GIT - Upper GI Flashcards
What are the two sections of the stomach and their functions?
secretory
- parietal cells = secrete hydrochloric acid
- chief cells = secrete pepsinogen
- mucus, water and bicarbonate
- intrinsic factor produced by parietal cells are essential for vitamin B12 absorption
motor
- regulates food intake = mixes, reduces particle size and empties into the duodenum
What are the cells in the gastric gland? What do they secrete and what is their function?
neck cells - mucus and bicarbonate
= protect the stomach lining from acid, neutralise acid
parietal cells - hydrochloric acid
G cell - gastrin = stimulates acid release
chief cell - pepsinogen
= is inactive but is activated by low pH into pepsin which starts protein hydrolysis
enterochromaffin cells (ECL) - histamine
= stimulate acid secretion
D cell - somatostatin
= reduce acid secretion
How does gastric acid secretion occur?
gastrin-ECL-parietal cell
gastrin is released from G cell
gastrin binds to cholecystokinin receptors (CCK2) on the ECL cell causing histamine release
histamine binds to histamine 2 receptors (H2) on parietal cells activating them
acetylcholine can bind to muscarinic 3 receptors (M3) directly on parietal cells causing their activation
- innervation via the parasympathetic system
How is gastric acid secretion regulated?
somatostatin binds to somatostatin 2 receptos (SST2) on the G cells, ECL cells and parietal cells
- G cells = inhibits gastric release
- ECL cells - inhibits histamine release
- parietal cells = inhibits acid release
prostaglandin E2 binds to receptors (EP2/3) on the ECL cell to inhibit histamine release
How does the H+/K+ ATPase pump work in acid secretion?
chloride ions are exchanged for bicarbonate ions
- Cl in, HCO3 out
chloride ions are actively secreted out with potassium ions
- co-transport
potassium is exchanged for hydrogen ions
- K+ in, H+ out
= K+ is recycled due to movement in AND out
carbon dioxide and water react to form carbonic acid
carbonic anhydrase breaks it down to bicarbonate and hydrogen ions
- these hydrogen ions are the ones exchanged for potassium
hydrogen ions and chloride ions join outside the cell to form hydrochloric acid
What is acute gastritis? What is chronic gastritis?
acute gastritis
- transient mucosal inflammatory process
- often erosive and can be haemorrhagic
= caused by irritants like drugs (NSAIDs), alcohol, infection, tobacco, caffeine
chronic gastritis
- chronic inflammation of the gastric mucosa
- common and often asymptomatic
- two types
= type A is autoimmune, type B is caused by a H.pylori infection
What are the peptic ulcers? What are the symptoms?
peptic ulcers are solitary ulcerated lesion in the mucosa of the
- stomach = gastric ulcer
- duodenum = duodenal ulcer
epigastric tenderness
sharp/burning/gnawing pain
dyspepsia
nausea/vomiting
belching
What is the pathogenesis of ulcers?
there is a break in the mucosal barrier
pepsin and hydrochloric acid irritate the mucosa
the irritated and inflamed mucosa may become necrotic and leave a hole
What are complications that can occur with peptic ulcers?
haemorrhage
- blood vessels can be damaged if the ulcer erodes into the stomach or duodenal wall
= hematemesis or melena
perforation
- the ulcer erodes through the entire wall
= digestive content enters the peritoneum causing inflammation
obstruction
- swelling and scarring can cause obstructions of food leaving the stomach causing repeat vomiting
What are risk factors for peptic ulcers?
H.pylori infection (bacterial)
- passed via faecal-oral or oral-oral route
Medications
- corticosteroids, NSAIDs
Lifestyle
- smoking, acidic drinks, caffeine, alcohol
= stimulate acid production
Age
- duodenal (30-50 yrs) or gastric (>60yrs)
Gender
- men are more likely
Genetic factors
- hereditary via Zollinger Ellison syndrome
= gastrinomas in the pancreas or duodenum cause excessive acid production
Other factors
- stress can worsen it but not cause it
What are the features linked to H.pylori virulence?
flagella
- allow bacterium to be motile in viscous mucus
adhesins
- enhance bacterial adherence to surface cells (epithelial cells)
urease
- generates ammonia from endogenous urea which elevates gastric pH
= allows bacterial survival
toxins
- damage stomach wall cells
How does H.pylori increase acid secretion?
increases urease activity
- raises gastric pH due to ammonia
- stimulates g cells to release gastrin who promotes acid secretion
release inflammatory mediators
- inhibit somatostatin production from d cells which stops inhibition of acid secretion
What is the role of prostaglandins? What effect do NSAIDs have on them?
enhance bicarbonate secretion
inhibit acid secretion
promote mucin synthesis
increase vascular perfusion
NSAIDs inhibit cyclooxygenases (COX-1 and COX-2) resulting in reduced prostaglandin synthesis
What is the difference between NSAIDs effect on COX-1 and COX-2 pathways?
COX-1 = inhibition causes
- reduces mucosal blood flow
- reduces mucus and bicarbonate secretion
- impairs platelet aggregation
COX-2 = inhibition causes
- reduced angiogenesis
- leukocyte activation
How can H.pylori infection be detected?
gold standard is oesophogastroduodenoscopy (OGD) and H.pylori infection screening
H.pylori detection
- 13C urea breath test
= H.pylori produces an enzyme urease that splits urea into carbon dioxide and water
= should detect 13 carbon dioxide if they swallow 13C urea
- faecal antigen test
- rapid urease test
- serology = does not differentiate between past and current infection
