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This Concept Map, created with IHMC CmapTools, has information related to: Liver Pathology II, Liver Pathology II Infectious D/Os BACTERIAL- extrahep infx can->liver inflam -proinf cytokines from Kupffer -due to endotoxins -S. aureus (TSS), S. typhi -Syphilis-secondary, tertiary can prolif in obstructed bil tree -gut flora->asc cholangitis US abscess-from asc chol, aa supply in immune deficiency -aa or portal spread->mult abscesses -direct extension-ɭ BIG abscess Can rupture through capsule-> peritonitis, peritoneal abscesses CLINICAL-abscesses->fever, RUQ pain, tender hep'meg Tx-ABX but DRAIN bigger ones High mort (30-90%) b/c found late, Liver Pathology II Infectious D/Os HAV-infectious hep -incub: 2-6wks -NO CHRONIC, RARE FULM -50% sero(+) by 50yo in US (IgG) -25% of clinically evident hep WW -contagious til 1wk post jaundice onset -IgM first, then decreases after mos, Liver Pathology II Malignant Tumors RARE HEPATOBLASTOMA -young kids-fatal if not resected early 2 types: epith; mixed epith & mesenchyme -latter w/ osteoid, cartilage, striated m ANGIOSARCOMA -PVC, ARSENIC, THOROTRAST -several decades after exposure -kill w/in a year, Liver Pathology II Infectious D/Os PARASITIC malaria, schistosomiasis, strongyloidosis, crypto, leishmaniasis Liver flukes: Fasciola hepatica, Clonorchis sinensis, Opisthorchis viverrini Abscesses in developing countries from amebic dz -can burrow into thor cavity, Carrier-w/out apparent dz or w/ chronic -esp HBV at early age, impaired immunity -HCV-w/ chronic hep (-)Sx infx-serologic, min elevated AST/ALT Acute hep-anicteric or icteric -1.incub 2.Sx, pericteric 3. Sx, icteric, 4. convalescence (wks-mos) -peak infective b/w 1, 2 -Sx-constitutional; Sx abate w/ jaundice Jaundice+dark urine (hyperbili) -icteric phase in HAV (adults), half HBV, few HCV Chronic-w/ or w/o progression to cirrhosis ɲmos w/ inflam, necrosis -also from Wilson dz, a1-AT def, EtOHism, drugs, AI -HCV especially progresses to cirrhosis -Sx:fatigue, malaise, anorexia, mild jaundice -spider angiomas, palmar erythema, hep/splen'meg -elevated bili, alk phos, inc PT -HBV, HCV can->immune complexes->GlomN, vasculitis -HCV-cryoglobulinemia in 35% Fulminant-submassive-massive hep necrosis -onset to hep enceph-2-3wks -subfulminant up to 3 mos -hep A-E (50-65%) or drugs, chem (25-30%) -acetaminophen, INH, MAOIs, halothane, methyldopa, Amanita phalloides toxin Clinical ACUTE, CHRONIC Course: variable -can ->cirrhosis in few years -death via cirrhosis, liver failure, hep enceph, varices -OR hepatocellular CA - HBV (esp neonatal) or HCV FULMINANT -jaundice, enceph, fetor hepaticus -NO gynecomastia, spider angiomas -mort 25-90% w/out xplant -complications: bleeding, CV instability, renal failure, ARDS, Carrier-w/out apparent dz or w/ chronic -esp HBV at early age, impaired immunity -HCV-w/ chronic hep (-)Sx infx-serologic, min elevated AST/ALT Acute hep-anicteric or icteric -1.incub 2.Sx, pericteric 3. Sx, icteric, 4. convalescence (wks-mos) -peak infective b/w 1, 2 -Sx-constitutional; Sx abate w/ jaundice Jaundice+dark urine (hyperbili) -icteric phase in HAV (adults), half HBV, few HCV Chronic-w/ or w/o progression to cirrhosis ɲmos w/ inflam, necrosis -also from Wilson dz, a1-AT def, EtOHism, drugs, AI -HCV especially progresses to cirrhosis -Sx:fatigue, malaise, anorexia, mild jaundice -spider angiomas, palmar erythema, hep/splen'meg -elevated bili, alk phos, inc PT -HBV, HCV can->immune complexes->GlomN, vasculitis -HCV-cryoglobulinemia in 35% Fulminant-submassive-massive