Classification of Gastric Carcinoid tumors

Gastric carcinoids are rare tumours. Clinical setting: -  Type I  - Associated with chronic atrophic gastritis with or without pernicious anemia. In autoimmune gastritis progressive destruction of the specialised parietal and chief cell zone leads to atrophy , intestinal metaplasia , hypochlorhydria and hypergastrinemia. - Type II - In Zollinger Ellison syndrome, particularly in patients associated with multiple endocrine neoplasia type 1.           - Type III - Sporadic tumours    - Not related to hypergastrinemia    - In the antrum or corpus    - Larger lesion, may be ulcerated.    - May have an aggressive course.

http://www.ncbi.nlm.nih.gov/pubmed/15362575

Hypergastrinemia

Non-Ulcerogenic causes:
- Renal failure
- Atrophic gastritis
- Pernicious anemia
- Previous vagotomy
- Short-gut syndrome
- PPI

Ulcerogenic causes:
- ZES
- Retained or excluded antrum
- G-cell hyperplasia
- Gastric Outlet Obstruction

Gastric Ulcer Classification

Type I: Lesser curve at or proximal to incisura
Type II: 2 ulcers, Type I and an active or chronic duodenal ulcer
Type III: Located 2cm from pylorus
Type IV: Proximal stomach or gastric cardia
Type V: NSAID induced (diffuse)

Types II and III are associated with high-acid states.

Upper GI premalignant screening recommendations

American society of gastroenterologists recommendations:

http://www.guideline.gov/summary/summary.aspx?doc_id=9306


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DDx: Elevated Gastrin Levels

GRAZ RAPPS:
- GOO
- Retained antrum
- Antral G cell hyperplasia
- Zollinger-Ellison Syndrome

- Renal Failure
- Atrophic gastritis
- Pernicious anemia
- Previous vagotomy
- Short gut

Gastrointestinal Stromal Tumors (GIST)

- Can arise from any mesenchymal component of gastric wall (hence previous designation of leiomyoma/leimyosarcoma)
- 3% of all gastric malignancies
- 50% of GIST in the stomach
- Carney triad: nonhereditary syndrome in young females (children) - gastric GIST, paraganglioma, pulmonary chondroma.
- increased incidence of GIST in pts with NF1
- Main route of metastasis is hematologic.  Lymphatic dissemination rare (<10%) therefore extensive lymphadenectomy not indicated
- presentation will largely depend on whether mass enalrges intraluminally or extraluminally

Metastases:
- 50% present with mets
- metastases can present as multiple serosal nodules throughout the peritoneal cavity or nodules in the liver. Extra-abdominal mets are rare.

Diagnosis:
- needle biopsy is not indicated, risks seeding or tumor rupture: soft and fragile tumor
- ? if unresectible then perhaps consider biopsy to justify upfront imatinib ?make the lesion resectable
- low risk metastases: <5cm, <5 mitoses/50 HPF

Pathology:
- Firm gray-white masses.
- often have a pseudocapsule that separates tumor from normal smooth muscle
- 80% have gain of function mutation of tyrosine kinase c-KIT, 8% have mutation that activates tyrosine kinase PDGFRA
- common stem cell - interstitial cells of Cajal

Adjunctive Therapy:
- NOT radiosensitive
- traditional chemo does not improve survival
- Imatinib: small molecule inhibitor of c-kit receptor

Survival:
- 5 year survival is 42% with complete resection
- survival drops to 9% with incomplete resection (?pre-Gleevec era)

Stress ulceration

Gastric pH needs to be >4 to prevent stress ulcer formation
- incidence of bleeding is 2-3%
- most common indication for stress ulcer prophylaxis is respiratory failure (followed by shock/hypotensions, sepsis and neurotrauma)

Agents used for prophylaxis are:
- H2 blockers
- sucralfate (higher incidence of bleeding compared to H2 blocker)
- PPIs

- H2 and PPIs are equally effective in stress ulcer prophylaxis and have no difference in nosocomial pneumonia

Sucralfate vs. Ranitidine:
- RCT performed NEJM 1998
- ranitidine has 50% decreased ulcer rate (1.7 vs 3.8%) compared to sucralfate
- does not significantly increase ventilator associated pneumonia rate (16 vs 19%)