1. CIRRHOSIS Ahmed Salam Lectures Medical Student “TSU”

2. Definition: G.S.M MEDICAL LECTURES/ Cirrhosis
AHMED SALAM
MD STUDENT
Definition:
Cirrhosis is a condition in which the liver does not function properly due to long-term damage . This damage is characterized by the replacement of normal liver tissue by scar tissue.
Typically, the disease develops slowly over months or years. Early on, there are often no symptoms, As the disease worsens.

3. Causes: G.S.M MEDICAL LECTURES/ Cirrhosis
AHMED SALAM
MD STUDENT
Causes:
Alcoholic liver disease (ALD). Alcoholic cirrhosis develops for 10–20% of individuals who drink heavily for a decade or more. Alcohol seems to injure the liver by blocking the normal metabolism of protein, fats, and carbohydrates.
Non-alcoholic steatohepatitis (NASH). In NASH, fat builds up in the liver and eventually causes scar tissue. This type of hepatitis appears to be associated with obesity (40% of NASH patients) diabetes.
Chronic hepatitis C , hepatitis B virus .
Primary biliary cholangitis (also known as primary biliary cirrhosis). The bile ducts become damaged by an autoimmune process.

4. G.S.M MEDICAL LECTURES/ Cirrhosis
AHMED SALAM
MD STUDENT
Autoimmune hepatitis: This disease is caused by an attack of the liver by lymphocytes .
Hereditary hemochromatosis: Usually presents with a family history of cirrhosis .
Glycogen storage disease type IV
Cystic fibrosis
Hepatotoxic drugs or toxins

5. Symptoms: G.S.M MEDICAL LECTURES/ Cirrhosis AHMED SALAM MD STUDENT
Cirrhosis often has no signs or symptoms until liver damage is extensive. When signs and symptoms do occur, they may include:
Fatigue
Bleeding easily
Bruising easily
Itchy skin
Yellow discoloration in the skin and eyes (jaundice)
Fluid accumulation in your abdomen (ascites)
Loss of appetite
Nausea
Swelling in your legs
Weight loss
Confusion, drowsiness and slurred speech (hepatic encephalopathy)
Spiderlike blood vessels on your skin
Redness in the palms of the hands

6. Portal hypertension: G.S.M MEDICAL LECTURES/ Cirrhosis
AHMED SALAM
MD STUDENT
Portal hypertension:
Liver cirrhosis increases resistance to blood flow and leads to higher pressure in the portal venous system, resulting in portal hypertension. Effects of portal hypertension include:
Splenomegaly (increase in size of the spleen) is found in 35% to 50% of patients.
Esophageal varices result from collateral portal blood flow through vessels in the stomach and esophagus (a process called portacaval anastomosis). When these blood vessels become enlarged, they are called varices and are more likely to rupture .  Variceal rupture often leads to severe bleeding, which can be fatal.
Caput medusa are dilated periumbilical collateral veins due to portal hypertension. Blood from the portal venous system may be shunted through the periumbilical veins and ultimately to the abdominal wall veins

7. CIRRHOSIS APPERANCE G.S.M MEDICAL LECTURES/ Cirrhosis AHMED SALAM
MD STUDENT
CIRRHOSIS APPERANCE

8. CIRRHOSIS APPERANCE G.S.M MEDICAL LECTURES/ Cirrhosis AHMED SALAM
MD STUDENT
CIRRHOSIS APPERANCE

9. Pathophysiology: G.S.M MEDICAL LECTURES/ Cirrhosis
AHMED SALAM
MD STUDENT
Pathophysiology:
Cirrhosis is often preceded by hepatitis and fatty liver (steatosis), independent of the cause. If the cause is removed at this stage, the changes are fully reversible.
The pathological hallmark of cirrhosis is the development of scar tissue that replaces normal parenchyma. This scar tissue blocks the portal flow of blood through the organ, raising the blood pressure and disturbing normal function. Recent research shows the pivotal role of the stellate cell, a cell type that normally stores vitamin A, in the development of cirrhosis. Damage to the hepatic parenchyma (due to inflammation) leads to activation of stellate cells, which increases fibrosis (through production of myofibroblasts) and obstructs hepatic blood flow. In addition, stellate cells secrete TGF-β1, which leads to a fibrotic response and proliferation of connective tissue. Furthermore, it secretes TIMP 1 and 2, naturally occurring inhibitors of matrix metalloproteinases, which prevents them from breaking down the fibrotic material in the extracellular matrix.

