chronic hepatitis Flashcards
1
Q
definition
A
chronic polyetiological inflammatory process of the liver parenchyma which lasts > 6 mths
2
Q
etiology
A
- Viral infections
- Toxicochemical – heavy metal & chemical agents.
- Toxicoallergic agents – NSAIDs, tetracycline, diuretics, steroids, TB, aminoglycosides, hormones
- Alcohol
- Autoimmune diseases
- Hereditary - α1 antitrypsin deficiency, Wilson-Kanovalov‘s Disease, Hemochromatosis
- Mushroom poisoning
- inflmtory bowel disease (ulcerative colitis)
- Idiopathic
- Non specific reactive hepatitis
- Secondary biliary hepatitis superimposed upon extrahepatic cholestasis
3
Q
types
A
- Viral hep A
- Epidemical hepatitis/ infectional jaundice/ Botkin‘s disease.
- benign acute, self lmited disorder tht does x lead to chronic/ carrier state.
- water-borne, fecal oral transmission, short incubation / latent period
- Cytolysis w/out persistence of virus in cells.
- diff morphological structures
- no serological markers
- acute hep with healing w/out complicatns of cirrhosis - Viral hep B
- parenteral route, sexual contact, downwards transmission fr mother to fetus
- relapsing, progressive, sometimes no remissions, leads to liver failure (chronization)
- chronization (acute to chronic Hep B) :
a. if asso with Hep D (delta)
b. if alcoholic & b4 has acute/chronic alcoholic hepatitis
- Markers: (HBs Ag- surface Ag), (HBc Ag, Hbe Ag- core Ag) - Viral hep C
- parenteral, sexual intercourse, downwards transmission from mother to fetus
- Progressive, leads to liver failure, cirrhosis, hepatocellular carcinoma, death
- Has direct hepatotoxic activity
- Not constant structure, mobile, < active clinical pic during the years
- After appearance of 1st sign → fast progression → death
- silent killer (non visible in progression) - Viral hep D
- Causes coinfection & superinfection.
- Superinfectn occurs in person with HBV & may manifest as acute exacerbation of chronic hep B.
- Direct hepatotoxic effect
- Ability for replication only with viral hep B or C
- By direct contact, blood transfusion
- Stimulates fibrotic septa formation (fast & irreversible → transformation into cirrhosis) - Viral hep E
- Sporadic & epidemic forms of acute hep.
- water-borne, fecal oral transmission & no risk of subsequent chronic liver disease.
4
Q
pathogenesis
A
- Persistent hepatitis :
- Parenchymal: dystrophic changes, Mesenchymal: inflmtory changes
Inflmtn of periportal areas (interstitial, reticuloendothelial tissue, bile ducts, vssls of portal syst, arteries)
- Affection → infiltration of lymphocytes & monocytes → produce enzymes → inflmtn (effusion, edema, infiltration, immune response) but no sclerosis
- Serous effusion is slight (liver enlargemt 3-5 mm) → no affection of metabolic funct of liver → may persists for years without changes of liver (benign form of disease)
- May ↓ after treatment /↓ of etiological factor - Aggressive hepatitis
- ↓ metabolic activity, ↓ synthetic function, ↓detoxification functn
- Acute attack of virus → stay long time in organism (in DNA) → virus disturb funct of m‘brane → cell dystrophy (direct degradation & necrotic changes) → virus activated by DNA polymerase → replication of virus → affected cells secreting special Ag (liver specific lipoproteins) → organism produce Ab → delayed hypersensitivity → macrophages infiltrate into lobule → produce enz → cell affectd
- Later if hyperactivity of lymphocytes → affection of whole liver
- Cell damage is due to infiltration & autoAb causes necrotic changes → free spaces occupied by collagenic tissues → liver fibrosis → Imbalance btw parenchyma & fibrotic tissues → sclerosis - Lupoid type of hepatitis (Autoimmunological)
- If T lymphocytes ↓ → autoimmune rxn against liver specific lipoproteins → auto Abs against liver structure - Biliary hepatitis
- Bile tract pathology → stasis of bile btw lobules → transudation of bile from duct to periportal spaces → bile acids affect periportal spaces → inflmtn, edema, increased permeability, infiltration → necrotic changes (lobules are affected later) - Alcoholic hepatitis
- Direct toxic effect
- Indirect - ↓ parenchymal activity; inactivation of cytochrome P450; hyperuricemia; block Vit B12 absorption; hyperlactermia in bowels
5
Q
classification
A
- acc to activity
- Mild – ↑ed ALT <3X
- Moderate – ↑ed ALT 3-10X
- Severe – ↑ed ALT >10X - acc to duration
- active phase – mild, moderate, severe
- non active phase
- acute & chronic - Los Angeles classification
- Chronic hepatitis B
- Chronic hepatitis C
- Chronic hepatitis D
- Autoimmune hepatitis
- Drug hepatitis
- Insufficiency of α1 antitrypsin
- 1‘ biliary hepatitis
- 1‘ sclerotic cholangitis
- Wilson-Kanovalov disease - Acc to etiology – viral hep A,B,C,D,E,F,G
- Acc to morpho changes
- Hep with 1‘ affection in periportal area
- Hep with affection of lobules (hepatocytes)
- Mixed - Acc to clinical form
- Persistent hepatitis (alcoholic, drugs)
- Aggressive hepatitis: viral; autoimmune; non viral non autoimmune
- Lobular (mix)
- Autoimmune - Acc to biliary affection (biliary hepatitis)
- Persistent: asso with periportal tract
- Aggressive: total involvemt of periportal & lobules
6
Q
main syndromes
A
Main clinical
1. Pain syndrome
- Discomfort, dull pain & heavy feeling in projection of the liver
- Prolonged for hours, mild & moderate, no radiation.
