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50 Cards in this Set
- Front
- Back
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Diverticulum
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- blind pouch leading off alimentary tract that communicates with gut lumen
- most are acquired and termed "false" because they lack or have an attenuated muscularis externa - most often in SIGMOID colon TRUE = all 3 gut wall layers FALSE = only mucosa and submucosa outpouch - occur occasionally where vasa recta perforate muscularis externa |
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Diverticulosis
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- MANY DIVERTICULA
- common (about 50% of people older than 60yrs) - caused by increased intraluminal pressure with FOCAL WEAKNESS in colon wall - associated with LOW-FIBER DIET - SIGMOID Colon - most common - often asymptomatic or assoc with vague discomfort and/or rectal bleeding |
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Diverticulitis
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inflammation of diverticula classically causing:
- LLQ pain - fever - leukocytosis - may perforate --> peritonitis, abscess formation, bowel stenosis - give abx! - may cause bright red rectal bleeding |
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Zenker's diverticulum
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false diverticulum
- herniation of mucosal tissue at jtn of pharynx and esophagus presents with: - halitosis (entrapped food) - dysphagia - obstruction |
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Meckel's diverticulum
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- persistence of VITELLINE DUCT OR YOLK STALK
- may contain ectopic acid-secreting gastric mucosa! and/or pancreatic tissue - MOST COMMON congenital anomaly of GI tract --> bleeding, intussuseption, volvulus, obstruction near terminal ileum contrast this with omphalomesenteric cyst = dilatation of vitelline duct DX: Tc99m nuclear scan - identifies parietal cells of ectopic gastric mucosa "10 year old male complains of intermittent abd pain and has no evidence of gastritc ulcer or gastritis - may also have black, tarry stool" The five 2's: - 2 inches long - 2 feet from ileocecal valve - 2% of population - presents in 1st 2 years of life - may have 2 types of epithelia (gastric/pancreatic) |
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intussusception
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"telescoping" of 1 bowel segment into distal segment
- can compromise blood supply - often due to intraluminal mass - usually in infants |
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volvulus
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- twisting of portion of bowel around its mesentery
- can lead to obstruction and infarction - may occur at sigmoid colon where there is redundant mesentery - usually in elderly |
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Hirschsprung's disease
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congential megacolon caused by lack of ganglion cells/enteric nervous plexuses (Auerbach's and Meissner's plexuses) in segment on intestinal biopsy
- due to FAILURE OF NERUAL CREST CELL MIGRATION - presents as chronic constipation early in life - dilated portion of colon proximal to aganglionic segment --> a "transition zone" - involves rectum - usually - FAILURE to PASS MECONIUM - you see constricted aganglionic segment and dilated megacolon with "transition zone" in b/t Cx: abdominal distention and bilious vomiting - increased risk with Down syndrome! Signmoid colon most often involved - RECTUM ALWAYS INVOLVED! |
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duodenal atresia
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causes early bilious vomiting with proximal stomach distention
- "double bubble" - FAILURE OF RECANALIZATION of small bowel - associated with DOWNS SYNDROME |
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Meconium ileus
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in CF, meconium plug obstructs intestine - preventing stool passage
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Necrotizing enterocolitis
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necrosis of intestinal mucosa and possible perforation
- colon usually involved but can involve entire GI tract - in neonates, more common in preemies (b/c decreased immunity) |
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Ischemic colitis
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reduction in intestinal blood causes ischemia
- typically affects ELDERLY - consequences include sepsis, bowel infarction and death |
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adhesion
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acute bowel obstruction
- commonly from recent surgery - can have well-demarcated necrotic zones |
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angiodysplasia
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- tortuous dilation of vessels--> bleeding
- most often found in CECUM and ASCENDING COLON - more common OLDER pts - confirm with ANGIOGRAPHY |
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Juvenile polyps
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AD disorder
- seen in first decade - increase risk of colorectal cancer - seen in rectum - smooth surface with cystic spaces - associated with germline mutation of SMAD4/BMP1A |
