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Cirrhosis of the Liver

Cirrhosis of the Liver. Hepatic Cirrhosis It is a chronic progressive disease characterized by: - replacement of normal liver tissue with diffuse fibrosis

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Cirrhosis of the LiverCirrhosis of the Liver

Hepatic CirrhosisHepatic Cirrhosis

• It is a chronic progressive disease characterized by:

- replacement of normal liver tissue with diffuse fibrosis that disrupts the structure and function of the liver

• It is a chronic progressive disease characterized by:

- replacement of normal liver tissue with diffuse fibrosis that disrupts the structure and function of the liver

– Extensive parenchymal cell degeneration

– Destruction of parenchymal cells

– Extensive parenchymal cell degeneration

– Destruction of parenchymal cells

Etiology and PathophysiologyEtiology and Pathophysiology

• Four types of cirrhosis:–Alcoholic (Laennec’s) cirrhosis–Postnecrotic cirrhosis–Biliary cirrhosis–Cardiac cirrhosis

• Four types of cirrhosis:–Alcoholic (Laennec’s) cirrhosis–Postnecrotic cirrhosis–Biliary cirrhosis–Cardiac cirrhosis

A. Alcoholic or Laennec’s Cirrhosis• In which the scar tissue characteristically

surrounds the portal areas• This is the most frequently caused by

chronic alcoholism, common type of cirrhosis

• Preceded by a theoretically reversible fatty infiltration of the liver cells

A. Alcoholic or Laennec’s Cirrhosis• In which the scar tissue characteristically

surrounds the portal areas• This is the most frequently caused by

chronic alcoholism, common type of cirrhosis

• Preceded by a theoretically reversible fatty infiltration of the liver cells

Etiology and PathophysiologyEtiology and Pathophysiology

B. Post necrotic cirrhosis–Complication of toxic or viral hepatitis–Accounts for 20% of the cases of cirrhosis–Broad bands of scar tissue form within

the liver

B. Post necrotic cirrhosis–Complication of toxic or viral hepatitis–Accounts for 20% of the cases of cirrhosis–Broad bands of scar tissue form within

the liver

• Etiology and Pathophysiology• Etiology and Pathophysiology

C. Biliary Cirrhosis• In which scarring occurs in the liver around

the bile ducts. • This type of cirrhosis usually results from

chronic biliary obstruction and infection (cholangitis)

• Accounts for 15% of all cases of cirrhosis

C. Biliary Cirrhosis• In which scarring occurs in the liver around

the bile ducts. • This type of cirrhosis usually results from

chronic biliary obstruction and infection (cholangitis)

• Accounts for 15% of all cases of cirrhosis

• Etiology and Pathophysiology• Etiology and Pathophysiology

Etiology and PathophysiologyEtiology and Pathophysiology

D. Cardiac Cirrhosis –Results from longstanding severe right-

sided heart failure

D. Cardiac Cirrhosis –Results from longstanding severe right-

sided heart failure

Diagnostic FindingDiagnostic Finding1. serum albumin• Decrease in level

2. liver enzymes• SGPT(ALT),SGOT(AST) increases

3.Serum bilirubin• Increases

4. Prothrombin time• prolong

1. serum albumin• Decrease in level

2. liver enzymes• SGPT(ALT),SGOT(AST) increases

3.Serum bilirubin• Increases

4. Prothrombin time• prolong

5. Ultrasound scanning• Used to measure the difference in density of

parenchymal cells and scar tissue.

6. CT-scan, MRI• It gives information about liver size, hepatic

blood flow and obstruction

7. Liver biopsy

8.ABG• May reveal a ventilation-perfusion imbalance

and hypoxia

5. Ultrasound scanning• Used to measure the difference in density of

parenchymal cells and scar tissue.

