GIT Flashcards
SCC sites?
Anywhere with squamous epithelium (floor of mouth, tongue, hard palate)
Can have multiple primaries due to field effect of local acting carcinogens
Gross features of SCC
Masses with necrosis, ulcers and rolled borders
Histologically, keratinizing growth patterns, atypia at base, irregular stromal invasion
Risk factors of SCC
Smoking, alcohol
Tobacco, betel nut chewing
HPV (esp 16)
Prognosis of SCC
5y disease free survival in px <40 yo is 76%
Treatment via surgery or radiation therapy
Metastases of SCC
LN: bilateral if primary close to midline, spreads from upper to middle to lower LNs (except anterior oral cavity, goes straight to middle)
Lungs, liver, bone, mediastinum
What is chronic gastritis
Chronic mucosal inflammatory changes causing mucosal and epithelial metaplasia, usually without erosion
Causes of chronic gastritis
H pylori (90%)
Autoimmune (pernicious anemia)
Toxic (alcohol, smoking)
Post-surgical (bile reflux)
Motor and mechanical causes (prev stomach surgery)
H pylori associated diseases
Chronic gastritis
Peptic ulcers
Gastric carcinomas
Gastric MALT lymphomas
H pylori pathogenicity
Colonisation damages epithelial and endothelial cells, more permeable to leakage of tissue nutrients to sustain bacteria
Bacterial platelet-activating factor causes thrombotic occlusion of capillaries
Produces urease, converting endogenous urea to free ammonia
Produces protease, breaking down glycoproteins in gastric mucus
Produces phospholipase, damaging endothelial cells and may release bioactive leukotrienes
Attracts neutrophils, releases myeloperoxidase
Other antigens recruit inflammatory cells, making mucosa more susceptible to acid injury
Causes of peptic ulcers
H pylori
Complications of peptic ulcers
Bleeding: ulcer extends deeper and damages large BV
Perforation: contents enters abdominal cavity, causing inflammation and infection
Obstruction: edema obstructs pylori canal/duodenum
Malignancy: adenocarcinoma
