesophagus (predicts vomit coming up)
Saliva Inhibition
Sleep
Sympathetic ANS
4 Contents of Salvia
- HCO3- = Basic
- Mucin = Lube
- Amylase = Starch -> Smaller Carbs
- Lysozyme = Anti-bacterial
Antrum Role
Grinding mill of stomach
Pylorus Role Stomach
Regulates size of particles that pass to duodenum (must be small)
Osmolaloity change of contents in stomach
Bolus -> Chyme
= More watery
Control of Gastric Emptying
Feedback mechs from duodenum: Acid, fat, amino acids, osmolarity
Rapid Gastric Emptying (eg. Diarrhoea, prokinetic drugs) causes
Food moves too quickly through stomach = not completely digested, chyme hyperosmolar
Gastric Acid Functions
- Sterilises stomach
- Denatures proteins
- Absorption of B12 and Iron
Parietal Cell Function
- H+ Cl- ion secretion to lumen
- HCO3- into blood
Parietal Cell secretion mechanism
H+/K+ Proton Pump
Carbonic anhydrase needed to catalyse HCO3- production
Stomach pH during night
Lowest (1-2) as no dilution from food etc
Stomach pH after eating
Highest (5-6) as buffered and diluted
What protects gastric mucosa from acid
Mucous
Bicarbonate buffer
ACh Role in Regulating Gastric Acidity
DECREASES PH / INCREASED ACID SECRETION
Stimulates
1. Parietal Cell release HCl
2. ECL Cell release histamine = stim parietal
3. G Cell release gastrin = stim parietal and ECL
ECL Cells Secretion
Histamine
Histamine Role Acidity
Paracrine activity = stimulates Parietal Cells to release ACh
ECL Cell Location
Stomach Body
G Cell Secretes
Gastrin
G Cell Location
Stomach ANtrum
Gastrin Function
Endocrine
Stimulates histamine release from ECL cells
Stimulates HCL release from Parietal Cells
D Cell Secretes
Somatostatin
D Cell Location
Antrum Stomahc
Somatostatin Function
Inhibits Gastrin secretion (= decreased HCl secretion)
3 Phases of Digestion
- Cephalic
- Gastric
- Intestinal
Cephalic Phase
Thought, sight, smell of food -> ACh released by Vagus Nerve -> Stimulation of G ECL Parietal -> HCl
Gastric Phase
Distension of stomach body and antrum causes acid secretion
Protein in antrum stimulates G cells -> gastrin -> HCL
What occurs in stomach during intestinal phase of digestion
HCl in antrum -> D cells release somatostatin -> gastrin inhibited -> less HCl
HCl in duodenum -> Secretin -> less HCl
Proteins/fats in duodenum -> CCK -> less HCl
Helicobacter Pylori impact on gastric acid
Increased secretion
Chief Cell secretion
Pepsinogen
Pepsinogen function
Cleaved in acid to become Pepsin
Pepsin function
Hydrolysis of proteins
How do you stop a gastric bleed
Must inhibit acid secretion, as otherwise acidic environment activates pepsin which destroys clot
Prostaglandins Function
Protection / repair of gastric mucosa
Are gastric ulcers pain better / wrose with food
Worse
Are duodenal ulcers better / worse with food
Better
Peptic Ulcer Symtpoms
Epigastric Pain
Bleeding -> blood in stool
Perforation
Obstruction = swelling / scarring
Treatment of Peptic Ulcer Disease
Proton Pump Inhibitors
(Historically surgery to decrease acid secretion)
Peptic Ulcer Disease Cause
Increased Acid
- Helicobacter pylori
Decreased prostaglandins
- Aspirin
- NSAIDs
H pylori risk factors
Poor childhood living conditions
= Devleoping world, low SES, Maori
H pylori causes
Break down of stomach mucous barrier -> mucosa
Achlorhydria
Low/no stomach acid
How does H pylori impact duodenum
H pylori -> increased gastrin -> increased acid -> gastric metallisation -> H pylori can migrate into duodenum
Treatment for H pylori
First line triple therapy (antibiotics)
Gastric Cancer Two Types
Intestinal
Diffuse
Intestinal gastric adenocarcinoma
Antrum
Glandular pattern
Diffuse gastric adenocarcinoma
Gastric Wall
No glandular formation