6. CT-scan, MRI• It gives information about liver size, hepatic

blood flow and obstruction

7. Liver biopsy

8.ABG• May reveal a ventilation-perfusion imbalance

and hypoxia

Manifestations of Liver CirrhosisManifestations of Liver Cirrhosis

Clinical ManifestationsEarly Manifestations

Clinical ManifestationsEarly Manifestations

• Onset usually insidious• GI disturbances:

–Anorexia –Dyspepsia –Flatulence –N-V, change in bowel habits

• Onset usually insidious• GI disturbances:

–Anorexia –Dyspepsia –Flatulence –N-V, change in bowel habits

Clinical ManifestationsEarly Manifestations

Clinical ManifestationsEarly Manifestations

• Abdominal pain• Fever• Lassitude• Weight loss• Enlarged liver or spleen

• Abdominal pain• Fever• Lassitude• Weight loss• Enlarged liver or spleen

Clinical ManifestationsLate Manifestations

Clinical ManifestationsLate Manifestations

• Two causative mechanisms–Hepatocellular failure–Portal hypertension

• Two causative mechanisms–Hepatocellular failure–Portal hypertension

Clinical ManifestationsJaundice

Clinical ManifestationsJaundice

• Occurs because of insufficient conjugation of bilirubin by the liver cells, and local obstruction of biliary ducts by scarring and regenerating tissue

• Occurs because of insufficient conjugation of bilirubin by the liver cells, and local obstruction of biliary ducts by scarring and regenerating tissue

Clinical ManifestationsJaundice

Clinical ManifestationsJaundice

• Intermittent jaundice is characteristic of biliary cirrhosis

• Late stages of cirrhosis the patient will usually be jaundiced

• Intermittent jaundice is characteristic of biliary cirrhosis

• Late stages of cirrhosis the patient will usually be jaundiced

Clinical ManifestationsSkin

Clinical ManifestationsSkin

• Spider angiomas (telangiectasia, spider nevi)

• Palmar erythema

• Spider angiomas (telangiectasia, spider nevi)

• Palmar erythema

Clinical Manifestations Endocrine DisturbancesClinical Manifestations Endocrine Disturbances

• Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver

• Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver

Clinical Manifestations Endocrine DisturbancesClinical Manifestations Endocrine Disturbances

• Alteration in hair distribution–Decreased amount of pubic hair–Axillary and pectoral alopecia

• Alteration in hair distribution–Decreased amount of pubic hair–Axillary and pectoral alopecia

Clinical Manifestations Hematologic Disorders

Clinical Manifestations Hematologic Disorders

• Bleeding tendencies as a result of decreased production of hepatic clotting factors (II, VII, IX, and X)

• Bleeding tendencies as a result of decreased production of hepatic clotting factors (II, VII, IX, and X)

Clinical Manifestations Hematologic Disorders

Clinical Manifestations Hematologic Disorders

• Anemia, leukopenia, and thrombocytopenia are believed to be result of hypersplenism

• Anemia, leukopenia, and thrombocytopenia are believed to be result of hypersplenism

Clinical Manifestations Peripheral Neuropathy

Clinical Manifestations Peripheral Neuropathy

• Dietary deficiencies of thiamine, folic acid, and vitamin B12

• Dietary deficiencies of thiamine, folic acid, and vitamin B12

Steatorrhea• Fatty stool• The passage of abnormally increase

amounts of fats in the feces (more than 5g/day) due to reduced absorption of fat by intestine

• The feces are pale, smell offensive, look greasy

Steatorrhea• Fatty stool• The passage of abnormally increase

amounts of fats in the feces (more than 5g/day) due to reduced absorption of fat by intestine

• The feces are pale, smell offensive, look greasy

Pruritus• Due to biliary obstruction leading to

retention of bile salts.• Patients may develop vascular spider

angiomas on the skin usually above the waistline

• These are numerous small vessels resembling a spider’s leg

Pruritus• Due to biliary obstruction leading to

retention of bile salts.• Patients may develop vascular spider

angiomas on the skin usually above the waistline

• These are numerous small vessels resembling a spider’s leg

ComplicationsComplications

• Portal hypertension and esophageal varices

• Peripheral edema and ascites• Hepatic encephalopathy• Hepato-renal Syndrome

• Portal hypertension and esophageal varices

• Peripheral edema and ascites• Hepatic encephalopathy• Hepato-renal Syndrome

Complications Portal Hypertension

Complications Portal Hypertension

• Characterized by:– Increased venous pressure in portal

circulation–Splenomegaly–Esophageal varices–Systemic hypertension

• Characterized by:– Increased venous pressure in portal

circulation–Splenomegaly–Esophageal varices–Systemic hypertension

Complications Portal Hypertension

Complications Portal Hypertension

• Primary mechanism is the increased resistance to blood flow through the liver

• Primary mechanism is the increased resistance to blood flow through the liver

Complications Portal Hypertension

Splenomegaly

Complications Portal Hypertension

Splenomegaly

• Back pressure caused by portal hypertension chronic passive congestion as a result of increased pressure in the splenic vein

