ALCOHOLIC LIVER DISEASE

INTRODUCTION
Definition and causes

Liver disease related to alcohol consumption fits into one of three categories—fatty liver,
alcoholic hepatitis, or cirrhosis. Fatty liver, which occurs after acute alcohol ingestion, is
generally reversible with abstinence and is not believed to predispose to any chronic form of
liver disease if abstinence or moderation is maintained. 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. 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.
Table 1: Forms of Alcoholic Liver Disease

Parameter Fatty Liver Alcoholic Hepatitis Cirrhosis

Histologic specificity for alcoholic cause No Yes No
Prognosis Excellent Variable Guarded
Reversible Yes Variable Generally, no

Prevalence and risk factors

The prevalence of alcoholic liver disease is influenced by many factors, including genetic factors
(e.g., predilection to alcohol abuse, gender) and environmental factors (e.g., availability of
alcohol, social acceptability of alcohol use, concomitant hepatotoxic insults), and is therefore
difficult to define. In general, however, the risk of liver disease increases with the quantity and
duration of alcohol intake. Although necessary, excessive alcohol use is not sufficient to promote
alcoholic liver disease. Only one in five heavy drinkers will develop alcoholic hepatitis, and one
in four will develop cirrhosis.

Different alcoholic beverages contain varying quantities of alcohol . Although fatty liver is a
universal finding among heavy drinkers, up to 40% of those with modest alcohol intake (up to 10
g per day) will also exhibit fatty changes. Based on an autopsy series of men, a threshold daily
alcohol intake of 40 g was necessary to produce pathologic changes of alcoholic hepatitis.
Consumption of more than 80 g per day was associated with an increase in the severity of
alcoholic hepatitis, but not in the overall prevalence. There is a clear dose-dependent relation
between alcohol intake and the incidence of alcoholic cirrhosis. A daily intake of more than 60 g
of alcohol in men and 20 g in women significantly increases the risk of cirrhosis. In addition,
steady daily drinking, as compared with binge drinking, appears to be more harmful.
Table 2: Alcohol Content of Some Common Beverages

Drink Amount (oz) Absolute Alcohol (g)

Beer 12 12
Wine 5 12
Liquor (80 proof) 1.5 12

Pathophysiology and natural history

The liver and, to a lesser extent, the gastrointestinal tract, are the main sites of alcohol
metabolism. Within the liver, there are two main pathways of alcohol metabolism, alcohol
dehydrogenase and cytochrome P-450 2E1. Alcohol dehydrogenase is a hepatocyte cytosolic
enzyme that converts alcohol to acetaldehyde. Acetaldehyde subsequently is metabolized to
 ALCOHOLIC LIVER DISEASE

acetate via the mitochondrial enzyme, acetaldehyde dehydrogenase. Cytochrome P-450 2E1 also
converts alcohol to acetaldehyde.

Liver damage occurs through several interrelated pathways. Alcohol dehydrogenase and
acetaldehyde dehydrogenase cause the reduction of nicotinamide adenine dinucleotide (NAD) to
NADH (reduced form of NAD). The altered ratio of NAD/NADH promotes fatty liver through
the inhibition of gluconeogenesis and fatty acid oxidation. Cytochrome P-450 2E1, which is
upregulated in chronic alcohol use, generates free radicals through the oxidation of nicotinamide
adenine dinucleotide phosphate (reduced; NADPH) to NADP. Chronic alcohol exposure also
activates hepatic macrophages, which then produce tumor necrosis factor a (TNF-α). TNF-α
induces mitochondria to increase the production of reactive oxygen species. This oxidative stress
promotes hepatocyte necrosis and apoptosis, which is exaggerated in the alcoholic individual
who is deficient in antioxidants such as glutathione and vitamin E. Free radicals initiate lipid
peroxidation, which causes inflammation and fibrosis. Inflammation is also incited by
acetaldehyde that, when bound covalently to cellular proteins, forms adducts that are antigenic.
Histologically, the earliest changes in alcoholic hepatitis are located predominantly around the
central vein. Alcohol is known to cause an exaggerated gradient of hypoxia from the portal vein
to the central vein, suggesting that the hypoxia induced by chronic alcohol use may contribute to
hepatic damage.

