this presentation consists of information about alcoholic liver disease like introduction, risk factors, treatments, and many other things. so stay tuned

1. -ADITYA PANDEY
(A4513319071)
2ND SEMESTER
B.PHARM
ALCOHOLIC LIVER DISEASE

2. INTRODUCTION
Alcoholic liver disease (ALD), also called alcohol-related
liver disease (ARLD), is a term that encompasses
the liver manifestations of alcohol overconsumption,
including fatty liver, alcoholic hepatitis, and
chronic hepatitis with liver fibrosis or cirrhosis.
It is the major cause of liver disease in Western
countries. Although steatosis (fatty liver) will develop in
any individual who consumes a large quantity of
alcoholic beverages over a long period of time, this
process is transient and reversible.
 More than 90% of all heavy drinkers develop fatty liver
whilst about 25% develop the more severe alcoholic
hepatitis, and 15% cirrhosis.

3. Continued.….
Liver disease related to alcohol consumption fits into one
of three categories:
• Fatty liver
• Alcoholic hepatitis
• Cirrhosis .
Fatty liver, which occurs after acute alcohol ingestion, is
generally reversible with abstinence .
Alcoholic hepatitis is an acute form of alcohol-induced
liver injury that occurs with the consumption of a large
quantity of alcohol over a prolonged period of time; it
encompasses a spectrum of severity ranging from
asymptomatic derangement of biochemistries to
fulminant liver failure and death.

4. Continued….
Cirrhosis involves replacement of the normal hepatic
parenchyma with extensive thick bands of fibrous
tissue and regenerative nodules, which results in the
clinical manifestations of portal hypertension and
liver failure.

6. RISK FACTORS
Quantity of alcohol taken: Consumption of 60–80g per
day for 20 years or more in men, or 20g/day for women
significantly increases the risk of hepatitis and fibrosis by
7% to 47%.
Pattern of drinking: Drinking outside of meal times
increases up to 3 times the risk of alcoholic liver disease.
Sex: Women are twice as susceptible to alcohol-related
liver disease, and may develop alcoholic liver disease
with shorter durations and doses of chronic
consumption. The lesser amount of alcohol
dehydrogenase secreted in the gut, higher proportion of
body fat in women, and changes in fat absorption due to
the menstrual cycle may explain this phenomenon.

7. Continued….
 Hepatitis C infection: A concomitant hepatitis C infection
significantly accelerates the process of liver injury.
 Genetic factors: Genetic factors predispose both to
alcoholism and to alcoholic liver disease. Both monozygotic
twins are more likely to be alcoholics and to develop liver
cirrhosis than both dizygotic twins. Polymorphisms in the
enzymes involved in the metabolism of alcohol, such as
mitochondrial dysfunction, and cytokine polymorphism etc.
 Diet: Malnutrition, particularly vitamin A and E deficiencies,
can worsen alcohol-induced liver damage by preventing
regeneration of hepatocytes. This is particularly a concern as
alcoholics are usually malnourished because of a poor diet,
anorexia, and encephalopathy.

8. SYMPTOMS
• There may be symptoms. This depends on how well
the liver is working. Symptoms tend to be worse
after a period of heavy drinking.
• Early symptoms include:
 Loss of energy
 Poor appetite and weight loss
 Nausea
 Belly pain
 Small , red spider like blood vessels on the skin

9. Continued….
• As liver functions worsens , symptoms include:
 Fluid build up of the legs and abdomen
 Yellow color in the skin , mucous membrane , or eyes
 Redness on the palms of the hands
 Shrinking of testicles (in male) and breast swelling (in
female)
 Abnormal bleeding
 Confusion or problems thinking
 Pale or clay colored stools

10. PATHOPHYSIOLOGY

11. Hepatic steatosis, alcoholic hepatitis, and cirrhosis are
often considered separate, progressive
manifestations of alcoholic liver disease. However,
their features often overlap.
Hepatic steatosis (fatty liver) is the initial and most
common consequence of excessive alcohol
consumption. Hepatic steatosis is potentially
reversible. Macrovesicular fat accumulates as large
droplets of triglyceride and displaces the hepatocyte
nucleus, most markedly in perivenular hepatocytes.
The liver enlarges.

12. Alcoholic hepatitis (steatohepatitis) is a combination
of hepatic steatosis, diffuse liver inflammation, and
liver necrosis (often focal)—all in various degrees of
severity. The damaged hepatocytes are swollen with
a granular cytoplasm (balloon degeneration) or
contain fibrillar protein in the cytoplasm (Mallory or
alcoholic hyaline bodies). Severely damaged
hepatocytes become necrotic. Sinusoids and
terminal hepatic venules are narrowed. Cirrhosis may
also be present.

13. Alcoholic cirrhosis is advanced liver disease
characterized by extensive fibrosis that disrupts the
normal liver architecture. The amount of fat present
varies. Alcoholic hepatitis may coexist. The feeble
compensatory attempt at hepatic regeneration
produces relatively small nodules (micronodular
cirrhosis). As a result, the liver usually shrinks. In
time, even with abstinence, fibrosis forms broad
bands, separating liver tissue into large nodules.

14. Hepatic encephalopathy (HE): Is a central nervous
system disturbance with a wide range of
neuropsychiatric symptoms, and which is associated
with hepatic insufficiency and liver failure
Thrombocytopenia:Thrombocytopenia (generally
defined as a platelet count less than 150,000) is a
common feature of chronic liver disease found in
30% to 64% of cirrhotic patients.

15. TREATMENT
• Abstinence is essential.
• Agents to suppress inflammation(corticosteroids).
• Nutritional improvement(supplimental amino acids).
• Promoters of hepatic regeneration(insulin , glucagon).
• Modifiers of metabolism (propylthiouracil).
• Fibrosis inhibitors(colchicine).
• Correct potassium , magnesium and phosphate
deficiency.
• Transfusions of packed red cells,plasma are
necessary.