Gastric Pathology - Nelson Flashcards
Describe the difference between a mucosal erosion and a mucosal ulcer.
Erosion: Loss and necrosis of surface epithelium confined to the lamina propria, i.e. mucosa.
Mucosal Ulcer: necrotizing process extending beyond mucosa → submucosa and through the muscular wall.
List the main causes of acute gastric ulceration.
*Acute Helicobacter infection
*First time use of large dose NSAID/Aspirin (cyclooxygenase inhibitors)
*Large quantities of EtOH (direct toxic effect)
*Shock, trauma, sepsis, uremia, severe burn (curlings ulcers in duodenum), and intracranial disease (CNS injury – Cushing’s Ulcer) => Stress ulcers
Describe, in one sentence, the most common pathologic finding in H. pylori gastritis.
Also describe the complications of H. pylori infection.
The most common pathological finding in H.pylori gastritis is: active chronic gastritis. Begins in antrum and can progress to fundus (see helpful picture to the right).
*High H+ (low pH) → Mucosal erosion + peptic ulcer *MALTlymphoma and Adenocarcinoma are other complications.
Describe how one typically acquires H. heilmannii
gastritis.
Reservoirs include cats, dogs, pigs, and nonhuman primates, it causes a similar disease to H. pylori.
Which H. Pylori diagnostic tests indicate active infection?
Endoscopic biopsy (immunohistochemically stained)
Stool antigen
urea breath test
serology
rapid urease on tissue biopsy
What is the pathogenesis of autoimmune gastritis?
What kinds of results do we see from cellular damage
Autoimmune CD4+ T-cell mediated destruction of parietal cells
Chief cells are also destroyed
Results:
- Decreased acid secreation (achlorhydria)
- Hypergastrinemia and hyperplasia of G cells to try and compensate
- Vit B12 deficinecy (loss of intrinsic factor)
- Reduced pesiongen
- Inflammatory mucosal damage and atrophy in body/fundus (antrum and cardia are spared)
Clinical findings of autoimmune gastritis?
Clinical findings develop after many years and are related to vitamin B12 deficiency:
(1) Megaloblastic anemia (macrocytic anemia)
(2) Atrophic glossitis
(3) Malabsorptive diarrhea
(4) Peripheral neuropathy: secondary to subacute combined degeneration of the dorsal and lateral columns. Present with paresthesias and ataxia and can progress to severe weakness, spasticity, clonus and fecal and urinary incontinence
(5) CNS alterations (personality changes, memory loss, and psychosis)
Common causes of reactive gastropathy?
Chemical mucosal injury associated with:
NSAIDS, aspririn, bile reflux, ETOH ingestion
3 main complications of peptic ulcer disease?
Bleeding
Perforation
Obstruction
Describe, in just a few sentences for each, the key pathologic and clinical features of eosinophilic gastritis.
Eosinophil-rich inflammation without known cause. Thought to be secondary to allergic or food allergy.
Patient present with esoinophilia and high IgE in blood.
Lesion present as mass, ulver, or pyloric obstruction
Describe, in just a few sentences for each, the key pathologic and clinical features of granulomatous gastritis.
Gastritis with granulomatous inflammation.
Most are 2ndary to disorder like Chrohns, Sarcoidosis, Mycobacterial/fungal infection, foreign body rxn, or cancer
Describe, in just a few sentences for each, the key pathologic and clinical features of lymphocytic gastritis.
Gatritis with intrepithelial lymphocytic inflammation. (CD8 T-cells)
40% associated with Celiac’s
Your patient has a very rare disorder caused by excessive secretion of TGF-alpha.
This leads to diffuse hyperplasia of the foveolar epithelium of the body/fundus of the stomach. As seen in this picture:
What does your patient have?
Any future risks?
Menetrier’s Disease
At risk for gastric adenocarcinoma
Your patient has elevated gastrin and a mrked increase in parietal cells along with HCl secretion.
Histological evaluation reveals that she also has hyperplasia of mucus neck cells with lots of mucus being produced.
Originally she sough care core peptic ulcers and diarrhea.
Whatmight you be thinking after these results?
Zollinger Ellison Syndrome
Let’s talk polyps.
This polyp, pictured below is often associated with PPI use, secondary to increased gastrin secretion following decreased HCl.
Cystic fundic gland polyp
Let’s talk polyps.
This polyp, pictured below is often associated with chronic gastritis (from H. Pylori, chronic reactive gastropathy, or autoimmune)
Usually found in gastric antrum, its an exagerated response to tissue injury and inflammation
hyperplastic polyp
Let’s talk polyps.
This polyp, pictured below is NEOPLASTIC.
Its incidence increases with age. Often occur with chronic gastritis and intestinal metaplasia
Gastric adenoma
A child is delivered normally. Everything is going well until 2 or 3 weeks post-partum. Child has new onset regurgitation and persistent, projectile vomiting. The vomit is non-bilious. On exam, child has firm abdominal ovoid mass.
Diagnosis?
Tx?
Congenital Hypertrophic Pyloric Stenosis
Surgical Myotomy is curative
(Pathology is hyperplasia of the pyloric muscularis propria)
A homeless Japanese man who only eats smoked fish presents in your clinic with some serious gastric issues. Just from these associations you should be thinking about something….
Gastric Adenocarcinoma
Most common malignancy of the stomach (90%). Japan 4 times more!
Risk factors:
Chronic gastritis: H. pylori gastritis and autoimmune gastritis
Dietary carcinogens too many nitrosamines and smoked foods
Menetrier’s disease
Diets lacking in fruits/vegetables: lacking antioxidants
Patients with familial adenomatosis polyposis
Gastric adenoma can present as
Intestinal Type: an invasive mass of ulcer, glandular cells present
OR
Diffuse Type: Thickening of gastric wall (leather bottle appearance), see signet-ring cells micoscopically
What type is shown in this picture?
Diffuse Type
Arrows are pointing to the signet-ring cells that are diagnostic
Most common location for GIST tumor (KIT)** ?
Type of cell these tumors differentiate to?
The key genetic defect?
Effective Treatment?
Location: stomach (60%) followed by jejunum, ileum, and duodenum
Differentiation: interstitial cells of Cajal – these are specialized cells involved in gut peristalsis (remember Amy P. from intro lecture)
Genetics: 85% = oncogenic, gain of function mutations of receptor tyrosine kinase (KIT) gene 8% = plateletderived growth factor receptor alpha (PDGFRA) (related to tyrosine kinase receptor)
Treatment: Gleevec (Rational = tyrosine kinase inhibitor)
Describe the most common risk factor for gastric MALT lymphoma and the remarkably simple first line therapy used for primary treatment.
Risk Factor: Chronic inflammation – in the stomach this means H. pylori
Treatment: Antibiotics will cause regression in 60-90% of cases
Translocations: unresponsive to treatment
Describe the key pathologic features and clinical presentation of “carcinoid syndrome” and a helpful diagnostic test that can assist in diagnosis.
Pathology: Tumor secretes serotonin, histamine, and bradykinin and the liver usually gets rid of them… not this time because you likely are talking about a metastatic disease
How do I get this?: Most of the neuroendocrine tumors producing carcinoid syndrome are of midgut origin (jejunum and ileum, appendix, ascending colon)
Clinical: flushing, sweating, bronchospasm, colicky abdominal pain, diarrhea, and right sided valvular fibrosis
Diagnostic test: 24 hour urinary 5-hydroxyindoleacetic acid (5-HIAA): this is a serotonin metabolite (a key player in the symptoms seen with carcinoid syndrome)
