1. CASE STUDY ON
ALCOHOLIC LIVER
CIRRHOSIS

2. Aswini Chand Paruchuri
Reg no: 611171602018
IV/VI – Pharm-d

3. INTRODUCTION
LIVER
ALCOHOLIC LIVER
DISEASE
CASE STUDY

4. LIVERLiver is one of the largest organ
in our body.,weighs upto 1500
grams in adults.
With the exception of the
brain, the liver is the most
complex organ in the body
 And it has morethan 500
different vital functions in our
body.
Some of the more well-known
functions include the following:
Production of bile, which helps
carry away waste and break down
fats in the small intestine during
digestion

5.  Production of certain proteins for blood plasma
 Production of cholesterol and special proteins to help carry
fats through the body
 Conversion of excess glucose into glycogen for storage
(glycogen can later be converted back to glucose for energy)
 Regulation of blood levels of amino acids, which form the
building blocks of proteins
 Processing of haemoglobin for use of its iron content (the
liver stores iron)
 Conversion of poisonous ammonia to urea (urea is an end
product of protein metabolism and is excreted in the urine)
 Regulating blood clotting
 Resisting infections by producing immune factors and
removing bacteria from the bloodstream

6.  And yet, when your liver is damaged, you generally won’t
know about it – until things get serious.
 Liver disease is defined as acute or chronic liver on the basis
of whether the history of disease is lessthan/greater than
6months, respectively.
 The hepatocyte is the functioning unit of the liver.
 Liver is the only organ which is readily regenerate.
 Viral infections and paracetamol overdose are the leading
causes of acute liver disease, but a significant number of
patients have no defined aetiology.
 Alcohol abuse and chronic viral hepatitis(B and C) are the
major causes of chronic liver disease.

7. ALCOHOLIC LIVER
CIRRHOSIS
 Alcoholic liver disease is a term that encompasses the
hepatic manifestations of alcohol overconsumption,
including fatty liver, alcoholic hepatitis, and chronic
hepatitis with hepatic fibrosis or cirrhosis.
 It is the major cause of liver disease in Western
countries.
 Term was 1st coined by Laennec in 1826
 Primary histologic features:
1. Marked fibrosis
2. Destruction of vascular & biliary elements
3. Regeneration
4. Nodule formation

9. About Alcohol :
 Alcohol beverage is a drink that contains ethanol
 In the bloodstream, from the stomach, alcohol is absorbed between
5-10 minutes
 Fact : females absorb alcohol faster than males because their bodies
contain less water
 Problem With Alcohol Beverages:
 Alcohol beverages are being consumed everyday, but consuming too
much can bring problems
 An example would be alcoholic liver disease(cirrhosis),heart
disease, cancer and strokes
 Cause addiction

10. Stages Of ALD :
There are three main stages of alcoholic liver disease, although
there is often an overlap between each stage. The three stages
are explained below.
Alcoholic fatty liver disease
 Alcoholic fatty liver disease is the first stage of alcoholic liver disease.
 Drinking a large amount of alcohol, even for only a few days, can lead to a
build-up of fatty acids in the liver.
 Fatty liver disease rarely causes any symptoms but it is an important
warning sign that you are drinking at a level that is harmful to your health.
 Fatty liver disease is reversible. If you stop drinking alcohol for two weeks,
your liver should return to normal.
Alcoholic hepatitis
 Alcoholic hepatitis (not related to infectious hepatitis) is the second, more
serious stage of alcoholic liver disease.

11.  Prolonged alcohol misuse over many years can cause the
tissues of the liver to become inflamed. This is known as
alcoholic hepatitis. Less commonly, alcoholic hepatitis can
occur if you drink a large amount of alcohol in a short period
of time (binge drinking).
 Alcoholic hepatitis is usually reversible, although you may
need to stop drinking alcohol for several months or years.
Cirrhosis
 Cirrhosis is the final stage of alcoholic liver disease.
Cirrhosis happens when prolonged inflammation causes
scarring of the liver and loss of function. Loss of liver function
can be life threatening.
 The damage caused by cirrhosis is not reversible. In mild to
moderate cases, stopping drinking alcohol immediately should
prevent further damage and lead to the gradual recovery of
liver function. In more severe cases, a liver transplant may be
required.

