Pathology of the Stomach Flashcards
What cells line the entire surface of the stomach? What do they contain?
Simple columnar, mucous-secreting foveolar cells which contain bicarbonate critical for gastric mucosal protection
What special cells are found primarily in the fundus and body of the stomach vs primarily the antrum?
Fundus / body:
Parietal cells - Pink cells, secrete acid and IF
Chief cells - secrete pepsinogen - basophilic due to RER
Antrum: enteroendocrine cells at base of glands:
D cells - somatostatin
G cells - gastrin
How does spread of cancer from the stomach differ from colon and why?
Spreads much easier from stomach than colon because the lamina propria of the stomach DOES contain lymphatic tissue -> can metastasize with this little invasion of mucosa
What is the difference between an erosion and an ulcer?
Erosion - loss of mucosa of the stomach, not into the submucosa (last layer of mucosa is muscularis mucosa)
Ulcer - Penetration into the submucosa or deeper
What is contained in the muscularis propria of the stomach?
Three layers of smooth muscle:
Innermost oblique
Inner circular
Outer longitudinal
Auerbach (myenteric) plexus sits between inner circular and outer longitudinal
What stimulates gastrin release and what is its action?
Stimulated by: Antral distension, alkalinization of the stomach, amino acids
Action: Increased HCl secretion and increased gastric motility
What stimulates histamine release in the stomach, what releases it, and what is its action?
Gastrin stimulates histamine production via enterochromaffin-like-cells (ECL cells)
Histamine acts on parietal cells to increase HCl secretion
What stimulates CCK, what releases it, and what are its actions?
Increased fatty acids in duodenum stimulates secretion by I cells in the duodenum / jejunum
Actions: Increased pancreatic secretions, gallbladder contractions, decreased gastric emptying, and relaxation of sphincter of Oddi
What stimulates secretin, what releases it, and what are its actions?
Acidic chyme in duodenum stimulates release by S cells
Actions - increase pancreatic and brunner’s glands bicarbonate secretions, decrease gastric acid secretion
What stimulates somatostatin, what releases it, and what are its actions?
Stimulated by increased acid or loss of vagal stimulation
Released by D cells of pancreas and stomach / duodenum, as well as hypothalamus -> widespread inhibitory action on release of hormones, including gastrin and histamine
What are the three broad etiologies of acute gastritis?
- Increased mucosal injury
- Decreased mucosal protection
- Decreased mucosal regenerative ability - i.e. chemotherapy
What things cause increased mucosal injury to cause acute gastritis?
- Ingestion of toxic chemicals or excessive alcohol
- Radiation / chemotherapy
- Bile reflux - biliary contents, post-surgery
What things cause decreased mucosal protection to cause acute gastritis?
- Advanced age - decreased mucus production
- NSAIDS - loss of PGE2, which is needed to maintain blood flow to mucosa, and maintain production of HCO3- / mucin
- Uremia - acidosis will allow less bicarbonate to be excreted
- Low O2 -> shock, high altitudes, severe burns
What is mild vs severe acute gastritis characterized by?
Mild = Nonerosive gastritis - neutrophils and slight edema
Severe = Erosive hemorrhagic gastritis - extensive inflammation, superficial ulcerations limited to mucosa (erosions)
What are the clinical manifestations of acute gastritis?
Range from asymptomatic to nausea/vomiting/epigastric pain and upper GI bleed (causing hematemesis or melena)
What things tend to induce acute gastric ulcers?
- NSAIDs
- Intracranial trauma - stimulation of vagal nerve increases gastric acid secretion
- Major physiologic stress - shock, sepsis, burns leads to decreased perfusion of mucosa (decrease nutrients) and systemic acidosis (Decrease bicarbonate excretion)
What is it called when you have an ulcer due to intracranial injury vs significant burns?
Intracranial injury = vagal stimulation -> Cushing ulcer (think of Cushing’s triad)
Burns = hypovolemia -> Curling ulcer (think of Curling irons are hot)
What are the potential complications of acute gastric ulceration and do these tend to occur alone?
Potential for significant blood loss and perforation
-> often happen in groups due to major inciting events, may be groups of ulcers and erosions