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Step 1 12.21.12

GI III

QuestionAnswer
What is the usual location and what distrobution pattern is seen in Crohn's disease? any portion of GI tract usually terminal ileum or colon. see Skip lesions and rectal sparing
What is the gross morphology of Crohn's disease? transmural inflammation. Cobblestone mucosa, creeping fat, bowel wall thickening, linears ulcers, fissures, fistulas
A "string sign" on barium swwallow X ray is associated with what disease? Crohn's disease
What is the microscopic morphology of Crohn's disease? non caseating granulomas and lymphoid aggregates (Th1) mediated
What are some major complications of Crohn's disease? strictures, fistulas, perianal disease, malabsorbtion, nutritional depletion, colorectal cancer
What is the intestinal manifestation of Crohn's disease? diarrhea that may or may not be bloody
What are the extraintestinal manifestations of Crohn's disease? migratory polyarthritis, erythema nodosum, immunologic disorders, kidney stones
What is the tx for Crohn's disease? corticosteroids, infliximab
What is a possible etiology for ulcerative colitis? might be AID
What is the location and distrobution of ulcerative colitis? colon inflammation. contiunous colonic lesions always with rectal invovlement
What is the gross morphology of ulcerative colitis? mucosal and submucosal inflammation only. friable mucosal pseudopolyps with freely hanging mesentery. Loss of haustra--> lead pipe appearance on imaging
What is the microscopic morphology of ulcerative colitis? crypt absesses and ulcers, bleeding with no granulomas. TH2 mediated
What are some major complications of ulcerative colitis? malnutrition, sclerosising cholangitis, toxic megacolon,COLORECTAL CARCINOMA (worse if right sideds or pan colitis)
What is the intestinal manifestation of ulcerative colitis? bloody diarrhea
What are some extraintestinal manifestations of ulcerative colitis? polyderma gangrenosum, primary sclerosing cholangitis, ankylosing spondylitis, uveitis
What is the Tx for ulcerative colitis? ASA pereparations ( sulfasalazine), 6 mercaptopurine, infliximab, colectomy
What is a mneominc to remeber the presentation of Crohn's disease? think of a FAT GRANny and old CRONE SKIPPING down a COBBLESTONE road way away from the WRECK (rectal sparing)
How is the Dx of iriitable bowel syndrome? at least 2 of: 1. pain improving with defaction 2. change in stool frequency 3. change in appaearance of stool
How does iritable bowel present? How do you tx it? usually diarrhea or constipation, or alternating. Tx the sx as the etiology is unclear
What is a key association of acute appendicitis in children? lymphoid hyperplasia after a viral infection
What is a key association of acute appendicitis in adults? obstruction, fecalith
What is the presentation and progression of acute appendicitis? initial diffuse periumbilical pain-->localized pain at McBurney's point( 1/3 distance from ASIS to umbilicus). get nausea fever and if it perforates--> peritonitis
What are some other things that must be considered in acute appendicitis? How do you rule them out? divertivculitis in the elderly. ectopic pregnancy ( use Beta-HCG to rule out)
What is a diverticulum? What features do they have? Where are they most often found? blind pouches protruding from the alimentary tract, false and have attenuated muscularis externa. Most often seen in the sigmoid colon
What is a true vs a false diverticulum? True: all 3 gut wall layers out puch. False: diverticulum or pseudodiverticulum- only the mucosa and submucosa outpuch. occur especially where vasa rect perforate muscularis externa
What is diverticulosis and what causes it? many diverticula. common in elderly. caused by incr intraluminal pressure and focal weakness in colonic wall. associated with .low fiber diets. most often in signmoid colonm
What are some possible presentations of diverticulosis? often ASx, or associated with vague discomfort or painless rectal bleeding
What is the cassic presentation of diverticulitis? inflammation of diverticula classically causing LLQ pain, fever, leukocytosis.
What can diverticulitis lead to? c an perforate leading to peritonitis, abscess formation, or bowel stenosis. Give abtx
What are some common associations of diverticulitis? may cause bright red rectal bleeding. may also cause colovesical fistula (fistula with bladder0--->pneumaturia. Called left sided appendicits due to clinical piucture sometimes
What is Zenker's diverticulum? flase diverticulum. Herneation of mucosal tissue at junction of pharynx and esophagus.
