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138 Cards in this Set
- Front
- Back
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Intestinal Atresia most common location
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Duodenum
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Types of anorectal anomalies
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Low (below puborectalis m)
Intermediate (at puborectalis m) High (above puborectalis m) |
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Types of malrotation
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Nonrotation
Incomplete rotation -can lead to volvulus & Ladd Bands |
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Hirschsprung Disease
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Absence of ganglion cells in Meissner & Auerbach plexuses
Short segment agangliosis - more common; usually boys Long segment agangliosis - less common; usually girls |
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Major manifestation of Gastroenteritis & Enterocolitis
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Diarrhea; These are both inflammation of the GI tract
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Symptoms of Dysentery
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diarrhea w/ blood & mucus
Associated w/ pain, tenesmus. fever |
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Types of Diarrhea
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Secretory - isotonic, voluminous, non-inflam, no associated fever
Exudative - Dysentery, feces w/ blood & mucus, pain Osmotic - hyperosmolar, voluminous caused by laxatives and other agents -Malabsorptive - Unabsorbed matl draws water into colon; subclass of osmolar |
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Secretory Infectious Diarrhea
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Viral: Rotavirus; Norwalk
Toxigenic Bacteria: ETEC; Vibrio cholera Parasites: Giardia; Cryptosporidium |
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Exudative Infectious Diarrhea
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Invasive bacteria: Campylobacter (US); EIEC; Shigella; Salmonella; Yersinia
Toxigenic bacteria: EHEC; Shigells; C. difficile |
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Hemolytic Uremic Syndrome
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Caused by EHEC (O157:H7)
Causes micorangiopathic hemolytic anemia Platelets becomed trapped in small capillaries causing renal failure Also caused by Shigella, and other Shiga-like toxins |
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Reiter Syndrome
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Combo of arthritis, urethritis, conjugtivitis
Caused by Shigella, Salmonella, Campylobacter |
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Protozoa Infection Location
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Giardiasis - mostly duodenum
Cryptosporidium - mostly SI Entamoeba Histolytica - mostly colon (flask shaped ulcers) |
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Types of Enterocolitis
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Necrotizing Enterocolitis
Pseudomembranous colitis Microscopic colitis IBD (Crohn Disease, Ulcerative colitis) |
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Necrotizing Enterocolitis
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Transmural gangrenous necrosis of intestine
Suspected of being caused by immature gut immune system being exposed to normal flora toxins |
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Pseudomembranous colitis
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Overgrowth of Clostridium difficile
Produces exotoxins A & B See plaques/membrane overlying colonic mucosa Treat w/ vancomycin |
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Microscopic colitis
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Chronic watery diarrhea; normal gross appearance; idiopathic
Collangeous colitis - band like collagen deposit under epithelium Lymphocytic colitis - prminent intraepithelial infiltrate of lymphocyte |
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IBD
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chronic inflammatory recurrent attacks of diarrhea
Exaggerated response to normal flora Defects in epithelium border Women>Men Left side colon - CD Right side colon - UC |
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Crohns Disease
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-segemental affected areas separated by unaffected areas
-Usually terminal ileum -Antisaccharomyces cerevesia Ab is marker -Transmural lymphoid aggregates -Deep slit like ulcers -Thickened intestinal wall w/ narrowed lumen -Smoking worsens (and is risk) -Malabsorption of B12 & bile salts Associated: Polyarthritis (sacroilitis & ankylosing spondylitis); Erythema nodosum; Uvetis; Primary sclerosing cholangitis; GI cancer |
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Ulcerative Colitis
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-Limited to colon (normal rectum -> no UC)
-Always start rectum move proximal -Mucosa & submucosa -No skip lesions -Walls not thickened -Broad based ulcers -Can lead to toxic megacolon -Onset early 20s -Smoking HELPS -Associated: Polyarthritis; erythema nodosum; primary sclerosing cholangitis (more than CD); Cancer |
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Whipple Disease
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-Rare SI disease w/ malabsorp
-Macrophages w/ bacilli (T whippelii) expand the lamina propria -Macrophages can be in lymph nodes, synovial membrane; brain -White Male 30-40 |
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Abetalipoprotein
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-Inabiliity to synthesize Apolipoprotein B
-No chylomicrons, VLDL, LDL -Free FA in enterocytes,b ut cannot be moved (vacuolation of enterocytes and steatorrhea) -Causes spiky RBCs (Burr cells) -Auto recessive |
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Celia sprue
