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105 Cards in this Set
- Front
- Back
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Mechanisms of esophagus preventing reflux?
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-competent LES
-gastric esophageal junction acting as valve -diaphragmatic muscle tone |
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Mechanisms of esophagus preventing reflux?
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-competent LES
-gastric esophageal junction acting as valve -diaphragmatic muscle tone |
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Secondary causes of achalasia?
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-Chagas disease (trypanosoma cruzi)
-diabetic autonomic neuropathy -infiltrative disorders like amyloidosis and sarcoidosis |
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HSV versus CMV infectious esophagitis?
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HSV results in multinucleated cells with nuclear viral inclusions; CMV just has large cells with nuclear and cytoplasmic viral inclusions NO multinucleations
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Plummer-Vinson syndrome?
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esophageal mucosal webs, iron deficiency anemia, glottitis, and cheilosis
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Risk factors for esophageal squamous cell carcinoma?
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alcohol, tobacco, achalasia, hot beverages, Plummer-Vinson syndrome
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Congenital hypertrophic pyloric stenosis?
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3:1 male to female, present with projectile non-bilious vomiting, firm mass felt in stomach
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Mechanism of atrophic or autoimmune gastritis?
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-antibodies to parietal cells and intrinsic factors (so causes pernicious anemia)
-reduced gastric secretion followed by secondary hypergastrinemia due to G-cell hyperplasia induction -potential for developing carcinoid tumor due to ECL-cell hyperplasia in the body and fundus |
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Menetrier's disease?
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-idiopathic condition, caused by excessive TGF-alpha secretion
-hyperplasia of superficial mucinous layer; so get GIANT RUGAL FOLDS -protein losing enteropathy due to making so much mucin -increased risk of carcinoma |
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Zollinger-Ellison syndrome?
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-gastrin secreting tumor/gastinoma (in pancreas or duod.)
-benign or malignant -PRIMARY hypergastrinemia -GIANT rugal folds from PARIETAL HYPERPLASIA -hyperchlorhydria -present with multiple duodenal ulcers |
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Gastric lymphoma?
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-stomach one of most common sites for extranodal lymphoma
-majority are marginal B-cell lymphomas aka MALT -associated with H. pylori, has characteristic lymphoepithelial lesions |
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Gastric carcinoid?
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-associated with autoimmune gastritis, ZE, MEN, or de novo
-carcinoid syndrome (flushing, sweating, ab pain, diarrhea) associated with metastatic disease usualmente |
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GI Stromal Tumors (GIST)??
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-most common mesenchymal OR stromal tumor
-submucosal polypoid mass in stomach -originate from interstitial cells of Cajal (C-kit+) -can be treated by tyrosine kinase inhibitor! (gleevac) |
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Meckel diverticulum?
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-true diverticulum containing all layers of bowel wall resulting from failure of Vitelline duct (yolk sac) involution
-rule of 2s (2% of population, 2 ft from IC valve, 2 in long, 2x common in men) -rarely symptomatic -may contain gastric/pancreatic heterotropia |
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Hirschsprung disease?
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constipation since birth due to aganglionosis, affects rectum and variable length of colon, failure to relax
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Clinical manifestations of malabsorption syndrome?
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-GI: diarrhea, steatorrhea
-Heme: anemia (vit b12, folic acid, iron) -skeletal: osteopenia (calcium, vit D) -skin: purpura, keratosis (vit A,K, zinc) -neurologic: peripheral neuropathy (vitB12,A) |
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Causes of malabsorption by defective digestion?
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-pancreatic insufficiency
-ZE syndrome (excess acid) -Biliary obstruction -disaccharidase deficiency (lactose intolerance) |
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Causes of malabsorption by defective mucosal absorption?
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-gluten sensitivity (celiac)
-Crohn's disease (IBD) -chronic infectious enterocolitis -bowel resection |
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Secretory diarrhea?
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-increased intestinal fluid secretion
-persists during fasting -causes: viral (rota), cholera, E. Coli, C. perfringes, laxatives |
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Osmotic diarrhea?
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-increased osmosis by luminal solutes
-abates on fasting -causes: lactase deficiency, gut lavage |
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Exudative diarrhea?