What are the presenting sx of Zenker's diverticulum? halitosis ( due to trapped food) , dysphagia, obstruction
What is Meckel's diverticulum? true diverticulum. persistance of the vitelline duct or yolk sac. May contain ectopic acid secreting gastric mucosa and or pancreatic tissue. MOST COMMON CONGENITAL LESION OF GI
What are some presenting sx of Meckel's diverticulum? melena, RLQ pain, intussecption, volvulus or obstruction near the terminal ileum.
What is a major difference between Mckel's diverticulujm and an omphalomesenteric cyst? cystic dilation of the mitelline duct
What are the 5 2's of Meckel's diverticulum? 1. 2 inches long 2. 2 feet from ileocecal valve 3. 2% of pupulation 4. first 2 years of life 5. may have 2 types of epithelia (gastric/pancreatic)
How do you Dx Meckel's diverticulum? pertechnetate study for ectopic uptake
What is intussusception? telescoping of 1 bowel segment into a distal segment, commonly at ileocecal junction
What Sx can intussusception cause? currant jelly stools, can comprimise the blood supply,
Who gets intussusception? unusual in adults but could be secondary to intraluminal mass or tumor. seen most often in chjildren perhaps associated with viral infection
what is volvulus? twisting of portion of bowel around its mesentery, can lead to obstruction and infarction. may occur at cecum and sigmoid colon where there is redundant mesentary. usually in elderly
What is the congenital derangement in Hirschsprung's disease? congential megacolon characterized by lack of ganglion cells/enteric nervoius plexus in segment on biopsy. Due to Failure of migration of neural crest cells
How Does Hirschsprung's disease present? chronic constipation early in life. dilation portion of colon proximal to aganglionic segment resulting in a transition zzone. involves rectum. usually failure to pass meconium
What other conegenital problem is associated with Hirshsprung's disease? Down syndrome
What is duodenal atresia? What is it associated with? causes early bilious vomiting with proximal stomach distention due to failure of recanalization of small bowel. Associated with Down Syndrome.
What us meconium ileus? in cystic fibrosis, meconium plug blocks the intestine preventing stool passage at birth
What is necrotizing enterocolitis? necrosis of intestinal mucosa and possible perforation. colon is usually invovled but can invovle entire GI tract. in neonates, more common in premies (decr immunitiy)
What is ischemic colitis? reduction in intestinal blood flow causes ischemia (pain out of proportion with physical findings). pain after eating leading to weight loss. commonly occurs at splenic flexure and distal colon. usually seen in elderly
What is adhesion? acute bowel obstruction, commonly from a recent surgery. can have well demarcated necrotic zones
What is angiodysplasia? tortuous dilation of vessels--> bleeding. most often found in cecum, terminal ileum, and ascending colon. common in older pt. confired via angiography
What are colonic polys? Where do they appear? How many are malignant? masses protruding into the gut lumen, saw tooth appearance. 90% are none neoplastic. often rectosignoiod
What types of polyps are precancerous? What are they assoicated with? adenomatous polyps. malignant risk is associated with incr size, villous histology, incr epithelial dysplasia. precursor to colorectal cancer. more villous = more malignant
What are the Sx of colonic polyps? often ASx, but can have lower GI bleed, partial obstruction or secondary diarrhea
What is a hyperplastic colonic polyp? most common non neoplatic
What is a juvenile colonic polyp mostly sporadic lesion in children. if single = no malignant potential
What is juvenile polyposis syndrome? multiple juvenile polyps in the GI tract, incr risk of adenocarcinoma
What is Peutz-Jeghers? and what is it associated with? autoD featuring multiple nonmalignant hamartomas throughout the GI tract, along with hyperpigmented mouth, lips, hands, genitalia. assoicatated with incr risk of CRC and other visceral malignancies
What is the epidemilogy of colorectal cancer? 3rd most common, 3rd most dealy. most are >50 y/o and 25% have a family Hx
What is familial adenomatous polyposis (FAP)? AutoD mutation of APC gene on chr 5q. 2 hit hypothesis. 100% progress to CRC. thousands of polyps; pan colonic always invovles the rectum
What is Gardner's syndrome? FAP + osseuos and soft tissue tumors with rectal hyperplasia
What is Turcot's sydrome? FAP + malignant CNS tumor. turcot=turban
What is hereditary nonpolyposis colorectal cancer (Lynch syndrome)? autoD mutation of DNA mismatch repair. 80% proceed to CRC. proximal colon is always invovled
What are some major RF for CRC? IBD, streptococcus bovis bacteremia, tobacco use, large villous adenomas, juvenile polyposis syndrome, Peutz-Jeghers