10. G.S.M MEDICAL LECTURES/ Cirrhosis
AHMED SALAM
MD STUDENT
As this cascade of processes continues, fibrous tissue bands (septa) separate hepatocyte nodules, which eventually replace the entire liver architecture, leading to decreased blood flow throughout. The spleen becomes congested, which leads to hypersplenism and the spleen's retention of platelets, which are needed for normal blood clotting. Portal hypertension is responsible for the most severe complications of cirrhosis.

11. Diagnosis: G.S.M MEDICAL LECTURES/ Cirrhosis Thrombocytopenia
AHMED SALAM
MD STUDENT
Diagnosis:
Thrombocytopenia
Aminotransferases – AST and ALT are moderately elevated.
Bilirubin – Levels normal when compensated but may elevate as cirrhosis progresses.
Albumin – levels fall as the synthetic function of the liver declines with worsening cirrhosis

12. G.S.M MEDICAL LECTURES/ Cirrhosis
AHMED SALAM
MD STUDENT
Prothrombin time – increases, since the liver synthesizes clotting factors.
Leukopenia and neutropenia – due to splenomegaly with splenic margination.
Coagulation defects
Imaging:
Ultrasound is routinely used in the evaluation of cirrhosis.
Endoscopy:
Gastroscopy (endoscopic examination of the esophagus, stomach, and duodenum) is performed in patients with established cirrhosis to exclude the possibility of esophageal varices.

13. G.S.M MEDICAL LECTURES/ Cirrhosis
AHMED SALAM
MD STUDENT
 liver biopsy:
Accumlation of connective tissue(fibrosis) and show yelleow color due to fat( steatosis)

14. Complications: G.S.M MEDICAL LECTURES/ Cirrhosis
AHMED SALAM
MD STUDENT
Complications:
High blood pressure in the veins that supply the liver (portal hypertension).
Swelling in the legs and abdomen.
Enlargement of the spleen (splenomegaly).
Bleeding.
Other complications:
Infections.
Malnutrition.
Buildup of toxins in the brain (hepatic encephalopathy).

15. Do not drink alcohol if you have cirrhosis. Eat a healthy diet.
G.S.M MEDICAL LECTURES/ Cirrhosis
AHMED SALAM
MD STUDENT
Jaundice.
Bone disease.
Increased risk of liver cancer.
Acute-on-chronic liver failure.
Prevention:
Do not drink alcohol if you have cirrhosis.
Eat a healthy diet.
Maintain a healthy weight.

16. Treatment: G.S.M MEDICAL LECTURES/ Cirrhosis
AHMED SALAM
MD STUDENT
Treatment:
Treatment for cirrhosis depends on the cause and extent of your liver damage. The goals of treatment are to slow the progression of scar tissue in the liver and to prevent or treat symptoms and complications of cirrhosis. You may need to be hospitalized if you have severe liver damage.
Treatment for the underlying cause of cirrhosis:
Treatment for alcohol dependency
Weight loss.
Medications to control hepatitis.

17. G.S.M MEDICAL LECTURES/ Cirrhosis
AHMED SALAM
MD STUDENT
Treatment for complications of cirrhosis:
Excess fluid in your body.
Portal hypertension. 
Infections.
Hepatic encephalopathy.

18. G.S.M MEDICAL LECTURES/ Cirrhosis
AHMED SALAM
MD STUDENT
Liver transplantation:
In advanced cases of cirrhosis, when the liver ceases to function, a liver transplant may be the only treatment option. People usually need to consider this option when they develop symptoms from cirrhosis, such as jaundice, significant fluid retention (ascites), bleeding varices, hepatic encephalopathy, kidney dysfunction, or liver cancer. A liver transplant replaces your liver with a healthy liver from a deceased donor or with part of a liver from a living donor. Cirrhosis is the most common reason for a liver transplant.