CASE STUDY ON ALCOHOLIC LIVER CIRRHOSIS

Aswini Chand ParuchuriReg no: 611171602018

IV/VI – Pharm-d

INTRODUCTION

LIVERALCOHOLIC LIVER DISEASE

CASE STUDY

LIVERLiver 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

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

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.

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

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

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.

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.

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

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

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.

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.

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.

Signs

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

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

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

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.

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

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

Patient Medical History :

Not a k/c/o : HTN\BA\DM

Past Medication History :

Not available

Social History :

Alcoholic,

Smoker,

Belongs to low economic status,

Married ,

Non-Allergic

Lab Investigations

CBC

Hb – 12g/Dl (↓)

RBC – 3.2 M/micro L (↓)

WBC – 6700 /mm3

ESR – 20mm/hr (↑)

LFTSGOT-169 microL (↑)

SGPT-162 microL (↑)

ALP – 58 microL (↑)

Albumin – 3.1 gm/dl (↓)

Globulin – 21gm

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

Drug ChartS.No

Drug Name ROA Frequency Duration10 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

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.

Assessment :

Based upon the above abnormalities,patient was assessed to be suffering from alcoholic liver cirrhosis.

Plan :

Refer to Drug Chart

Drug ChartS.No

Drug Name ROA Frequency Duration10 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(cyproheptadine HCL)

PO BD Y Y Y Y

Day 1

B.P-120/80 mm Hg RR-20 b/m PR- 80b/m CVS-S1S2

+ve

Day 2

B.P-120/80 mm Hg RR-20 b/mPR- 78b/m CVS-S1S2 +ve

Day 3

B.P-120/80 mm Hg RR-20 b/m

PR- 80b/m CVS-S1S2 +ve

Day 4

B.P-120/80 mm Hg RR-20 b/m

PR- 78b/m CVS-S1S2 +ve

Goals to be achieved

TO reduce abdominal distention.

To reduce patient weakness.

To increase appetite.

To reduce weight loss.

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

Goals achieved

Weakness reduced by day 2

Abdomen distension was reduced

Apetite was increased

SGOT ,SGPT ,ALP levels were normalised on day3 and day4.

Monitoring parameters:

RBC levels

ESR levels

SGOT levels

SGPT levels

ALP levels

BUN levels

These levels was monitored.

Problems Identified

Most common interactions experienced by people in the use of Pantoprazole Sodium, Ceftriaxone:

Anxiety

Dyspnoea

Renal failure Acute

anaemia

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.