138. Pathology Gastric Disorders Flashcards
What are the functions of mucin in the stomach?
Main: mucosal protection against auto-digestion
Mucin: prevents food from directly touching epithelium neutral pH (bicarb secretion by surface epithelium)
Continuous layer of epithelial cells form physical barrier
3-7 day replacement of surface foveolar cells
Parietal cells secrete acid to lumen, bicarb to vessels (Alkaline Tide)
Rich vasculature washes away acid that back-diffuses from LP
Definitions of
- Gastritis
- Acute vs. Chronic Gastritis
- Helicobacter pylori gastritis
- Gastropathy
Gastritis: inflammation of gastric mucosa
Acute: ACTIVE gastritis (neutrophils present)
Chronic: chronic inflammation (lymphocytes, plasma cells)
HP gastritis: chronic gastritis with ACTIVITY (neutrophils present)
Gastropathy: rare inflammatory cell presence, but reactive mucosal changes present
Acute Gastritis
- causes
- sx
- mechanism
- list the two subtypes
Cause: acute hemorrhagic/erosive gastritis, infections (CMV), med injury (NSAIDs), iatrogenic (gastrostomy tube, post-surgery, chemoradiation)
Sx: asx or variable pain, N/V
Mechanism: more damage (gastric acidity, peptic enzymes, meds/toxins/infection) and less defenses (less mucus barrier, ischemia/shock) leads to PEPTIC ULCERATION
- Acute hemorrhagic erosive gastritis
- Stress Related Mucosal Ulcer
Acute hemorrhagic erosive gastritis
- what it is
- causes
- histo
sudden stress-induced imbalance b/w injurious/protective factors = diffuse mucosal hyperemia, bleeding, erosions/ulcers
causes: NSAIDs (decrease mucosal protective agents - PGs, mucins, bicarb), Alcohol (increase damage, less defenses - NSAID synergy), Bile Acids (mucous damage), Shock/Vascular Compromise (hypoperfusion, stasis, VC, high vascular permeability)
Histo: erosion of superficial mucous layer w/ increased neutrophils and vascular congestion
Stress-Related Mucosal Ulcer
- what it is
- Curling ulcer (location, mechanism)
- Cushing ulcer (location, mechanism)
critically ill pts with trauma/shock/sepsis/burns/intracranial disease/surgery
Curling: proximal duodenum, assoc w/ severe burns/trauma: hypovolemia -> mucosal ischemia
Cushing: gastric/duodenal/esophageal, assoc w/ intracranial disease, high risk of perforation
vagal stimulation -> acid production
Chronic Gastritis
- most common cause
- most common noninfectious cause
- sx
- Histo
HP most common cause
autoimmune gastritis most common noninfectious cause
sx: less severe than acute but more persistent (N/V, pain)
Histo: superficial plasmacytic infiltrate, lymphoid aggregates
HP Gastritis
- what HP is, pathogenicity
- dx
- histo
HP: G- curved rod, fecal-oral contamination, 20% prevalence in N America, attaches to epithelium but does NOT penetrate surface mucosal cells - affects antrum and assoc w/ increased acid production
Dx: Biopsy/Path, Urease breath test, Antibody test (can’t distinguish past infection)
Histo: lymphoid infiltration of LP (lymphoid follicle formation) - CAN INDUCE MALT LYMPHOMA, neutrophils in b/w glands/expanding LP (mucosal inflammation), GNRods in surface epithelium (seen on Warthin Starry Silver Stain)
Autoimmune Gastritis
- what it is
- assoc
- pathogenesis
- histo (4)
DESTRUCTION OF PARIETAL CELLS by antibodies against parietal cells and IF - causes hypochlorhydria and high serum gastrin levels
Assoc: increased risk of dysplasia/carcinoma (and gastrinoma), other autoimmune conditions (hashimoto’s, addison’s disease)
