Liver cirrhosis aetiology, pathogenesis, clinical features, treatment

2. INTRODUCTION
•HEPATIC CIRRHOSISISACOMMONDISEASECHARACTERISEDBYDIFFUSEHEPATIC
FIBROSISANDNODULEFORMATION.
•OCCURSATANYAGEANDHASSIGNIFICANTMORBIDITY ANDISANIMPORTANT
CAUSEOFPREMATUREDEATH.
•MOSTCOMMONCAUSE-CHRONICVIRALHEPATITISANDPROLONGEDEXCESSIVE
ALCOHOLCONSUMPTION.
•MOSTCOMMONCAUSEOFPORTALHYPERTENSIONANDITSASSOCIATED
COMPLICATIONS

4. ALCOHOLIC CIRRHOSIS
• EXCESSIVECHRONICALCOHOLUSECANCAUSESEVERALTYPESOFCHRONICLIVERDISEASE
INCLUDINGALCOHOLICFATTYLIVER,ALCOHOLIC HEPATITIS,ALCOHOLIC CIRRHOSIS.
•CONTRIBUTESTOLIVERDAMAGEINPATIENTSWITHOTHERLIVERDISEASESUCHASHEPATITIS C
HEMOCHROMATOSIS ANDFATTYLIVERDISEASERELATEDTOOBESITY.
• ITCANPRODUCEFIBROSISINTHEABSENCEOFACCOMPANYING INFLAMMATION ANDNECROSIS.

5. • FIBROSISCANBECENRILOBULAR,PERICELLULAR,PERIPORTAL.
• WHENFIBROSISREACHESCERTAINDEGREETHEREISDISRUPTIONOFNORMALLIVERARCHITECTURE
ANDREPLACEMENTOF LIVERCELLSBYREGENERATIVENODULES.
• NODULES–MICRONODULES-<3MMDIAMETER
MACRONODULES->3MMDIAMETER

6. PATHOGENESIS

7. CLINICAL SYMPTOMS:
• NON SPECIFIC SYMPOMS: RIGHT UPPER QUADRANT ABDOMINAL PAIN, FEVER,
NAUSEA, VOMITING, DIARRHEA, ANOREXIA AND MALAISE.
• SPECIFIC SYMPTOMS: ASCITES, EDEMA, UPPER GASTROINTESTINAL
HEMORRHAGE.
• MANY PRESENT INCIDENTALLY AT THE TIME OF AUTOPSY OR ELECTIVE SURGERY.
• OTHERS : JAUNDICE OR ENCEPHALOPATHY.

8. • ON PHYSICAL EXAMINATION LIVER AND SPLEEN MAY BE ENLARGED WITH LIVER
EDGE BEING FIRM AND NODULAR.
• OTHER FREQUENT FINDINGS INCLUDE SCLERAL ICTERUS, PALMAR ERYTHEMA,
SPIDER ANGIOMAS, PAROTID GLAND ENLARGEMENT, DIGITAL CLUBBING, MUSCLE
WASTING.
• MEN –DECREASEDBODY HAIR, AND GYNECOMASTIA AS WELL AS
TESTICULAR ATROPHY.
• WOMEN-ADVANCED ALCOHOLIC CIRRHOSIS MENSTURAL IRREGULARITIES ,SOME
WOMAN MAY BE AMENORRHEIC THIS CHANGES ARE OFTEN REVERSIBLE
FOLLOWING CESSATION OF ALCOHOL.

9. • LAB TESTS NORMAL IN EARLY CASES , ABNORMAL IN ADVANCED STAGES.
• ANEMIC-CHRONIC GI BLOOD LOSS, NUTRITIONAL DEFICIENCY, HYPER SPLENISM
RELATED TO PORTAL HYPERTENSION, DIRECT SUPPRESSIVE EFFECT OF ALCOHOL ON
BONE MARROW.
• ZIEVE’S SYNDROME-HAEMOLYTIC ANEMIA WITH SPUR CELLS AND
ACANTHOCYTES.
• PLATELETS REDUCED EARLY IN THE DISEASE REFLECTIVE OF PORTAL HYPERTENSION.
• TOTAL SERUM BILIRUBIN NORMAL OR ELEVATED.

10. • DIRECT BILIRUBIN MILDLY ELEVATED, PROGRESSES AS DISEASE WORSENESS.
• PROTHROMBIN TIME PROLONGED, NOT RESPOND TO IV VIT-K.
• SERUM SODIUM LEVELS NORMAL UNLESS PATIENT HAVE ASCITES AND DEPRESSED
LARGELY DUE TO INGESTION OF EXCESS OF FREE WATER.
• ALT,AST ELEVATED IN PATIENTS WHO CONTINUE TO DRINK,WITH AST LEVELS
HIGHER THAN ALT,2:1RATIO.
• LIVER BIOPSY CAN BE HELPFUL TO CONFIRM DIAGNOSIS BUT WHEN PATIENTS
PRESENT WITH ALCOHOLIC CIRRHOSIS AND ARE STILL DRINKING LIVER BIOPSY IS
WITHHELD UNTIL ABSTINENCE FOR ATLEAST 6MONTHS TO DETERMINE NON-
REVERSIBLE DISEASE.

11. TREATMENT
• ABSTINENCE IS THE CORNER STONE OF THERAPY.
• GOOD NUTRITION AND LONG TERM MEDICAL SUPERVISION TO
MAINTAIN UNDERLYING COMPLICATIONS.
• COMPLICATIONS REQUIRES SPECIFIC MANAGEMENT.
• GLUCOCORTICOIDS IN THE ABSENCE OF INFECTIONS.
• DF-DISCRIMINANT FUNCTION VALUE – SERUM TOTAL BILURUBIN +
DIFFERNCE IN PATIENT’S PROTHROMBIN TIME COMPARED TO
CONTROL (IN SECONDS) Х 4.6

12. • TREATMENT IS RESTRICTED TO PATIENT’S WITH DF VALUE MORE THAN 32, WITH
USE OF GLUCO CORTICOIDS IMPROVED SURVIVAL AT 28 DAYS.
• ORAL PENTOXIFYLLINE- DECREASE PRODUCTION OF TNFΑ AND OTHER
PROINFLAMMATORY CYTOKININS, EASY TO ADMINSTER WITH FEW SIDE
EFFECTS.
• RECENT STUDIES USED PARENTERALLY ADMINSTERED INHIBITORS OF TNFΑ
SUCH AS INFLIXIMAB OR ETANERCEPT.
• ANABOLIC STEROIDS, PROPYLTHIOURACIL,
ANTIOXIDANTS,COLCHICINE,PENICILLAMINE USED BUT NO CLEAR CUT BENEFITS.
• MEDICATIONS THAT REDUCE CRAVING FOR ALCOHOL SUCH AS ACAMPROSATE
CALCIUM HAVE BEEN FAVOURABLE.
• THEY CAN TAKE OTHER MEDICINES IN THE PRESENCE OF CIRRHOSIS

13. • ACETAMINOPHEN IS DISCOURAGED IN PATIENTS WITH LIVER DISEASE,
HOWEVER IF NO MORE THAN 2GRAMS PER DAY ARE CONSUMED, THERE
GENERALLY ARE NO PROBLEMS.