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-Gluten sensitive enteropathy
-Hereditary -Toxicity related to Gliadin fraction -SI injury (more proximal) and malabsorption -Sensitized intramucosal T cells to gliadin protein -Remove gluten from diet, symptoms resolve -Associated: Dermatitis herpetiformis (chronic blistering symmetrical pruritic eruptions of vesicles); malignant disease (Intestinal Tcell lymphoma, GIST, breast cancer) |
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Tropical Sprue
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-Chronic malabsorption w/i days of diarrheal enteric infection
-All areas of SI -Folate and B12 deficiency |
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Ischemic Bowel Disease (acute vs Chronic)
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Acute: sudden sever abdominal pain; sudden bloody bowel evacuation; shock & vascular collapse
Chronic: No visible effect (mucosa & submucosa); intermittent episoded of bloody diarrhea |
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Angiodysplasia
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-Dilated submucosal and mucosal vessels in cecum and right colon
-Attributed to wall tension, vascular degeneration due to increased age -20% of significant lower intestinal bleeding |
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Hemorrhoids
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External - below pectinate line; not prone to bleed due to SC lining; painful
Internal - above pectinate line; Prone to bleed (columnar epithelium); painless |
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Diverticulosis
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-Common factors: age, low fiber diet
-Left side (Western) simulates appendicitis -Rt side (Asian) Complications 10-25% - diverticulitis (most common), perferation, pericolonic abcesse, fistula, hemorrhage |
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Ladd bands
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An intestinal adhesion
Associated with malrotation of the colon Congenital |
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Intestinal adhesions
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most often seen with endometriosis
mentrual bleeding (ectopic mucosa) -> inflammation -> repair (fibrosis) -> adhesion |
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Intestinal intussuseption
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Most common caus of intestinal obstruction in children
Most common in terminal ileum Have currant jelly stools Male infants more common |
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Inflammatory polyp
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Pseudopolyp
Made of granulation tissue and is a reactive hyperplastic epithelium rxn |
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Hyperplastic poylp
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Hyperplasia of intestinal crypts
Usually sessile (very common) More common in males Glandular lumens have star-shapped or serrated profiles |
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Juvenile polyp (hamartomatous polyp)
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Large and pedunculated
Abundant stroma which is disproportionate to # of glands Smooth, momlobulated surface; ulcerated Multiple can be part of Juvenile polyposis syndrome Children younger than 5 Most occur in rectum and can cause Hematochezia, Melena |
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Peutz-Jerghers polyps
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Arborizing proliferation of muscularis mucosae
Large and pedunculated Lobulated and not ulcerated When multiple seen part of A dominant Peutz-Jerghers syndrome (mutation STK11 gene; polyps from stomach to butt; see pigmented macules face, genitals, hands/feet) |
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Adenomatous polyps
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Left side in whites and young
Right side in blacks and elderly |
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Serrated adenoma
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Combined features fo hyperplastic and adenomatous polyps
Have characterisitics of dysplasia w/ serrated outline |
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Familia Adenomatous polyposis
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Auto Dom defect in adenomatous polyposis coli (APC) gene on chrom 5
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Lynch syndrome
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-Hereditary Nonpolyposis Colorectal cancer
-Auto Dom mutation in DNA repair genes -Results in microsatellite instability -Proximal to splenic flexure -Associated with extraabdominal cancer like endometrial cancer |
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CEA
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Carcinoembryonic Antigen
-Maker for colorectal caner mainly -Also for gastric, pancreatic, lung, and breast carcinoma |
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Carcinoid Tumor
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-Majority in appendix and ileum
-Most common tumor of small intestine -submucosal -Tumors are very indolent |
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Carcinoid syndrome
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-Carcinoid tumors that secrete hormones in such a quantity as to overwhelm liver ability to metabolize them
-Vasomotor disturbances, diarrhea, cramps, nauseas, vomiting, asthma-like attacks, endocardial fibrosis (rt vent), thickening of valves (P, T) |
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GI Lymphomas
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-In extranodal lymphoid tissues
-Most common are B cell lymphomas -H pylori -> gastric lymphoma -Campylobacter jejuni -> SI lymphoma (Mediterranean lymphoma, Alpha heavy chain disease) - |
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Appendiceal Tumros
