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86 Cards in this Set
- Front
- Back
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Liver
A. anatomy |
- portal vein and heptaic artery enter porta hepatis
- portal veins, hepatic arteris and bile ducts travel in parallel portal tracts - hepatocytes in plates extending from portal tracts to terminal hepatic vein - hepatocytes bathed on two sides by portal venous & hepatic arterial blood |
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Liver
A. special cells in liver |
- deep to endothelial cells lies space of Disse
- Kupffer cells attach to endothelial cells = macrophages - fat containing hepatic stellate cells in space of Disse |
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Liver
A. drainage of bile |
- btw abutting hepatocytes = bile canaliculi formed by groves in plasma membrane and separated form vascular space by tight junctions
- drain into canals of Hering that connect to bile ductules in periportal region - ductules empty into terminal bile duts within portal tracts |
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Liver
A. Hepatic lobular model B. acinar model |
A. terminal hepatic vein is at center (centrilobular) and portal tracts at periphery (periportal)
B. three zones based on blood flow. zone 1 closest to blood supply and 3 fartherest |
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Liver diagram
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Hepatic failure
A. acute B. chronic C. hepatic dysfxn without overt necrosis |
A. assoc with encephalopathy = fulminant liver failure
- cause by massive hepatic necrosis usus induced by drug or hepatitis virus B. cirrhosis C. hepatocytes unable to perfomr nl metabolic fxn but viable (tetracycline toxicty, acute fatty liver of preg) |
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Hepatic failure
A. sx |
- hypoalbumninemia --> peripheral edema
- hyperammonemia: cerebral dysfxn - fetor hepaticus: musty, sweet and sour body oder - impaired estrogen metabolism --> hyperestrogenemia --> spider angioma in female, hypogonadism /gynecomastia in males - coagulopathy |
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Hepatic failure
A. complications |
- Hepatic encephalopathy: fluctuating neuro sings (rigidity, asterixis assoc elevated ammonia)
- hepatorenal syn: renal fxn abl = Na retention, impired water secretion, decr renal perfusion & GFR - hepatopulmonary syn: liver dz, hypoxemia, intrapulm vascular dilations (causes cutaneous spider nevi). hypoxemia b/c less time for O2 exchange b/c of dilated vessels |
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Cirrhosis
A. hallmark morphology |
- bridging fibrous septa linking portal tracts
- parenchymal nodules = hepatocytes encircled by fibrosis. nodularity from cycles of hepatocyte regen & scaring - disruption of architecture |
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Cirrhosis
A. pathogenesis |
- death of hepatocytes, ECM deposition, vascular reorganization
- nl: Collagen I, III in porta tracts; IV in Disse - cirrhosis: I and III in Disse - new vascular channels connect vessels in portal to terminal hepatic veins= shunt blood frm parenchyma - hepatic stellate cells proliferate --> become fibrogenic cells --> contractile cells = constrict sinusoidal vascular channles = resistance - surviving hepaocytes stimulated to regen as spherical nodules within fibrous septa = FIBROTIC NODULAR LIVER with deliver y of blood to hepatocyes and ability to secrete substances compromised |
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Portal hypertension
A. preheptaic B. intraheptaic C. posthepatic |
A. obstructive thrombosis, massive splenomegaly with incr splenic vein blood flow
B. cirrohsis C. right heart failure, constrictive pericarditis, hepatic vein outflow obstruction |
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Portal hypertension
A. pathophysiology |
- incr R to portal flow caused by contraction of myofibroblasts and disruption fo flow by scarring
- incr in portal venous blood flow (vaso diation) resulting from hyperdynamic circ |
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Portal hypertension
A. clincial consequences |
- ascites: splanchnic vasodiation --> low perfusion --> RAAAS, ADH secretion --> HTN + Na and H20 retention --> extravasation of fluid into abdomen
