Cirrhosis ppt

1. Cirrhosis
PRESENTED BY
MR.ROMAN BAJRANG
RELIANCE INSTITUTE OF NURSING

2. CIRRHOSIS

3. 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.
Edited by:- MR. ROMAN BAJRANG

4. Cirrhosis
End stage complication of liver disease
“Diffuse disorder of liver characterised
by; Complete loss of architecture,
Replaced by extensive fibrosis with,
Regenerating parenchymal nodules.

5.  Cirrhosis is common end result of many chronic
liver disorders.
 Starts as hepatocellular necrosis & inflammation
 Proceeds to bridging fibrous septa.
 Regeneration of remaining hepatocytes form
nodules.
 Loss of normal architecture & function.
INTRODUCTION

7. Normal Liver Histology

8. Edited by:- MR. ROMAN BAJRANG

9. DEFINITION
• Cirrhosis is defined as a diffuse process characterized by
fibrosis and the conversion of normal liver architecture
into structurally abnormal nodules .
• Cirrhosis is a generic term for an end stage of CLD
characterized by destruction of hepatocytes &
replacement of normal hepatic architecture with fibrotic
tissue & regenerative nodules.
(*kirros = orange, osis = condition – Greek)

10. 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

11. • 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

12. Morphological Classification
 Macronodular (parenchymal nodules >3mm)
Etiology Frequency
Chronic viral hepatitis 10-20%
Wilson’s disease Rare
Alpla1 antitrypsin ↓ Rare
Cryptogenic Common
Various drugs & toxins Rare
 Micronodular (parenchymal nodules <3mm)
Etiology Frequency
Alcohol 60-70%
Primary biliary 5%
Hemochromatosis 5%
Cystic fibrosis Rare

14. 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

15. 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

16. • 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

17. Edited by:- MR. ROMAN BAJRANG

18. Clinical presentation

19. CirrhosisClinicalFeatures

20. CLINICAL FEATURES & COMPLICATIONS
• Fatigue
• Generalized pruritus
• Loss of appetite & weight
• Intermittent jaundice
• Loss of libido & testicular atrophy (men)
• Gynecomastia
• Menstrual abnormalities (females)
• Bleeding tendencies (↓protein for
clotting)
• Ecchymoses
• Edema & ascites (↓intravascular
colloidal pressure & ↑capillary
hydrostatic pressure)
• Fetor hepaticus

21. Contd…
• Asterixis (flapping hand tremors)
• Portal HTN (scar tissue blocks normal
flow of blood & ↑pressure in the portal
vein)
• GI bleed (d/t esophageal varices
/hemorrhoids)
• SBP (d/t long-standing ascites)
• Splenomegaly (portal HTN can
cause spleen to enlarge & retain
WBCs & platelets)
• Hepatic encephalopathy (↑accumulation
of toxins like Ammonia in the brain)
• Gallstones & CBD stones (d/t
biliary stasis)

22. • Insulin resistance & Type 2 DM
• Metabolic bone diseases
• Palmar erythema
• Pigmentation
• Digital clubbing
• Caput medusae
• Spider angioma
• Hepatorenal syndrome
• Hepatopulmonary syndrome
• Hepatic Hydrothorax
• Hepatocellular carcinoma
Contd…

23. Pathogenesis of clinical features
Jaundice
Dark urine
Pale stools
Oedema
Steatorrhoea
Pruritis
Ascites
Bleeding
Haematemesis
Encephalopathy
Foetar hepaticus
Impaired conjugation or obstruction.
Conjugated hyperbilirubinemia (vs. acholuric)
Biliary obstruction
Low albumin – low oncotic pressure.
Bile obstruction.
Bile obstruction  Bile salt in blood.
Portal hypert, low alb, hyper aldosterone
Coag. factor synthesis
Oesophageal varices. (hemorrhoids)
Toxic nitrogen products – gut bacteria.
Musty odor (mercaptans by gut bacteria)

24. Clinical Features
Hepatocellular failure
Malnutrition, low albumin & clotting factors,
bleeding.
Hepatic encephalopathy.
Portal hypertension.
Ascites, Porta systemic shunts, varices,
splenomegaly.

25. Bleeding tendencies
Decreased synthesis of prothrombin complex
Thrombocytopenia
Epistaxis, bleeding gums, ecchymosis,
Upper GI bleed
Lower GI bleed

26.  Ascites
Accumulation of free fluid in peritoneal cavity
Hypoalbuminemia
Portal hypertension
Decreased effective intravascular volume
hyperaldosteronism

27. Hepatic encephalopathy
Portosystemic shunting of portal blood
Precipitating factors
Protein over load
Upper GI bleed
Constipation
Drugs
Diuretics / large volume peritoneocentesis
alkalosis

28. Portal hypertension
Splenomegaly
Hypersplenism
Porto-systemic anastomosis
Caput medusae
Esophageal varices
Hemorrhoids
Hepato-pulmonary syndrome

29. 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

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

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

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

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

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

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

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

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

40. Edited by:- MR. ROMAN BAJRANG

41. 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

42. 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
3.Plt count-alcoholic thrombocytopaenia 4.UGI
endoscopy-variceal bleeding
Hepatocellular damage

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

44. Test category Serum measurement
Hepatocyte integrity AST ↑ (AST/ALT ratio >1)
ALT ↑
LDH ↑
Biliary excretory function S.Bil ↑ (total/direct) Urine Bil.
↑
S. Bile acids ↑
S. GGT ↑
S. 5-nucleotidase ↑
S.ALP ↑
Hepatocyte function S. Albumin ↓ PT ↑
S. Ammonia ↑
LAB. EVALUATION

45. Radiological Evaluation
 Ultrasound
• Surface nodularity
• Coarse & heterogenous echotexture
• Segmental hypertrophy/atrophy
• Signs of Portal HTN
Enlarged p/vein (>13 mm)
Slow portal venous flow (<15cm/sec)
Portal vein thrombosis
• Splenomegaly
• Ascites
• Fatty change
• Cork screw appearance of hepatic arteries

46.  CT Scan
• Surface nodularity (regenerative>siderotic)
• Fatty change
• Segmental hypertrophy/atrophy
• Signs of portal HTN
 MRI
• Morphologic changes (same as USG & CT)
• Regenerative or cirrhotic nodules

47. Other Ix
 Transient Elastography (Fibro-scan)
• New, non‐invasive, rapid & reproducible method
• In cirrhotic patients, liver stiffness measurements
range from 12.5 to 75.5 kPa
 Liver Biopsy
• regenerative nodules of hepatocytes
surrounded by fibrous connective
tissue that bridges between portal
tracts
• Mallory's hyaline material within
hepatocytes

48. Management
1.Supportive Management
2.Treatment for specific etiology
3.Treatment for complications

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

50. 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

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

52. 1.Variceal bleeding

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

54. 2.Hepatic encephalopathy

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

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

57. 3.Hepatorenal Syndrome

58. Management
1. Liver transplantation
2. Agonists of vasopressin-ornipressin and terlipressin
3. Dopamine
4. Renal vasoconstrictor antagonists-Saralasin
5. Surgical shunts
Edited by:- MR. ROMAN BAJRANG

59. 4.Ascites

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

62. 5.Spontaneous bacterial peritonitis

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

64. Prognosis
Prognosis depends on the Child-Pugh
score

65. Edited by:- MR. ROMAN BAJRANG

66. Complications
Congestive splenomegaly.
Bleeding varices.
Hepatocellular failure.
Hepatic encephalitis / hepatic coma.
Hepatocellular carcinoma.

68. Edited by:- MR. ROMAN BAJRANG