3. DefinitionDefinition
Cirrhosis liver is chronic diffuse liverCirrhosis liver is chronic diffuse liver
disease of varied ethiology characteriseddisease of varied ethiology characterised
by hepatic cell necrosis, prolifiration ofby hepatic cell necrosis, prolifiration of
connective tissue (fibrosis),nodularconnective tissue (fibrosis),nodular
regeneration,altered intrahepaticregeneration,altered intrahepatic
circulation with desordes archtectoniccirculation with desordes archtectonic
structure of liver.The main signs of CL arestructure of liver.The main signs of CL are
syndrome liver cell failure,syndrome portalsyndrome liver cell failure,syndrome portal
hypertention, cholestasis syndrome.hypertention, cholestasis syndrome.
4. EthiologyEthiology
ViralViral hepatitishepatitis B,C.DB,C.D
AlcocholAlcochol (an intake of about 80 mg(an intake of about 80 mg
dayly,for 15 years, may lead to cirrhosis)dayly,for 15 years, may lead to cirrhosis)
ProlongedProlonged cholestasischolestasis (chronical(chronical
hepatitis,cholestatic variant)hepatitis,cholestatic variant)
CardiacCardiac failurefailure of long duration inducesof long duration induces
fibrosis fround the central veinfibrosis fround the central vein
DrugsDrugs: methyldopa,tetracyclin,: methyldopa,tetracyclin,
methotrexate, isoniazid, othermethotrexate, isoniazid, other
5. EthiologyEthiology
CongenitalCongenital
disorders:hemachromatosis(desordersdisorders:hemachromatosis(desorders
iron absorbtion and deposition in the liver leadsiron absorbtion and deposition in the liver leads
to cirrhosis),to cirrhosis),
Wilson-Konovalov’s disease (desordersWilson-Konovalov’s disease (desorders
exchange copper), galactosemia, alfa-1-exchange copper), galactosemia, alfa-1-
antitripsin deficiency.antitripsin deficiency.
InfectionsInfections: Malaria, Kala-Asar, Sshistosomiasis: Malaria, Kala-Asar, Sshistosomiasis
AutoimmunityAutoimmunity
Vienoclusive diseasesVienoclusive diseases
Criptogenic (ideopathicCriptogenic (ideopathic
6. PathogenesisPathogenesis
Chronical viral hepatatis and other causes areChronical viral hepatatis and other causes are
lead to necrosis hepatocyts, fibrosis,lead to necrosis hepatocyts, fibrosis,
regenerating nodules, altered circulation,regenerating nodules, altered circulation,
desorders anatomical structure (architectonic)desorders anatomical structure (architectonic)
and all function of the liver. Regeneratingand all function of the liver. Regenerating
nodules, by compressing the blood supply of thenodules, by compressing the blood supply of the
liver cause ichemic damage of the nomal heticliver cause ichemic damage of the nomal hetic
cells, leadin his necrousis and new fibrosiscells, leadin his necrousis and new fibrosis
nodul. We may show chain reaction:necrosis –nodul. We may show chain reaction:necrosis –
fibrosis – nodule regenerating – compressionfibrosis – nodule regenerating – compression
nomal hepatocyts – necrosis – fibrosis- nodulesnomal hepatocyts – necrosis – fibrosis- nodules
regenerating ...........regenerating ...........
7. PathogenesisPathogenesis
Desorders of ciculation liver is the causeDesorders of ciculation liver is the cause
of syndrom portal hypertention.Decreasesof syndrom portal hypertention.Decreases
quantity hepatocyts leads to developquantity hepatocyts leads to develop
syndrom liver cell failure, decreasesyndrom liver cell failure, decrease
syntesis of albumins (hypoalbuminemia,syntesis of albumins (hypoalbuminemia,
oedema),protrombin(gemorragicoedema),protrombin(gemorragic
diathesis,stomatorrhagia).diathesis,stomatorrhagia).
8. MorphologyMorphology
The liver is firm,has gritty border andThe liver is firm,has gritty border and
fibrous bands surrounding nodules offibrous bands surrounding nodules of
various sizes.various sizes.
Microscopic examination would showMicroscopic examination would show
necrosis,collapse,fibrosis,regeneration,necrosis,collapse,fibrosis,regeneration,
regenerating nodules and alteredregenerating nodules and altered
circulation.circulation.
10. Histologic examinationHistologic examination
The most common histologic classificationThe most common histologic classification
divides cirrhosis into micronodular,divides cirrhosis into micronodular,
macronodular and mixed.macronodular and mixed.
In micronodular cirrhosis (typical of alcocholicIn micronodular cirrhosis (typical of alcocholic
liver diseases),the regenerating nodules are noliver diseases),the regenerating nodules are no
larger than the original lobules,ie, aproximately 1larger than the original lobules,ie, aproximately 1
mm in diameter or less.mm in diameter or less.