What is the presentation of colorectal cancer? rectosignmoids> ascending>descending. 1. ascending: exophytic mass, iron deficiency, weight loss 2. Descending: infiltrating mass, partial obstruction, colicky pain, hematochezia
What are some key ways to Dx colorectal cancer? iron deficiency anemia in males esp if > 50 y/o. and post menopausal females. Screen Pt with stool occult blood test and colonoscopy
What be seen in CRC in a barium enema XR? apple core lesion
What is a tumor marker for colorectal cancer? CEA
What are the 2 major molecular pathways leading to CRC? 1. microsatelllite instability pathway: DNA mismatch repiar gene as in sporadic and HNPCC 2. APC/Beta carenin (chromosomal instabity (85%). loss of APC gene--<KRAS mutation (makes adenoma)--> loss of p53 leads to carcinoma
What is a carcinoid tumor and where are they most commonly found? What do they produce? tumor of neuroendocrine cells. 50% of small bowel tumors. most common sites are appendix, ileum and rectum. most commonly malignant in SI. might produce 5-Ht leading to carcinoid syndrome
What is seen on EM in a carcinoid tumor? "dense core bodies"
What are the classic Sx of carcinoid tumor? wheezing, right sided heart murmurs, diarrhea, flushing. If tumor is confined to GI there is no carcinoid syndrome. but see carcinoid syndrome if there are metastses
What is cirrhosis? diffuse fibrosis and nodular regenration destroys the normal arhitecture of the liver. incr risk of hepatocellular carcinoma
What are the major etiologies of cirrhosis? EtOH (60-70%), viral hepatic biliary disease, hemochromatosis
What are some major effects of portal hypertension? esophageal varices, peptic ulcer, melena, splenomegaly, splenomegaly, caput medusae, ascites, hemerroids
What are the major effects of liver cell failure? coma, scleral icterus, fetor hepaticus, spider nevi, gynecomastia, jaundice, anemia, ankle edema
What is the major diagnositic use of aminotransferase like AST, ALT? Liver enzymes. ALT>AST in viral hepatitis. AST>ALT in alcoholic hepatitis
What is the diagnostic use of GCT (gamma glutamyl transpeptidase)? various liver disease. incr with heavy EtOH consumption
What is the diagnostic use of akaline phosphatase? obstructive liver disease (hepaticellular carcinoma), bone disease, bile duct disease
What is the major diagnostic use of amylase? acute pancreatitis, mumps
What is the major diagnositc use of lipase? acute pancreatitis
What is the major diagnositc use of ceruloplasmin (decr)? Wilson's disease
What is Reye's syndrome and what are the major findings? often fatal childhood hepatoencephalopathy. Findings: mitochondrial abnormalities, gatty liver, hypoglycemia, vomiting, hepatomegaly, coma.
What is Reye's syndrome associated with? viral infections esp VZV and influenza B treated with salicylaters
What is the mech of Reye's syndrome? aspirin metabolites decr beta oxidation by reversibly inhibitng mitochondrial enxzymes. DONT GIVE ASIRIN TO KIDS. acetominophen with caution
What is hepatic steatosis and what is seen? short term change with moderate EtOH intake. macrovsicular fatty change that may be reversible with EtOH cessation
What is alcoholic hepatitis? requires sustaine long term consumption. swollen and necrotic hepatocytes with Mallory bodies ( intracytoplasmic eosinophilic inclusions) are present
What is the AST ALT ratio seen in alcoholic hepatitis? AST>ALT
What is alcoholic cirrhosis? final and irreversible. micronodular irregularly shrunken liver with hobnail appearance. sclerosis around central vein (zone III). manifestation of chonic liver disease
What is hepatocellular carcinoma/hepatoma and what is it associated with? most common liver tumor in adults primary. incr incidence with Hep B, Hep C, Wilson's disease, hemochromatosis, alpha 1 antitrypsin defiencym allcoholic cirrosis and carcinogen like aflatoxin from aspergillus.
What are the key findings in hepatocellular carcinoma/hepatoma? jaundice, tender hepatomegaly, ascites, polycythemia, hypoglycemia
How does hepatocellular carcinoma/hepatoma spread? WHat is a key marker? What can it lead to? commonly spreads hematogenously. incr alpha fetoprotein, may lead to Budd-Chiari syndrome
What is a cavernous hemangioma? common bening liver tumor. 30-50y/o. biospy is contraI due to risk of hemmorhage
What is nutmeg liver? What causes it and what can it lead to? due to backup of blood to liver. commonly caused by right sided heart failure and Budd-Chiari syndrome. if it persits centrilobular conjestion and necrosis can result in cardiac cirrhosis
What is Budd-Chiari syndrome? occlusion of IVC or hepatic veins with contrilobular conjestion and necrosis leading to congestive liver diesease (hepatomegaly, ascites, abdominal pian and eventual failure.