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colonic polyps
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90% are benign hyperplastic hamartomas, not neoplasms
- often rectosigmoid - sawtooth appearance - MORE VILLOUS the polyp - more likely it's malignant!!! |
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Colorectal cancer
- char - risk factors - ba swallow imaging results - - tumor marker - R vs. L sided differences |
3rd most common cancer
- most sporadic - mainly due to chromosomal instability (85%) or microsatellite instability (15%) Risk factors: - colorectal villous adenomas - chronic IBD (especially UC) - increased age - FAP - HNPCC - FHx - screen pts >50 with stool occult blood test and colonoscopy - "apple core" lesion on barium enema x-ray - CEA tumor marker R sided - bleeding - polypoid appearance - Iron deficiency anemia - less obstructive effect because right colon has increased caliber for distention than left L sided - obstructive - "napkin-ring" appearance - weight loss - progressive fatigue` |
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FAP
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familial adenomatous polyposis
- AD - mutation of APC gene (which normally inhibits B-catenin and in doing so inhibits growth signal) on chromosome 5q - TWO HIT hypothesis - Thousands of polyps - PANcolonic - ALWAYS involves rectum - ALL PATIENTS develop colon cancer - 35-40 yr - prophylactic colectommy recommended |
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Gardner's syndrome
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AD
- FAP with osseous and soft tissue tumors - retinal hyperplasia - osteomas/desmoid tumors - |
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Turcot's syndrome
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AR
- FAP with possible brain involvement (GLIOBLASTOMA) |
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HNPCC
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AD
- mut in MSH gene - normally involved in DNA MISMATCH REPAIR pathway - mut --> microsatellite instability - 80% progress to CRC - proximal colon always involved - commonly RIGHT-SIDED colon cancer - 60% risk in females of ENDOMETRIAL CANCER!!! |
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Peutz-Jeghers syndrome
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AD
- benign polyposis syndrome - associated with increased risk of CRC and other visceral malignancies (panceras, breast, ovary, stomach) Findings: hamartomatous polyps of colon and small intestine - hyperpigmented mouth, lips, hands, genitalia - mainly in small bowel - increased risk benign sex cord stromal, ovarian tumor |
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Carcinoid
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tumor of ENDOCRINE cells
- 50% of small bowel tumors - most common site = small intestine - "Dense core bodies" on EM - often produce 5-HT (depending on location --> CARCINOID SYNDROME) Classic sx's of carcinoid syndrome: - sheezing - Right-sided murmurs - diarrhea - flushing |
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Cirrhosis and portal HTN
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- diffuse fibrosis of liver - destruction of normal architecture
- NODULAR REGENERATION Micronodular - nodules < 3mm, uniform in size - due to METABOLIC insult - alcohol, hemochromatosis, Wilson's disease Macronodular - nodules> 3mm, varied sizes - usually due to significant liver injury leading to hepatic necrosis (eg - post-infectious, drug-induced hepatitis) - increased risk of HCC!!! - portacaval shunt between splenic vein and left renal vein may relieve portal HTN |
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effects of portal HTN
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esophageal varices --> hematemesis
espohageal varices and peptic ulcers--> melena splenomegaly caput medusae ascites hemorrhoids |
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effects of liver cell failure
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coma
scleral icterus fetor hepaticus (breath smells like a freshly opened corpse) spider nevi gynecomastia jaundice testicular atrophy liver "flap" - asterixis (coarse hand tremor) bleeding tendancy (decreased prothrombin and clotting factors) Anemia Ankle edema |
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Enzyme markers of GI pathology - name what each signals:
AST/ALT GGT Alkaline phosphatase (ALP) Amylase Lipase Ceruloplasmin decrease |
AST/ALT
- viral hepatitis: ALT>AST - alcoholic hepatitis: AST>ALT - MI (AST) GGT (gamma-glutamyl transpeptidase) - various LIVER diseases ALP - obstructive liver disease (HCC) - bone disease - bile duct disease Amylase - acute pancreatitis - mumps Lipase - acute pancreatitis Ceruloplasmin (decreased) - Wilson's disease |
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Reye syndrome
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rare, often fatal childhood HEPATOENCEPHALOPATHY
- fatty liver (microvescicular steatosis - fatty change) - hypoglycemia - coma associated with viral infection (esp VZV and influenza B) that has been treated with SALICYLATES - Aspirin NOT recommended for children (use acetaminophen, with caution) because of MITOCHONDRIAL DYSFTN OF OXID. PHOS. |