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-inflammatory mucosal injury
-persists during fasting -causes: shigella, salmonella, campylobacter, clostridium difficile, amoeba, inflamm. bowel disease (IBD) |
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Malabsorption diarrhea?
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-improper absorption of normal nutrients
-abates on fasting -causes: celiac, giardia |
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Altered motility diarrhea?
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-disorder of neuromuscular function
-diagnosis of exclusion -cause: irritable bowel syndrome |
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Celiac disease?
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-immune mediated sensitivity to gluten (protein component of gliadin)
-long term risk of T cell lymphoma, enteropathy-associated T cell lymphoma (EATL) -increased risk of adenocarcinoma |
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Crohn's disease?
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-F slightly higher, peak age 20-25
-smoking a risk factor -affects any part of GI tract but discontinuous -thickened wall, strictures, and fissures -fistulas and perforations -cobblestoning of muscosa with aphthous and fissuring ulcers -ab pain, fever, anemia, mild diarrhea -lower incidence than UC |
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Does Crohn's disease spare the rectum?
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YES
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What are aphthous ulcers?
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very superficial ulcer above lymphoid tissue
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What is "creeping fat" and what is it associated with?
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extension of mesenteric fat on serosal surface, in crohn's disease
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Ulcerative colitis?
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-slightly higher incidence than CD
-affects each sex equally, does not favor Jews, same peak 20-25 -get clinically recurring bloody mucoid diarrhea -stree related flare ups -smoking may be protective -limited to colon |
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Gross path of ulcerative colitis?
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-starts at rectum (b/c CD spares it) and extends proximally without skipping
-exclusively colon, rarely backwash ileitis -NO mural thickening, serosal surface normal -inflamm, pseudopolyps (NOT neoplasia) -MEGACOLON - toxic dilation, distension due to paralysis |
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Ulcerative colitis microscopic features?
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-diffuse mucosal inflammation, sometimes deeper
-crypt distortion, mucodepletion -cryptitis and crypt abscesses -ulceration only in severe cases (ironic) -inflammatory polyps -4 fold inc risk of colon carcinoma -basically, disorganization of crypts, glands destroyed |
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Crohn's disease microscopic features?
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-perilymphoid - patchy inflammation
-aphthous and fissuring ulcerations -focal cryptitis (neutrophils) -uncommonly granulomas |
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Peutz-Jeghers polyps?
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hamartomatous polyps and pigmentation around the mouth (because they are a sleutz with jeigger)
also intussusception and risk of non-GI tumors also autosomal dominant |
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Non-neoplastic colorectal polyps?
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-hyperplastic polyps - small invaginated floral appearance
-hamartomatous polyps - tumor like malformations with abnormal growth |
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Tumors of small intestine are rare, but what is most common place to find one??
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duodenal ampulla
associated with FAP and inc risk with HNPCC, celiac, crohn's |
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Familial Adenomatous Polyposis??
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-Dominant germline mutation of APC gene on 5q21
-polyps at puberty, cancer at 40 or earlier - >100 polyps - adenomas elsewhere (duodenum) |
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Lynch or HPNCC??
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-dominant mutations in DNA repair genes, microsatellite instability
-mimics sporadic carcinoma -more often right sided and mucinous -risk of colon and other cancers (endometrium, stomach, renal) |
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What is the difference between right and left sided colorectal adenocarcinoma?
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-RIGHT: slow blood loss leading to anemia
-LEFT: altered bowel function (cause on the side where poop is about to leave), bleeding |
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Sporadic colorectal carcinoma?
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-70% left colon
-30% right -50% survival |
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Carcinoid tumor?
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-well differentiated neuroendocrine (NE) carcinoma
-ALL potentially malignant - NE cells throughout GI and lung, gallbladder, panc, thyroid -may secrete hormone (serotonin) which causes carcinoid syndrome and indicates metastasis -even with metastasis prognosis is better than carcinoma |
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Which prognosis is better: primary B or T cell type lymphoma??
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B cell lymphoma has better prognosis (duh, B for Better)
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Pseudomyxoma peritonei??
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mucin secreting appendiceal adenocarcinoma
causes jelly belly! |
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Different types of degeneration and intracellular accumulation in hepatic injury?
