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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