- portosystemic venous shunts: most imp = esophagogastric varices = hematemesis - congestiv esplenomegaly - hepatic encephalopathy |
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Jaundice
A. fxn of bile |
1. emulsification of dietary fat in lumen of gut through detergent action
2. elimination of bilirubin, excess cholesterol that are insuf water-soluble into urine |
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Bilirubin formation/excretion
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- bilirubin in blood bound to albumin --> liver
- UDP glucuronyltransferase --> conjugated form - in gut, deconjugated by bacteria & degraded to urobilinogens --> excreted in feces - small amount of urobilinogen excreted in urine |
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Bile acid vs bile salt
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- bile salt most common = conjugation of bile acids with taurine or glycine
- bile acid are highly effectiv edetergents |
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Jaundice
A. pathophysio |
- unconjugated bilirubin is bound to albumin = not excreted in urine
- if unconjugated high, more in free ion form, diffuse into tissues particularly the brain - three mechanisms: 1. excessive extrahepatic production 2. reduced hepatocyte uptake 3. impaired conjugation (1-3 = unconjugated) 4. decr hepatocellular excretion 5. impaired bile flow (4-5 = conjugated) |
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Neonatal jaundice
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- hepatic machinery no fully mature
- exacerbated by breastfeeding b/c bilirubin-deconjugating enzymes in breast milk |
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Hereditary hyperbilirubinemia
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- Crigler-Najjar type 1: enzyme completely absent
- Crigler-Najjar type II: transferase activity reduced - Gilbert: transferase 30% activity normal |
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Hereditary hyperbilirubinemia
A. dubin-johnson syndrome B. rotor syndrome |
A. chronic conjugated hyperbilirubinemia due to defect in hepatocellular excretion of bilirubin glucouronids across canalicular membrane
B. asym conjugated hyperbilirubinemia assoc with defects in hepatocellular uptake and excretion |
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Cholestasis
A. def B. causes |
A. impaired bile flow/excretion (not just bilirubin)
B. extrahepatic or intrahepatic obstruction - defects in hepatocyte bile secretion |
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Cholestasis
A. sx B. lab dx |
A. jaundice, pruritis, skin xanthomas (accum of cholesterol), intestinal malabs (vit def)
B. elevated alkaline phosphatase and GGT (enzymes on apical membranes of hepatocytes and bile duct) |
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Viral hepatitis
A. etiology |
- EBV (infectious mononucleosis)
- CMV - yellow fever - hepatic viruses A/B/C/D/E |
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Hepattis A virus
A. type of virus B. transmission C. sx D. titter |
A. hepatovirus
B. from raw/steamed shellfish. - virus shed in stool 2-3 weeks before, 1 week after onset of jaundice C. no chronic hepatitis, carrier state or fulminant hepa D. IgM or IgG antibody |
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Hepatitis B
A. virus type B. consequences |
A. hepadnaviridae
B. acute hepatitis - nonprog chronic hepatitis - prog chronic disease ending in cirrhosis - fulminant hepatitis - assymptomatic carrier state |
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Hep B
A. natural curse |
- HBsAg at onset of sx
- anti HB not rise until acute dz is over - HBeAg, DNA appear soon after HBsAG - Ig against HBeAg = acute infxn peaked & on wane - Ig HBsAg = vaccine, Ig HBcAg = infxn |
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Hep C
A. type of virus B. consequences C. hallmarks of infxn |
A. Flaviviridae
B. chronic dz --> cirrhosis C. persistent infxn and chronic hepatitis |
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Hep C
A. vaccine B. lab dx |
A. genomic instablity and antigenic variability hamper vaccine
B. episodic elevations in serum aminotransferases with intervening nl periods |
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Hep D
A. acute coinfection B. superinfection C. helper-independent latent infection D. dx |
A. HBV and HDV same time
