Flashcards in Week 4 - Functions of the stomach Deck (26):
What prevents a rise in intragastric pressure whilst eating? Explain how this works
-Receptive relaxation ->Vagally mediated relaxation of the orad of the stomach
-Rugae allow distension
What are the orad and caudad regions of the stomach?
-Orad is proximal portion consisting of fundus and part of body
-Caudad is the rest
What factors allow the stomach to disrupt food? Explain each one
-Peristalsis -> coordinated movements in muscular walls of antrum every 20s from proximal to distal allow mixing of stomach contents to create chyme
-Shape of stomach-> funnel arrangement causes separation of contents
-Acidic conditions ->unravels proteins, activates proteases and disinfects
What factor of the stomach aids separation of liquid chime and large contents?
-Shape of stomach -> Larger proximal to smaller distal creates a funnel type arrangement which allows contents to accelerate towards the pyloric sphincter, in such a way that separation of the large contents occurs and the small/liquid chyme is ejected into duodenum
-Occurs every 3 minutes
Name the importance cells of the stomach and their secretions
-Parietal cells -> HCL and Intrinsic factor
-Enterochromaffin like cells -> Histamine
-Chief cells -> pepsinogen
-G cells -> gastrin
-D cells -> somatostatin
-Mucus cells (surface and neck)
Where are parietal cells mainly located?
Where are G cells mainly located?
What is the function of histamine in the stomach?
-Acts via H2 receptors to mediate acid production
What is the function of somatostatin?
-Inhibits G cells and ECL cells to decrease acid production
What is the function of mucus?
-Protect epithelia from the acid
Describe the structure of a gastric gland and pit from deep to superficial
-Enteroendocrone cells at the bottom (G and D cells)
What 3 factors stimulate the parietal cells for HCL production?
-Histamine (chemical mediator)
What is histamines function of acid production?
-Fine tune acid production based on amounts of food entering stomach
What controls gastrin secretion?
-Presence of peptides and a'a in stomach lumen
-Vagal stimulation via Ach and gastrin-releasinf peptide
-Negative control by somatostatin produced by D cells
-Increasing pH in the stomach due to dilution by food
What inhibits HCl production?
-When food leaves stomach, pH drops and G cells inhibited
-When food leaves stomach, pH drops and D cells stimulated to inhbit G cells and ECL indirectly
-Stomach distension reduced-> Vagal activity reduced -> reduced stimulation of G cells and parietal cells
Describe the formation of HCl and its byproducts causing alkaline tide
-In the parietal cell, water split into OH and H
-H moved into stomach lumen
-Cl moved into stomach lumen (enters parietal cell from ECF in exchange for HCO3)
-OH combines with CO2 to form HCO3-
-HCO3 moved into bloodstream forming alkaline tide
How is H+ pumped into lumen by parietal cell?
-H+/K+ATPase (Proton pump)
What are the 3 phases of digestion?
Explain the cephalic phase of digestion
-Prepares stomach for digestion before food enters
-Produces 30% of total HCl
-Smelling, tasting, chewing, swallowing stimulates vagal activity
-Direct stimulation of parietal and G cells
Describe the gastric phase of digestion
-Produces 60% of total HCl
-Distension of stomach stimulates vagus (Parietal and G cells stimulated)
-Presence of a'a and small peptides stimulates G cells
-Food acts as a buffer in stomach and increases pH to remove inhibition on gastrin production
Describe intestinal phase of digestion
-10% of HCl production
-Chyme initially stimulates gastrin
-Short phase as soon overtaken by inhibition of G cells
What are the stomach defences to acid?
-Mucus/HCO3 forms thick alkaline viscous layer which adheres to epithelium -> epithelium kept at higher pH
-High turnover of epithelia helps to keep epithelia in tact
-Prostaglandins are vasodilators which help maintain mucousal blood flow supplying the epithelium with nutrients
Name 3 common factors which breach stomach defences
-Alcohol dissolves mucous layer
-NSAIDs inhibit PGs
Name 2 pharmacologic interventions of acid production
-H2 antagonist (ranitidine)
-Proton Pump Inhibitor (Omeprazole)
Why is a PPI better than H2 antagonist?
-H2 antagonist only removes histamine stimulation of parietal cells, Ach and gasrtin still causing production
-PPI blocks acid production after point of stimulation so all stimulants affected