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Liver and gallbladder MUDr. Michal Palkovič, PhD. Doc. MUDr. Ján Porubský, CSc.,

Liver and gallbladder - uniba.sk · obstruction 3 types: pre-hepatic –thrombosis v. portae, tumor, infection, hyperkoagulation disorders hepatic –cirrhosis post-hepatic –thrombosis

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  • Liver and gallbladder

    MUDr. Michal Palkovič, PhD.

    Doc. MUDr. Ján Porubský, CSc.,

  • Liver : human organ with complex structure and function

    1. Structure : epithelial tissue – hepatocytes, blood and biliary vessels, phagocytes – Kupffer cells, lipocytes

    main functional unit – lobulus, portal regions

    2. Function: metabolic – sugar metabolism and release

    synthesis – Ig, complement, blood coagulation, binding proteins (Fe), vitamin A

    deposition – glycogen, triglycerides, fat-soluble vitamins

  • catabolic (detoxic) –

    - endogenous – hormones, proteins

    - exogenous – xenobiotics –medications, toxins

    excretory – bile

    Liver dystrophy: eosinophilous (dehydratation)

    hydropic

    steatosis

    pigment deposition

  • Liver necrosis: - irreversible change

    etiology – toxins, viruses etc.

    according to extension : monocellular, focal, diffuse

    according to the type of necrosis:

    hepatodystrofia flava – yellow – icterus !!

    hepatodystrofia rubra – bleedings – icterus !!

    hepatodystrofia sivá – fibrotisation (chronic)

    Liver atrophy: most common: atrophia fusca (brown)

  • Liver inflammation:

    purulent – abscess

    non-purulent – alteration of hepatocytes, mesenchymal cell stimulation and proliferation, blunt infiltration (mainly mononuclear),

    diffuse or focal

    Virus hepatitis:

    1. Acute: Hepatitis A : picornavirus, orofoecal transmission, incubation period 20 – 45 days, intestinal spread, only acute

  • Hepatitis B (serous): DNA hepadnavirus, parenteral infection (body fluids except feces), incubation period 40 – 180 days, HBs Ag

    Hepatitis C (non A - non B): RNA virus, parenteral infection (infusions, dialysis, 10% - STD, incubation period 15 – 150 days, 75% asymptomatic !!!

    Hepatitis D: defect RNA virus, parenteral infection, incubation period 30 – 50 days, always confection with HBV

    Hepatitis E: orofoecal transmission, incubation period

    14 – 60 days, fulminant epidemic, 40% mortality in pregnant women

  • Hepatitis F: RNA, other name Toga virus (family Togaviridae), fulminant hepatitis, parenteral transmission, 1.5% prevalence in population

    Hepatitis G: RNA, flaviviridae family, parenteral transmission, fulminant, 12.9% prevalence in population

    (some sources: "orphan virus" with no causal links to any human disease)

    Hepatitis TT: ssDNA virus, parvovirus-like, parenteraltransmission, 10% prevalence in population

  • Clinical features: usual virus symptoms: joint pain, digestive disorders, skin exanthema, headache, dark urine, pale stool, icterus – anicteric form!

    Morphological changes:

    1. Dystrophic – necrotic hepatocyte changes (hydropic vacuole), if severe - irreversible

    2. Diffuse mesenchymal reaction – multiplication and enlargement of Kupffer cells, mononuclears

    3. Inflamatory cells in portal regions -Lymphocytes

  • Special forms of Hepatitis:

    hepatitis of infants – large-cell cholestasis

    cholestatic form

    necrotic – fulminant form (only HBV)

    anicteric – mild form (only HAV)

    2. Chronic hepatitis – inflammation longer than 6 months

    Criteria: etiology – non-viral agent

    grading – activity and inflammation degree, number of necrosis, 3 degrees

    staging – stage of fibrosis, 6 stages

    so called Knodell score

  • Division:

    Chronic non-biliary hepatitis

    Chronic hepatitis B, B and D, C – worst prognosis

    – HCV – cirrhosis in 30%, carcinoma in 7%

    Autoimmune hepatitis (lupoid)

