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Cirrhosis
PRESENTED BY
MR.ROMAN BAJRANG
RELIANCE INSTITUTE OF NURSING
CIRRHOSIS
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
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.
 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
Normal Liver Histology
Edited by:- MR. ROMAN BAJRANG
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)
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
• 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
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
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
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
• 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
Edited by:- MR. ROMAN BAJRANG
Clinical presentation
CirrhosisClinicalFeatures
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
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)
• 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…
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)
Clinical Features
Hepatocellular failure
Malnutrition, low albumin & clotting factors,
bleeding.
Hepatic encephalopathy.
Portal hypertension.
Ascites, Porta systemic shunts, varices,
splenomegaly.
Bleeding tendencies
Decreased synthesis of prothrombin complex
Thrombocytopenia
Epistaxis, bleeding gums, ecchymosis,
Upper GI bleed
Lower GI bleed
 Ascites
Accumulation of free fluid in peritoneal cavity
Hypoalbuminemia
Portal hypertension
Decreased effective intravascular volume
hyperaldosteronism
Hepatic encephalopathy
Portosystemic shunting of portal blood
Precipitating factors
Protein over load
Upper GI bleed
Constipation
Drugs
Diuretics / large volume peritoneocentesis
alkalosis
Portal hypertension
Splenomegaly
Hypersplenism
Porto-systemic anastomosis
Caput medusae
Esophageal varices
Hemorrhoids
Hepato-pulmonary syndrome
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
4. Symptoms due to complications
– Haemoptysis-UGI bleeding
– Altered behavior-HE
– Worsening abd pain-SBP
Signs
• Eyes and Face
1. Icterus
2. Cyanosis
3. Parotid enlargement
• Hands
1. Clubbing
2. Leukonychia
3. Dupuytren’s contraction
4. Palmar erythema
5. Spider naevi
6. Scratch marks
7. Pigmentation
• Chest
1. Los of axillary hair
2. Spider naevi
3. Gynaecomastia
• Abdomen
1. Hepatomegally
2. Splenomegally
3. Ascites
4. Caput medusae
• Legs
1. Oedema
2. Loss of hair on the shins
• Genitalia
1. Testiculat atrophy
Investigations
• 1. Investigations for diagnosis
• 2. Investigations for etiology
• 3. Investigations for
severity/complication
Investigations for diagnosis
1. USS abdomen
2. Liver biopsy
3. CT abdomen
Edited by:- MR. ROMAN BAJRANG
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
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
Peritoneal fluid
analysis-SBP 6.USS-
ascites, portal
hypertension
7.Renal function tests(SE,S.cre)-hepatorenal
syndrome
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
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
 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
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
Management
1.Supportive Management
2.Treatment for specific etiology
3.Treatment for complications
Supportive Management
1.Proper Nutrition
2.Manage bleeding-transfusion, fluid
3.Abdominal paracentesis
4.Tx for itching
5.Regular excersise
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
Treatment for complications
1.Variceal bleeding
2.Hepatic encephalopathy
3.Hepatorenal syndrome
4.Ascites
5.Spontaneous bacterial peritonitis
1.Variceal bleeding
Management
1. Initial rescitation
2. Vasopressin
3. Endoscopic band ligation
4. Sclerotherapy
5. Balloon tamponade
6. TIPSS
7. Proponalol
2.Hepatic encephalopathy
Risk factors
1. GIT bleeding
2. Infection
3. Constipation
4. Medication-opiates, antidepressants
5. Dietary protein
6. Renal failure
7. Portosystemic shunts
Management
1. Low protein diet
2. Lactulose
3. Antibiotis-neomycin, metranidazole
4. LOLA, Zinc
5. Sodium Benzoate
6. General measures
3.Hepatorenal Syndrome
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
4.Ascites
1. Sodium restriction
2. Diuretics-aldosteron, Frusemide
3. Terapeutic paracentesis
4. TIPSS
5.Spontaneous bacterial peritonitis
Management
• Start Tx with cefotaxime 2g 8 hrly
• Change antibiotic according to culture report
Prognosis
Prognosis depends on the Child-Pugh
score
Edited by:- MR. ROMAN BAJRANG
Complications
Congestive splenomegaly.
Bleeding varices.
Hepatocellular failure.
Hepatic encephalitis / hepatic coma.
Hepatocellular carcinoma.
Edited by:- MR. ROMAN BAJRANG

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Cirrhosis ppt

  • 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
  • 6.
  • 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
  • 13.
  • 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
  • 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
  • 32.
  • 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
  • 36.
  • 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
  • 53. Management 1. Initial rescitation 2. Vasopressin 3. Endoscopic band ligation 4. Sclerotherapy 5. Balloon tamponade 6. TIPSS 7. Proponalol
  • 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
  • 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
  • 60. 1. Sodium restriction 2. Diuretics-aldosteron, Frusemide 3. Terapeutic paracentesis 4. TIPSS
  • 61.
  • 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.
  • 67.
  • 68. Edited by:- MR. ROMAN BAJRANG