B. chronic carrier of HBV exposed to HDV C. liver transplant setting D. RNA in blood, IgM anti-HDV |
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Hepatitis E
A. virus group B. consequence |
A. hepevirus
B. high mortality in pregnant women |
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Clinicopatholgoic syndromes of viral hepatitis
A. dz assoc with HBV B. chronic hepatitis C. carier state D. increasing combination |
A. fulminant hepatitis
B. fatigue, spider angioma, palmar erythema C. assoc with hep B D. HIV and chronic viral hepatitis |
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Acute hepatitis
- morphology |
- diffuse swelling "ballooning degen = cytoplasm empty
- cholestasis: bile plugs from cessation of contractility - macrophage aggregates = sites of hepatocyte loss - bridging necrosis - fatty chang ein hep C; ground class hepatocytes in HBV |
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Chronic hepatitis
- morphology |
- inflamm limited to portal tracts w/ lymph * macro
- HCV = fatty change; HVBV = ground class hepatocytes - deposition of fibrous tissue = bridging fibrosis - cirrhosis: irreg sized nodules separated by broad scars |
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Fulminant Hepatic failure
A. def B. morphology |
A. hepatic insuf --> sx of hepatic encephalopathy within 2-3 wks
B. liver shink --> red organ covered by wrinkled too large capsule - destruction ofhepatocytes leaves collapsed reticulin framework and portal tracts |
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bacteiral infections
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- staph aureus in toxic shock syndrome
- salmonella typhi in typhoid fever - T. pallidum in secondary/tertiary syphilis |
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A. ascending cholangitis
B. liver abscess morphology |
A. infxn of biliary tree
B. bacteremic sprad = multiple small abscesses - direct extension --> solitary large abscesses - biliary abscesses = purulent material |
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Autoimmune hepatitis
A. hallmark B. assoc with other immune dz C/ tx |
A. clusters of plasma cell sin interface of portal tracts andhepatic lobules
B. SLE, celiac, rheumatoid arthritis - thyroiditis, Sjogren, Ulcerative colitis C. prednisone or with azathioprine |
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Drug/Toxin induced liver disease
A. most common cause B. etiology C. Reye syndrome |
A. acetaminophen, isonazid
B. direct toxicty - hepatic conversio fo xenobiotic to activ etoxin - immune mechanism C. mitochondrial dysfxn in liver, braine in children -fat droplets within hepatocytes |
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Alcoholic liver dz
A. forms: hepatic steatosis - morphology * patho |
- hepatic steatosis: microvesicular lipid droplts accumulate
- patho: excess H from alcohol and acetaldehyde dehydrogenase shunt substrats away from catabolism -> lipid biosyn |
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Alcoholic liver dz
A. forms: alcholic hepatitis - morphology and patho |
- alcoholic hepatitis: hepatocyte swelling * necrosis (fat, water, protein accum), mallory bodies (eosinophilic ctoplasmic clumps), fibrosis
patho: P450 prdouces ROS and alcohol impair glutathione levels = sensitize liver to oxidative injury |
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Alcoholic liver dz
A. natural course |
- steatosis
- hepatitis - progressive fibrosis - cirrhosis: fibrous septa --> univform micronodules - derangement of vascular perfusion: vasoconstriction = portal HTN b/c alcohl stimulates endothelin release |
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Metabolic live rdiz
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- nonalcoholic fatty liver disease
- hemochromatosis - wilson disease - alpha1 - antitrypsin deficiency - neonatal cholestasis |
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Nonalcoholic fatty liver disease
A. main components B. pathogenesis C. lab findings |
A. hepatocyte ballooning, lobular inflammation, steatosis
B. hepatic fat accumulation - hepatic oxidative stress that acts on the accum lipids = release lipid peroxides = ROS C. AST/ALT <1 (in contrast to alcoholic steatohepatitis |
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Steatohepatitis (NASH)
- morphology |
- steatosis
- multifocal parenchymal inflam - firbosis |
