• By :

• Mohamed adel
• Mohamed anwar
• Ahmed salah
• Abderhman raafat

• By :
• Ali gamal
• Mohamed ali
Liver diseases •
•
omar mohamed
Abderlhamn bendary
• Ahmed mansour
• Liver is a largest gland in body.
• It is located at right side of the abdomen, inferior to the
diaphragm and anterior to the stomach.
▪ Functions of the liver:
➢ Metabolism carbohydrate, protein and fat
➢ Defence against microbes.
➢ Detoxifies the blood to rid it of harmful substances such as
alcohol and drugs.
➢ Clearance of bilirubin .
➢ Stores some vitamins, iron and the sugar glucose.
Anatomy
1) Jaundice
▪ Definition:
• Jaundice is yellowish discoloration of the skin, sclera and
mucous membranes due to due to increase in serum
bilirubin above 2 mg/dl.

• Normal levels are:

➢ Direct (also called conjugated) bilirubin: up to to 0.3 mg/dL
➢ Total bilirubin: 0.3 to 1.9 mg/dL
 Mechanism of jaundice
▪ Hemolytic jaundice:
• Increased hemolysis of RBC’S causes increased hemobilirubin
• The liver can not pick all the excess hemobilirubin , so
hemobilirubin level increased in the blood (indirect bilirubin)
(water insoluble).
• Some hemobilirubin which will picked up by liver cells &
conjugated to glucuronic acid by the effect of glucoronyl
transferase enzyme forming cholebilirubin (direct bilirubin)
(water soluble) as mentioned before………..
▪ Hepatocellular jaundice:
• The liver can not pick up excess hemobilirubin & not excrete all
bile pigment (cholebilirubin)
• Direct & indirect bilirubin increased in blood.
• Urine: dark (cholebilirubin)
• Stool: pale (slightly diminished stercobilin).
▪ Post-hepatic jaundice (obstructive jaundice):
• Cholebilirubin is prevented from reaching the intestine so it
regurgirates into the blood stream
• Increased direct and total bilirubin
• Urine: dark (cholebilirubin)
• Stool: pale (bile not reach intestine)
 Types and causes of jaundice
1) Pre-hepatic jaundice (hemolytic jaundice):
• If an infection or medical condition makes the red blood
cells break down sooner than usual.
• The disruption occurs before the bilirubin has been
transported from the blood to the liver.
• Bilirubin levels rise
• Conditions which may trigger this include:
➢ Malaria
➢ Sickle cell anaemia.
➢ Thalassaemia.
➢ Hereditary spherocytosis.
➢ Haemolytic anaemia.
2) Intra-hepatic jaundice (Hepatocellular jaundice):
• If the liver is damaged (the disruption occurs inside the liver),
results in defective uptake, conjugation, and transport of
bilirubin.
• Conditions which may trigger this include:
➢ The viral hepatitis group of infections : hepatitis A, hepatitis B
and hepatitis C.
➢ Autoimmune hepatitis : a rare condition where the immune
system starts to attack the liver
➢ Alcoholic liver disease: where the liver is damaged as a result
of alcohol misuse.
➢ Obesity and non- alcoholic fatty liver disease.
➢ Cirrhosis of the liver.
➢ liver cancer.
➢ Acute drug hepatitis: halothane and paracetamol.
3) Post-hepatic jaundice (obstructive jaundice):
• Obstruction of biliary excretion of conjugated bilirubin leading
to increase in its amounts it passes back into the blood.

• This is caused by:

• Eating a high-fat diet: can raise your cholesterol levels and
increase the risk of having gallstones.
• Gall bladder or bile duct stones: obstructing the bile duct
system
• Gall bladder cancer or bile duct cancer.
• Pancreatitis : inflammation of the pancreas.
• Pancreatic cancer : an uncommon type of cancer that
develops inside the pancreas (a gland that helps with the
digestion of food)
▪ Symptoms and Signs of jaundice:
1. yellow discoloration of the skin
2. Yellow discoloration of mucous membranes
3. light-colored stools
4. Dark-colored urine
5. Abdominal pain
6. Nausea and vomiting
7. loss of appetite
8. weakness
9. Fever
10. Headache
11. Confusion
12. Itching of the skin due to retention of bile salts.
13. Swelling of the legs and abdomen.
▪ What are the complications of jaundice in adults?