With abstinence, morphologic changes of the fatty liver usually revert to normal. Although the
short-term prognosis in patients with alcoholic steatosis is excellent, with longer follow-up it has
been found that cirrhosis develops more commonly in alcohol abusers with fatty liver changes
than in those with normal liver histology. Morphologic features predictive of progression to
fibrosis, cirrhosis, or both include severe steatosis, giant mitochondria, and the presence of
mixed macrovesicular-microvesicular steatosis.

Historically,the 30-day mortality rate in patients with alcoholic hepatitis ranges from 0% to 50%.
Clinical and laboratory features are powerful prognostic indicators for short-term mortality.
Hepatic encephalopathy, derangement in renal function, hyperbilirubinemia, and prolonged
prothrombin time are seen more frequently in patients who succumb to their illness than in those
who survive. Both the discriminant function and the model for end-stage liver disease (MELD)
score can be used to predict short-term mortality in patients with alcoholic hepatitis. The MELD
score is calculated based on a patient's prothrombin time, serum creatinine, and bilirubin; a
calculator can be found on the United Network for Organ Sharing website. Long-term survival in
patients with alcoholic hepatitis who discontinue alcohol is significantly better than in those who
continue to drink, although it remains considerably below that of an age-matched population.
Three-year survival approaches 90% in abstainers, whereas it is less than 70% in active drinkers.

Cirrhosis has historically been considered to be an irreversible outcome of severe and prolonged
liver damage. However, studies involving patients with liver disease from many distinct causes
have shown convincingly that fibrosis and cirrhosis may actually have a component of
reversibility. For those patients with decompensated alcoholic cirrhosis who undergo
transplantation, survival is comparable with that of patients with other causes of liver disease
(approximately a 70% 5-year patient survival rate).

Signs and symptoms

Patients with fatty liver are typically either asymptomatic or present with nonspecific symptoms
that do not suggest acute liver disease. Supporting features on physical examination include an
enlarged and smooth, but rarely tender, liver. In the absence of a super-imposed hepatic process,
stigmata of chronic liver disease such as spider angiomas, ascites, or asterixis should be absent.

Alcoholic hepatitis is a syndrome with a spectrum of severity, and therefore manifesting

symptoms vary. Symptoms may be nonspecific and mild and include anorexia and weight loss,
abdominal pain and distention, or nausea and vomiting. Alternatively, more severe and specific
symptoms may include encephalopathy and hepatic failure. Physical findings include
 ALCOHOLIC LIVER DISEASE

hepatomegaly, jaundice, ascites, spider angiomas, fever, and encephalopathy. When alcoholic
hepatitis is more severe, the differential diagnosis includes autoimmune hepatitis, acute viral
hepatitis, acute Budd-Chiari syndrome, severe drug-induced liver injury, and an acute
manifestation of Wilson's disease.

Established alcoholic cirrhosis may manifest with decompensation without a preceding history of
fatty liver, alcoholic hepatitis, or any other alcohol-related diagnosis. Alternatively, alcoholic
cirrhosis may be diagnosed concurrently with acute alcoholic hepatitis. The symptoms and signs
of alcoholic cirrhosis do not help differentiate it from other causes of cirrhosis. Patients may
present with jaundice, pruritus, abnormal laboratory findings (e.g., thrombocytopenia,
hypoalbuminemia, coagulopathy), or complications of portal hypertension, such as variceal
bleeding, ascites, or hepatic encephalopathy.

Fatty liver is usually diagnosed in the asymptomatic patient who is undergoing evaluation for
abnormal liver function; results include usually mildly elevated aminotransferase levels lower
than twice the upper limit of normal. Laboratory tests are not diagnostic of fatty liver.
Characteristic ultrasonographic findings include a hyperechoic liver with or without
hepatomegaly. Liver biopsy is rarely needed to diagnose fatty liver in the appropriate clinical
setting, but may be useful in excluding steatohepatitis or fibrosis. Typical histologic findings of
fatty liver include fat accumulation in hepatocytes that is often macrovesicular, but may
occasionally be microvesicular The centrilobular region of the hepatic acinus is most commonly
affected. In severe fatty liver, however, fat is distributed throughout the acinus. Fatty liver is not
specific to alcohol ingestion; it is associated with obesity, insulin resistance, hyperlipidemia,
malnutrition, and various medications. Attribution of fatty liver to alcohol use therefore requires
a detailed and accurate patient history.