12. Epidemiology :
 In india, liver cirrhosis is one of the leading cause of death .
 12th leading cause of death in the united states
 On average about 27,000 deaths per year
 40% cases asymptomatic
 Additional 10,000 deaths due to liver cancer secondary to cirrhosis
 Overall, alcoholic liver disease accounts for well over a third (37%)
of liver disease deaths. And figures show victims of liver disease are
getting younger – more than 1 in 10 of deaths of people in their 40s
are from liver disease, most of them from alcoholic liver disease

13. Aetiology of liver cirrhosis
 Hepatitis C, fatty liver, and alcohol abuse are the most common causes
of cirrhosis of the liver., but anything that damages the liver can cause
cirrhosis, including:
 Fatty liver associated with obesity and diabetes
 Chronic viral infections of the liver (hepatitis types B, C, and D;
Hepatitis D is extremely rare)
 Blockage of the bile duct, which carries bile formed in the liver to
the intestines, where it helps in the digestion of fats; in babies, this can
be caused by biliary atresia in which bile ducts are absent or damaged,
causing bile to back up in the liver. In adults, bile ducts may become
inflamed, blocked, or scarred, due to another liver disease called
primary biliary cirrhosis.
 Repeated bouts of heart failure with fluid backing up into the liver

14.  Certain inherited diseases such as:
 Cystic fibrosis
 Glycogen storage diseases, in which the body is unable to
process glycogen, a form of sugar that is converted to glucose
and serves as a source of energy for the body
 Alpha 1 antitrypsin deficiency, an absence of a specific enzyme
in the liver
 Diseases caused by abnormal liver function, such as
hemochromatosis, a condition in which excessive iron is
absorbed and deposited into the liver and other organs,
and Wilson's disease, caused by the abnormal storage of copper
in the liver
 Although less likely, other causes of cirrhosis include reactions
to prescription drugs, prolonged exposure to environmental toxins,
or parasitic infections.

15. Risk Factors :
 The risk factors presently known are:
 Quantity of alcohol taken: consumption of 75–100 ml/day for 20 years or
more in men, or 25 ml/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 2.7
times the risk of alcoholic liver disease.
 Gender: females 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
 Genetic factors: genetic factors predispose both to alcoholism and to
alcoholic liver disease. Monozygotic twins are more likely to be alcoholics
and to develop liver cirrhosis than dizygotic twins. Due to polymorphisms in
the enzymes involved in the metabolism of alcohol.

16.  Iron overload (Hemochromatosis)
 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.

17. Signs
 Bleeding tendencies : deficiency of clotting factors
 Hyperpigmentation
 Hyperdynamic circulatory state
 Edema
 Hernia
 Testicular atrophy
 Delirium
 Constructional apraxia
 Flapping tremors
 Inversion of sleep rhythm

18. Symptoms
Symptoms vary based on how bad the disease is. You may not have
symptoms in the early stages. Symptoms tend to be worse after a
period of heavy drinking.
Digestive symptoms include:
 Pain and swelling in the abdomen
 Decreased appetite and weight loss
 Nausea and vomiting
 Fatigue
 Dry mouth and increased thirst

19. Skin problems such as:
 Yellow color in the skin, mucus membranes, or eyes
(jaundice)
 Small, red spider-like veins on the skin
 Very dark or pale skin
 Redness on the feet or hands
 Itching
Brain and nervous system symptoms include:
 Problems with thinking, memory, and mood
 Fainting and lightheadedness
 Numbness in legs and feet

20. Diagnostic tests
 Complete blood count (CBC)
 Liver biopsy
 Liver function tests
 Abdominal CT scan
 Blood tests for other causes of liver disease
 Ultrasound of the abdomen
And patient social history plays a vital role to
determine the disease.

21. Treatment
 The first treatment of alcohol-induced liver disease is
cessation of alcohol consumption. This is the only way to
reverse liver damage or prevent liver injury from worsening.
Without treatment, most patients with alcohol-induced liver
damage will develop liver cirrhosis
 Counseling may be necessary to break the alcohol addiction.
 Vitamins, especially B-complex and folic acid, can help
reverse malnutrition.
 Diet
 Liver transplantation

22. Case Study
 A 70 years old male patient was admitted in the hospital on
10/09/13.
Chief Complaints :
C/o: abdominal distention since 4days
weakness since 15days
decreased appetite since 15days
weight loss since 15days
On Examination :
 Patient is conscious and oriented
 No cyanosis/icterus/clubbing
 B.P-120/80 mm Hg RR-20 b/m
 PR- 80b/m CVS-S1S2 +ve

23. Patient Medical History :
Not a k/c/o : HTNBADM
Past Medication History :
Not available
Social History :
Alcoholic,
Smoker,
Belongs to low economic status,
Married ,
Non-Allergic

24. Lab Investigations
 CBC
Hb – 12g/Dl (↓)
RBC – 3.2 M/micro L (↓)
WBC – 6700 /mm3
ESR – 20mm/hr (↑)
 LFT
SGOT-169 microL (↑)
SGPT-162 microL (↑)
ALP – 58 microL (↑)
Albumin – 3.1 gm/dl (↓)
Globulin – 21gm

25.  RFT
BUN-12mg/dL
Sr.Cr-0.7mg/dL
Special investigations
Hbs Ag : -ve (impression)
USG Abdomen : coarse texture
Gall Bladder : wall thickening
Spleen : enlarged mass
Diagnosis :
Alcoholic liver cirrhosis