Macronodular cirrhosis (postnecrotic cirrhosis) isMacronodular cirrhosis (postnecrotic cirrhosis) is
characterized by larger nodules,wich measurecharacterized by larger nodules,wich measure
several sentimeters in diameter and may containseveral sentimeters in diameter and may contain
central viens.central viens.
11. Сlinical featuresСlinical features
Cirrhosis of liver may progress for many yearsCirrhosis of liver may progress for many years
before any clinical suspicion is eroused becousebefore any clinical suspicion is eroused becouse
even 10% of healthy liver tissue is adequate foreven 10% of healthy liver tissue is adequate for
metabolic functions and liver cells has ametabolic functions and liver cells has a
remarkable capacity to regenerate.remarkable capacity to regenerate.
The maine signs of cirrhosis liver are meteorism,The maine signs of cirrhosis liver are meteorism,
ascites, oedema, hematemesis, jaundice,hepaticascites, oedema, hematemesis, jaundice,hepatic
coma. Paine absent.coma. Paine absent.
The clinical features may be separated as thoseThe clinical features may be separated as those
due to Liver cells failure and those due to portaldue to Liver cells failure and those due to portal
hypertensionhypertension
12. Clinical featuresClinical features
SyndromSyndrom LiverLiver cellcell failurefailure
jaundice –usually mild, may be severejaundice –usually mild, may be severe
terminaleterminale
ascites, oedema, palmar erythema,ascites, oedema, palmar erythema,
spider nevus, gynecomastia,testicularspider nevus, gynecomastia,testicular
atrophy,loss of libido,flapping tremors,atrophy,loss of libido,flapping tremors,
alopecia, Dupuytren’s contracture,alopecia, Dupuytren’s contracture,
wasting, weakness,disturbed sleep,muscle crampswasting, weakness,disturbed sleep,muscle cramps
EncephalopathyEncephalopathy caracterized by day-night reversal,asterixis,caracterized by day-night reversal,asterixis,
tremor,dysarthria,delirium,drowsiness,ultimately coma also occur.tremor,dysarthria,delirium,drowsiness,ultimately coma also occur.
13. Clinical featuresClinical features
SyndromSyndrom PortalPortal HypertensionHypertension
*Ascites*Ascites
*Splenomegaly and hypersplenism*Splenomegaly and hypersplenism
* Delated veins over the chest wall,on* Delated veins over the chest wall,on
abdomen,into esophagus and rectumabdomen,into esophagus and rectum
* Hematemesis, melena,* Hematemesis, melena,
* Bleeding per rectum* Bleeding per rectum
15. Clinical featuresClinical features
OnOn examinationexamination
In 70% of cases,the liver isIn 70% of cases,the liver is
enlarged,palpable,firm,has gritty (blunt) edgeenlarged,palpable,firm,has gritty (blunt) edge
and nodular surface; the left lobe mayand nodular surface; the left lobe may
predominate.predominate.
Skin manifestations consist of spider neviSkin manifestations consist of spider nevi
(usually on the upper half of the body),palmar(usually on the upper half of the body),palmar
eythema(nottled redness of the thenar andeythema(nottled redness of the thenar and
hypothenar eminences) and evidence of vitaminhypothenar eminences) and evidence of vitamin
deficiencies (glossitis and cheilosis).Jaudicedeficiencies (glossitis and cheilosis).Jaudice
(usually not an initial sign)is mild at first,(usually not an initial sign)is mild at first,
increasing in severity during the later stagincreasing in severity during the later stag
16. On examinationOn examination
Ascites,perepheral oedema,pleuralAscites,perepheral oedema,pleural
effusions and ecchymotic lesionseffusions and ecchymotic lesions
Splenomegalia (35-50% cases)Splenomegalia (35-50% cases)
The superficial veins of the abdomen andThe superficial veins of the abdomen and
thorax may be dilated,reflecting thethorax may be dilated,reflecting the
intrahepatic obstruction to portal bloodintrahepatic obstruction to portal blood
flow.flow.
17. Diagnostic methodsDiagnostic methods
LaboratoryLaboratory findingsfindings::
GBAGBA --anemiaanemia (often macrocytic) is result of(often macrocytic) is result of
suppression erythropoiesis by alcohol +folate deficiencysuppression erythropoiesis by alcohol +folate deficiency
+ hemolysis +hypersplenism.+ hemolysis +hypersplenism.
Leycopenia.Trombocytopenia.ESRLeycopenia.Trombocytopenia.ESR is eccelerated.is eccelerated.
