Lek. Anna Skubała
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lek. Anna Skubała Department of Infectious , Tropical Diseases and Parasitoses . Infectious Diseases and Hepatology Clinic. JAUNDICE. Basic classificATION. MECHANICAL JAUNDICE. NON-OBSTRUCTIVE JAUNDICE. Bile ducts ( intra - or extrahepatic ) involved Mechanical blockage

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Jaundice

lek. Anna Skubała

Department of Infectious, TropicalDiseases and Parasitoses.

InfectiousDiseases and HepatologyClinic

JAUNDICE


Basic classification

Basic classificATION

  • MECHANICAL JAUNDICE

  • NON-OBSTRUCTIVE JAUNDICE


Mechanical jaundice

Bile ducts (intra- orextrahepatic) involved

Mechanicalblockage

Cholelithiasis(gall stones) – Cholecystolithiasis – Chledocholithiasis

Pancreatolithiasis

Neoplasmatic tumor aroundduodenum, caputpancreas, duodenalpapilla (Vater’spapilla)

Primarycholangiocarcinoma

Infectionsinthe same places

MECHANICAL JAUNDICE


Mechanical jaundice1

Mechanicaljaundice


Non obstructive jaundice

Infectious (HBV, HCV, HAV, otherhepatotropicviruseslike CMV, EBV)

Autoimmunologic (AIH, PBC, PSC)

Genetic (Wilson’sdisease, hemochromatosis, Gilbert’ssyndrome, Budd-Chiarisyndrome, Crigler-Najjarsyndrome)

Toxic (paracetamol, otherdrugs and chemicals, mushrooms, alcohol)

Non-obstructivejaundice


Non obstructive jaundice1

Alwaystakeintoconsideration a possibility of otherinternaldiseaseslike:

  • Heartinsufficieny

  • Hemolyticanaemia

  • Erytrocytes’ impairement (artificialheartvalve, hemodialysis, DIC, haemolytic-uraemicsyndrome)

  • Severeinfections (sepsis, malaria, toxoplasmosis)

  • Severeburns

  • Hipersplenism

    And oncologicdiseases:

  • HCC hepatocellular carcinoma

  • Metastases to hepar

  • Limphoproliferativesyndromes, lymphomas

Non-obstructivejaundice


Wilson s disease

Wilson’sdisease


Jaundice

copperaccummulation


Jaundice

Autosomalrecessive

Excessivecopperaccummulation, mainlyinliver, due to defectiveprotein, whichisresponsible for transport of Cu inthehepatocytes’ membrane

Cu is not excretedwith bile

Cu accumulateinliver, brain, kidneys and incornea – impairment of thoseorgans


Jaundice

First manifestationsinchildhoodorearlyadulthood

Differentconstelation of signsindifferentpatients

Hepatomegaly, hepatitis, livercirrhosiswithsigns of portal hypertension, acuteliverfailure

Parkinson’ssyndrome(intention tremor, bradykinesis, stiffness, dyzarthria), epilepticseazures, migrainheadache, hypersalivation, sleeplessness, personalitydisturbances, affectivedisturbances, psychoses

Kayser-Fleischer rings, cataract, Fanconisyndrome, cardiomiopathy, heartrythmdisorders, osteoporosis, arthritis, pancreatitis, retardedsexualmaturation, infertility, lack of menstruation, habitualmiscarriages, hypothyroidism, hypoparathyroidism, hemolysiswithjaundice


Jaundice

AST, ALT 

Serum ceruloplasmin 

Total serum copperconcentration 

In histologicexaminatoion – uncharacteristicchanges,  Cu concentration


Criteria

Kayser-Fleischer rings

Decreasedceruloplasminconcentration

Liverimpairmentsignsorneurologicmanifestations

Criteria:


Jaundice

liver biopsy with assessment of copper contentin the specimen


Jaundice

If the diagnosis is confirmed – test 1st degree family members


Treatment

alcohol abstinence

NO: nuts, chocolate, mushrooms, liver, mussels

continouspenicylamine treatment

zinc

Treatment:


Jaundice

In case of acute liver failure or in unstable cirrhosis resistant to treatment – liver transplantation

