L4- GIT Pathology II (stomach) Flashcards
discuss the distribution of cells in different areas of the gastric mucosa
Cardia, Antrum: mucus secreting cells
Corpus, Fundus (oxyntic): chief cells (pepsinogen) and parietal cells (acid, IF)
list the causes of Pyloric Stenosis
Congenital
Acquired: chronic antral gastritis, peptic ulcers, malignancies
Congenital hypertrophic pyloric stenosis:
- (1) defect/definition
- (2) associated Syndromes
- affects (males/females) more
1- concentric hypertrophy of circular muscle coat
2- Turner syndrome, Trisomy 18, Esophageal atresia
3- males (3:1)
Congenital hypertrophic pyloric stenosis:
- (1) clinical presentation
- (2) Tx
1- regurgitation, projectile vomiting, palpable epigastric mass, visible peristalsis
2- surgery: myotomy
list the categories of gastritis
Erosive:
- acute gastritis
- NSAID injury, EtOH gastritis, oral Fe, KCl
Chronic, non-erosive:
- H. pylori
- pernious anemia
describe acute gastritis (what occurs, how long it occurs, occurs in response to what)
- acute mucosal process transient nature
- occurs in severe stress (burns, shock)
-inflammation associated with hemorrhage, in severe cases erosion => GI bleed
how does EtOH affect the stomach
- direct injury
- inc acid secretion
-may lead to acute gastritis
list the clinical features (and complications) of gastritis
-maybe asymptomatic
- epigastric pain, n/v
- hematemesis, melena
-bleeding may be fatal
list some causes of Acute Gastritis
- NSAIDs
- excess EtOH
- heavy smoking
- ischemia, shock
- severe stress (burns, surgery)
- chemotherapy drugs
- systemic infections
- uremia
Acute Gastritis:
- can either be (1) or (2) type
- (3) is obvious on endoscopy, and they can lead to (4)
1- superficial mucosal injury = erosions (loss of surface epithelium)
2- full thickness mucosal injury = ulcer
3- erosions and hemorrhage
4- hyperemia, punctate areas of hemorrhage
Acute Gastritis, on histology:
- (1) in lamina propria
- (2) in epithelium, glands
1- edema, congestion (lamina propria)
2- neutrophil infiltration (surface epithelium, glands)
Chronic Gastritis:
- (1) definition
- (2) are the common causes
- (3) are the less common causes
1- chronic inflammation of gastric mucosa associated with epithelial injury, mucosal atrophy, or epithelial metaplasia
2- H. pylori, autoimmune disease
3- chronic bile reflux, post-surgical (antrectomy), Crohn’s, sarcoidosis, radiation
Chronic Gastritis appearance on endoscopy
- variable: from normal to patchy/diffuse erythema
- w/ or w/o hemorrhage to boggy with thick mucosal folds
Chronic Gastritis appearance on microscopy
- inflammatory infiltrates in lamina propria: lymphocytes, plasma cells
- PMNs / neutrophils in surface epithelium, glandular lumen
- reactive lymphoid aggregates (mainly superficial, marks H. pylori infections)
- intestinal metaplasia, glandular atrophy, dysplasia
H. pylori: classic bacterial features (hint- 5 important distinguishing features)
Gram- curvilinear shape motile: flagella non-invasive urease+
list the diseases associated with H. pylori
-Chronic gastritis: diffuse antral, multifocal atrophic
- peptic ulcer
- gastric adenocarcinoma
- gastric lymphoma
describe the basic progression of H. pylori infections into its associated diseases
1:
- enzymes: proteases, ureases, phospholipases
- -> direct mucosal damage
- -> induces inflammatory response (+ attraction of inflammatory cells)
- -> chronic gastritis, peptic ulcer
2:
- attracts PMNs + other inflammatory cells
- uncontrolled B cell proliferation
- lymphoma
list the diagnostic testing for H. pylori, indicate the most commonly used test
Non-Invasive:
- **urea breath test
- serology: IgG, IgA
- PCR in saliva, feces
Endoscopic based invasive:
- rapid urease test
- histopathology + culture
- PCR
Autoimmune gastritis:
- (1) definition
- destruction of (2), leading to (3) changes
- inc risk for (4), (5)
1- Ig’s against parietal cell Ags/IF
2- oxyntic glands
3- achlorhydria (dec HCl in stomach) + inc gastrin levels
4- gastric carcinoma
5- neuroendocrine tumors / carcinoids
Autoimmune gastritis has the presence of (1) to cause gland destruction and (2) in the (3) part of the stomach. As a result of the destruction / (2), there is a loss of (4) and a loss of (5), where (5) leads to (6).