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Hemochromatosis
A. def B. hemosiderosis C. characteristic sx |
A. the hereditary diz of excessive accum of body iron
B. acquired deposition of iron in tissues C. micronodular cirrhosis - DM, skin pigmentation |
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Hemochromatosis
A. pathogenesis B. most common cause |
- incr iron --> lipid peroxidation
- stimulation of collagen formation by hepati stellate cells - ROS with Fe act on DNA B. ineffective erythropoiesis, myelodysplastic syndrome |
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Hemochromatosis
A. what increases hepcidin B. what decreases hepcidin |
A. inflammation, Fe --> hepcidin prevent release of Fe from intestin and macrophages = lower plasma level
B. Fe def, hypoxia, ineffective erythropoiesis --> iron overload |
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Hemochromatosis
A. morphology |
- hemosiderin deposition (stains blue
- cirrhosis (micronodular pattern) - pancreatic firbosis --> DM - heart enlarged, skin pigmentation - in joint synovial lining = acute synovitis = pseudo-gout - no inflam b/c iron = direct hepatotoxin |
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Wilson dz
A. def B. nl metabolic pathway |
A. impaired cooper excretion into bile
- failure to incorporate copper into ceruloplasmin - accum in liver, brain, eye B. copper bas in duodenum, complex w/ albumin - free Cu form ceruloplasmin --> secreted in blood - excess Cu in bile and also ceruloplasmin degraded in lysosomes |
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Wilson dz
A. morphology |
- Liver: steatosis
- brain: injury to basal ganglia (putamin) - eye lesions: kayser-Fleischer rings (Cu in Descemet's membrane) |
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Wilson's dz
A. sx B. dx |
A. acute or chronic liver dz
- parkinson-diz like syn B. decr serum ceruloplasmin - incr hepatic cooper content - incr urinary excretion of copper |
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alpha1-antitrypsin def
A. pathogenesis B. assoc dz C. morphology |
A. inzyme inhibit proteases released by neutorphiles
B. pulmonary emphysema, bronchiectasis, arterial aneurysm, Wegener's granulomatosis C. round-to-oval cytoplasmic globular inclusions in hepatocytes, PAS positive |
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Intraheptaic biliary tract dz
- name |
- secondary biliary cirrhosis
- primary biliary cirrhosis - primary sclerosing cholangitis |
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Secondary biliary cirrhosis
A. etiology B. morpholgy |
A. extrahepatic cholelithiasis
- maliganices of biliary tree or pancras head - strictures from surgeries B. icteric discoloration - feathery degeneration in parenchyma |
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primary biliary cirrhosis
A. primary feature B. lab dx C. sx |
A. nonsuppurative, inflam destruction of medium-sized intrahepatic bile duct
B. elevated alkaline phosphatase, cholesterol, gama-glutamyltransferase C. pruritus, fatigue, skin pig, xanthelamas, steatorrhea - incr risk of hepatocellular carcinoma, Sjogren syn = dry eyes& mouth - antimitochondrial Ig |
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Primary bilirary cirrhosis
A. morphology |
- small duct biliary fibrosis/cirrhosis
- interlobular bile ducts infiltrated by lymphocyts and noncaseating granulomatous infam - prog stasis --> liver green and capsule turns granular = deposition of firbous septa - end result: micronodular cirrhosis |
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Primary sclerosing cholangitis
A. primary features B. Ig found |
A. inflam, dilation of preserved segments
- obliterative fibroiss of intra/extrahepatic bile ducts - assoc w/ inflam bowel dz B. anti-smooth muscle Ig, ANA, rheumatoid factor, pANCA |
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Primary sclerosing cholangitis
A. morphology B. sx |
A. concentric fibrosis = onion skin fibrosis --> disappear --> leave cordlike firbous scar
B. elevated serum alkaline phosphatase - fatigue, pruritius, jaundice - incr risk of chronic pancreatitis, hepatocellular carcinoma |
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Anomalies of biliary trees
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- von meyenburg compled: bile duct hamartomas. need to differentiate from metastases to liver