What might someone with Budd-Chiari have on PE and what are some key associations for this condition? develop varices and have visible abdominal and back veins. absence of JVD. associated with hypercoagulable state, polycythemia vera, pregancy, and hepatocellular carcinoma
What is the protein derangement in alpha 1 antitrypsin deficency? misfolded gene products aggregates in hepatocellular ER-->cirrhosis with PAs postive globules in liver. In the lungs the lact of a functioning enzyme causes decr eleastic tissue and panancinar ephysema. codominany
What is jaundice and what are 3 major cuases? yellow skin and or sclerae resulting from elevated bilirubin. 1. direct hepatocellular injury 2. obstruction to bile flow 3. hemolyisis
What is the hyperbilurubinemia, urine bilirubin and urine urobilinogen for hepatocellular jaundice? hyperbilirubinemia: direct/indirect urine bilirubin: incr urine urobilinogen: normal to decr
What is the hyperbilurubinemia, urine bilirubin and urine urobilinogen for obstructive jaundice? hyperbilirubinemia: direct urine bilirubin: incr urine urobilinogen: decr
What is the hyperbilurubinemia, urine bilirubin and urine urobilinogen for hemolytic jaundice? hyperbilirubinemia: indirect urine bilirubinL absent (acholuria) urine urobilinogen: incr
What causes physiologic neonatal jaundice? How do you Tx it? immature UDP glucoronyl transferase-->unconjugated hyperbiliorubinemia--> jaundice/kernicterus. Tx: phottherapy ( converts UCB to a water soluable form)
What is Gilbert's syndrome? mildly decr UDP glucoronyl transferase or decr bilirubin uptake, Asx
What labs might be seen in Gilbert's syndrome? elevated unconmjugated bilirubin without over hemolyisis. bilirubin with incr with fasting and stress
What is Crigler-Najjar syndrome, type I? absent UDPglucornyl transferase. presents early in life and pt die w/in a few years.
What are the major findings in Crigler-Najjar syndrome, type I? jaundice, kernicterus (bilirubin deposition in brain), incr unconjugated bilirubin
How do you tx Crigler-Najjar syndrome, type I? plasmaphoresis and phototherapy
What is Crigler-Najjar syndrome, type II? how is it tx? less severe than 1, responds to phenobarbital which incr liver enzymes
What is Dubin-Johnson syndrome? conjugated hyperbilirubinemai due to defective liver excretion. grossly black liver. benign.
What is Rotor's syndrome? milder version of Dubin-Johnson but no black liver
What type of bilirubin builds up in Gilbert's syndrome? issue is with bilirubin uptake-->unconjugated bilirubin
What type of bilirubin builds up in Crigler-Najjar syndrome? problem with bilirubin conjugation--> unconjugated bilirubin
What type of bilirubin builds up in Dubin-Johnson syndrome? problem is with excretion of conjugated bilirubin--> conjugated bilirubin
What is the pathophysiology of Wilson's disease? inadequate hepatic copper excretion and failure of copper to enter circulation as ceruloplasmin
What does Wilson's disease lead to? copper accumulation esp in liver, brain, cornea, kidneys, joints
What is a menomic for the key characterizing features of Wilson's disease? Copper is Hella BAD: 1. Ceruloplasmin decr, cirrosis, corneal depositis (Kayser-Fleischer rings), copper accumulation, carcinoma 2. hemolytic anemia 3. basal ganglia degenration (parkisons sx) 4. asterixis 4. demetia, dyskinesia, dysarthria
What is hemochromatosis? depostion of hemosiderin (hemochromatosis causes hemosiderosis)
What is the presentation of hemochromatosis? triad: 1. cirrhosis 2. DM 3. skin pigmentation "bronze DM). Can have enoguh iron to set off airport metal detectors
What does hemochromatosis cause? CHF, testicular atrophy and incr risk of hepatocellular carcinoma. can be primary or secondary
What are some causes of secondary hemochromatosis? chronic transfusion (Beta thalsemmia major), incr ferritin, incr iron, decr TIBC leading to incr transferrin saturation
what is a genetic association of hemochromatosis? HLA A-3
how do you tx hereditary hemochromatosis? phlebotomy, deferoxamine
Created by: tjs2123