1- Ig's against parietal cells +/- Ig against IF 2- atrophy 3- stomach body, fundus 4- acid production (= achlorhydria) 5- Intrinsic Factor 6- vitB12 def --> pernicious anemia
Autoimmune gastritis histology:
-list the 3 main features and describe their individual presentations
- chronic inflammation: deep inflammatory infiltrates composed of lymphocytes
- gastric atrophy
- intestinal metaplasia: goblet cells in foveolar pits
Gastric Ulcers:
- (1) definition
- (2) common locations
- heals (better/worse) than an erosion
1- loss of mucosa that extends thru muscularis mucosa or deeper
2- antrum (gastric), duodenal
3- worse, longer healing time
Acute gastric ulcers:
- (1) major causes
- Curling ulcers via (2)
- Cushing ulcers via (3)
- can develop while in (4), 5-10% of the time
1- severe trauma, major surgeries
2- extensive burns
3- head injury, intracranial lesions
4- ICU
Acute gastric ulcers:
-usually presents with (1), although can present as (2)
-pathogenesis is related to (3) and (4)
1- multiple ulcers, asymptomatic
2- massive upper GI bleed
3- systemic acidosis, hypoxia (trauma, burns)
4- vagal stimulation (intracranial lesions)
describe the appearance of an acute gastric ulceration
- multiple, small, circular
- normal gastric rugae (folds)
- base is not usually indurated (fibrotic changes)
-adjacent gastric mucosa is either normal or has reactive changes
list the sites of Peptic Ulcer Disease (by decreasing popularity)
- duodenum
- stomach
- gastroesophageal junction
- margins of gastrojejunostomy
- Meckel’s diverticulum
- stomach, duodenum, jejunum in Zollinger-Ellison syndrome (gastric tumor / gastroma)
Peptic Ulcer Disease appearance:
- (1) usual size
- (2) shape
- (3) edges / margins
- (4) depth
- (5) base appearance
- (6) surroundings
1- 50% <2cm
2- round/oval, punched out, straight walls
3- sharp, raised (not everted)
4- variable, may penetrate entire wall
5- smooth, clean base
6- radiating surrounding mucosal folds – typical features of chronic gastritis
peptic ulcer disease zones
(4 zones)
- necrotic fibrinoid debris
- nonspecific inflammatory infiltrate (predominately neutrophilic)
- granulation tissue
- fibrosis, collagenous scar
list the many causes of peptic ulcer disease (hint- 6)
- H. pylori: 70% gastric, 90% duodenal
- NSAIDs (inhibits PGs)
- smoking (impairs mucosal blood flow)
- alcohol
- psychological stress
- Zollinger Ellison syndrome (multiple ulcers via gastric tumor)
list the clinical features seen in Peptic ulcer disease
- burning epigastric pain 1-3 hours after meals
- relieved by food, alkali
- worse at night
- associated with weight loss
- gastric outlet obstruction
list the clinical complications seen in Peptic ulcer disease
- bleeding
- perforation
- gastric outlet syndrome
- malignant transformation (unknown reason in duodenal, rare in gastric)
H. pylori
Gastric Ulcer:
-epigastric pain (1) after meals
-pain (worse/better) with food
Duodenal Ulcer:
- epigastric pain (3) after meals
- pain (worse/better) with food
-(gastric/duodenal) is worse at night
1- 1-3 hrs
2- worse
3- 3-5 hrs
4- relieved with food
5- duodenal is worse at night
list the causes of reactive gastropathy (+ definition)
Defn: minimal inflammatory reaction of stomach in response to chemicals
- NSAIDs
- other meds: Fe, kayexalate
- alcohol, acid, alkali
- duodenopancreatic reflux (bile into stomach)
NSAID gastric injury:
- inhibition of (1) limits production of (2) which is responsible for (3- include all functions)
- NSAIDs are also considered (4), causing (5) in the stomach upon ingestion
1- COX / cyclo-oxygenase
2- PGs
3- (gastric mucosa protection) maintain blood flow, inc mucus / HCO3 production, augment epithelial defenses
4- direct irritant
5- denudation of surface epithelial (removal of layers), inc mucosal permeability to ions
(1) is the most common malignant tumor of the stomach, with highest occurrence in (2) geographic areas. It generally has a (good/bad) prognosis and comes in (4) subtypes.