hep necrosis -onset to hep enceph-2-3wks -subfulminant up to 3 mos -hep A-E (50-65%) or drugs, chem (25-30%) -acetaminophen, INH, MAOIs, halothane, methyldopa, Amanita phalloides toxin Morph HBV-ground-glass hep'cytes -HBsAg aggregates -sanded nuclei Acute hepatitis: diffuse hep'cyte swelling =ballooning degeneration -sometimes cholestasis, bile plugs -fatty change in HCV -cytolysis (see macs) and apoptosis present -necrosis can->bridging necrosis -inflam-Kupffer cells w/ hypertrophy, -plasia -w/ hemosiderin -bile duct prolif, esp in HCV Chronic-smoldering necrosis, arch preserved -lymphoid aggregates in HCV -interface hepatitis, bridging necrosis->fibrosis -portal tract fibrosis->periportal, bridging Fulminant-entire liver or just parts -collapsed reticulin framework, intact tracts, Liver Pathology II Benign Tumors ADENOMAS -in young women using BCP -regress w/ discontinued use -if subcapsular, can rupture, esp if preg -can harbor hep CA rarely MORPH-pale, yellow-tan, bile-stained -often subcapsular, well-demarcated -can reach 30 cm -sheets, cords of ‘NL’ hep’cytes -vasc supply but no portal tracts, Liver Pathology II Malignant Tumors HEPATOCELLULAR-90% -10x higher risk in Mediterranean -highest in Korea, Taiwan, Moz, China -blacks 4x higher rate, MALES -linked to HBV infx prevalence Western-most w/ cirrhosis-EtOH, HCV Developing-most w/out cirr-HBV PATHOGENESIS-synergistic HBV/HCV->cell death, regen->mutate HBV-DNA integration->clonal, instability -HBV X protein-bind p53 Aflatoxins-activated in liver, integrate-p53 HCV, EtOH, hemochromatosis->cirrhosis HIGHEST RISK-hereditary tyrosinemia MORPH-uni-, multifocal, or diffuse -paler, can have green hue -often invade vv. – portal, IVC->heart -well-diff-acinar or trabecular Fibrolamellar CA-20-40yos -scirrhous-hard w/ fibrous bands -well-diff, good prognosis Mets-infrequent-lung, LNs CLINICAL-elevated alpha-fetoprotein -false (+) w/ yolk sac gonad tumors -jaundice,fever, GI bleed, pain, full abd Death w/in 10mos of Dx-cachexia, bleeds, liver failure/hep coma, tumor rupture, Liver Pathology II Malignant Tumors METASTATIC TUMORS Far more common than primary -BREAST, LUNG, COLON, leuk, lymph Can replace 80% of liver paren, hep’meg -often only sign-LFTs usually NL -jaundice or enz elevation sometimes, Liver Pathology II Transplantation GVHD->cholestasis Acute GVHD-10-50d post xplant -direct attack of donor lymphos on liver epith ->hep w/ necrosis, inflammation -parenchyma & portal tracts Chronic GVHD d -inflamed portal tracts, esp bile ducts ->fibrosis -endotheliitis, Liver Pathology II Malignant Tumors CHOLANGIOCARCINOMA -Thorotrast exposure, not other risks -Opisthorchis liver fluke MORPH-not bile-stained -firm, gritty due to desmoplasia -resemble adenoCA -most mod-diff, sclerosing, dense stroma Mets in ½ -Lung,bone (vert), adrenal, brain -LNs in half CLINICAL-late detection, poor prognosis, Liver Pathology II Transplantation BONE MARROW TRANSPLANT Drug Toxicity->”Liver Toxicity” អ% pts -from cytoreductive drugs BEFORE xplant -onset just after xplant ->wt gain, tender hep’meg, edema, ascites, hyperbili, dec. urine Na secretion ->CL necrosis -> veno-occlusive dz Persistent severe liver dysfcn ->death -septicemia, pneumonia, bleeding, multiorgan failure, Liver Pathology II Infectious D/Os HCV(flaviviridae)-inoculation/xfusions -90-95% xfusions hep - 2-26wk incub -in 50-90% IVDAs ᡪ% rate of->chronic, cirrhosis -leading infx cause of chronic liver dz -acute usually (-)Sx -chronic-episodic transaminase elevations -unstable virus->multiple types->no vax ->anti-HCV IgG doesn't confer immunity, Liver Pathology II Infectious D/Os HDV-RNA-replication defective -infects only when inside HBsAg -depends on HBV -Acute coinfx-after exposure to both -fulm more likely than HBV alone -Superinfx-HDV in chronic HBV carrier -mild HBV->fulminant -acute, severe hep erupts in carrier -chronic, progressive develops (cirr) HDV common in Africa, middle E, S. Italy US-in IVDAs, hemophiliacs Serology-look for IgM for both for timing, Liver Pathology II Transplantation HVGD - Liver Rejection Acute cellular rejection like all solid organ -inflam cells into portal tracts, bile duct & hep’cyte injury, endotheliitis Chronic Rejection -severe obliterative arteritis->ischemia -OR bile ducts obliterated via dec blood, Liver Pathology II Infectious D/Os HEV-enteric, water-borne-incub 6 wks -ssRNA, sim to HCV, w/ HEV Ag -shed in stool during acute illness -HEV RNA, virions detected before onset -illness, AST/ALT, IgM simultaneous elev -young-middle aged -Epidemics: Asia, India, Africa, Mexico -high mortality among pregnant women =20% -mostly self-limiting, not chronic or carrier -persistent IgG anti-HEV, Liver Pathology II Infectious D/Os HBV (hepadnaviridae)->serum hep-4-26 wk incub ->acute, chronic (progressive, nonprog), fulminant, (-)Sx carrier state, CA (w/ D) -in all fluids but stool -can be spread to fetus->carrier state -HBsAg (before Sx), HBcAg, HBeAg, DNA pol w/ RT; HBX->CA HBV DNA, HBcAg, DNA pol soon after HBs IgM andti HBc just before Sx, replaced by IgG Anti-HBe soon after HBe disappearance IgG anti HBs rises wks-mos after HBs disappears (window-IgG=Ag)-"carrier" w/ HBsAGɲmos Chronic-HBsAg, HBeAg, HBV DNA persist w/ anti-HBc -can->progressive liver dmg -2 phases: Prolif (CTLs activated); Integrative (incorporate DNA in live cells) -w/ ABs, infectivity/liver dmg ends Fulminant: mutant w/ no HBe, but HBcAg, Liver Pathology II Pregnancy Conditions ACUTE FATTY LIVER -mostly in 3rd trimester Sx-bleeding, nausea, vomiting, jaundice -can ->hep failure, coma, death -often Sx coexist w/ preeclampsia MORPH-biopsy necessary -microves fatty hepatocytes -mostly mild course -severe->hep’cyte dropout, disarray -portal tract inflam (sim to viral) Tx-terminate pregnancy, Liver Pathology II Pregnancy Conditions INTRAHEPATIC CHOLESTASIS -3rd trimester -BENIGN Sx-pruritus, dark urine, light stools, jaund Slightly elevated ALK PHOS Conj bili seldom ɱmg (high) Bx-mild cholestasis w/out necrosis Estrogenic hormones inhibit bile secretion Risk-stones, malabsorption -fetal distress, stillbirth, premies, Liver Pathology II HEPATITIS SYNDROMES Carrier-w/out apparent dz or w/ chronic -esp HBV at early age, impaired immunity -HCV-w/ chronic hep (-)Sx infx-serologic, min elevated AST/ALT Acute hep-anicteric or icteric -1.incub 2.Sx, pericteric 3. Sx, icteric, 4. convalescence (wks-mos) -peak infective b/w 1, 2 -Sx-constitutional; Sx abate w/ jaundice Jaundice+dark urine (hyperbili) -icteric phase in HAV (adults), half HBV, few HCV Chronic-w/ or w/o progression to cirrhosis ɲmos w/ inflam, necrosis -also from Wilson dz, a1-AT def, EtOHism, drugs, AI -HCV especially progresses to cirrhosis -Sx:fatigue, malaise, anorexia, mild jaundice -spider angiomas, palmar erythema, hep/splen'meg -elevated bili, alk phos, inc PT -HBV, HCV can->immune complexes->GlomN, vasculitis -HCV-cryoglobulinemia in 35% Fulminant-submassive-massive hep necrosis -onset to hep enceph-2-3wks -subfulminant up to 3 mos -hep A-E (50-65%) or drugs, chem (25-30%) -acetaminophen, INH, MAOIs, halothane, methyldopa, Amanita phalloides toxin