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Cirrhosis-
Tawny
Lecture 20
Yellowish
brown
color
Tawny
Introduction
• The term cirrhosis was first used by Rene
Laennec (1781-1826) to describe the
abnormal liver color of individuals with
alcohol induced liver disease.
• Derived from Greek word Kirrhos means
Yellowish brown color.
Definition
• Cirrhosis is defined as a diffuse process
characterised by fibrosis and the conversion
of normal liver architecture into structurally
abnormal nodules.
Morphology
• Its three main morphologic characteristics
are:
• 1.Bridging fibrous septa
• 2. Parenchymal nodules- micro & macro
• 3. Disruption of the architecture of the entire
liver.
Common Causes
1. Chronic alcoholism
2. Chronic hepatitis B& C
3. Biliary disease
4. Hemochromatosis
5. Cryptogenic 10%
6. Wilson's disease,
7. alpha-1 anti-trypsin deficiency.
• Obesity
• Nonalcoholic fatty liver disease
• Autoimmune hepatitis
• Diseases that damage or destroy bile ducts.
• Inherited diseases
• Drugs, toxins & toxins
Types of Cirrhosis
• 1. Alcoholic Cirrhosis (Laennec)
• 2. Post necrotic Cirrhosis (macronodular)
• 3. Billiary Cirrhosis
• 4. Cardiac Cirrhosis
Pathogenesis
1. Hepatocellular death
2. Regeneration
3. Progressive fibrosis
4. Vascular reorganization
Pathophsiology :
Liver insult due to alcohol ingestion, viral hepatitis,
exposure to toxin
Hepatocyte damage
Liver inflammation - ↑WBCs, nausea, vomiting, pain,
fever, anorexia, fatigue
Alteration in blood and lymph flow
Cont..
Liver necrosis →liver fibrosis and scarring → portal
hypertension
- Ascities, edema,
- Spleenomegaly ( thrombocytopenia, leucopenia)
- Varices (esophageal varices, hemorrhoids, anemia)
↓ billirubin metabolism – hyperbilirubinemia,
jaundice
Cont..
• ↓ bile in gastrointestinal tract – light colored stool
• ↑ urobilinogen – Dark Urine
• ↓ vit K absorption- bleeding tendency
• ↓ metabolism of protein, carbohydrate, fats→
hypoglycemia,
• ↓ plasma protein- ascites and edema
• ↓androgen and estrogen detoxification(↓
hormone metabolism)- ↑ estrogen and androgens
hormone – Gynecomastia, loss of body hair,
menstrual dysfunction, spider angioma, palmer
erythema, testicular atrophy
Cont..
• ↓ Aldesterone metabolism so ↑ levels – sodium
and water retention-- edema
• Biochemical alteration - ↑ AST, ALT levels, ↑
bilirubin, low serum albumin, prolong prothombin
time, elevated alkaline phosphatase.
• Liver failure
• Hepatic encephalopathy
• Hepatic coma
• Death
Clinical manifestations
Early manifestations
• No symptoms
• GI disturbances: anorexia, dyspepsia,
flatulence, weakness, fatigue, nausea,
vomiting, weight loss, abdominal pain,
bloating, diarrhea, constipation
• Abdominal pain, dull and heavy feeling
• Fever, lassitude, weight loss, enlargement of
liver and spleen.
Cont…
Later manifestations:
Results from liver failure and portal
hypertension
• Jaundice
• Peripheral edema
• Ascites
• Others: Skin lesion, hematological disorders,
endocrine disturbances, and peripheral
neuropathy
• Advanced stage: small and nodular liver
Clinical Manifestations
Complications
• The ultimate mechanism of deaths in most
cirrhotic patients is
• (1) progressive liver failure,
• (2) a complication related to portal
hypertension, or
• (3) the development of hepatocellular
carcinoma.
Complication
Portal hypertension
• The nodules and scar tissue can compress
hepatic veins within the liver.
• This causes the blood pressure within the liver to
be high, a condition known as portal
hypertension.
• Portal venous pressure is more than 15mmHg or
20 cm of water (normal 5-10mm Hg)
Cont…
• Is characterized by ↑venous pressure in the
portal circulation, spleenomegaly, large collateral
vein, ascites, systemic hypertension, and
esophageal varices.
• The common area to form collateral channels are
in the lower esophagus( the anastomosis of the
left gastric vein and azygos vein), the parietal
peritoneum, rectum.
• High pressures within blood vessels of the liver
occur in 60% of people who have cirrhosis.
L20 cirrhosis sr
L20 cirrhosis sr