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hepatic steatosis
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- short-term change with moderate alcohol intake
- REVERSIBLE macrovesciular fatty change upon alcohol cessation |
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Alcoholic hepatitis
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- requires sustained, long-term consumption
- swollen necrotic hepatocytes with neutrophilic infiltration - MALLORY bodies (intracytoplasmic eosinophilic inclusions) seen AST>ALT (you're toASTed with alcoholic hepatitis!) wherease ALT>AST in viral hepatitis |
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alcoholic cirrhosis
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fatal and irreversible form
- micronodular irregularly shrunken liver with "hobnail" appearance - sclerosis around central vein (zone III) - has manifestations of chronic liver disease (eg - jaundice, hypoalbuminemia) |
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HCC/hepatoma
- what increases risk? - presentation? - marker? - may lead to what condition? |
most common primary malingant tumor of liver
- increased incidence of HCC is associated with: HBV HCV (NOTE: HBV and HCV are most common risk factors!) Wilson's diasese hemochromatosis alpha-1-antitrypsin deficiency (as in panacinar emphysema) alcoholic cirrhosis carcinogens (eg: aflatoxin in peanuts) can present with: - tender hepatomegaly - ascites - polycythemia - hypoglycemia marker - elevated alpha-fetoprotein! may lead to: - BUDD-CHIARI SYNDROME |
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Budd Chiari Syndrome
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OCCLUSION OF IVC or HEPATIC VEINS
- with centrilubular congestion and necrosis - leads to congestive liver disease (hepatomegaly, ascites, abdominal pain, eventual liver failure) - may develop varices and have visible abdominal back veins - absence of JVD associated with - polycythemia vera - pregnancy - HCC can test for it with hepatic venography |
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alpha1-antitrypsin deficiency
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misfolded gene product protein accumulates in hepatocellular ER
- decreased elastic tissue in lungs --> emphysema PAS+ globules in liver!!! (key if given a picture - see pink globules!) codominant inheritance mutant AAT can't be secreted by liver!!! |
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jaundice
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normally, liver converts unconjugated (indirect) bilirubin to conjugated (direct)
Direct/Conjugaged - water soluble - can be excreted into urine and by liver into bile to be converted by gut bacteria to urobilinogen (some of which is resorbed) - some urobilinogen is formed directly from heme metabolism! |
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Gilbert's Syndrome
- defect - cx - unconj bilirubin level - associated with? |
mildly decreased UDP-glucuronyl transferase or decreased bilirubin
uptake asymptomatic elevated unconjugated bilirubin without overt hemolysis associated with stress NO CLINICAL CONSEQUENCES |
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Crigler-Najjar syndrome, type I
- defect - when it presents - lifespan? - findings? - type II - how is it different? tx? - tx for type I? |
ABSENT UDP-glucuronyl transferas
- presents early in life - pateints die w/in a few yrs - muscle rigidity - lethargy - seizures findings: - jaundice - kernicterus - increased unconjugated bilirubin Tx: plasmapheresis and phototherapy Type II - less severe - responds to Phenobarbital which increases liver enzyme synthesis |
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Dubin-Johnson syndrome
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- conjugated hyperbilirubinemia
- due to defective liver excretion - grossly black liver - benign |
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Rotor's syndrome
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similar to Dubin-Johnson syndrome
- dueto difective liver excretion - does not cause black liver however! |
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Wilson's disease
- inheritance pattern? - pathophysiology - Cx - Tx |
AR
inadequate hepatic copper excretion - failure of copper to enter cirulation as CERULOPLASMIN! - so we see decreased ceruloplasmin in Wilson's disease - copper accumulates in liver brain cornea (Kayser-Fleischer rings) kidneys joints - aka - hepatolenticular degeneration Cx: ABCD - Asterixis - Basal ganglia degeneration (parkinsonian symptoms) - Ceruloplasmin decrease - Cirrhosis - Corneal deposits (Kayser Fleischer rings) - Copper accumulation - Carcinoma (hepatocellular - Choreiform movements - Dementia Tx: PENICILLAMINE!!! |
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hemochromatosis
- pathophys - cx - ferritin, iron, TIBC, transferrin saturation levels? - tx - HLA assoc? |
HEMOSIDEROSIS = deposition of hemosiderin (iron)
HEMOCHROMATOSIS = disease caused by this iron deposition Classic triad of sx's: - Cirrhosis - DM - skin pigmentation --> bronze diabetes - results in CHF and increased risk of HCC disease may be primary (autosomal recessive) or secondary to CHRONIC TRANSFUSION THERAPY - may set off metal detectors at airport!!! - Tx: repeated phlebotomy, DEFEROXAMINE - assoc: HLA-A3 |
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Primary sclerosing cholangitis