The diagnosis of alcoholic hepatitis is based on a thorough history, physical examination, and
review of laboratory tests. Characteristically, the aspartate aminotransferase–to–alanine
aminotransferase ratio (AST/ALT) is approximately 2:1, and the absolute value of the
aminotransferase levels does not exceed 300 U/L unless a superimposed hepatic insult exists,
such as acetaminophen toxicity. Other common and nonspecific laboratory abnormalities include
anemia and leukocytosis. Liver biopsy is occasionally necessary to secure the diagnosis. The
classic histologic features of alcoholic hepatitis include inflammation and necrosis, which are
most prominent in the centrilobular region of the hepatic acinus. Hepatocytes are classically
ballooned, which causes compression of the sinusoid and reversible portal hypertension. The
inflammatory cell infiltrate, located primarily in the sinusoids and close to necrotic hepatocytes,
consists of polymorphonuclear cells and mononuclear cells. In addition to inflammation and
necrosis, many patients with alcoholic hepatitis will have fatty infiltration and Mallory bodies,
which are intracellular perinuclear aggregations of intermediate filaments that are eosinophilic
on hematoxylin-eosin staining. Neither fatty infiltration nor Mallory bodies are specific for
alcoholic hepatitis or necessary for the diagnosis.

The diagnosis of alcoholic cirrhosis rests on finding the classic signs and symptoms of end-stage
liver disease in a patient with a history of significant alcohol intake. Patients tend to underreport
their alcohol consumption, and discussions with family members and close friends may provide a
more accurate estimation of alcohol intake. Patients may present with any or all complications of
portal hypertension, including ascites, variceal bleeding, and hepatic encephalopathy. The
histology of end-stage alcoholic cirrhosis, in the absence of acute alcoholic hepatitis, resembles
that of advanced liver disease from many other causes, without any distinct pathologic findings

The overall clinical diagnosis of alcoholic liver disease, using a combination of physical
findings, laboratory values, and clinical acumen, is very accurate. However, liver biopsy can be
justified in select cases, especially when the diagnosis is in question. In addition to confirming
the diagnosis, liver biopsy is also useful for ruling out other unsuspected causes of liver disease,
better characterizing the extent of the damage, providing prognosis, and guiding therapeutic
 ALCOHOLIC LIVER DISEASE

decision making. As emphasized in the recent practice guidelines for alcoholic liver disease from
the American College of Gastroenterology), liver biopsy is a relatively safe procedure, with
morbidity lower than 0.6% and mortality lower than 0.03%. With a typical presentation, liver
biopsy is not mandatory to diagnose alcoholic liver disease.

DEMOGRAPHIC DATA
Patient’s name: Patient Girlush

Address: N/A

Sex: Female

Age: 48 y.o.

Civil Status: Married

Religion: Roman Catholic

Nationality: Filipino

Date of admission: March 6, 2010

Chief complaint: Vomiting and fever

Final Diagnosis: Alcoholic liver disease secondary to AGE with some dehydration

NURSING HISTORY
PRESENT HEALTH HISTORY

March 2, 2010 that was Monday at around 8:00 in the morning when patient Girlush experienced
episode of nausea and vomiting until it persist up to five days and it was already accompanied by a high
degree of fever that’s why her husband decided to brought her at the hospital.

PAST HEALTH HISTORY

According to the client she completed her immunization during childhood. She usually
experienced cough, colds and fever and her husband usually brought a solmux for her cough, neozep for
her colds, and paracetamol for her fever.

At the age of 43 according to the client she was hospitalized at Cagayan Valley Medical Hospital
due to of convulsion.

FAMILY HISTORY

According to the S.O. there is no hereditary disease can be attributed from the patient’s
father’s side, but the patient’s mother had a family health history of hypertension, Heart disease,
and Diabetes mellitus.

SOCIAL HISTORY

According to the patient’s son his mother usually watches T.V and sometimes she went to her
neighbors with same age just to have mingled with them and sometimes she played with her grandson and
granddaughter.
 ALCOHOLIC LIVER DISEASE

GORDON’S FUNCTIONAL HEALTH PATTERN

1. Health perception and health management

>Before hospitalization
Health for her is important but she has no sufficient knowledge on how to take
care of herself.
>After hospitalization
The S.O. now views how important health management is.