• Anemia
• Chronic hepatitis
• Cancer
• Liver failure
• Kidney failure
• Hepatic encephalopathy (brain dysfunction)
• Death
INVESTIGATION
Function Pre-hepatic Hepatic Post-hepatic
test Jaundice Jaundice Jaundice
Total Normal /
Increased
bilirubin Increased
Conjugated
bilirubin Normal Increased Increased
(Direct)
Unconjugate
bilirubin Increased Increased Normal
(Indirect)

Dark ( Dark
Urine Color Normal conjugated (conjugated
bilirubin) bilirubin
 Pre-hepatic Hepatic Post-hepatic
Function test
Jaundice Jaundice Jaundice
Alkaline
phosphatase Normal Increased
levels

ALT & AST Normal Increased Increased

Splenomegaly Present Present Absent

▪ Other investigation:
• Albumin decreased in cirrhosis
• Prothrombin time prolonged
• Blood cholesterol: raised in obstructive jaundice.
• CBC : anemia with reticulocytosis (immature red blood cells) in
hemolysis .
▪ Imaging tests:
• Abdominal ultrasonography: hepatomegaly , splenomegaly,
ascites, cirrhosis, gall bladder stones , cancer head of pancreas
• Upper endoscope for cirrhosis.
• Computerised tomography (CT) scan , magnetic resonance
imaging (MRI) scan .

• Liver biopsy: If it's suspected that your liver has been damaged by
a condition such as cirrhosis or liver cancer, and recommended to
assess the condition of the liver tissue.
 Treating jaundice
▪ Pre-hepatic jaundice:
• Blood transfusions may be required to replace the red blood cells
such as genetic blood disorders (sickle cell
anaemia or thalassaemia.
▪ Intra-hepatic jaundice:
• Anti-viral medications may be used to help prevent further liver
damage.
▪ Avoiding any further exposure to the harmful substances such as
alcohol or chemicals.
▪ Post-hepatic jaundice:
• Surgery is recommended to remove stone .
• Supplementary measures in cholestasis:
➢ Diet restriction of fat
➢ Vitamin as A,D,E,K.
2) Viral hepatitis
• Hepatitis means inflammation of the liver
• Viral hepatitis is a group systemic infection affecting
the liver predominantly caused by 5 kinds of viruses as
A, B, C, D and E.
 Mode of transmission
Types of Viral Hepatitis
▪ 5 types:
A: Fecal-oral transmission
B: Sexual fluids & blood to blood
C: Blood to blood
Vaccine
D: Travels with B Preventable
E: Fecal–oral transmission
Adapted from Corneil, 2003
❑Hepatitis B virus
▪ Persons at risk:
• Medical staff (dentists, surgeons, nurses, Lab staff).
• I.V. drug absuers - Dialysis units
• Babies of infected mothers: as the virus can pass from mother
to baby (Vertical transmission).
❑Hepatitis D virus:
• It is an incomplete virus, it requires hepatitis B virus for
replication. Diagnosis depends on detection of anti-HDV
antibodies in serum.
 HAV HBV HCV HDV HEV

Genome RNA DNA RNA RNA RNA

Transmission oral Blood blood blood oral

I.P 2-8W 4-24W 4-24W 4-24W 2-8W

Acute attack mild Mild, Severe mild Mild, Severe Mild

Chronicity No May be usually May be No

Cancer liver No May be May be ? No

Prophylaxis Pre/ post Pre/ post Blood donor Pre/ post Ensure safe
exposure exposure screening, exposure drinking
immnization immnization risk immnization water
behaviour
modification
❑ Investigation: A) Liver function tests:
• ALT & AST: increased
• Serum bilirubin: increased
• Alkaline phosphatase: increased
B) Urine: albuminuria & hematuria.
C) Stool: pale with steatorrhea.
D) Viral markers:
• Hepatitis B markers : HBsAg (detection of Hepatitis B
surface antigen in serum).
• Hepatitis A markers (HAV IgM & HAV IgG): detecting
circulating antibodies as (Anti-HAV IgM) which suggests
recent infection).
❑ Complication:
1) Complete recovery
2) Relapses (recurrent).
3) Fulminant hepatic failure.
4) Prolonged cholestasis (patient condition improve but
jaundice deepens
5) Chronic hepatitis.
❑ Treatment:
• Rest: complete bed rest
• Diet: restricted protein , fat and alcohol
• Prophylactic measures:
✓ Hygiene measures
✓ HBV vaccine given to groups at high risk or travelers to
endemic areas
 Chronic hepatitis
❑ Aetiology:
• HBV and HCV
• Autoimmune hepatitis
• Alcohol
• Metabolic disorder: Wilson disease