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L20 cirrhosis sr

  • 3. Introduction • The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with alcohol induced liver disease. • Derived from Greek word Kirrhos means Yellowish brown color.
  • 4. Definition • Cirrhosis is defined as a diffuse process characterised by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules.
  • 5.
  • 6. Morphology • Its three main morphologic characteristics are: • 1.Bridging fibrous septa • 2. Parenchymal nodules- micro & macro • 3. Disruption of the architecture of the entire liver.
  • 7. Common Causes 1. Chronic alcoholism 2. Chronic hepatitis B& C 3. Biliary disease 4. Hemochromatosis 5. Cryptogenic 10% 6. Wilson's disease, 7. alpha-1 anti-trypsin deficiency.
  • 8. • Obesity • Nonalcoholic fatty liver disease • Autoimmune hepatitis • Diseases that damage or destroy bile ducts. • Inherited diseases • Drugs, toxins & toxins
  • 9. Types of Cirrhosis • 1. Alcoholic Cirrhosis (Laennec) • 2. Post necrotic Cirrhosis (macronodular) • 3. Billiary Cirrhosis • 4. Cardiac Cirrhosis
  • 10. Pathogenesis 1. Hepatocellular death 2. Regeneration 3. Progressive fibrosis 4. Vascular reorganization
  • 11.
  • 12. Pathophsiology : Liver insult due to alcohol ingestion, viral hepatitis, exposure to toxin Hepatocyte damage Liver inflammation - ↑WBCs, nausea, vomiting, pain, fever, anorexia, fatigue Alteration in blood and lymph flow
  • 13. Cont.. Liver necrosis →liver fibrosis and scarring → portal hypertension - Ascities, edema, - Spleenomegaly ( thrombocytopenia, leucopenia) - Varices (esophageal varices, hemorrhoids, anemia) ↓ billirubin metabolism – hyperbilirubinemia, jaundice
  • 14. Cont.. • ↓ bile in gastrointestinal tract – light colored stool • ↑ urobilinogen – Dark Urine • ↓ vit K absorption- bleeding tendency • ↓ metabolism of protein, carbohydrate, fats→ hypoglycemia, • ↓ plasma protein- ascites and edema • ↓androgen and estrogen detoxification(↓ hormone metabolism)- ↑ estrogen and androgens hormone – Gynecomastia, loss of body hair, menstrual dysfunction, spider angioma, palmer erythema, testicular atrophy
  • 15. Cont.. • ↓ Aldesterone metabolism so ↑ levels – sodium and water retention-- edema • Biochemical alteration - ↑ AST, ALT levels, ↑ bilirubin, low serum albumin, prolong prothombin time, elevated alkaline phosphatase. • Liver failure • Hepatic encephalopathy • Hepatic coma • Death
  • 16. Clinical manifestations Early manifestations • No symptoms • GI disturbances: anorexia, dyspepsia, flatulence, weakness, fatigue, nausea, vomiting, weight loss, abdominal pain, bloating, diarrhea, constipation • Abdominal pain, dull and heavy feeling • Fever, lassitude, weight loss, enlargement of liver and spleen.
  • 17. Cont… Later manifestations: Results from liver failure and portal hypertension • Jaundice • Peripheral edema • Ascites • Others: Skin lesion, hematological disorders, endocrine disturbances, and peripheral neuropathy • Advanced stage: small and nodular liver
  • 19. Complications • The ultimate mechanism of deaths in most cirrhotic patients is • (1) progressive liver failure, • (2) a complication related to portal hypertension, or • (3) the development of hepatocellular carcinoma.
  • 20. Complication Portal hypertension • The nodules and scar tissue can compress hepatic veins within the liver. • This causes the blood pressure within the liver to be high, a condition known as portal hypertension. • Portal venous pressure is more than 15mmHg or 20 cm of water (normal 5-10mm Hg)
  • 21. Cont… • Is characterized by ↑venous pressure in the portal circulation, spleenomegaly, large collateral vein, ascites, systemic hypertension, and esophageal varices. • The common area to form collateral channels are in the lower esophagus( the anastomosis of the left gastric vein and azygos vein), the parietal peritoneum, rectum. • High pressures within blood vessels of the liver occur in 60% of people who have cirrhosis.

Notas do Editor

  1. Pressure exceeding greater than 22 mm Hg in the portal vein or a pressure difference between the portal vein and the hepatic vein of greater than 12 mm Hg will result in portal hypertension. Measuring portal pressure involves inserting a catheter into the portal vein. The internal jugular, femoral, or medial antecubital vessels are the best way to access the hepatic and portal veins.