2. Nutritional-metabolic pattern

>Before hospitalization
The client takes three meals a day which compose commonly fish, vegetable, and
meat and she only consume one cup of rice every meal. She drinks 3 to 4 glasses of water
every day, 1 bottle of soft drink particularly coke, sprite, pop, royal or sparkle every
week, 3-4 bottles of liquor particularly red horse every week, 2-3 glasses of juices
particularly eight o’clock every week and a cup of coffee a day.

>During hospitalization
Her physician ordered her a BRAT diet and last March 10, 2010 the physician
ordered her to temporarily not to take any foods for 1 hour in preparation for ultra sound.
3. Elimination pattern

>Before hospitalization
The patient urinates three to five times a day ranging 4 glasses or 960ml and it is
a light yellow in color and defecates once a day every morning with yellow color and in
soft consistently.

>During hospitalization
The patient is able to urinate 4 times a day ranging 2 and ½ glasses or 600ml it is
a light yellow in color and defecates once a day.

4. Activity exercise pattern

>Before hospitalization
The patient was able to perform activities such as bathing, toileting, dressing and
tooth brushing 2 times a day and other self care activities. She did household chores in
their house as her daily exercise during her vacant hours. She was able to watch
television for about six hours.

>During Hospitalization
The patient is able to perform self care activities without the assistance of her
S.O.

5. Sleep rest pattern

>Before hospitalization
The client usually sleeps for about 8 hours every day from 11:00 in the evening
to 7:00 in the morning and she doesn’t have an afternoon nap.

>During hospitalization
The client has an intermittent sleep, she begins to sleep at 9:00 in the evening and
woke up due to the ward stimuli and then continue to sleep again. The patient has an
afternoon nap at 3:00 in the afternoon.

6. Cognitive perceptual pattern

 ALCOHOLIC LIVER DISEASE

>Before hospitalization
She can speak tagalong and Ilocano as her primary dialect. The patient can
interact and express herself clearly and she doesn’t have any hearing difficulties or visual
problem.

>During hospitalization
The patient can still follow instructions. She is still able to read and write letters
and still able to express herself.

7. Self perception-self concept pattern

>Before hospitalization
According to the client she was loved by her husband and two children. Her two
children were her inspiration and her and she wants a bright future for her grandson and
granddaughter.

>During hospitalization
According to the client she is still loved by her family and she stated that she at
her age is still strong to do her routine activities.

8. Role relationship pattern

>Before hospitalization
According to the patient she was the only one who did household chore like;
cooking, cleaning their house, fetch water and the like. She also takes her grandson and
granddaughter a bath before going at her work and shower before sleeping.

>During hospitalization
According to the client she is unable to do household chores because of her
condition and she is also unable in taking care her grandson and granddaughter.

9. Sexuality reproductive pattern

>Before hospitalization
According to the patient they did sexual activity with her husband and as the fruit
of their love they are able to have two children.

>During hospitalization
According to the client she cannot express her love to her husband due to her
condition.

10. Coping stress tolerance

>Before hospitalization
According to the client she manages her stress through bonding with her children
during dinner time, playing with her grandson and granddaughter and watching TV for
about six hours every day.

>During hospitalization
According to the patient she manages her stress through having a nap at around
3:00 in the afternoon.
 ALCOHOLIC LIVER DISEASE

11. Values and belief pattern

>Before hospitalization
She doesn’t attend the Sunday mass but her faith to God is still on her.

>During hospitalization
According to the patient she cannot attend the Sunday mass because of her
situation but she is praying for her condition.
 ALCOHOLIC LIVER DISEASE

PHYSICAL ASSESSMENT
General appearance: weak looking, ecteric sclera, flabby soft abdomen, afebrile.

Vital Signs:

 Temperature: 38.9⁰C
 Respiratory Rate: 32cpm
 Pulse Rate: 90bpm
 Blood Pressure: 120/80mmhg

BODY PARTS METHOD NORMAL ABNORMAL ANALYSIS

USE FINDINGS FINDINGS
Head
 Hair >inspection >black hair,
evenly
distributed
 Scalp >inspection >no infection or
infestation
>rounded in
shape
>palpation >no mass and
tenderness
 Face >inspection >no facial
asymmetry
 Skin >inspection >dark
complexion
EYES
 Eyebrows >inspection >hair evenly
distributed and
equal in
movement
 Eyelid >inspection >upper lid
covers, small
portion of the
iris and cornea;
lower lid
margin is just
below the
cornea and
sclera
 Eyelashes >inspection >equally
distributed with
Black eyelashes
and curled
slightly
outward
 Conjunctiva >inspection >shiny, smooth
and pink