❑Clinical pictures: see diagram

❑ Investigation
A) Liver function tests:
• ALT & AST: increased
• Serum bilirubin: increased
• prothrombin time: prolonged.
• ↓Albumin: In avanced cirrhosis
B) Viral markers: HCV AB & HBs Ag
✓ PCR can show HCV-RNA in blood (can be quantitative).
C) Abdominal U/S: Normal finding & Hepatomegaly &
Splenomegaly.
D) Liver biopsy: is diagnostic.
E) Assess autoimmune hepatitis: ANA(antinuclear antibody)
 Treatment
▪ Treatment of autoimmune hepatitis:
• Prednisolone.
• Azathioprine.
▪ Treatment of HCV: Combined therapy using
• Alpha interferon: SC once week for 12 month.
• Ribavarin: (viracure): 800-1200mg orally per day
6month
▪ Treatment of HBV : Lamuvidine 100mg oral daily for
3 year at least.
 Natural History

Chronic Cirrhosis Liver

Hepatitis 20-30% Cancer
1-4%/year

Most symptoms begin to show only when liver is more severely

damaged
 HCV is not Transmitted via..
Swimming pools
• Coughing or sneezing
• Kissing
• Mosquito or animal bites
• Sharing food
3)liver Cirrhosis
❑ What is cirrhosis?
• End stage complication of liver disease.
• Diffuse process characterized by liver necrosis and
fibrosis and conversion of normal liver structure into
abnormal regenerating nodules.
• Morphological:
1) Micro nodular: small nodules of the same size.
2) Macro nodular: big nodules of variable size.
3) Mixed.
▪ Causes of liver cirrhosis:

1) Fatty liver associated with obesity and diabetes.

2) Chronic viral infections of the liver (hepatitis types B, C).

3) Blockage of the bile duct, which carries bile formed in the

liver to the intestines, where it helps in the digestion of
fats.

4) Repeated attack of heart failure .

5) Metabolic disease: inherited diseases such as:
– Cystic fibrosis.

– Glycogen storage diseases, in which the body is unable to

process glycogen ( form of sugar) and converted it to glucose
(source of energy for the body). The glycogen or one of its
related starches can build up in the liver, causing problems.

– Hemochromatosis: excessive iron is absorbed and deposited

into the liver and other organs.

– Wilson's disease: abnormal storage of copper in the liver

 Clinical Manifestations of liver cirrhosis
A) Early Manifestations
▪ GIT disturbances:
• Abdominal pain.
• Anorexia , nausea and vomiting.
• Diarrhea.
• Weight loss
• Fatigue.
• Enlarged liver or spleen
B) Late Manifestations
▪ Hepatocellular failure: Hepatic encephalitis / hepatic coma.
▪ Portal hypertension
▪ Hepatocellular carcinoma.
▪ Shrunken liver & splenomegaly.
 ARCHITECTURAL LIVER DISRUPTION IS THE MAIN MECHANISM THAT LEADS TO AN INCREASED INTRAHEPATIC RESISTANCE

Cirrhotic Liver
Portal
systemic
collaterals

Distorted
sinusoidal
architecture
leads to
increased
resistance
Portal
vein

Splenomegaly
▪ Diagnosis:
1) The gold standard for diagnosis of cirrhosis is a liver biopsy.
2) Laboratory findings:
• Aminotransferases : AST and ALT are moderately elevated.
• Alkaline phosphatase: usually slightly elevated.
• Albumin : decrease
• Bilirubin : may elevate as cirrhosis progresses.
• Coagulation defects: the liver produces most of the
coagulation factors and thus coagulopathy correlates with
worsening liver disease.
• CBC: Anemia, Leukopenia and thrombocytopenia due to
splenomegaly
3) Radiological investigation: Ultrasound is routinely used in the
evaluation of cirrhosis and screen for hepatocellular carcinoma
 Treatment and Prevention
▪ Prevention:
• Stop drinking alcohol (or don’t start at all)
• Limit salt in the diet
• Eat a nutritious diet
• Get vaccinated for hepatitis A and B.
• Stop alcohol drinking.
▪Treatment:
▪ Antibiotics: for infections as cefotaxime and amoxicillin-
clavulanic acid.

▪ Laxatives, such as lactulose, decrease risk of constipation;

their role in preventing encephalopathy .

▪Treatment for hepatitis: such as interferon for viral

hepatitis and corticosteroids for autoimmune hepatitis.

▪ Diuretics: to remove extra fluids from the body, as

furosemide(lasix)

▪Liver transplant