BloodBlood chemicalchemical teststests::
Bilirubin – progressive elevationBilirubin – progressive elevation
AST, alcolane phosphotase, j-globulin areAST, alcolane phosphotase, j-globulin are
encreaseencrease
Protrombin index, albumin level is decreaseProtrombin index, albumin level is decrease
18. Diagnostic methodsDiagnostic methods
LiverLiver biopsybiopsy::
fibrosis with regenerative nodules andfibrosis with regenerative nodules and
disorders architectonics liver.Necrosisdisorders architectonics liver.Necrosis
hepatocyts, mononuclear infiltration may behepatocyts, mononuclear infiltration may be
present.present.
LaparoscopyLaparoscopy
surface of the liver is changes on collor andsurface of the liver is changes on collor and
has many micro or macronoduleshas many micro or macronodules
(tuberous).Hepatic and splening enlargement.(tuberous).Hepatic and splening enlargement.
22. Diagnostic methodsDiagnostic methods
X-rayX-ray examinationexamination oror EGendoscopyEGendoscopy::
may reveal the presence of esophagealmay reveal the presence of esophageal
or gastro varices.or gastro varices.
UltrasoundUltrasound examinationexamination
is helpful for assessing liver and splenis helpful for assessing liver and splen
size,hepatic noduls, ascites,portal andsize,hepatic noduls, ascites,portal and
splenic, hepatic veins dilatation.splenic, hepatic veins dilatation.
23. ComplicationsComplications
Gastrointestinal bleeding may occur fromGastrointestinal bleeding may occur from
varicesvarices
CardiomyopathyCardiomyopathy
Ascites, ascites-peritonitisAscites, ascites-peritonitis
Hepatocellular insurfficiecyHepatocellular insurfficiecy
HypersplenismHypersplenism
Hepatic comaHepatic coma
Hepatocellular carcinomaHepatocellular carcinoma
24. TreatmentTreatment
1.1. Regime:Regime:
may be freedom or ward, when function ofmay be freedom or ward, when function of
liver is very severe abnormalliver is very severe abnormal
2.2. Diet №5Diet №5
excluding alcohol, spicy, fried and fattyexcluding alcohol, spicy, fried and fatty
food, roasted fish and meat, sausage,food, roasted fish and meat, sausage,
swine.Administer vitaminscontant foodswine.Administer vitaminscontant food
products.products.
25. TreatmentTreatment
EthiologicalEthiological treatmenttreatment::
Antiviral therapy,if the patient has positiveAntiviral therapy,if the patient has positive
result of serologycal viruses markersresult of serologycal viruses markers
Prednisolon 10-20 mg dayly,if patient hasPrednisolon 10-20 mg dayly,if patient has
positive serological autoimmune markerspositive serological autoimmune markers
Exclude intaking alcoholExclude intaking alcohol
26. Patogenetic therapyPatogenetic therapy or drugs, areor drugs, are
normalizing metabolism in livernormalizing metabolism in liver
Essencial phospholipidEssencial phospholipid
““Essenciale”Essenciale”
““Lipostsbil”Lipostsbil”
HepatoprotectorsHepatoprotectors
““Silibor”, “Silimarin”, “Carsil”Silibor”, “Silimarin”, “Carsil”
“Liv-5, “Legalon”“Liv-5, “Legalon”
Administer on 1 tab 3 time dailyAdminister on 1 tab 3 time daily
3-5 weeks.3-5 weeks.
27. **
TreatmentTreatment Symptomatic therapySymptomatic therapy
a)a) Ascites, odemaAscites, odema
◄◄ Diuretic drugs: furasemide 40 mg 1Diuretic drugs: furasemide 40 mg 1
daily in the morning, fasting withdaily in the morning, fasting with
spironolacton 100 mg dallyspironolacton 100 mg dally
This drugs should be administed withThis drugs should be administed with
careful monitoring of blood pressure,careful monitoring of blood pressure,
urine output, serum electrolytes (Na,urine output, serum electrolytes (Na,
K, Ca)K, Ca)
◄◄Drip transfusion albuminum 100 – 200Drip transfusion albuminum 100 – 200
ml intravenousml intravenous
◄◄ ParacentesisParacentesis
28. **
**
Treatment cholestasis syndromesTreatment cholestasis syndromes
““Cholestiramine” 4g three time dailyCholestiramine” 4g three time daily
with water or juicewith water or juice
““Cholestipol” 5 gCholestipol” 5 g
orally and intravinous adsorbentsorally and intravinous adsorbents
““Polysorb” orallyPolysorb” orally
““Hemodesis” intravenousHemodesis” intravenous
Fencarol (anti-hystamine drugs)Fencarol (anti-hystamine drugs)
PhenobarbitalPhenobarbital
Ursodesoxycholic acid 10-15 mg/kgUrsodesoxycholic acid 10-15 mg/kg