• Back pressure caused by portal hypertension chronic passive congestion as a result of increased pressure in the splenic vein

Complications Portal Hypertension Esophageal Varices

Complications Portal Hypertension Esophageal Varices

• Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus and produces varices

• Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus and produces varices

Complications Portal Hypertension Esophageal Varices

Complications Portal Hypertension Esophageal Varices

• Varices have fragile vessel walls which bleed easily

• Varices have fragile vessel walls which bleed easily

Complications Portal Hypertension

Internal Hemorrhoids

Complications Portal Hypertension

Internal Hemorrhoids

• Occurs because of the dilation of the mesenteric veins and rectal veins

• Occurs because of the dilation of the mesenteric veins and rectal veins

Complications Portal Hypertension

Caput Medusae

Complications Portal Hypertension

Caput Medusae

• Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins around the umbilicus

• Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins around the umbilicus

Complications Peripheral Edema and Ascites

Complications Peripheral Edema and Ascites

• Ascites:- Intraperitoneal accumulation of watery

fluid containing small amounts of protein

• Ascites:- Intraperitoneal accumulation of watery

fluid containing small amounts of protein

Complications Peripheral Edema and Ascites

Complications Peripheral Edema and Ascites

• Factors involved in the pathogenesis of ascites:- Hypoalbuminemia- Levels of aldosterone- Portal hypertension

• Factors involved in the pathogenesis of ascites:- Hypoalbuminemia- Levels of aldosterone- Portal hypertension

Complications Hepatic Encephalopathy

Complications Hepatic Encephalopathy

• Liver damage causes blood to enter systemic circulation without liver detoxification

• Liver damage causes blood to enter systemic circulation without liver detoxification

Complications Hepatic Encephalopathy

Complications Hepatic Encephalopathy

• Main pathogenic toxin is NH3 although other etiological factors have been identified

• Frequently a terminal complication

• Main pathogenic toxin is NH3 although other etiological factors have been identified

• Frequently a terminal complication

Complications Fetor HepaticusComplications Fetor Hepaticus

• Musty, sweetish odor detected on the patient’s breath

• From accumulation of digested by-products

• Musty, sweetish odor detected on the patient’s breath

• From accumulation of digested by-products

Hepatorenal syndromeHepatorenal syndrome

• acute renal failure coupled with advanced hepatic disease (due to cirrhosis or less often metastatic tumor or severe alcoholic hepatitis)

• characterized by:– Oliguria– benign urine sediment– very low rate of sodium excretion– progressive rise in the plasma creatinine

concentration

• acute renal failure coupled with advanced hepatic disease (due to cirrhosis or less often metastatic tumor or severe alcoholic hepatitis)

• characterized by:– Oliguria– benign urine sediment– very low rate of sodium excretion– progressive rise in the plasma creatinine

concentration

Hepatorenal SyndromeHepatorenal Syndrome

• Reduction in GFR often clinically masked

• Prognosis is poor unless hepatic function improves

• Nephrotoxic agents and overdiuresis can precipitate HRS

• Reduction in GFR often clinically masked

• Prognosis is poor unless hepatic function improves

• Nephrotoxic agents and overdiuresis can precipitate HRS

Diagnostic StudiesDiagnostic Studies

• Liver function tests• Liver biopsy• Liver scan• Liver ultrasound

• Liver function tests• Liver biopsy• Liver scan• Liver ultrasound

Diagnostic StudiesDiagnostic Studies

• Esophagogastroduodenoscopy• Prothrombin time• Testing of stool for occult blood

• Esophagogastroduodenoscopy• Prothrombin time• Testing of stool for occult blood