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Mucinous cystadenoma
Mucinous cystadenocarcinoma Psudomyxoma peritonei |
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Normal Liver Percussion size
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6-12 midclavicular
4-8 midsternal |
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Zones of liver metabolic activity
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Zone 1 - periportal (around portal space); highest O2 tension
Zone 2 - Midzonal area Zone 3 - pericentral; lowest O2 tension (most susceptable to ischemia) |
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Epithelium of bile ductule
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Cuboidal cells
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Patterns of Hepatocelluar injury
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Ballooning
Foamy Degeneration Steatosis (micro-, macrovesicular) Focal lytic dropout Apoptosis Piecemeal necrosis (interface hepatitis) Bridging necrosis Submassive/massive necrosis Fibrosis Cirrhosis |
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Mallory bodies
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Cytokeratin tangles
Seen in balloning hepatic cellular injury (as well as other things) |
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Foamy hepatic degeneration
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Related to chronic cholestasis
Characterisitically periportal Cytoplasm becomes clear/foamy but are not necessarily distended |
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Steatotic hepatic injury
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Macro - nuclei are pushed to side; more common
Micro - nuclei are central; more serious; mitochondrial injury |
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Nucleus changer
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Pyknotic - condensed nucleus
Karyolysis - nucleus fades Karyorrhexis - nucleus breaks down |
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Councilman body
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Compact cytoplasm in apoptotic cell after the nucleus is gone
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Regeneration of massive hepatic necrosis
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Can occur as long as the architechture is preserved, b/c bile duct can produced new hepatocytes
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Stages of fibrosis
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Portal fibrosis (increased collagen but still limited) ->
Periportal fibrosis (portal space is expanded and collagen no longer limited to protal space) -> Bridging fibrosis -> Cirrhosis (only abnormal nodules of hepatocytes left in b/w fibrous bands; these nodules are regenerative parenchyma) |
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Types of cirrhosis
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Diffuse (requirement to be called cirrhosis)
Macronodular (>3mm; most common) Micronodular (<3mm) |
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Hepatocellular carcinoma
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Will be a large mass in the liver in a background of cirrhosis!
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Heme -> Biliverden
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Heme oxygenase
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Biliverden -> Unconjugated Bilirubin
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Biliverden reductase
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Unconjugated bilirubin -> congujated bilirubin
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UDP-glucuronosyl transferase
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Level at which jaundice is clnically seen
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Total bilirubin levels reach 2.0-2.5 mg/dL
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Kernicterus
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Unconjugated bilirubin levels >20-25 mg/dL
Injury to basal ganglia, pons, cerebellum Causes lethargy, opisthotonos, death, cerebal palsy, hearing loss, and mental retardation |
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Crigler-Najjar Type I
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Hereditary unconjugated bilirubin
Complete absence of UGT Kernicterus Always fatal unless liver transplant |
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Crigler-Najjar Tpye II
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Reduced UGT activity (only works on mono glucuronic bilirubin)
Nonfatal, but can lead to kernicterus |
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Gilbert Syndrome
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Reduced UGT activity (30# of normal)
Mild hyperbilirubinemia with fasting or stress Common |
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Hereditary conjugated hyperbilirubinemia
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Impaired bilirubin excretion
Rotor syndrome - liver is not pigmented Dubin-Johnson syndrome - defect in canalicular organic ion transport protein; liver is darkly pigmented |
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Hereditary unconjugated hyperbilirubinemia
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-Excess bolirubin production, Failure to take up bilirubin, failure to conjugate bilirubin
-Erythroblastosis fetalis -Physiologic jaundice of newborn |
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Resorption of bile salts
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95% in terminal ileum
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Only effective method of excretion of cholesterol
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Excretion in bile
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Vitamin K dependent clotting factors
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2, 7, 9, 10
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2 requirements for cirrhosis