Pathogenesis: low parietal cells = hyperplasia of G cells in antrum = hypersecretion gastrin = overstim ECL cells = ECL hyperplasia = hypersecretion histamine
Histo: 1. Atrophy of body/fundus glands w/ deep+diffuse lymph infiltrates w/ glandular infiltration; 2. Extensive metaplasia (Goblet cells), pancreatic acinar metaplasia; 3. Neuroendocrine cell hyperplasia (ECL Cells); 4. NO HP
Complications of Chronic Gastritis (3)
- sites/RFs/pathogenisis/histo of one key one
Gastric Adenocarcinoma Gastric Lymphoma (MALT Lymphoma): due to lymphoid follicle formation of HP Gastritis
Peptic Ulcer Disease: in proximal duodenum, stomach antrum, lower esophagus, meckel’s diverticulum
- caused by acid+pepsin on GI mucosa causing ulceration
RF: HP, smoking, COPD, illicit drugs, NSAIDs, alcoholic cirrhosis
Pathogenesis: imbalance b/w mucosal defense & injurious agents = ulcer
Histo: ulcerated mucosa + nearby mucosa with chronic inflammation
Key Gross sign of hypertrophic gastropathies
Giant “Cerebriform” enlargement of RUGAL FOLDS due to epithelial hyperplasia without inflammation
Menetrier Disease
- what it is
- cause
- sx
- peds vs adult disease
- gross
- histo
diffuse hyperplasia of foveolar epithelium of body/fundus and hypoproteinemia due to protein-losing enteropathy
cause: excessive secretion of TGFalpha
sx: weight loss, diarrhea, peripheral edema
peds: self-limiting disease following URI
adult: increased risk of gastric adenocarcinoma
gross: prominent gastric folds, thickened mucosa
histo: thickened mucosa w/prominent folds, cystic dilation at base of gastric glands; foveolar hyperplasia, tortuous pits, cystic glandular dilatation
Zollinger-Ellison Syndrome
- cause
- sx
- tx
- detection
- gross
- histo
Cause: gastrin-secreting tumor (in small intestine/pancreas)
sx: duodenal ulcers, chronic diarrhea, stomach (doubling of mucosal thickness due to high parietal cells)
tx: PPI: block acid hypersecretion; surgically resect gastrinoma
60-90% gastrinomas are MALIGNANT (75% sporadic/isolated, 25% MEN type 1)
detection: Somatostatin receptor scintigraphy, endoscopic ultrasound
Gross: enlarged gastric rolds
Histo: marked oxyntic gland hyperplasia (high parietal cell hyperplasia)
Inflammatory and Hyperplastic Polyps
- RF
- epidemiology and age
- size
- dysplasia risk
- Histo
MOST COMMON POLYP TYPE (75%) RF: chronic inflammation, HP infection age: 50-60yo size: <1cm and multiple higher risk of dysplasia with increased size
Histo: LP edema, inflammation, surface erosion, with irregular cystically dilated elongated foveolar glands
Fundic Gland Polyps
- etiology
- prevalence
- sx, number
- histo
- risk of cancer
sporadic or pts with Familial Adenomatous Polyposis (FAP)
Higher prevalence due to increased PPI use in US (blocking acid increased gastrin secretion = fundic gland growth)
Often asx, single or multiple in number
No risk of cancer if sporadic, increased risk in FAP-assoc polyps
Gastric Adenoma Polyp
- Epidemiology/Prevalence
- where do they occur
- risk of cancer
- histo
Epi: increased freq with age (50-60yo, M>F), increased prevalence in ppl with FAP
Occur on background of chronic gastritis with atrophy and intestinal metaplasia
Higher size = increased risk of adenocarcinoma (>2cm bad)
Carcinoma may be present in 30% adenomas (need to be removed)
Histo: no mucin glands visible, elongated nuclei, darker cells, high N:C ratio, intestinal columnar epithelium + dysplasia
