cirrhosis of liver Flashcards
defintion
Liver cirrhosis is polyetiological irreversible fibrosis with total destruction of liver with appearance of false lobules (changes of architectonics of liver tissue), blocking normal filtration of hepatocytes, loss of function and formation of macro/ micronodules with portal hypertension development.
etiology
- Alcohol
- Infections:
- Virus (hepatitis B,C,D, E,F,G)
- Parasites – Giardia lambia etc
- Bacterial
- fungal - Hepatotoxic chemicals: tetracyclines, mushroom poisoning (amonitine), anabolic hormones (contraceptives, estrogens etc), heavy metals
- secondary hepatitis → peptic ulcer and cholecystitis
- Biliary cirrhosis. Biliary diseases of liver
- biliary duct disease- intra and extrahepatic
- autoimmune disorders
- Autoimmune hepatitis
- Hereditary haemochromatosis
- Hepatic venous congestion
- Budd-Chiari - syndrome
- hereditary disorders- Wilson disease, alpha-1 antitrypsin deficiency
- metabolic and electrolytes disorders- iron and copper.
- alimentary disorders
- cryptogenic
Pathogenesis
Pathogenesis
Etiological factor cause irritation of hepatocytes, there is constant inflammation and infiltration of immune cells to liver parenchyme, necrosis as a result of ischemia due to abnormal circulation resulting in formation of nodules, release of growth factors and cytokines which stimulate fibroblast development and fibrosis development→ scarring and eventually cirrhosis (Chronic injury to liver: inflammation, necrosis, fibrosis, scarring and eventually cirrhosis)
Classification
Classification
1. Anatomically / Morphologically :
- Micronodular – <3mm, common cause is alcohol
- Macronodular – >3mm, common cause is viral hepatitis
- Mixed
- Incomplete septal fibrosis/cirrhosis
2. Clinical picture:
- Quick progressing
- Slow progressing
- Latent
- Not progressive
3. Phase:
- Active
- Remission
4. Stages
- Compensation – liver functions compensated by healthy hepatocytes, only morphological changes can be seen.
- Subcompensation
- Decompensation – liver insufficiency and failure
5. By etiologically
- Alcoholic cirrhosis
- Viral cirrhosis
- Biliary cirrhosis – primary (autoimmune) and secondary (disturbed bile flow)
Main clinical & laboratory syndromes
Main clinical & laboratory syndromes
1. Pain syndrome
- Dull and heavy in projection of liver
- Prolonged for hours
- No radiation
- Triggering factors include – eating, stress, physical activity, drugs and alcohol.
2. Dyspeptic syndrome
- Gastric : nausea, vomiting, loss appetite, bitter taste of mouth and dryness
- Intestinal : meteorism and flatulence, unstable stool, bleeding
3. Asthenic syndrome
4. Mesenchymal inflammatory syndrome
- Fever, arthralgia, lymphoadenopathy, splenomegaly, vasculitits, myocarditis etc.
- Labs : ↑ ESR, ↑ WBC ↑ C-reactive proteins
5. Syndrome of cytolysis
6. Edematous syndrome – Ascitis, ↓ Urine output
7. Hemorrhagic syndrome
8. Cholestatic syndrome
9. Liver insufficiency syndrome
- ↓ albumin, bilirubin, prothrombin, cholesterol, coagulating factors (V, VIII), Fibrinogen
- In late stage → dev encephalopathy or coma
10. Non -liver signs syndrome
- Liver hands – palmar erythema
- Clubbing of fingers
- Zone by Decholte – presence of spider nevi in chest and neck
11. Syndrome of dirty grey skin - disorder of metabolism of lipids and cholesterol
12. Portal hypertension syndrome
a. 1st stage:
- Pressure 150 mmHg
- No splenomegaly, no caput medusa, no collaterals, no ascitis
b. 2nd stage:
- 160-300mmHg
- Splenomegaly
- Osophageal vein varicose absent with caput medusa
- Collaterals visible
- No ascitis
c. 3rd stage
- 300 – 700mmHg
- Splenomegaly, all collaterals pronounced even with complications like bleeding
- Ascites
treatment
Diet No.5, don‘t eat fat, spices and substances which stimulate liver, stop alcohol, reduce salt intake, aspirin and NSAIDS should be avoid. Low protein diet
Drugs:
- Antiviral- interferon alpha, lamivudine and ribavarin; reverse transcriptase inhibitors, acyclovir
- Hepatoprotectors – carcil, ligalone, acid glutamidase, riboxin, vitamins and Phospholipids, interferon, carbile, lipamid
- Diuretics, aldosterone antagonist, vasopressin to stop ascites
- Symptomatic treatment – antidyspeptic drugs, immune regulators
- Detoxication - 5% glucose IV infusion
- liver metabolism improver- glucocorticosteroids
- immunosuppressive agents - Corticosteroids – prednisolone, triamcinolon, dexamethasone
- infusion therapy of plasma and albumin in case of catabolic syndrome.
indications to immunosuppresion
- Predisposition to infection
- Pancytopenia esply with decrease in leukocyte, lymphocyte and monocyte counts
- Cirrhosis caused by autoimmune disorder - autoimmune hepatitis or idiopathic (non-viral hepatitis)
- Serum antimitochondrial or self antibodies in blood investigation.
complications
- Portal hypertension complications – variceal bleeding, hepatic encephalopathy, ascites
- Hepatocellular carcinoma
- Progressive liver failure→death
- Cirrhosis, liver decompensation.
- jaundice
- inflammatory syndrome
- detoxicating syndrome- hepatic coma
- liver insufficiency
- gastro-esophageal bleeding
- haemorrhagic problems- coagulopathy, anemia, hemophilia
- hepatopulmonary syndrome
- spontaneous bacterial peritonitis
- Hepatic encephalopathy.