- Trigger factors: eating, catch cold, stress, physical activity, drugs, alcohol.
- Dyspeptic syndrome
- Stomach dyspepsia: nausea, vomiting, LOA,
- Intestinal dyspepsia meteorism, flatulence, belching, unstable stool, LOW
- epigastric discomfort and regurgitation and constipation
- Laboratory signs: low counts and changed function of thrombocyte, decreased synthesis of blood coagulating factors II, V and VII - Asthenic syndrome
- Weakness, malaise, ↓ working ability, restlessness, oss of interest in everything - Immunoinflammatory syndrome
Clinically:
- Arthralgia
- Fever
- Vasculitis
- Lymphadenopathy
- Spleen enlargement
Lab:
- High γ-globulins
- ↑ ESR, ↑ed Ig M, A, G
- Specific Ab against nucleus, mitochondria & sm mm
- Increased leukocytes
- Decreased albumins
- Decreased reaction of leucocyte migration inhibition
- If it‘s alcoholic liver, ↑ lupoid (LE) cells marker
- Cholestasis syndrome
Clinically:
- Itching (bile acids accum in skin) – can‘t sleep
- Icterus, dark urine, pale stool
- skin pigmentation, xanthelasmas, fever
- To evacuate bile, antidote is used :
a. non specific enterosorbance: enterogel, interstopan
b. specific: bile acid sequestrants
Laboratory signs: high level of conjugated bilirubin, cholesterol, γ glutamate transpeptide, ↑ alkaline phosphatase (cholestasis) - Hemorrhagic syndrome
- Epistaxis (nasal bleeding), Gingival bleeding, Metrorrhagia, petecchiae/ecchymosis after injectn
Lab:
- ↓ production of coagulative factors, Vit K defic – prothrombin & fibrinogen ↓
- low level of thrombocytes, high spleen activity - Cytolysis syndrome
Weight loss, fever, jaundice, hemorrhagic diathesis, changes in CNS, extrahepatic signs. Laboratory signs:
- low albumin, prothrombin, cholesterol, cholinesterase and factors V and VII
- ↑ AST, ALT (transaminases), LDH5, alkaline phosphatase
- ↑ glutamate transpeptidase / γ-glutamine transpeptidase
- ↑ bilirubin (conjugated) - Splenomegaly syndrome
- Hepatomegaly syndrome
- Hypersplenism syndrome
- ↑ function of spleen/liver activity – destruction of all blood cells (pancytopenia)
- thrombocytopenia → hemorrhagic syndrome
- leukocytopenia → infections ↑
- anemia - Abnormal pigments syndrome
- Jaundice with or w/o cholestasis- xanthelasma
- Skin icterus, itching, dark urine, light feces color
- ↑ CNS disturbances → ↑ toxicity → sleeplessness - Hepatodepression syndrome
- ↓ albumins & ↑ γglobulins → dysproteinemia
- ↓bromsulfurin - Portal hypertension syndrome – meteorism, splenomegaly, hepatomegaly, varicose esophagus vein, caput medusa, ascitis
- Non liver/small liver Signs
- Liver hand - hyperemia of thenar & hypothenar, clubbing, palmar erythema, pale nail
- Vascular stars - zone by Dekolte (neck, upper part of chest), small dots which disappear after pressing
- Trophic disorders (syndrome of dirty grey skin) lipid & CLTRL metab disorder→ accumulation in skin
- Teleangioectasia, gynecomastia, red tongue, xanthoma, xanthelasma
7
Q
laboratory markers
A
Lab
- ↓Albumin production
- ↓ prothrombin, fibrinogen
- ↓ Cholesterol, cholinesterase
- ↓ bilirubin, ↑ toxins in blood
- ↓ V, VII clotting factors (HRgic syndrome)
- ↑ γ globulin