26. Drug Chart
S.N
o
Drug Name ROA Frequency Duration
10 11 12
13
1 Inj.Monocef (1g)
(cephalosporin–antibiotic
)
IV BD Y Y -
-
2 T.Udiliv(600mg)
(ursodeoxycholic acid)
po TDS - Y Y -
3 Inj.pantoprazole(40mg)
(proton pump inhibhitors)
IV BD Y Y y
Y
4 Tab.Hepameez(10mg)
(L-ornithine+ L-aspartate)
PO OD Y Y Y
Y
5 Inj.Metronidazole(160mg)
(anti-helmenthic)
IV OD _ Y _ _
6 Syp.duphalac (2tsp)
Biscodyl - laxative
PO SOS Y Y Y Y
7 SYP. Cypon
(cypoheptadine HCL)
PO BD Y Y Y Y

27. SOAP NOTES
 SUBJECTIVE :
A 7OYrs old male patient was admitted in the
hospital on 10/9/13, with c/o: abdominal distension since
4days, weakness since 15days, decreased appetite since
15days, weight loss since 15days,past medical & medication
history nil, Social history -Alcoholic, Smoker, Belongs to
low economic status, Married , Non-Allergic.
 OBJECTIVE :
patient was to be found, abnormalities of LFT,
CBC& social history &US Abdomen : coarse texture,
Gall Bladder : wall thickening, Spleen : enlarged mass.

28.  Assessment :
Based upon the above abnormalities,patient
was assessed to be suffering from alcoholic liver
cirrhosis.
 Plan :
Refer to Drug Chart

29. Drug Chart
S.N
o
Drug Name ROA Frequency Duration
10 11 12
13
1 Inj.Monocef (1g)
(cephalosporin–antibiotic
)
IV BD Y Y -
-
2 T.Udiliv(600mg)
(ursodeoxycholic acid)
po TDS - Y Y -
3 Inj.pantoprazole(40mg)
(proton pump inhibhitors)
IV BD Y Y y
Y
4 Tab.Hepameez(10mg)
(L-ornbthine+ L-aspartate)
PO OD Y Y Y
Y
5 Inj.Metronidazole(160mg)
(anti-helmenthic)
IV OD _ Y _ _
6 Syp.duphalac (2tsp)
Biscodyl - laxative
PO SOS Y Y Y Y
7 Syp.cypon(cyproheptadi
ne HCL)
PO BD Y Y Y Y

30. Day 1
 B.P-120/80 mm Hg RR-20 b/m
 PR- 80b/m CVS-S1S2
+ve

31. Day 2
B.P-120/80 mm Hg RR-20 b/m
PR- 78b/m CVS-S1S2 +ve

32. Day 3
 B.P-120/80 mm Hg RR-20 b/m
 PR- 80b/m CVS-S1S2 +ve

33. Day 4
 B.P-120/80 mm Hg RR-20 b/m
 PR- 78b/m CVS-S1S2 +ve

34. Goals to be achieved
 TO reduce abdominal distention.
 To reduce patient weakness.
 To increase appetite.
 To reduce weight loss.

35. Treatment options
 Vit-k
 Hepato protective agents:
silymarin
 anti viral drugs:
Interferons, such as interferon alfa-2b and pegylated interferon alfa-2a
Nucleoside reverse transcriptase inhibitors (NRTIs) such as adefovir, entecavir, lamivudine,
telbivudine, and tenofovir
 Corticosteroids:
Hydrocortisone , methylprednisolone , dexamethasone
 Aminoglycoside:
Amikacin,
 Anti amoebic:
Metrogyl
 Other drugs:
ceftriaxone , udiliv , pantoprazole , Hepameez ,syp cypon , syp duphalac

36. Goals achieved
 Weakness reduced by day 2
 Abdomen distension was reduced
 Apetite was increased
 SGOT ,SGPT ,ALP levels were normalised on day3
and day4.

37. Monitoring parameters:
 RBC levels
 ESR levels
 SGOT levels
 SGPT levels
 ALP levels
 BUN levels
 These levels was monitored.

38. Problems Identified
 Most common interactions experienced by
people in the use of Pantoprazole Sodium,
Ceftriaxone:
 Anxiety
 Dyspnoea
 Renal failure Acute
 anaemia

39. Lifestyle modifications:
 Lifestyle changes are key to treating ALC. The most
important thing to do is to stop all alcohol intake. This
should be done under the supervision of a physician
to prevent complications of withdrawal .
 Smoking speeds up liver damage, so quitting smoking
is important.
 Maintaining a normal weight is also helpful. Obesity
can cause non-alcoholic fatty liver, which is similar to
alcoholic hepatitis.
 Eating a balanced diet and taking certain vitamins
and minerals can correct nutritional deficiencies
caused by alcohol abuse.