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-Ballooning generation (ETOH); basically the cells grow beer bellies!
-Foamy or feathery degeneration (bile stasis); bile has fatty cholesterol, so foamy -steatosis, macro and microvesicular (ETOH, obesity, diabetes, drugs etc) |
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Some causes of cirrhosis???
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-ETOH and NASH
-viral hepatitis -PBC -autoimmune hepatitis (AIH) -hemochromatosis -alpha 1 AT def -Wilson's disease -cryptogenic -PSC |
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There are 3 groups of viral hepatitis, what are they?
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-hepatotropic viruses (A,B,C,D,E,G)
-part of systemic viral infection (EBV, yellow fever) -immunosuppression related (adeno, CMV,HSV) |
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Microscopic features of acute viral hepatitis????
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-mainly lobular injury
-individual cell necrosis (acidophil body) -focal or spotty necrosis -hepatocyte degeneration |
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Autoimmune hepatitis??
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-symptoms and presentation similar to chronic viral hepatitis
-Type I: elevated ANA and/or ASMA, more common in females with wide age range (perimenopausal), elevated IgG -Type II: childhood type, antiLKM |
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Primary Biliary Cirrhosis associated with which antibody??
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AMA - anti mitochondrial antibody (PBC more common in women because B for Breast, and since your mom gives you her mitochondria you have AMA with this)
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Symptoms of hereditary hemochromatosis??
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-present after 40 yrs (need time to accumulate 20g of iron)
-homozygotes have the symptoms, related to deposition in liver, pancreas, heart, and skin -hepatomegaly, skin pigmentation, diabetes, arthritis, cardiac arrhythmias |
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In the late stages you get the classic triad of hereditary hemochromatosis, which is..?
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cirrhosis
skin pigmentation diabetes mellitus (bronze diabetes) |
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Wilson's disease?
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-toxic accumulation of copper in liver, eye, and brain
-AR, chromosome 13, ATP7B gene -mean age of onset:12 -total body copper 50-150mg (only 2-5 absorbed daily) -use copper chelation therapy with D-Penicillamine -increased serum, liver, and urinary copper -reduced ceruloplasmin |
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What is the liver like in Wilson's disease??
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-cirrhosis without specific morphological features
-chronic active hepatitis -acute hepatitis (mimicking viral or autoimmune hepatitis) -fulminant hepatitis -majority present with either cirrhosis or chronic hepatitis - |
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Other symptoms in Wilson's, besides the liver?
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-neurological symptoms usually seen after liver disease
-mild behavior changes like psychosis or parkinson's -Kayser-Fleischer rings in the eye, no vision problems |
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PiMM, PiSS, PiZZ?
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forms of A1AT gene as defined by migration on gel
-PiMM is medium, normal -PiSS is slow, low A1AT but no symptoms -PiZZ is no migration (post-JiZZ so no migration), very low levels, 10% are symptomatic |
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A1AT structural versus functional defect?
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-structural: accumulates in liver causing liver disease (at early age like Wilson's)
-functional: causes destructive lung disease and pulmonary emphysema |
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Primary biliary cirrhosis?
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-autoimmune liver disease with AMA
-early stages NOT cirrhotic (misnomer) -more in females (B for Breast) -pruritis is classical symptom because cholangitis is primary symptom -increased alk phos and cholesterol -other extrahepatic diseases coexisting: Sjogren's, thyroiditis, rheumatoid arthritis, celiac, etc. |
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Primary sclerosing cholangitis?
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-inflammatory obliterative fibrosis of extrahepatic and intrahepatic bile ducts
-characteristic "beading" radiologically (like balls) -more common in men (PenisScrotumCock) -association with IBD -symptoms and LFTs similar to PBC -increased risk of cholangiocarcinoma |
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Budd-Chiari?
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occlusion of hepatic veins, triad of ab pain, ascites, and hepatomegaly
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Hepatic artery compromise versus portal vein compromise?
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portal vein supplies 70% so more likely to cause diffuse hepatic ischemia (centilobular)
rapid hepatic artery compromise may cause localized infarct |
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polyarteritis nodosa?