Regular follow-up visits


Hemochromatosis

Hemochromatosis


Jaundice

iron accumulation


Jaundice

autosomalrecessive

mutation in the gene responsible for membrane protein

impairment of hepcidine production – protein inhibiting iron absorption in GI tract and iron release from the macrophages

excessive iron absorption causes its accumulation in organs like: liver, pancreas, heart, joints


Jaundice

clinicalmanifestations – more often in men

firstsymptoms > 20 years of age in men and > 40 years of age in women

early symptoms: weakness, libido decline, arthralgia (hands, wrists)

later signs: the effect of chronic hepatitis or liver cirrhosis, cardiomiopathy, pancreas impairment, hormonal disorders (hypopituiarismus, hypothyroidism)

progressive disease

liver cirrhosis

1/3 of the patients reveal hepatocarcinoma (HCC)


Jaundice

Fe, ferritin

AST, ALT  (ALT > AST)

CT, MRI – liver cirrhosis


Jaundice

liver biopsy– assessment of disease advance, fibrosis (prognosis); excessive iron accumulation in hepatocytes, fibrosis, cirrhosis

genetic tests – mutations searched by PCR (also 1st degree family members of patients with hemochromatosis)


Treatment1

restrictive meat consumption

alcohol abstinence

avoiding dietary supplements containing iron and vit. C

bloodletting

deferoxamine

Treatment:


A lcoholic l iver d isease

Alcoholicliverdisease


Jaundice

alcohol – (oxygenation) – acetic aldehyde – acetic acid


Stages

Alcohol-relatedsteatosisof theliver (fattydegeneration)– asymptomatic; reversible

Alcohol-relatedhepatitis – fatigue, nausea, vomiting, pain in right subcostal area, hepatomegaly, tenderness of liver (>80%), ascites (up to 80%), jaundice (> 60%), hepatic encephalopathy (45%), temperature (up to 30%)

Cirrhosisof liver due to alcohol abuse

Stages:


Jaundice

Women are more susceptible to negative effects of alcohol

smaller dose

faster progress


Diagnosis

GGTP 

ALT, AST – sometimes (AST/ALT >= 2)

ALP, Fe , bilirubin

prothrombintime – elongation

electrolytedisorders (hypoNa, hypoK; hypoMg)

leucocytosis, macrocyticanaemia, trombocytopaenia

Diagnosis:


Criteria1

rule out other possible causes of liver dysfunction

history of alcohol abuse

GGTP 

ultrasonographic picture of liver

Criteria:


Treatment2

alcohol abstinence

treatment of malnutrition and other defficiences connected with alcohol abuse

treatment of electrolytes disorders

glycocorticosteroidsif severe course of the disease with encephalopathy

treatment of cirrhosis and liver failure complications

Treatment:


N on a lcoholic s teato h epatitis

Non-alcoholicsteatohepatitis


Jaundice

chronic, progressive hepatitis in people who do NOT abuse alcohol

histopatologicchanges similar to those in alcoholic liver disease


Causes

Causes:

A. Metabolic disorders:

  • metaboicsyndrome

  • DM

  • obesity

  • protein malnutrition

  • excessive weigh loss (zespoleniaomijającejelitacienkiegoiżołądka, excision of a large part of intestine, long-lasting starvation, malabsorption syndrome, celiakia, unspecific enteritis, pancreas diseases)

  • total, long-lasting parenteral feeding

  • lipids metabolism disorders

  • chorobyspichrzeniowe (Wolmans disease, Niemann-Pick disease)

  • Tay-Sachs disease

  • Gaucherdisease

  • Wilson's disease

  • hemochromatosis

  • glikogenoses

B. Drugs:

  • Amiodaron

  • Diltiazem

  • Tamoxifen

  • GKS

  • Warfarin

  • ARV drugs

  • antibiotics (tetracycline, bleomycin)

