Flashcards in Gastric Digestion and Disease Deck (35):
Functions of the stomach
- food reservoir
-food digestion (antrum mixes/grinds)
-controls passage of food to SI (pylorus regulates size/timing)
-Gastric acid secretion (+ other secretions for protection against acid)
What is required to have normal function of gastric emptying
-intact atrum, pylorus and duodenum
-Normal vagal function to co-ord activity
-normal hormonal function
How does food move through the stomach?
1- Fundus (storage) relaxes when food is about to enter, (vagus nerve), causing reflex
2- body & antrum contract together allowing food to be moved to the distal stomach
3- Pylorus is contracted (stops spillage)
4- mixing of food in antrum (retropulsion)
Abnormal Gastric emptying
Rapid GE: common post-gastric surgery, when antrum/pylorus removed> "dumping Syndrome"
Delayed GE: eg) diabetic gastroparesis due to vagal nerve damage, usually due to ANS neuropathy
Role of Gatric Acid
main role is to sterilise food, make the stomach environment hostile to bacteria (par H.pylori)
Dumping syndrome is?
nausea vomiting cramping, poop as food moves too fast stomach > duodenum, food not completely digested.
-Hyperosmolar chyme = fluid shift = intestinal distention = pain =diarrhoea
absent or low gastric acid, often related to pernicious anaemia
How is acid secreted in the stomach?
Parietal cells. Located in the body, with proton pumps to secrete HCL. Secrete ~2L/day
how does the H/K ATPase pump in the Parietal cells work and what is it for
A proton pump that actively pumps H+ from cells into stomach
H20 + CO2 >> H+ + HCO3
in exchange K enters cell, HCO3 transported out of cell into bloodstream exchanged with Cl-.
H20 + CO2 >> H+ + HCO3
is catalysed by what enzyme
Why does HCO3 swap for Cl- and H+ swap for K+
because pH and osmolarity need to stay in equilibrium.
How exactly does the parietal cells secrete acid?
Tubovesicles fuse with canaliculus, increased SA and proton pump numbers increase acid secretion into lumen and gut, against a 3 mill fold conc gradient
Protective factors of the gastric mucosa?
What happens if these protective factors results in?
Damage to these = ulceration
ECL cells are?
-located body of stomach, secrete histamine (paracrine activity)
Stimulates acid secretion from adjacent parietal cells
antrum of stomach
(enters blood circ. binds to ECL, > histamine release > HCL release)
antrum of stomach
endocrine & paracrine
inhibits acid secretion by acting on adjacent G cells
neurotransmitter, released by vagus and enteric neurons
Stimulates parietal, ECL and gastrin cells
Abnormal Gastric Secretion
Increased : 'Gastrinoma', cancer with tumours that produce gastrin> ulcers and destruction of gastric mucosa
-'Pernicious anaemia' AB against parietal cells and/or IF
-gastric surgey, body or antrum removed
-vagotomy: loss of vagus nerve > less ACh
What are other gastric secretions
from Chief cells
cleaved to form pepsin
pepsin degrades protein
Lipid molecules to repair mucosa due to acid damage
brain stimulates vagus/enteric nerve
Parietal, HCL and G cells released
-when food starts to enter the stomach
-physical digestion + AA release (stimulate G cells)
-food causes distention, stimulates enteric nerves > ACh > parietal, ECL and G
too much acid in stomach, time to turn off acid secretion
- Excessive HCl > D cells
-G cells inhibited (stopping HCl)
- Fats + HCl in duodenum release 'secretin' & 'cholecystokinin
-inhibit cid secretion
Why is Secretin released. extra job other then inhibiting acid secretion?
due to HCl
-also stimulate pancreas and bile ducts to release HCO3
Why is cholecystokinin. Extra job other then inhibiting acid secretion?
due to partially digested fats and proteins.
-also stimulate release of pancreatic enzymes and gallbladder contraction to release bile to digest the fats
What does Helicobacter pylori cause?
-Gastritis (non-specific inflammation post infection)
-Gastric MALToma - lymphoid tissue lymphoma cancer
Who does H.pylori infect and where?
Only humans in the antrum of the stomach. Via person-to-person transmission (oral-oral or faecal-oral)
Tends to be childhood infection (1-5 yrs), and is caused by living conditions, ethnic group, country of birth
Treatment for H.pylori
'triple therapy' as single AB doesn't work
-omeprazole, clarithromycin and amoxycillin for 14 days
-is resistance, 2nd regime
Causes of Peptic Ulcer Disease (stomach or duodenum)
Mainly H.pylori and aspirin and NSAIDs
How did they initially treat peptic ulcers
gastrectomy (remove antrum)
Vagotomy (part of vagus nerve)
Pyloroplasty: cut and resuture pylorus
Symptoms of peptic ulcers
non-specific epigastric pain
obstruction due to scarring/fibrosis
2 main types of Gastric Cancer
1) Intestinal : well differentiated and cells arranged in a tubular/glandular pattern
2) Diffuse: Poorly differentiated cells, lack of glandular formation. Can infiltrate gastric wall