- polycystic liver dz - congential hepatic fibrosis: persistence of embryonic biliary tree --> portal tracts enlarged by collagenous bands = liver divided into irregular islands - Carolii disease: assoc w/ above. larger ducts dilated and contain insipissate bile |
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Alagille syndome
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- AD = absence of bile ducts in portal tracts
- pentad of chronic colestasis - peripheral stenosis of pulmonary artery - butterfly-like vertebral arch defects - posterior embryotoxon - hypertelic facies |
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Impaired blood inflow to liver
A. etiology B. manifestation |
A. hepatic artery compromise
- portal vein obstruction - intra- hepatic thrombosis: no ischemia but see red-blue discoloration = infarct of zahn. no necrosis but hepatocellular atrophy and hemostasis in sinusoids - extrahep thrombosis: pylephlebitis, hypercoag, trauma B. esophageal varices, splenomegaly - intestinal congestion - ascites not common b/s presinusoidal |
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Impaired intrahepatic blood flow
A. etiology B. manfestation |
A. cirrhosis, sinusoid occlusion by DIC or tumor cells
- right sided cardiac decompensation : passive congest - left "": hypoperfusion + hypoxia --> centrilobular (cl) necrosis --> CL hemorrhagic necrosis = nutmeg liver - peliosis hepatis: dilation primary B. cirrhosis --> ascites, esophageal varices - hepatomegaly, elevated aminotransferases |
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Hepatic vein ouflow construction
A. etiology B. manifestation |
A. hepatic vein thrombosis (Budd Chiari syn) assoc w/ myeloprolif disorder, coag inherited disorder, paroxysmal nocturnla hemoglobinuria = CL congestion & necrosis
- IVC thrombosis - sinusoidal obstructive syndrome: after allogeneic bone marrow transplant = obliteration of hepatic vein radicles by reticulated collagen B. ascites, hepatomegaly - elevated aminotransferases - jaundice |
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Graft-vs-host dz
A. acute graft vs host dz B. chronic "" C. actue rejection of trasplanted livers D. chronic "" |
A. <50 days after bone marrow transplant, donor lymph attack liver epithelium
B. > 100 days, portal tract inflam, bile duct destruct, fibrosis C. intiltratio of mixed inflam cells (eosinophiles) + endothelitis D. arteriopathy = obliterative arteritis |
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Hepatic dz associated with preganncy
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- preeclampsia
- acute fatty liver of preganncy - intrahepatic cholestasis of pregnancy |
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Preeclampsia
A. primary features B. assoc syndrome |
A. HTN, proteinuria, pheripheral edema
- coagulation abl, seminated intravascular coagulation B. HELLP syndrome: hemolysis, elevated liver enzymes, low platelets |
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Acute fatty liver of pregnancy
A. sx B. morphology C. tx |
A. hepatic failure, bleeding nausea, vomiting, jaundice
B. microvesicular steatosis with oil red O C. termination of pregnancy |
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Intrahepatic cholestasis of pregnancy
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- pruritus begining in 3rd trimester --> darkening of urine, jaundice (conjugated)
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Nodular hyperplasias
A. focal nodular hyperplasia B. nodular regenerative hyperplasia C. common feature |
A. well-demarcated, poorly encap nodule = central stellate scar
B. liver transformed into sphericla nodules in absence of fibrosis C. alteration in hepatic blod supply due to obliteration of portal vein radicles + compensatory augmentation of arterial blood supply |
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Benign neoplasms
A. cavernous hemagioma B. hepatic adenoma |
A. red-blue, soft nodules = should not be mistake for metastastic tumor
B. hepatic adenoma: subcap ones can rupture --> intraperitoneal hemorrhage; rarely transform to cancer |
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Malignat tumor: hepatoblastoma
A. epidemio B. assoc |
A. children
B. familial adenomatous polyposis syn - beckwith-wiedmann syndrome |
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Hepatocellular carcinoma
