Chronic Hepatitis.

Liver Cirrhosis.

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Liver function

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Liver function

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 International classification of
disorders… -10 - about liver diseases

 К 70: Alcoholic liver disease

 К 71: Тoxic liver disprders
 К 72: Hepatic failure and acute hepatitis
 К 73: Chronic hepatitis
 К 74: Liver fibrosis and cirrhosis

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 Chronic hepatitis
a series of liver disorders of
varying causes and severity in
which hepatic inflammation
and necrosis continue for at
least 6 months
 the end of the process – liver
cirrhosis
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 History
 1937 – J.M.Findlay, F.O.McCallum – first
investigation of “serum” hepatitis

 1956 - F.O.McCallum - first finding about

viral hepatitis A and B and its transmission
mechanisms

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 Classification
Now
 By Cause (aetiology)
 By Grade (activity)
 By Stage

Late
 Histologic Classification (chronic active,
lobular and persistent hepatitis)
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 Classification by Cause
Aetiology
 chronic viral hepatitis, caused by
hepatitis B, hepatitis B plus D, hepatitis C,
or other viruses
 autoimmune hepatitis
 drug-associated chronic hepatitis
 cryptogenic chronic (idiopathic)
hepatitis
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 Classification By Grade

 histologic assessment of
necroinflammatory activity
 is based upon examination of the
liver biopsy

 Clinically - mild, moderate, or

severe degree of CH
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Normal picture of the liver tissue

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Hepatitis

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Liver cirrhosis

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Hepatitic steatosis

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 Classification By Grade:
degree of
 periportal necrosis
 bridging necrosis
 hepatocyte degeneration
 focal necrosis within the lobule
 portal inflammation

 numerical histologic activity index (HAI),

based on the work of Knodell and Ishak
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 Classification By Stage
 0 = no fibrosis

 1 = mild fibrosis

 2 = moderate fibrosis

 3 = severe fibrosis, including bridging fibrosis

 4 = cirrhosis
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 Pathogenesis
 Liver tissue damage by aetiologic factor

 Cellular and humoral immune response

 Autoimmunoaggression

 Progression of chronic liver tissue inflammation

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 Clinical syndromes
 > 70% - without complaints, symptomless
 Not acute onset
 Asthenic s. (weakness, fatigue,…)
 Dyspeptic s.
 Aching s.
 Inflammatory s.
 Haemorrhagic s.
 Fever
Also - See the lecture of previous term
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 Examination
 Jaundice (желтуха)
 Paleness (anemia)
 “Vascular stars” =spider naevi (сосудистые
звездочки)
 “Hepatic palms of the hand” (печеночные
ладони) = palmar erythema
 Stratches due to Pruritus (расчесы)
 Bruises and petechieae (синяки и петехии)
 Xanthomas and xanthelasmas (deposits of
cholesterol)
 Gynaecomastia
 Loss of body hair in men or hirsutism in women 18
Hepatic marks

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 Examination
 Liver enlargement
 Low liver margin rounding (закругление
нижнего края печени)
 Tenderness with palpation of liver area

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Chronic Viral
Hepatitis

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 Chronic Viral Hepatitis
 hepatitis A and E, are self-limited and do
not cause chronic hepatitis
 the entire clinicopathologic spectrum of
chronic viral hepatitis occurs in patients
with chronic B and C as well as in patients
with chronic hepatitis D superimposed on
chronic hepatitis B
 HBV may leads to liver cancer

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 Particularity of clinical features
 ranging from asymptomatic infection to
fatal hepatic failure
 Fatigue is a common symptom
 persistent or intermittent jaundice is a
common feature in severe or advanced
cases
 Appetite loss
 Arthralgia and arthritis
 Skin rash 23
 Particularity of chronic HBV
 Replicative phase : very contagious
 - in the serum - markers of HBV replication
(hepatitis B e antigen (HBeAg)and HBV DNA)
 - in the liver - detectable intrahepatocyte
nucleocapsid antigens - primarily hepatitis B core
antigen (HBcAg)
 Nonreplicative (latent) phase : not
contagious
 - absence of HBeAg and HBV DNA
 - presens of anti-HBe (antibodies)
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 Particularity of chr. HBV
 In young age – after acute hepatitis in 1%
 Majority of adults never had acute НBV
 Spontaneous remission in 30%
 All depend on immunity!

 AsAT increased: from 100 to 1000 units

 Moderate elevations in serum bilirubin (51.3 to
171 umol/L) (3 to 10 mg/dL)
 Hypoalbuminemia
 Prolongation of the prothrombin time 25
 Particularity of chronic HCV
 chronic hepatitis follows acute hepatitis C in 50
to 70 % of cases
 almost 60 % of patients are asymptomatic
 in 25 % of patients hepatitis C will progress
eventually to end-stage cirrhosis
 Clinical features of chronic hepatitis C are similar
to chronic hepatitis B
 aminotransferase levels tend to fluctuate more
and to be lower, especially in patients with long-
standing disease –compare with HBV
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 TREATMENT
 Chronic Hepatitis B and C:
- Interferon - alpha : A 4-month course
of subcutaneous injections, daily at a dose
of 5 million units or 3 times a week at a
dose of 10 million units
 Chronic Hepatitis D (Delta Hepatitis) -
management is not well defined
 Symptomatic treatment

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 Prevention of chronic hepatitis
 Vaccination against HBV

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 Chronic
AUTOIMMUNE
HEPATITIS

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 Chronic AUTOIMMUNE
HEPATITIS
 is a chronic disorder characterized by
continuing hepatocellular necrosis and
inflammation, usually with fibrosis, which
tends to progress to cirrhosis and liver
failure.

