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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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slide1
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
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
slide11

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

slide12

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

slide14

AST, ALT 

Serum ceruloplasmin 

Total serum copperconcentration 

In histologicexaminatoion – uncharacteristicchanges,  Cu concentration

criteria

Kayser-Fleischer rings

Decreasedceruloplasminconcentration

Liverimpairmentsignsorneurologicmanifestations

Criteria:
treatment

alcohol abstinence

NO: nuts, chocolate, mushrooms, liver, mussels

continouspenicylamine treatment

zinc

Treatment:
slide19

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

Regular follow-up visits

slide22

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

slide23

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)

slide24

Fe, ferritin

AST, ALT  (ALT > AST)

CT, MRI – liver cirrhosis

slide25

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:
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:
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:
slide35

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:
slide41

hepatic veins thrombosis

could also contain VCI thrombosis

impaired blood drainage from the liver

causes1

myeloproliferativeneoplsms (polycythaemia, nadpłytkowość)

stanynadkrzepliwości

oral contraceptives

idiopathic

Causes:
slide43

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

treatment4

causative– ifpossible

chronicanticoagulanttreatment

acute: liver transplantation

Treatment:
slide47

chronic necrotico-inflammatory process of liver

unknownethiology

increased serum gamma-globulin concentration

presenceof autoantibodies

slide48

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

4 times more common in women

slide49

asymptomatic

acute or chronic hepatitis

slide50

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:
slide55

Unknownetiology

Chronic, progressive

Associated withdestruction of small bile ducts

slide56

Asymptomatic

Fatigue, pruritus

slide57

Hepatomegaly

Xanthelasma

Jaundice

Liverfailuresymptomsinadvanceddisease

slide58

ALP, GGTP 

ALT, AST 

Bilirubin 

Hypercholesterolaemia

Characteristicautoantbodies AMA

IgM

Liverbiopsy

slide60

Osteoporosis

Fat-solublevitaminsdeficiency

HCC

slide62

congenitalhyperbilirubinaemia

1,5-7x moreoftenin men

usuallyasymptomatic

slightjoundiceperiodically

accidentaldiagnosis

do not needtreatment

slide64

congenital, autosomalrecessive

Severejaundicein first daysafterbirth

otherlabolatorytests – normal

jaundice of subcorticalnuclei

neonataldeath

treatment: long-lastongphototherapy, plasmapheresis, livertransplantation

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