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Diffuse fibrosis
Regenerated nodule parenchyma |
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Neonatal cholestasis
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Results from prolonged conjugated hyperbilirubinemia
Obstruction (Extrahepatic biliary atresia; congenital bile duct anomalies) or hepatocellular (congenital metabolic disorderd; Infections; Drugs, idiopathic) -> all are considered cause of neonatal (giant cell) hepatitis |
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Liver Failure - Massive necrosis
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Acetaminophen overdose (40% of time)
Other drugs or toxins Viral hepatitis A or B |
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Liver Failure Classifications
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-Massive necrosis
-Acute dysfunction w/o overt necrosis (acute fatty liver) -Decompensation of chronic hepatitis & cirrhosis -Unidentified cause |
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Hyperestrogenemia
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Caused by liver failure (live is responsible for processing them)
Causes palmar erythema, spider angiomas, gynecomastia |
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Fetor Hepaticus
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Patients exude musty smell
Due to buildup of mercaptans due to shunting them away from liver (mercaptans come from metabolism of methionine by intestinal bacteria) |
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Hyperammonemia
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aka Hepatic enceophalopathy
Abnormal neurotransmission and brain edema causing confusion, stupor, coma Causes rigidity, hyperreflexia,, asterixis |
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Manifestations of liver failure
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-Jaundice
-Hypoalbuminemia -Coagulopathy/bleeding disorder -Hyperestrogenemia -Fetor Hepaticus -Hyperammonemia -Renal failure -Respiratory failure |
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Causes of infectius hepatitis
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-2nd involvement due to sepsis is most common
-miliary TB, 2nd/3rd Syph, malaria, flukes, echinococcis amebiasis |
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Liver Abscess Routes
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-Biliary tract (ascending cholangitis)
-Arterial (sepsis) -Portal vein (pylephlebitis) -Direct extension -Penetrating injuries |
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Hepatitis A
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Unenveloped (A & E)
Can cause fulminant liver failure (A & B) SS RNA (A, C, D, E) -F to O previous exposure leads to IgG Anti HAV Ab (lifelong immunity) 1st stage - constitutional symptoms 2nd stage - icterus appears with IMPROVEMENT |
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Hepatitis E
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-Unenveloped (A & E)
-Enzootic/zoonotic -young and middle aged; pregos in 3rd tri have 20-30% mortality) -SS RNA (A, C, D, E) -previous exposure leads to IgG Anti HEV Ab (poorly lasting immunity) -F to O |
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Hepatitis B
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-DS DNA (long incubation time)
-Can cause fulminant liver failure (A & B) -Enveloped (B, C, D) -In general the more aggressive the less likely chronicity -Can either resolve, become carrier, or lead to chronic disease -Close contact spread -As age goes up, chance of chronicity goes down (<5% in ICT, >50% in ICD) |
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HBV structure
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Mature HBV virion (Dane particle):
HBsAg - surface Ag; made in excess HBcAg - nucleocapsid core Ag HBeAg - nonstructural e Ag DNA Pol HBV DNA |
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HBV phases
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Proliferative - actively replicating
Integrated - non replicating; intregrated into host genome; HBsAg still being produced in excess |
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Distinguishing vaccine from infection Hep B
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-Prior infec will have IgG anti-HBsAg and anti-HBcAg
-Vaccine will have ONLY IgG anti-HBsAg |
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Hepatitis D
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-ss RNA (A, C, D, E)
-Deficient in HBsAg, so it need HBV around (making excess HBsAg) to make functional Dane particle |
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2 ways of HDV infection
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Coinfection with HBV -> more likely fulminant; chronicity not likely
Superinfection of HBV carrier - lower chance of fulminicity; higher chance of chronicity |
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Hepatitis C
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-ss RNA
-Long incubation -Acute infection commonly subclinical; high rate of chronicity -Risk factors: IvDA; Sexual; Health care workers -No vaccine |
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Hepatitis G (GB Virus Type C)
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-RNA virus
-Not Hepatotrophic -Coinfection w/ HIV and HGV may improve pronosis of HIV infection |
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Autoimmune hepatitis
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-Similar to viral hepatitis
-F>M -Plasma cell infiltrate -High frequency of cirrhosis -Concurrent w/ other autoimmune diseases -Responds to immunosuppresive therapy |
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Types of liver drug toxicity
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Direct toxicity - drug is directly toxic to liver
Indirect toxicity - drug must be modified before it is toxic Immune injury - drug acts as a hapten |
