Cirrhosis is a chronic liver disease characterized by fibrosis and loss of liver function, with types including micronodular and macronodular cirrhosis, often due to factors like alcohol, viral infections, and metabolic disorders. Clinical presentation varies and includes non-specific symptoms like malaise and jaundice, alongside distinct physical signs and complications. Management encompasses supportive care, addressing specific etiologies, and treatment of complications, with prognosis evaluated via the Child-Pugh scoring system.

1. Cirrhosis
Harindu Udapitiya,
Temporary Lecturer,
Division of Pharmacology.

2. Overveiw
1. What is cirrhosis
2. Types
3. Etiology
4. Clinical presentation
5. Investigations
6. Complications
7. Management

3. 1.What is Cirrhosis
• Cirrhosis is a consequence of chronic
liver disease, characterized by
replacement of liver tissue by
fibrosis, scar tissue and regenerative
nodules leading to loss of liver
function and disruption of the liver
architecture.

5. 2.Types of cirrhosis
1.Micronodular cirrhosis.
• Regenerating nodules are usually <3 mm in size
and the liver is involved uniformly.
• This type is
often caused
by ongoing
alcohol
damage or
biliary tract
disease

6. • 2. Macronodular Cirrhosis
• The nodules are of variable Size and normal
acini may be seen within the larger nodules.
• This type is
often seen
following
chronic viral
hepatitis

7. 3. Etiology

8. 1. Drugs and toxins
Alcohol, methotrexate, isoniazid,
methyldopa
2. infections
Hepatitis B and C , Schistosoma japonicum
3. autoimmune
PBC, autoimmune hepatitis, PSC
4. metabolic
Wilson’s disease, haemochromatosis, alpha
1 antitrypsin, porphyria

9. 5. Biliary obstruction
Cystic fibrosis, atresia, strictures, gall stones
6. vascular
Chronic right heart failure, Budd Chiari
syndrome
7. miscellaneous
Sarcoidosis, intestinal by- pass surgery for
obesity
8. unknown
cryptogenic

10. • Alcoholic liver disease 60-70%
• Viral hepatitis 10%
• Biliary disease 5-10%
• Primary hemochromatosis 5%
• Cryptogenic cirrhosis 10-15%
• Wilson’s, alpha 1AT def rare

12. 4. Clinical presentation

13. Symptoms
1. Non specific symptoms-
– Lethargy
– Malaise
– Abd pain
– loss of appetite
2. Symptoms due to elevated bilirubin-
– Yellowish discoloration of eyes
– Pruritus
3. Symptoms due to liver failure-
– Leg edema
– Abdominal distension
– Loss of hair

14. 4. Symptoms due to complications
– Haemoptysis-UGI bleeding
– Altered behavior-HE
– Worsening abd pain-SBP

15. Signs
• Eyes and Face
1. Icterus
2. Cyanosis
3. Parotid enlargement

16. • Hands
1. Clubbing
2. Leukonychia
3. Dupuytren’s contraction
4. Palmar erythema
5. Spider naevi
6. Scratch marks
7. Pigmentation

17. • Chest
1. Los of axillary hair
2. Spider naevi
3. Gynaecomastia

18. • Abdomen
1. Hepatomegally
2. Splenomegally
3. Ascites
4. Caput medusae

19. • Legs
1. Oedema
2. Loss of hair on the shins
• Genitalia
1. Testiculat atrophy

20. 4. Investigations
• 1. Investigations for diagnosis
• 2. Investigations for etiology
• 3. Investigations for
severity/complication

21. 1. Investigations for diagnosis
1. USS abdomen
2. Liver biopsy
3. CT abdomen

22. 2. Investigations for etiology
1.Viral hepatitis
– Hepatitis B and C serology
2.Autoimmune hepatitis
– Anti LKM antibody, anti smooth muscle antibody, IgG
3.Alpha 1 antitrypsin deficiency
– Alpha 1 antitrypsin level, phenotype testing
4.Wilson’s disease
– Reduced serum Cu and Caeruloplasmin; increased 24 hr
Cu excretion
5.haemochromatosis
– s. ferritin
6.Hepatocellular carcinoma
– Alpha feto protein level
– USS
7.Primary billiary cirrhosis
-serum IgM level

23. 3. Investigations for
severity/complication
1.liver function tests
Serum Albumin
Coagulatory profile/PT
Serum billirubin
2.Liver biochemistry
AST(SGOT)
ALT(SGPT)
ALP-biliary canaliculi damage
Gamma GT-hepatobilliary damage
Hepatocellular damage
3.Plt count-alcoholic thrombocytopaenia
4.UGI endoscopy-variceal bleeding

24. 5.Peritoneal fluid analysis-SBP
6.USS-ascites, portal hypertension
7.Renal function tests(SE,S.cre)-hepatorenal
syndrome

25. 5. Management
1.Supportive Management
2.Treatment for specific etiology
3.Treatment for complications

26. 1.Supportive Management
1.Proper Nutrition
2.Manage bleeding-transfusion, fluid
3.Abdominal paracentesis
4.Tx for itching
5.Regular excersise

27. 2.Treatment for specific etiology
1.Viral-antivirals
2.Alcohol-stop alcohol
3. Wilson's disease-chelation therapy
4.Billiary obstruction-relieve obstruction
5.Vascular-manage HF

28. 3.Treatment for complications
1.Variceal bleeding
2.Hepatic encephalopathy
3.Hepatorenal syndrome
4.Ascites
5.Spontaneous bacterial peritonitis

29. 1.Variceal bleeding

30. Management
1. Initial rescitation
2. Vasopressin
3. Endoscopic band ligation
4. Sclerotherapy
5. Balloon tamponade
6. TIPSS
7. Proponalol

31. 2.Hepatic encephalopathy

32. Risk factors
1. GIT bleeding
2. Infection
3. Constipation
4. Medication-opiates, antidepressants
5. Dietary protein
6. Renal failure
7. Portosystemic shunts

33. Management
1. Low protein diet
2. Lactulose
3. Antibiotis-neomycin, metranidazole
4. LOLA, Zinc
5. Sodium Benzoate
6. General measures

34. 3.Hepatorenal Syndrome

35. Management
1. Liver transplantation
2. Agonists of vasopressin-ornipressin and terlipressin
3. Dopamine
4. Renal vasoconstrictor antagonists-Saralasin
5. Surgical shunts

36. 4.Ascites

37. Management
1. Sodium restriction
2. Diuretics-aldosteron, Frusemide
3. Terapeutic paracentesis
4. TIPSS

39. 5.Spontaneous bacterial peritonitis

40. Management
• Start Tx with cefotaxime 2g 8 hrly
• Change antibiotic according to culture report

41. 6. Prognosis
Prognosis depends on the Child-Pugh
score

43. Summery
1. Pathology
2. Etiology
3. Clinical presentation
4. Investigations
5. Complications
6. Management
7. Prognosis