    Chronic hepatitis in drug addicts and medication over-dose

    Chronic non-purulent destructive cholangoitis

    inflammatory destruction of biliary pathways, ends as biliary cirrhosis (mainly women)

  • Primary sclerotising cholangitis

    chronic liver and biliary pathways inflammation –mainly men,

    prognosis is bad – rapid cirrhosis

    Minimal chronic hepatitis

    minimal changes, blunt cellulisation, rare necrosis,

    only monocellular, reticular skeleton intact

    Mild to severe chronic hepatitis

    reticular skeleton damage, inflammation spreads into portobiliar space of liver

  • Granulomatous hepatitis – specific inflammation

    Liver damage induced by alcohol

    Alcohol detoxication: alcohol dehydrogenase (ADH)

    microsomal alcohol oxidation

    Liver damage: changes to mitochondria, microtubules,

    cytoplasmatic membrane, collagen production

    stimulation, reduced degradation, lipocyte activation, fibrotisation

  • Alcoholic liver disease : reversible changes –

    centroacinary steatosis (reparation after abstinence)

    Alcoholic hepatitis: long-term alcohol abuse -massive steatosis, liver capsule fibrotisation, hepatocyte necrosis, Mallory body (hyalin), granulocytes, fibrosis in portal spaces =

    liver cirrhosis

  • Liver cirrosis:

    irreversible changes – full loss of morphological liver structure (pseudo lobulisation)

    1. liver cells destruction and necrosis

    2. connective tissue proliferation and inflammation,

    psudocanaliculus

    3. pseudo lobulisation

    Division: etiology: sure – viruses, alcohol, medication etc.

    unsure – autoimmune, nutrition, unknown

  • Division according to nodule size a. micronodular (portal, septal) - until 3 mm

    etiology: alcohol, chronic hepatitis, metabolic disorders

    b. macronodular (posthepatitic), 3mm to xx cm

    etiology: virus hepatitis, toxins

    c. biliary – primary – chronic non-purulent cholangitis

    secundary – diseases of biliary pathways

  • Portal hypertension

    Definition: hypertenzion in v. portae, due to blood flow obstruction

    3 types: pre-hepatic – thrombosis v. portae, tumor,

    infection, hyperkoagulation disorders

    hepatic – cirrhosis

    post-hepatic – thrombosis of hepatic veins

    Complication:

    Esophageal varices – bleedings – 40% mortality

    Anorectal varices – external hemorrhoids

  • Caput medusae – paraumbilical veins

    Bleeding disorders – low prothrombin and fibrinogen production,

    Splenomegaly – ↑ 1000g

    Ascites – bad prognostic factor

    pathogenesis: hypertension in v. portae,

    hypalbuminemia, low blood volume,

    high sodium resorption = vicious circle

    Spider nevi – dilatation of subcutaneous veins

  • Liver tumors :

    1. Primary: a. mesenchymal – hemangioma

    b. epithelial – hepatocellular adenoma

    hepatoblastoma (children)

    hepatocellular carcinoma

    cholangiocellular carcinoma

    2. Secondary – MTS hru v. portae, non-lymphatic route

    Hepatocellular Carcinoma: in 80-90 % cirrhosis, alcohol, HCV, contraceptives, steroids, hormones

  • Inflammation of gallbladder:

    acute: acute purulent, phlegmonose

    etiology: mechanical factors (stenosis or occlusion)

    ductus cysticus, E. coli, enterococcus,

    complications: empyema, perforation, diffuse

    peritonitis

    chronic: wall hypertrophy, Rokitansky-Aschoff sinuses

    etiology : recurrent inflammations, stones

    complications : same as in acute

  • Hydrops: usualy associated with inflammation

    Cholelithiasis: women

    types: cholesterole, pigmented, mixed

    etiology: bile pH change, rase, gender (estrogens)

    high cholesterol and bilirubin concentration in bile bilirubínom, nutrition status

    complictions: purulent inflammation, empyema, perforation, hydrops, biliary pathways obstruction (icterus, acute pancreatitis)

    Tumors: adenocarcinoma – MTS to LN and in to liver

    Klatskin tumor- ductus hepaticus communis