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Treatment for Acetominophen
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N-acetyl cysteine; restores glutathione
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Reye syndrome
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Children given aspirin for virus induced fever. Causes oxidation of mitochondrial fatty acid oxidation. Eventually can cause hepatic encephalopathy and death
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Drugs causing Macrovesicular steatosis
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-Methotrexate
-Ethanol -Amiodarone |
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Drugs causing Microvesicular steatosis
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-Tetracycline
-Salicylates (Reye syndrome) |
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Drugs causing Centrilobar necrosis
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-Carbon Tet (CCL4)
-Acetominophen |
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Drugs causing Massive necrosis
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-Isoniazid
-Acetominophen -Halothane -Amanita phalloides |
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Drugs causing Chronic hepatitis
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-Nitrofurantoin
-Methyldopa -Isoniazid -Phenytoin -Oxyphenisatin |
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Drugs causing Granulomatous hepatitis
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-Phenylbutazone
-Sulfonamides -Hydralazine -Allopurinol -Quinidine |
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Drugs causing Cholestasis
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-Erythromycin estolate
-Chlorpromazine -Anabolic steroids -Contraceptives |
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Metabolism of EtOH
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EtOH -> Acetaldehyde
(alcohol dehydrogenase) Acetaldehyde -> acetate (aldehyde dehydrogenase) NADH+H is byproduct of both rxns |
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Mechanism of alcoholic steatohepatitis
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-Excess NADH shunts metabolism to lipid biosynthesis
-Impaired synthesis and secretion of lipoproteins (liver not func properly) -Increased peripheral catabolism of fat -Steatosis begins centrilobularly |
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Nonalcoholic steatosis
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Similar to alcohol steatosis
Risk factors are DM Type 2 and obesity |
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Wilson's Disease
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-Hepatolenticular degeneration
-Auto rec -Abnormal copper accumulation -Copper promotes generation of free radicals -Injury to basal ganglia (uncoordination; dystonia) -hemolytic anemia -Kayser Fleischer rings (copper in eyes) chronic hepatitis -> cirrhosis or actue massive liver necrosis ATP7B (chrom 13) - responsible for copper to golgi (ceruloplasmin) or copper to bile caniliculi (two places copper goes) |
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alpha 1 antitrypsin def
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-Auto rec
-a1 antitrp inhibits neutrophil elastase -PiMM to PiZZ genotype (PiMM is normal) -Only 10 % of PiZZ get disease -Pi (protease inhibitor) protein is misfolded cannot be delivered -Hepatitis to Cirrhosis -Emphysema |
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Fe in body
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-Fe is absorbed in Duodenum and jejunum
-Fe transported by transferrin -Fe stored as ferritin, hemosiderin -Excess Fe produces free radicals and causes lipid peroxidation, stimulation of collagen formation, direct interaction w/ DNA |
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2nd Hemochromatoses
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-Most common from ineffective erythropoeisis (thalassemia, sideroblastic anemia, pyruvate kinase def, myelopdysplastic syndrome)
-Can be parenteral admin or large PO |
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1st Hemochromatoses
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-Auto rec
-Excessive Fe absorp in intestine -C282Y & H62D (gene mutations) -See cirrhosis, DM, bronze skin pigmentation -Also arthralgia, cadiomyopathy, arrhythmia, heart failure, thyroid/adrenal insuff, hypogonadism, impotence, amenorrhea |
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Primary Biliary Cirrhosis
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-Autoimmune hepatitis
-Destruction of bile ducts leading to chronic hepatitis and biliary cirrhosis -Associated w/ other autoimmune dz -Antimitochondial Ab -F>M -Cholestasis & portal HTN -micronodular dz |
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Primary sclerosizing cholangitis
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-Segmental fibrosis w/ eventual intra/extra hepatic bile duct obliteration
-Segmental constriction of affected areas, dilation of unaffected areas (chain of lakes) -M>F -Stronly associated with UC -Theory: damage to GI mucosa in UC allows increased absoption of organisms/toxins -Progress to liver failure 100% |
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Von Meyenburg's complex
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-Common
-Microhamartomatous changes in bile duct -see disorderly arrangement of bile ducts w/ fibrous tissue surrounding them |
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Polycystic kidney dz Auto dom
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-Multiple cyts that DONT communicate w/ biliary tree
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Polycystic kidney dz Auto rec
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-Congenital hepatic fiborsis
-Liver is divided by fibrous tracts w/ no nodular regeneration (aka not cirrhosis) -Bile ducts do communicate with hepatic duct (can become infected and inflamed; inc risk cholangiocarcinoma) |