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vasculitis of medium size arteries, swollen and damage due to attack by immune cells, could lead to hepatic artery compromise
another nodosa: erythema nodosa, fat inflammation leading to red nodules on skin, extraintestinal manifestation of IBD |
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Budd-Chiari syndrome?
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-myeloproliferative disorders (polycythemia vera, chronic myelogenous leukemia)
-paroxysmal nocturnal hematuria -oral contraceptives -tumor embolism |
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Non-neoplastic liver masses?
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-focal nodular hyperplasia
-nodular regenerative hyperplasia -benign cysts |
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Benign neoplasm of the liver?
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liver cell adenoma
hemangioma |
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Malignant neoplasm of the liver?
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-hepatocellular carcinoma (HCC)
-fibrolamellar HCC -cholangiocarcinoma -hepatoblastoma (occur in children) -angiosarcoma (last two are very rare) |
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Which is more common, primary or secondary malignant neoplasms of the liver?
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SECONDARY (cause liver has Kupffer cells who like sloppy seconds, thats why they accumulate the most iron in secondary iron overload conditions)
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von Meyenburg complexes?
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bile duct hamartoma, benign
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Hamartoma?
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benign focal malformation that resembles a neoplasm, grows at same rate as surrounding tissue and composed of same tissue elements but it is just a disorganized mass
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Focal nodular hyperplasia?
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-non-neoplastic mass with central stellate scar that radiates with almost-cirrhotic looking tissue surrounding
-female bias, young to mid-aged -growth around a vascular proliferation -may be confused with hepatocellular adenoma radiologically -usually solitary |
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Nodular regenerative hyperplasia?
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-nodularity but NO fibrosis
-NO gender/age BIAS because nonspecific nodular adaptation of liver to ANY abnormality in total hepatic blood perfusion -diffuse involvement of liver with fine nodularity, but remember no fibrosis |
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Causes of nodular regenerative hyperplasia?
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-connective tissue diseases (vasculitis)
-kidney and BM transplants -chemotherapy |
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Is nodular regenerative hyperplasia symptomatic?
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usually no, may cause portal hypertension
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Liver cell adenoma or hepatocellular adenoma?
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-women over 30 who use OCs for >7yrs
-may be mistaken for FNH or HCC -subcapsular adenomas can rupture and cause hemorrhage -hemorrhaging is the biggest problem with this -usually single, can be large but usually benign -looks like normal liver tissue BUT bile ducts missing!! |
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Most cases of hepatocellular carcinoma have increased serum levels of.....?
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Alpha fetoprotein (AFP)
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Fibrolamellar variant of HCC aka fibrolamellar carcinoma?
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-young patient (20-40) [remember HCC >60]
-occurs in non-cirrhotic liver without HBV -NO increase in AFP -better prognosis -central scar just like FNH -characterized by very dense collagen bands |
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Intrahepatic cholangiocarcinoma?
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-histo-wise similar to any metastatic adenocarcinoma
-primary needs to be ruled out -risk factors: PSC, biliary anomalies, liver fluke worm in far east -POOR prognosis |
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Common primary sites for metastatic liver tumors?
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colon, lung, breast
surface umbilication is characteristic |
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empyema?
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collection of pus within a naturally existing anatomical cavity, such as the lung pleura. It must be differentiated from an abscess, which is a collection of pus in a newly formed cavity.
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Complications of gallstone disease?
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-colicky biliary pain
-cholecystitis -empyema -perforation -peritonitis -pancreatitis -mucocele -intestinal obstruction -gallbladder carcinoma |
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Carcinoma of extra hepatic bile ducts?
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-greater incidence in males (in their 70s)
-little/no role of gallstones -IBD/PSC predisposing (thats why there is more men with this) -periampullary tumors clinically mimic pancreatic head carcinoma -progressive deep jaundice |
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Gallbladder carcinoma?
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-more common in women in their 70s
-60-90% have gallstone disease -adenocarcinomas with variable differentiation -poor prognosis -extension to liver common -symptoms similar to gallstone disease so often goes undiagnosed |
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Pancreatic pseudocyst?
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-localized collection of necrotic material
-NO lining epithelium -after acute or chronic pancreatitis -usually on surface of panc |
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Benign or borderline cystic tumors of pancreas?