A. etiology B. morphology |
A. chronic viral infxn (HBV, HCV), chronic alcoholism
- non-alcoholic steatohepatitis (NASH) - fod contaminants (aflatoxin) B. propensity fo rinvasion of vascular structures - can be unifocal, multifocal or diffusely infiltrative |
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Hepatocellular carcinoma
A. sx |
- upper abd pain, malaise, fatigue
- wt loss, abdominal fullness - elevated serum alpha-fetoprotein |
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Cholangiocarcinoma (maligant)
A. extrahepati cCCA B> intrahepatic CCA |
A. small lesions at tiem of dxx
- abundant fibrous stroma accompaniens epithelial proliferation B. vascular invasion - propagation along portal lymphatics = intrahepatic metastsis - desmoplastic |
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Disorders of gallbladder
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- cholelithiasis (gallstones)
- cholecystitis |
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Cholelithiasis
A. types B. patho of cholesterol stones C patho of pigment stones |
A. cholesterol stones, pigment stones (bilirubin calcium salts)
B. cholesterol concn > solubilization capacity of bile --> nucleates - combo of supersat, hypomotility, nucleation, hypersecretio of mucus traps nucleated crystals C. elevated unconguated bilirbin - infection w/ E. coli, ascaris, liver fluke increase risk |
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Cholelithiasis morphology
A. cholesterol stones B. pigment stones C. sx |
A. yellow, ovoid, radiolucent
B. black/brown, mostly radiopaque C. biliary pain, empyema, perforation - incr risk for carcinoma of gallbladder - gallstone ileus or Bouveret's syndrome (large size) |
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Cholecystitis
A. acute cholecystitis pathogenesis B. "" morphologyi |
A. calculous cholecystits form irritation/inflam: absence of bacteria --> mucus layer disrupted --> epithelium to bile salt --> prostaglandins = inflam
- acute acalculous cholecytitis: ischemia |
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Acute cholecystitis: sx
A. common B. acalculous |
A. RUQ pain, anorexia, tachycardia, sweating, vomiting
B. insidious b/c sx obscured by underlying conditions precipitating attacks (DM, infex, sepsis with hypotension, SALMONELLA) |
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Chronic cholecystitis
A. assoc B. sx C. morphology |
A. cholelithiasis
B. similar to acute: biliary colic (sporadic) to indolent RUQ pain and epigastric distress C. thickened wall, serosa fibrotic - porcelain gallbladder (dystrophic calcification) - xanthogranulomatous cholesystitis: shrunken, thick wall, inflamed with necrosis, hemorrage - hydrops of gallbladder: gbcontain only clear secretions |
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Disorders of extrahepatic bile duct
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- choledocholithiasis
- ascending cholangitis - biliary atresia - choledochal cyst |
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Choledocholithiasis
A. def B. consequences |
A stones within bile duct of biliary tree (not GB)
B. pancreatitis, cholangitis, hepatic abscess - secondary biliary cirrhosis, actue calculous cholecystitis |
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Cholangitis
A. def B. def of ascending cholangitis C. etiology D. sx |
A. bacterial infxn of bile ducts as result from obstruction to flow (choledocholithiasis or biliary strictures)
B. ifxn of intrahepatic biliary radicles C. E.coli, klebsiella, enterobacter, catheters |
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Biliary atresia
A. def, epidemio B. patho |
A. compelte/partial obstruction of lumen of extrahepatic biliary tree withn 1st 3 months of life
B. fetal form assoc with anomalies (malrot, polysplenia) C. perinatal form: nl biliary tree destroyed after birth |
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Choledochal cyst
A. def |
A. congenital dilation of common bile duct
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Carcinoma of gallbladder (cholangiocarcinoma)
A. risk factor B. morphology C. sx |
A. cholelithiasis
B. infiltrating patter: diffuse thickening and induration - exophytic patter: grows into lumen as califlower mass - when discovered, most invaded liver centrifugally C. abd pain, jaundice, anorexia, nausea, vomiting |
