Gi Flashcards
Gastric adenoma risk
Chronic gastritis
- H pylori
- meds
- alcohol
Age >50
Gastric adenome px
Premalignant
Good it caught at this stage
Risk gastric adenoma →adenocarcinome
Flat lesion
Large > 2 cm
Highly dysplastic
-Irregular_architecture
_Cytologic atypia
Gastric Adenocarcinoma genes
-50%e-cadherin CDH1 LOF
Fap
β - catenin LOF dt-microsatellite_instability or hyper methylation
Tp53
Mx h pylori’s → cancer
Ros, proinflammatory cytokines
Decades
Virulence factor CagA → unregulated growth - not presentin all h. Pylori
Mx EBV → gastric c
~10% of gastric tumors
Poorly defined Mx
Tp53 mutation
Lymphocytic infiltrate
Lifestyle fx gastric cancer
Smoking
Alcohol
Obesity
High salt
Nitrate consumption - processed meatand fish
Birth outside US.
Asian, South American East Europe
Diffuse type gastric cancer
Younger pt
Fewer risk fx
Less likely precursor lesion
More likely e-cadherin orβ - catenin
Massintestinal type gastric AC
Distal stomach
Exophytic
Heaped up borders
Central ulceration
Typically mucousgland dysplasia
Diffuse type gastric Ac path
No focal site of origin
Infiltrative pattern
Excess collagen, fibroblasts 7 “ leather bottle” stomach
“Iceberg” small apparent mass bc deep infiltration
Tx gastric cancers
Total orpartial gastrectomy
Chemo in late stage, survival <20%
Malt lymphoma
Most often in stomach
H pylori → B cell proliferation →acquired mutations
Malt histology
Marginal zone b-cell lymphomas.
Mature lymphocytes
Invasion and destruction of gastric glands
Malt px/tx
W eradication of H pylori ‘ crr > 70%
Often noother tx but chemo, radiation, surgery in advanced
Gist
Gastrointestinal_stromal tumors
Tyr k mutations- go f
Interstitial cells of cajal
Gists site
Mostly stomach and si
Submucosal
Well circumscribed solitary mass
Gist histo
Interstitial cells of cajal
Submucosal
Spindle alls
Esophageal Ac
Often progression from barret’s esophagus
Distal 1/3 ofesophagus
Risk:
- chronic GERD
- obesity
- achalasia
Esophageal SCC
More common
Upper 2/3 of esophagus
Risk:
- smoking
- alcoho
- hot Bev
R caustic agents
-Plummer Vinson syndrome:esophageal web
Hepatic adenoma risk, demo
F 20-45 yo
OcPs and anabolic steroids
Glycogen storage disease
Dt Er on hepatocyses
Hc_adenoma p x
Usually benign
Can → HCC or cause intraperitoneal hemorrhage
Bleeding in trauma
Resect
HCC risk
Hep B, c ~75%
Any cirrhosis
Alcohol
Nafld
Aspergillus_toxins
Primary biliary cholangitis
Hereditary hemochromatosis
Wilson disease
α-1- antitrypsin def.
Paraneoplastic syx in HCC
Insulin-like gf → hypoglycemia
EPO → erythrocytosis
PTHrP → hypercalcemia, osteoporosis
Watery diarrhea
Biopsy HCC
Don’t do it, hemorrhage risk
HCC tx 1px
Surgery
Chemo, radiation not generallyhelpful
30-50% 5 yr Os if resectable <6 mo if not
Cholangiocarcinoma
Biliary tree, not gall bladder
Mucin-producing, moderate-to-poor differentiation
Cholangiocarcinome risk
Primary sclerosing cholangitis
Clonorchis sinensis- Chinese liver fluke
Thorotrast-dc’d contrast dy e
Congenitalcholedochal cysts
Cholangiocarcinoma st
Obstructive jaundice
Hepatonegoly
Palpable gall bladder
Pancreatic carcinoma risk fx
Smoking
FHx
Obesity
Chronic pancreatitis
Alcoholism
Genetics
Genetic syndromes pancreatic c
BRCA 1 and 2
PRSS1 -familial pancreatitis
Lynch-MLH1, MSH2, MSH6, PMS2, EPCAM
STK11 peutz jeghers
VHL - Von hippel lindau
Mutations pancreatic c
KRAS, p16, p53
DPC4/SMAD4
HER2 ~50%
Pancreatic c sx
If obstructing pancreatic duct
-Pain
- jaundice
- indigestion
- pruritis
- pale, smelly stools
- malabsorption
Tail = silent
Often d x stage 4 → metastatic sx
Pancreatic c px marker
CA 19-9
Chemo pancreatic.
Most common:
5-fu
Paclitaxel
site of folate absorption
jejunum
site of B12 absorption
ileum
site of bile salt absorption
ileum
