Liver Cirrhosis

Dr. Mpondo B
 Introduction
The liver:
Largest gland in the body
Produces bile, different proteins
Contains bile salts, pigments, phospholipids,
cholesterol and a variety of electrolytes
Involved in metabolism of different organic
compounds
Normal liver
 Definition of Cirrhosis:

Diffuse disorder of liver characterised by;

1.Complete loss of normal architecture,
2.Replaced by extensive fibrosis with,
3.Regenerating parenchymal nodules.
 In other words:
 A chronic, degenerative disease
characterized by replacement of normal
liver tissue with diffuse fibrosis that
disrupts the structure and function of
the liver
 Repeated destruction of hepatic cells
causes the formation of scar tissues
 Cirrhosis is common end result of many
chronic liver disorders.
 Diffuse scarring of liver – follows
hepatocellular necrosis of hepatitis.
 Inflammation
 Loss of normal architecture & function.
 Major types of Cirrhosis
a. Alcoholic Cirrhosis ( Laennec’s Cirrhosis)
 Most common type of liver cirrhosis
 Caused by chronic alcoholism

b. Postnecrotic cirrhosis
 Late result of a previous bout of acute viral
hepatitis

c. Biliary cirrhosis
 Resulted from chronic biliary obstruction and infection
 Least common type
Normal Liver
Cirrhosis
Micronodular cirrhosis:
Alcoholic Hepatitis
Macronodular Cirrhosis
Nutmeg Liver-Cardiac Sclerosis
 Predisposing/ Precipitating
factors:
 malnutrition
 effects of alcohol abuse
 chronic impairment of bile excretion –
biliary obstruction in the liver and common
bile duct (gallbladder stones)
 necrosis from hepatotoxins or viral
hepatitis
 Congestive heart failure
 Pathophysiology:
 liver cell damage result in inflammation &
hepatomegaly
 attempts at regeneration eventually result
to fibrosis and a small nodular liver
 hepatic function is slowly impaired
 obstruction of venous channels blocks
hepatic blood flow and cause portal
hypertension
Stages
Prevalence of Liver Cirrhosis
around the world
 Prevalence Based on Etiology
 Alcoholic liver disease 60-70%
 Viral hepatitis 10%
 Biliary disease 5-10%
 Primary hemochromatosis 5%
 Cryptogenic cirrhosis 10-15%
 Pathogenesis:
 Hepatocyte injury leading to necrosis.
 Alcohol, virus, drugs, toxins, genetic etc..

 Chronic inflammation - (hepatitis).

 Bridging fibrosis.
 Regeneration of remaining hepatocytes
Proliferate as round nodules.
 Loss of vascular arrangement results in
regenerating hepatocytes ineffective.
 Clinical presentation

 Anorexia and wt. loss

 Early morning nausea and vomiting (with
blood)
 Flatulence and changes in bowel habits
 Emaciation
 fatigue
 Signs
 Jaundice

 Abdominal pain and tenderness

 Ascites

 Peripheral edema
 Dry skin and rashes

 Petechiae

 ecchymosis
 Spider angiomas (nose, cheeks, upper thorax
and shoulders)

 Hepatomegaly

 Protruding umbilicus

 Dilated abdominal veins

 Fetor hepaticus

 Asterixis

 delirium
 Males (increase estrogen)

 Gynecomastia

 Impotence

 Fall of body hair

 Atrophy of testicles
Females (increase androgren)

 Hirsutism

 Acne

 Deepening of voice

 Increase virilism
Cirrhosis
Clinical
Features
 Pathophysiology
Liver insult
Alcoholic Ingestion, Viral hepatitis
Exposure to toxins

Increase Hepatocyte
wbc pain
damage

fatigue liver
fever
Inflammation
Nausea Alterations in anorexia
vomiting blood and
lymph flow
 Liver
necrosis

liver Liver fibrosis

failure And scarring
Decrease ADH Palmar Spider Loss of
edema Erythema angiomas Body hair
Dec.androgen/
Estrogen p.
Testicular
Dec.met.of CHON Gyneco Menstrual
Plasma atrophy
And Carb./ mastia changes
CHON
Dec.Fat
Edema
Hypoglycemia Acites

Vit.k absop. Bleeding

tendencies
bile
Clay-colored
Bilirubin excretion stool
Dark urine
In urine
hyperbilirubinemia jaundice
Bilirubin metabolism
 ascites
edema
Esophageal
varices
hemorrhoids
bleeding
Superficial
Liver fibrosis Portal HPN
Abdominal
varices

splenomegaly
bleeding
Delayed
Wound
Anemia
healing
Thrombocytopenia infection
leukopenia
Esophageal varices
 Increase
serum Alterations
ammonia In Foul breath
sleep

Inability to
Hepatic
Liver failure Metabolize
encephalopathy
ammonia
Confusion to
Hepatic
Respiratory coma
Asterexis acidosis

DEATH
Pathogenesis of Hepatic
Encephalopathy

Brain

Liver

N2 wastes
Hepatic encephalopathy Rx
 ammonia production
 dietary protein to 20-40 g/day, maintain adequate calories
  ammonia formation in the intestine – give laxative, enema
as ordered and Neomycin -  bacterial ammonia production
•Protect pt. from injury
 side rails up
 turning to side
 assess mental status, LOC
 proper positioning (semi-Fowler’s)
 prevent aspiration
•Prevent further episodes of encephalopathy
 low protein diet
 prescribed medications
 avoid constipation ( to  ammonia production by bacteria in
the GIT)
 early signs of encephalopathy (restlessness, slurred speech,
dec. attention span)
Liver Biopsy – Cirrhosis
Liver Biopsy – Cirrhosis:
MRI Cirrhosis
 Complications:

 Congestive splenomegaly.
 Bleeding varices.
 Hepatocellular failure.
 Hepatic encephalitis / hepatic coma.
 Hepatocellular carcinoma.
Hepatocellular Carcinoma
 Conclusions:
 Common end result of diffuse liver damage.
(Viral hepatitis, Alcohol, congenital, drugs, toxins & Idiopathic)

 Characterised by diffuse loss of architecture.

 Fibrous bands & regenerating nodules distort
and abstruct blood flow. (inefficient function)
 Hepatocellular insufficiency & portal
hypertension.
 Shrunken, scarred liver, ascitis,
spleenomegaly, liver failure, CNS toxicity.
Thank you and
May God be
Glorified