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Caroli's dz
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-Associated w/ congenital hepatic fibrosis
-Bile ducts are dilated and grossly cystic (cysts communicate) -Complicated w/ cholangitis, intrahepatic lithiasis, abscesses -Eventually develop cholangiocarcinoma |
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Infarct of Zahn
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-Thrombosis of porta vein radical
-Results in ischemia, dilatation and paradoxical congestion of sinusoids |
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Budd-Chiari Syndrome
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-Hepatic vein thrombosis (2 or more)
-Massive hepatomegaly -Severe portal HTN -Severe ascites -Can be caused by hypercoagulable states -Terminal venules and large vv may be thrombotic with necrosis and eventually fibrosis |
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Causes of pylephlebitis
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Appendicitis, diverticulitis, pancreatitis
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Shunt through gastric veins
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esophageal varices
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Shunt throuh splenic vv
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congestive splenomegaly
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Shunt through inf mesenteric vv
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hemorrhoids
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Shunt through falciform ligament-periumbilical vein
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caput medusa
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Veno-occlusive disease
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-Terminal obliteration (non thrombotic)
-Caused by: toxic endothelial damage; subendothelial swelling; Deposition of collagen; centrilobar congestion, necreosis and fibrosis -Acute: chemotherapy from bone marrow transplant -Chronic: Pyrrolizinde alkaloids (Jamaican bush tea) |
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Preeclampsia/eclampsia
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HTN, proteinuria, edema, coagulation disorders seizures (eclampsia)
-Can have a subcapsular hematoma -Periportal fibrin deposits and coagulative necrosis |
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HELLP Syndrome
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-Variant of preeclampsia
Hemolysis Elevated Liver enzymes Low Platelet count |
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Acute fatty liver of prego
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3rd trimester
Jaundice, acute liver failure w/o necrosis Microvesicular steatosis |
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Intrahepatic cholestasis of prego
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3rd trimester
Estrogen inhibts bile secretion (in predisposed individuals) Increased fetal distress, stillbirth, premature |
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Focal nodular hyperplasia
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-Well circumscribed nodule with central stellate scar
-Hyperplastic response to localized increased blood flow -F>M |
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Nodular regenerative hyperplasia
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-Regenerative nodules in absence of fibrosis
-Entire liver -Causes portal HTN |
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Cavernous hemangioma
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-Most common benign lesion
-Subcapsular (red-blue; soft;<2cm) -Percutaneous biopsys contraindicated, cause profuse bleeding |
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Hepatic adenoma
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-Well demarcated
-Often subcapsular -Related to oral contreceptives and anabolic steroids -Can rupture causeing hemoperitoneum -Do not change to malignant -F>M -Do not infiltrate |
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Hepatoblastoma
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-Infancy (<18 mo)
-M>F -Total resection of mass -See immature hepatocytes and stroma |
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Angiosarcoma
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From exposure: PVC, arsenic, thorotrast
-Highly aggressive and metastasizes widely |
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Hepatocellular carcinoma
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-Most common cancer in liver
- >85% have cirrhosis -ELevated AFP -M>F -Poor prognosis -Associated with HBV & HCV |
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Risk factors for hepatocellular carcinoma
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-HBV & HCV
-Alcohol related -Primary hemochromatosis -Hereditary tyrosinemia -Aflatoxin |
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Fibolamellar carcinoma
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-M=F
-Young adults -No association with chronic liver dz -No elevated AFP -Bands of fibrosis separating malignant hepatocytes |
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Cholangiocarcinoma
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-Extremely hard (desmoplastic)
-Poor prognosis (detected late; death w/i 6 mo) |
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Risk factors for Cholangiocarcinoma
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-Primary sclerosing cholangitis
-Congenital hepatic fibrosis -Carloi dz -Coledochal cysts -Thorotrast -HCV -Liver flukes |
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LIver metastatic tumors
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-Most common tumor in liver
-From colon, breast, lung -Noncirrhotic background!! -Striking hepatomegaly -Nodular feeling liver upon palpation -May retain normal liver function |