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 Chronic AUTOIMMUNE
HEPATITIS
 80 % of patients – women < 30 y.o. and
> 50 y.o
 idiopathic/autoimmune hepatitis is the
result of a cell-mediated immunologic
attack directed against liver cells
 predisposition to autoimmunity is
inherited, while the liver specificity of this
injury is triggered by environmental (e.g.,
chemical or viral) factors
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 Evidence to support an autoimmune
pathogenesis includes the following:

1. In the liver - cytotoxic T cells and plasma cells

2. Circulating autoantibodies (nuclear, smooth
muscle, thyroid, etc.), rheumatoid factor, and
hyperglobulinemia are common
3. In patients and in their relatives - other
autoimmune disorders (thyroiditis, rheumatoid
arthritis, autoimmune hemolytic anemia,
ulcerative colitis, proliferative
glomerulonephritis, juvenile diabetes mellitus,
and Sjogren's syndrome) 32
 Evidence to support an autoimmune
pathogenesis includes the following:

4. Histocompatibility haplotypes associated

with autoimmune diseases, such as HLA-
B1, -B8, -DRw3, and -DRw4, are common
5. This type of chronic hepatitis is responsive
to glucocorticoid/immunosuppressive
therapy, effective in a variety of
autoimmune disorders

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 Clinical features
 Many of the clinical features of
autoimmune hepatitis are similar to
chronic viral hepatitis

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 Treatment
 is glucocorticoid therapy - 12 – 18 month
and - with azathioprine
 Symptomatic treatment
 Unfortunately, therapy has not been
shown to prevent ultimate progression to
cirrhosis

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 Liver
Cirrhosis

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 Liver Cirrhosis

 chronic injury of the hepatic

parenchyma
 include extensive fibrosis in
association with the formation of
regenerative nodules

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 Aetiology and Classification
 Alcoholic
 Postnecrotic (Cryptogenic and Postviral)
 Biliary
 Cardiac
 Metabolic
 Inherited
 Drug-related
 Miscellaneous
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 Classification

 Micronodular
 Macronodular
 Mixed
 PRIMARY BILIARY CIRRHOSIS

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 Pathogenesis
 hepatocyte necrosis
 collapse of the supporting reticulin
network with subsequent
connective tissue deposition
 distortion of the vascular bed
 nodular regeneration of remaining
liver parenchyma
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 Clinical features
derive from the morphologic
alterations and often reflect
the severity of hepatic damage
rather than the etiology of the
underlying liver disease

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 Clinical features
 Loss of functioning hepatocellular mass
lead to jaundice, edema, coagulopathy,
and a variety of metabolic abnormalities
 fibrosis and distorted vasculature lead to
portal hypertension and its sequelae,
including gastroesophageal varices and
splenomegaly
 Ascites and hepatic encephalopathy result
from both hepatocellular insufficiency and
portal hypertension
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 Clinical features
 Aresimilar to chronic hepatitis +
portal hypertension signs

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 Portal hypertension signs
 Ascites
 Splenomegalia
 Bleeding esophageal varices and
hemorrhoid

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 Pathogenesis of
ascites

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 Complaints
 Appetite loss, Anorexia
 Weight loss
 Reduction in skeletal muscle mass
 Easy bruising
 Increasing weakness and fatigue

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 Examination data
 Jaundice
 Palmar erythema
 Spider angiomas (“vascular stars”)
 Parotid and lacrimal gland enlargement,
 Clubbing of fingers
 Splenomegaly
 Muscle wasting
 Ascites with or without peripheral edema

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 Examination data
 Men:
 - decreased body hair
 - gynecomastia
 - testicular atrophy (result from disturbances
in hormonal metabolism, including increased
peripheral formation of estrogren due to
diminished hepatic clearance of the
precursor androstenedione)
 Women:
 - signs of virilization
 - menstrual irregularities 49
 Examination data
A firm, nodular liver may be an early
sign of disease – deep palpation

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jaundice,
telangiectasis and
gynaecomastia

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 Laboratory Findings

 Elevations of AST, alkaline phosphatase

and bilirubin levels
 Hypoproteinemia
 Anemia, low WBC and thombocytes, incr.
ESR

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 Instrumental methods
 Sonography
 Endoscopy (esophageal
( varices)
 CT, MRI
 Laparoscopy
 Biopsy of the liver

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 Treatment of Liver Cirrhosis
 Diet – 5
 Glucocorticoids
 Beta-blockers
 Spironolactone and furosemide
 Ursodiol
 Cholestyramine
 Oral bile salt-sequestering resin
 Liver transplantation
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