  • Cytostatics

  • large doses of vit. A

  • Metotrexat

  • salicylanes, ASA

    C. Hepatotoxins:

  • carbon tetrachloride

  • Phosphorus

  • alpha-amanitin

    D. Infections:

  • HCV

  • HDV

    E. Other:

  • Reye's syndrome

  • pregnancy complication

  • eclampsia


Symptoms

usually asymptomatic

fatigue

weakness

discomfort in right upper abdominal quadrant

hepatomegaly(<75%) or splenomegaly (<25%)

other signs of portal hypertension (rarely)

Symptoms:


Diagnosis1

AST, ALT (AST/ALT <1)

dyslipidaemia

hyperglycaemia

hypoalbuminaemia

prothrombintime elongation

Fe, ferritin

GGTP, bilirubin

liver biopsy

Diagnosis:


Treatment3

causative – e.g. metabolicsyndrome

treatment of liver cirrhosis complications

Treatment:


Budd chiari syndrome

Budd-Chiarisyndrome:


Jaundice

hepatic veins thrombosis

could also contain VCI thrombosis

impaired blood drainage from the liver


Causes1

myeloproliferativeneoplsms (polycythaemia, nadpłytkowość)

stanynadkrzepliwości

oral contraceptives

idiopathic

Causes:


Jaundice

If comprises one of the hepatic veins and the collateralcirculation is well developed – asymptomatic

If all 3 hepatic veins involved – acute liver failure, with fast growing ascites

Usually sub-acute or chronic: hepatomegaly, ascites, jaundice, liver failure symptoms, peripheral oedema


Diagnosis2

dopplerultrasonography

CT

angio-MRI

Diagnosis:


Treatment4

causative– ifpossible

chronicanticoagulanttreatment

acute: liver transplantation

Treatment:


A uto i mmunologic h epatitis

Autoimmunologichepatitis


Jaundice

chronic necrotico-inflammatory process of liver

unknownethiology

increased serum gamma-globulin concentration

presenceof autoantibodies


Jaundice

no age limit, most common in okrespokwitana and between 40. - 60. years of age

4 times more common in women


Jaundice

asymptomatic

acute or chronic hepatitis


Jaundice

most common symptom – fatigue

jaundice

rarely acute liver failure

more aggressive and treatment resistant in children and young adults

co-existingotherautoimmunologicdiseases


Diagnosis3

AST, ALT 

bilirubina 

ALP – normalor

prothrombintime elongation

Hypoalbuminaemia

mild leucopenia, eosynophilia, normocyticanaemia, thrombocytopaenia

serum gamma-globulins (mainly IgG)

other autoantibodies: ANA, ASMA, anti-actin, anty-LKM1, pANCA

liver biopsy

Diagnosis:


Overlapping syndromes

AIH + PBC

AIH + PSC

AIH + chronic viral hepatitis

Overlapping syndromes:


Treatment5

immunosupresive– prednisolon, prednisone p.o.

Azathioprine (allows to reduce steroids doses)

liver transplantation

alcohol abstinence

Treatment:


P rimary b iliary c irrhosis

Primarybiliarycirrhosis


Jaundice

Unknownetiology

Chronic, progressive

Associated withdestruction of small bile ducts


Jaundice

Asymptomatic

Fatigue, pruritus


Jaundice

Hepatomegaly

Xanthelasma

Jaundice

Liverfailuresymptomsinadvanceddisease


Jaundice

ALP, GGTP 

ALT, AST 

Bilirubin 

Hypercholesterolaemia

Characteristicautoantbodies AMA

IgM

Liverbiopsy


Jaundice

Onlyapprovedtreatment: ursodeoksycholicacid

Livertransplantation


Jaundice

Osteoporosis

Fat-solublevitaminsdeficiency

HCC


Gilbert s syndrome

Gilbert’ssyndrome


Jaundice

congenitalhyperbilirubinaemia

1,5-7x moreoftenin men

usuallyasymptomatic

slightjoundiceperiodically

accidentaldiagnosis

do not needtreatment


Crigler najjar syndrome

Crigler-najjarsyndrome


Jaundice

congenital, autosomalrecessive

Severejaundicein first daysafterbirth

otherlabolatorytests – normal

jaundice of subcorticalnuclei

neonataldeath

treatment: long-lastongphototherapy, plasmapheresis, livertransplantation


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