GI Flashcards
Two types of hereditary colon cancer
- FAP (familial adenomatous poliposis) – APC mutation
2. Lynch Syndrome (HNPCC) – 4 muts possible (MLH-1 or 2, PMS2, MSH-6) –> all mismatch repair genes
Peripheral Appetite regulation signals
Stimulate nutrient/fat absorption: Leptin, insulin, CCK, PYY, ApoA4
Increase Lipolysis: cortisol, ghrelin
Central signaling molecs that regulate appetite
increase appetite: AgRP (NPY neurons) & orexin A
decrease appetite: a-MSH (POMC neurons), GLP-1, CRH, NE, 5-HT
Zones of liver most affected by
a) ischemia
b) toxins
c) infection (hepatitis)
Zone III (Pericentral/”Centrilobular”) affected 1st by ischemia & toxins
Zone I (Periportal) affected 1st by infection, last for ischemia
* (bc closest to hepatic a.)
Tumor in Parotid gland… what is the DDx? (3)
1: Pleiomorphic adenoma = benign, mobile, painless. w/ cartilage
- Warthin’s: benign, cystic w/ germinal centers
- Mucoepidermoid carcinoma: malignant, mucinous.
* Painful w/ CN VII involvement!
Squamous Carcinoma vs. Adenocarcinoma of esophagus
presentation, risk factors
Squamous Carcinoma: upper 2/3; w/ smoking, EtOH, nitrites, hot food
=> ulcerated, w/ keratin whorls
ADenocarcinoma: Distal 1/3; w/ GERD/Barret’s, obesity…etc.
=> glandular, messy/inflammatory
Gastric vs. Duodenal ulcers
(both = “peptic,” pain often worse at pm)
Gastric: pain Greater w/ food, *often from NSAID use. risk cancer.
Duodenal: pain Decreases w/ food, *H pylori infection ~100%!
*punched out border = benign
Pernicious Anemia
autoimmune destruction of parietal cells of stomach (body/fundus)
=> Chronic gastritis w/ anemia (low B12) & achlorhydria
(dead parietal cells = lack H+ & IF secretion)
*Chronic gastritis from H Pylori = at Antrum of stomach.
Case:
Older male patient with history of diarrhea, weight loss, weakness & joint pain, also non-specific heart & neuro Sxs for past 6 months.
= Whipple’s disease (chronic infection w/ tropheryma whipplei)
Histo: PAS+ foamy macrophages in intestinal lamina propria, and villus atrophy in sm. intestine
Note: malabsorption AND Cardiac, Arthralagia, & Neuro Sxs
Abetalipoproteinemia
AR mut in TG transfer protein => can’t synth/secrete VLDLs & chylomicrons –> lipid accumulation in intestinal enterocytes!
=> Fail to thrive, steatorrhea, acanthocytosis, ataxia, night blindness!
Special case Gastric cancer mets: (3)
- Virchow’s node: mets to L supraclavicular node
- Sister Mary Joseph nodule: subcutaneous periumbilical mets
- Krukenberg tumor: bilat. mets to ovaries *signet ring cells & mucus
Adenomatous vs. Hyperplastic polyps of colon
Adenomatous = Premalignant (=> Colorectal). more villous = bad.
("Villous = Villainous")
Hyperplastic = NON-neoplastic, common.> 1 Colonic polyps in child. What are the associated risks?
(single polyp = no malignant potential)
multiple polyps, no other Sx = Juv. polyposis => risk adenocarcinoma.
multiple benign GI Hamartomas = Peutx-Jeghers => risk CRC
*also hyperpigmentation of mouth/lips, hands, genitalia.
2 toxins in pathogenic Clostridium difficile
Toxin A (Enterotoxin): chemoattractant for neutrophils => diarrhea Toxin B (Cytotoxin): destroys cytoskeleton of enterocytes & depolymerizes actin => mucosal necrosis :(
Utility of GGT (Gamma glutamyl transpeptidase) as a Liver test
use GGT with Alk Phos (“ALP”) to distinguish btwn bone and liver disease.
Normal GGT w/ high ALP = bone problem
(GGT = liver/biliary specific, but not as good as ALP)
unique exposures that increase risk of liver cancer
for HCC & Angiosarcoma
#1. Hepatocellular Carcinoma: aflatoxins from aspergillus = carcinogens 2. Angiosarcoma (endothelial): exposure to arsenic (pesticides, glass manufacturing) or polyvinyl chloride (plumbers)
Hereditary Hyperbilirubinemias (3)
- Gilbert’s: mild UDP-glucuronyl transferase or bili uptake def.
=> ASx, but jaundice w/ stress or fasting. No hemolysis. - Crigler-Najar: NO UDP-GT (Unconjugated bilirubinemia)
=> jaundice & kernicterus, death as toddler - Dubin-Johnson: defective liver excretion of bilirubin (conj. bilir-emia)
=> black liver, intermittent jaundice, no other Sxs
Wilson’s disease vs. Hemochromatosis
Wilson’s: copper accumulation bc failed excretion (AR, CuATPase mut)
=> Kaiser-fleish. rings, hemolytic anemia, asterixis, HCC
*Putamen degen –> “Dementia, Dyskinesia, Dysarthria”
Hemochromatosis: Fe/hemosiderin deposition (AR or transfusions)
=> 1. micronodular cirrhosis, 2. DM, 3. bronze skin;
risks: CHF, HCC, testicular atrophy
Detection of this parasite = “scotch tape test”
use tape to pull up eggs in perianal area
Enterobius! (pinworms)
*esp. in am bc adults exit anus & lay eggs at pm
Eggs of this parasite are found in the patient’s stool.
Schistosomiasis (schistosoma mansoni or japonicum)
Rhabditidiform larvae of this parasite can be found in patient’s stool
Strongyloides (larvae via skin –> to lungs then swallowed, lay eggs in intestines –> larvae grow & exit in stool)
Proglotids found in stool. parasite = ?
tapeworms (Taenia solium, Diphyllobothium latum)
*proglotid = end segment of worm
trophozoites and/or cysts IDed in patient’s stool. Parasite = ?
Giardia or Enterobius histolica (protozoans)
Schilling test is for __?__
pernicious anemia! (give exogenous IF => B12 absorption improves)