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both intra and extra hepatic
- INFLAMMATION and FIBROSIS of bile ducts --> alternatic strictures and dilations with "beading on ERCP - concentric "onion skin" bile duct fibrosis - increased ALP - ASSOCIATED WITH UC!!! - can lead to secondary biliary cirrhosis!!! |
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biliary cirrhosis - primary
- cx - ALP level? serum mitochondrial Ab level? - associated conditions |
intrahepatic, AUTOIMMUNE disorder
- severe obstructive jaundice - steatorrhea - pruritus - hypercholesterolemia (xanthoma) - increased ALP - increased serum ANTI-MITOCHONDRIA Abs (most important marker) - associated with scleroderma and CREST |
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Biliary cirrhosis - secondary
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EXTRAhepatic biliary obstruction (as compared to primary which was INTRA hepatic autoimmune-related)
- increased pressure in intrahepatic ducts --> injury/fibrosis - often complicated by ascending cholangitis (bacterial infection), bile stasis, and "bile lakes" - increased ALP (as is often seen with biliary tract disease) - increased conjugated bilirubin (because it's obstructive jaundice |
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Gallstones
- how they form - risk factors - triad of sx's - cholesterol vs. pigment stones - sequelae - dx - tx |
Form when solubilizing bile acids and lecithin are overhwelmed by increased cholesterol and/or bilirubin
Risk factors - female, fat, forty, fertile! Cx: Jaundice, fever, RUQ pain ChoLesteroL stone: - radioLucent - 80% of gallstones - associated with: obesity, Crohns!!!, CF!!!, increased age, clofibrate, estrogens, multiparity, rapid weight loss, Native American origin Pigment stones - radioOPAQUE - seen in pts with chronic RBC hemolysis, alcoholic cirrhosis, advanced age, biliary infection cause: ascending cholangitis, acute pancreatitis, bile stasis, cholecystitis can also --> biliary colic - gallstones interfere with bile flow, causing bile duct contraction (may present without pain) Dx: ultrasoudn Tx: cholecystectomy |
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cholecystitis
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inflamm of gallbladder
- can be infectious (CMV, cryptococcus) or due to gallstone complication - increased ALP if bile duct becomes involved (as in ascending cholangitis) |
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Acute pancreatitis
- pathophys - causes - cx - labs - sequelae - chronic pancreatitis - chronic calcifying pancreatitis |
autodigestion of pancreas by pancreatic enzymes
- causes: GET SMASHeD Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia/Hyperlipidemia, Drugs Cx: epigastric abdominal pain radiating to back, anorexia, nausea Labs: elevated AMYLASE, LIPASE (lipase has higher specificity because it's only made in pancreas) sequelae - DIC, ARDS (pancreatic enzymes act on lung tissue), diffuse fat necrosis, hypocalcemia (Ca2+ collects in pancreatic Ca soap deposits) - pesuodcyst formation - hemorrhage - infection Chronic pancreatitis --> pancreatic insufficiency --> steatorrhea, fat-soluble vitamin deficiency, and DM Chronic calcifying pancreatitis - strongly associated with alcoholism |
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Pancreatic adenocarcinoma
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prognosis averages 6 mo of less
- very aggressive - usually already metastasized at presentation - tumors more common in pancreatic head (--> obstructive jaundice) - increaed risk in Jewish and Afr Amer males increased CEA and CA19-9 associated with cigarettes - NOT ALCOHOL!!! presentation: - abdominal pain radiating to back - weight loss - migratory thrombophlebitis - redness and tenderness on palpation of extremities (Trouseau's sign) - obstructive jaundice with palpable gallbladder (Courvoisier's sign) |
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describe each:
1. hyperplastic polyp 2. hamartomatous polyp 3. inflammatory polyp 4. lymphoid polyp 5. adenomatous polyp (villous and tubular) |
1. well-differentiated mucosal cells that form glands and crypts
2. mucosal glands, smooth muscle and connective tissue - occur sporadically in Peutz-Jeghers or juvenile polyposis 3. seen in UC and Crohns, composed of regenerating intestinal mucosa 4. in children - intestinal mucosa infiltrated with lymphocytes 5. adenomatous are NEOPLASTIC (unlike 1-4) - contain dysplastic mucosal cells and can tranform into adenocarcinoma - decree of malignant potential det by: - degree of dysplasia - histologic pattern: VILLOUS are MORE likely to undergo MALIGNANT xformation than tubular - size matters - adenomas >4 cm have 40% risk of becoming malignant and those <1cm are mostly benign |
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name the most likely associated diagnosis:
"make with long history of UC presenting with fatigue and high ALP" vs. "middle aged caucasian female with a long history of pruritis and fatigue who now develops a pale stool and xanthelasma" |
1st case pt most likely assoc with primary sclerosing cholangitis (an inflammation and fibrosis condition where bile ducts show beading on ERCP)
2nd case most likely primary biliary cirrhosis (and autoimmune obstructive jaundice condition with steatorrhea, pruritis and hypercholesterolemia) |