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-serous cystadenoma (watery)
probably benign but not always: -mucinous cystic neoplasm -intraductal papillary mucinous neoplasm (feathery gross appearance) -solid-pseudopapillary tumor (part solid, part cystic, almost exclusively in women_ |
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Most common type of pancreatic carcinoma?
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ductal adenocarcinoma
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Less common types of pancreatic carcinoma?
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acinar cell
adenosquamous undifferentiated mixed epithelial-neuroendocrine oncocytic |
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Pancreatic carcinoma of the head versus the body and tail?
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Head causes obstructive jaundice and carcinoma may project into duodenal mucosa
Body and tail generally silent; pain, weight loss, migratory thrombophlebitis |
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Pancreatic carcinoma and peutz-jeghers syndrome?
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people with PJS have increased risk
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Pancreatic carcinoma risk factors?
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M>F, 60-80 yrs
SMOKING only definite risk factor (grandma) PJS and inherited pancreatitis have increased risk |
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Endocrine pancreas?
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4 cell types:
-Beta: insulin -alpha: glucagons -delta: somatostatin -PP: pancreatic polypeptide other minor hormones:VIP and serotonin |
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Diagnosis of diabetes?
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-random >200mg/dL
-fasting >120 -OGTT >200 2hrs |
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Diabetes mellitus is leading cause of...?
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end-stage renal disease
leg amputations blindness |
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What is insulitis?
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T cell islet infiltration seen in type I diabetes
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Autoimmunity in Type II diabetes?
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NO, strong genetic role though
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Typical examples of islet cell tumors of pancreas?
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insulinoma
gastrinoma (ZE syndrome) MEN other rare ones:VIPoma, glucagonoma, somatostinoma |
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Characterisitics of islet cell tumors of the pancreas?
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-much less common than exocrine carcinomas
-just like other neuroendocrine tumors (carcinoid) -single or multiple -localized or matastatic -distributed throughout pancreas -functional or nonfunctional |
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Hemolytic jaundice would cause what levels of unconjugated and conjugated bilirubin?
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-indirect (unconjugated) elevated because jaundice results from accelerated breakdown of RBCs that exceeds liver's ability
-some spurious elevation of direct seen |
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Obstruction of biliary tract leads to what findings?
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-inc conjugated bili in blood (backs up into blood instead of being excreted in bile)
-coke colored urine from bili and clay colored stools from lack thereof -urobiliogen absent due to lack of bile intestine -itching |
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Jaundice due to hepatocellular destruction?
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-inc conjugated bili in serum with inc unconjugated as liver fails
-basically same as obstructive jaundice except urobiligen variably decreased rather than absent |
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Unconjugated hereditary hyperbilirubinemias?
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Gilbert syndrome: decreased bili UGT
Crigler-Najjar Type 1: absent UGT Crigler-Najjar Type 2: decreased UGT |
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Conjugated hereditary hyperbilirubinemias?
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Dubin-Johnson: impaired biliary excretion - canalicular defect
Rotor syndrome: decreased uptake/excretion |
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When is decreased lipid handling by the liver seen?
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in serious cases aka rarely
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AST/ALT?
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-AST in mito and cytoplasm and has longer half life so elevated longer
-ALT only in cytoplasm |
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Alkaline phosphate?
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-located on canalicular surface
-responsible for transport of bili into bile -elevations in obstructed disease (normal in children, seen with fractures, tumors) |
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Lactate dehydrogenase?
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-glycolytic enzyme found in nearly all cells with LD5 found in hepatocytes, but has short half life so not seen with liver disease
LDH elevations usually from heart, RBCs or tumor |
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Gamma glutamyltransferase (GGT)?
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-on canalicular surface and in microsomes: drug inducible
-not found in bone so used to diff ALP elevation of bone or liver (ALP alone=bone source) -GGT elevations may be caused by enzyme induction from chronic ETOH or anticonvulsant drugs |
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Alpha fetoprotein?
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major plasma protein in fetal life and inc in hepatocyte regeneration or proliferation in acute hepatitis, recovery from hepatitis, and liver neoplasm
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