1- adenocarcinoma
2- Japan, South Korea
3- bad
4- intestinal, diffuse types
intestinal gastric adenocarcinoma:
- (1) basic definition
- mainly associated with (2)
- neoplastic cells form (3), which is not seen in diffuse type
1- chronic gastritis with intestinal metaplasia
2- H. pylori infections
3- glands
diffuse gastric adenocarcinoma:
- (1) is the only known risk factor
- (2) are the hallmark upon investigation
- it has (3) or lack of (3) appearance in comparison with the intestinal type
1- E-cadherin mutation
2- signet ring cells (peripheral nucleus with mucin vacuoles)
3- no glands —- linitis plastica / Brinton’s disease
intestinal gastric adenocarcinoma:
- (1) gross appearance
- (2) histological appearance
1- elevated mass, raised borders with central ulcer
2- columnar gland forming cells infiltrating thru desmoplastic stroma (back-to-back glands)
diffuse gastric adenocarcinoma:
- (1) gross appearance
- (2) histological appearance
1- thickened gastric wall, loss of rugae (folds)
2- signet ring cells: mucin vacuoles, peripherally displaced crescent shaped nuclei
gastric adenocarcinoma prognostic classifications (indicate what it is based off of)
(based on depth of infiltration)
Early gastric CA:
-confined to mucosa, submucosa, regardless of regional LN involvement
Advanced gastric CA:
-invades beyond submucosa, +/- LN involvement
gastric adenocarcinomas:
- (1) common involved sites
- (2) growth patterns
- (3) routes of metastasis
1- pylorus/antrum 50-60%, cardia 25%
2- exophytic, excavated/ulcerative, flat/infiltrative
3- regional, transcoelomic, lymphatic, hematogenous
Gastric adenocarcinomas:
- usually present with (1)
- (2) nonspecific Sxs
- (3) is a common complication
- prognosis is based on (4)
1- asymptomatic
2- weight loss, anorexia, abdominal pain
3- pyloric outlet syndrome
4- depth of invasion, nodal status
_______ results from the spread of gastric adenocarcinomas to both ovaries
Krukenberg tumor
define Virchow node
L supraventricular lymph node
-can indicate metastasis of a gastric adenocarcinoma
(1) is a mesenchymal tumor of the GIT (anywhere), previously misdiagnosed as (2) tumors. (1) derives from (3) cells and is usually (benign/malignant).
1- GIST (GI stromal tumor)
2- leiomyoma or nerve sheath tumor
3- cells of Cajal (pacemaker cells)
4- either, based on size and mitoses
-found anywhere in GIT, but often in stomach
GIST = (1):
- (2) gross appearance
- often due to (3) mutation
- (4) histological appearance
1- GI stromal tumor
2- whorls / bundles of spindle shaped / epitheliod cells (protruding mass / fleshy tumor covered by intact mucosa)
3- Kit mutations
4- spindle shaped tumors cells in whorled pattern, high rate of angiogenesis (plenty of blood supply noted)
GIST = (1):
- malignancy is based on (2)
- (3) Tx
1- GI stromal tumor
2- site, size, mitotic count
3- imatinib/Gleevec, KIT inhibitor