 Sclera >inspection >whitish w/o >Ecteric >Due to

discoloration increased bile
circulating in
 ALCOHOLIC LIVER DISEASE

the blood

 Eyeballs >inspection >symmetrical

 Pupils >inspection >black in color ,

equal in size,
isometric 3-4
mm, round in
shape and iris
flat and round
.>inspection >reactive to
light

EARS
 Pinna >inspection >color same as
facial skin;
symmetrical
>palpation >firm and not
tender;
Recoils after it
is folded
 External canal >inspection >dry skin;
minimal
cerumen and
various shades
of brown
NOSE >inspection >symmetric and
straight

>palpation >not tender, no

lesions
MOUTH
 Lips >Inspection >Moist and
darker in color

 Gum >Inspection >No bleeding

and lesions
NECK
 Muscle >Inspection >Muscles are
equal in size;
Head centered
 Lymph nodes >palpation
SHOULDER >inspection >symmetrical
>palpation >no swelling

UPPER
EXTRIEMITIES >inspection >dark
 Skin complexion
 ALCOHOLIC LIVER DISEASE

>palpation >good skin

turgor
>inspection >convex
 Nails curvature

>palpation >prompt return

 muscle and of pink or usual
tone color

>inspection >equal size on

both sides of
the body

CHEST
>inspection >chest
symmetric
>palpation >no tenderness
or masses
>percussion >normal
percussion
sound
>auscultation

ABDOMEN
>inspection >uniform color; >Bloaty >Due to
flat abdomen abdomen excessive
peritoneal fluid
>auscultation >audible bowel
sounds
>percussion >dullness >Thumpy sound >Due to
specially in the excessive fluid
liver and spleen in the peritoneal
cavity
> Due to
>palpation >no tenderness >Soft excessive fluid
in the peritoneal
cavity

LOWER
EXTREMITIES
>inspection >dark
 Skin complexion
with good skin
 ALCOHOLIC LIVER DISEASE

turgor

>inspection >convex
 Toenails curvature

>inspection >prompt return

 muscle of pink or usual
color

>inspection >equal size on

both sides of
the body
 ALCOHOLIC LIVER DISEASE

LABORATORY AND DIAGNOSTIC EXAM

URINALYSIS

Date Ordered: March 7, 2010

Date Performed: March 10, 2010

Microscopic Exam Chemical Exam

Color: Orange Albumin: Trace

Characteristic: Turbid Sugar: Negative

Reaction pH: 5.0 (Normal: 7.35-7.45)

Specific Gravity: 1.025 (Normal: 1.010-1.025)

Bacteria: Positive

Pus Cells: 0.2

Epithelial Cells: Moderate

HEMATOLOGY

Date Performed: March 6, 2010

Result Reference Interpretation Significance

Values
Indicates
WBC 14.5 3.5 – 10 Increased presence of
infection
Indicates
HgB 9.1 11.0 -16.5 g/dl Decrease occurrence of
anemia
Platelet 170 150 – 390 x 09/L Decreased
Differential Count
Lymphocytes 42.2 17 - 48 Normal
Indicates
Monocytes 11.3 2.0 – 6.0 Increased presence of
infection
Granulocytes 56.5 43 - 76 Normal

HEMATOLOGY
 ALCOHOLIC LIVER DISEASE

Date Performed: March 8, 2010

Result Reference Interpretation Significance

Values
Indicates
WBC 16.0 3.5 - 10 Increased presence of
infection
Indicates
HgB 8.8 11.0 -16.5 g/dl Decrease occurrence of
anemia
Indicates
Platelet 142 150 – 390 x 09/L Decreased
hypercoagulation
Differential Count
Lymphocytes 42.2 17 - 48 Normal
Indicates
Monocytes 11.3 2.0 – 6.0 Increased presence of
infection
Granulocytes 56.5 43 - 76 Normal

Blood Chemistry

Date Performed: March 8, 2010

Result Reference Interpretation Significance

Values
Sodium 132 136 – 155 Decreased
Potassium 3.26 3.60 – 5.5 Decreased

Serology

Date Performed: March 06, 2010

Test Result Method

HBsAG Non-Reactive Immuno-chromatography

Fecalysis

Physical Characteristic: Soft

Color: Yellow

Bacteria:

WBC/HPF: 0 – 4

RBC/HPF:

Yeast Cells

Amoeba: None found

ALCOHOLIC LIVER DISEASE
 ALCOHOLIC LIVER DISEASE

REVIEW OF THE SYSTEM

Anatomy and physiology of the liver

The liver is the largest internal organ in the body, and weighs about 3 pounds in an adult. The
liver is located in the right upper quadrant of the abdomen, just below the diaphragm. A thick
capsule of connective tissue called Glisson's capsule covers the entire surface of the liver. The
liver is divided into a large right lobe and a smaller left lobe. The falciform ligament divides the
two lobes of the liver.

Each lobe is further divided into lobules that are approximately 2 mm high and 1 mm in
circumference.

These hepatic lobules are the functioning units of the liver. Each of the approximately 1 million
lobules consists of a hexagonal row of hepatic cells called hepatocytes. The hepatocytes secrete
bile into the bile channels and also perform a variety of metabolic functions. Between each row
of hepatocytes are small cavities called sinusoids. Each sinusoid is lined with Kupffer cells,
phagocytic cells that remove amino acids, nutrients, sugar, old red blood cells, bacteria and
debris from the blood that flows through the sinusoids. The main functions of the sinusoids are to
destroy old or defective red blood cells, to remove bacteria and foreign particles from the blood,
and to detoxify toxins and other harmful substances. Approximately 1500 ml of blood enters the
liver each minute, making it one of the most vascular organs in the body. Seventy-five percent of
the blood flowing to the liver comes through the portal vein; the remaining 25% is oxygenated
blood that is carried by the hepatic artery.

The liver is responsible for important functions, including:

 Bile production and excretion

 Excretion of bilirubin, cholesterol, hormones, and drugs
 Metabolism of fats, proteins, and carbohydrates
 ALCOHOLIC LIVER DISEASE

 Enzyme activation
 Storage of glycogen, vitamins, and minerals
 Synthesis of plasma proteins, such as albumin and globulin, and clotting factors
 Blood detoxification and purification

The liver synthesizes and transports bile pigments and bile salts that are needed for fat digestion.
Bile is a combination of water, bile acids, bile pigments, cholesterol, bilirubin, phospholipids,
potassium, sodium, and chloride. Primary bile acids are produced from cholesterol. When bile
acids are converted or "conjugated" in the liver, they become bile salts.

Bilirubin is the main bile pigment that is formed from the breakdown of heme in red blood cells.
The broken-down heme travels to the liver, where is it secreted into the bile by the liver.
Bilirubin production and excretion follow a specific pathway. When the reticuloendothelial
system breaks down old red blood cells, bilirubin is one of the waste products. This "free
bilirubin" is a lipid soluble form that must be made water-soluble to be excreted. The
conjugation process in the liver converts the bilirubin from a fat-soluble to a water-soluble form.
The liver also plays a major role in excreting cholesterol, hormones, and drugs from the body.

The liver plays an important role in metabolizing nutrients such as carbohydrates, proteins, and
fats. The liver helps metabolize carbohydrates in three ways:

 Through the process of glycogenesis, glucose, fructose, and galactose are converted to
glycogen and stored in the liver.
 Through the process of glycogenolysis, the liver breaks down stored glycogen to
maintain blood glucose levels when there is a decrease in carbohydrate intake.
 Through the process of gluconeogenesis, the liver synthesizes glucose from proteins or
fats to maintain blood glucose levels.

The liver synthesizes about 50 grams of protein each day, primarily in the form of albumin. Liver
cells also chemically convert amino acids to produce ketoacids and ammonia, from which urea is
formed and excreted in the urine. Digested fat is converted in the intestine to triglycerides,
cholesterol, phospholipids, and lipoproteins. These substances are converted in the liver into
glycerol and fatty acids, through a process known as ketogenesis.

Prothrombin and fibrinogen, substances needed to help blood coagulate, are both produced by
the liver. The liver also produces the anticoagulant heparin and releases vasopressor substances
after hemorrhage.

Liver cells protect the body from toxic injury by detoxifying potentially harmful substances. By
making toxic substances more water soluble, they can be excreted from the body in the urine.
The liver also has an important role in vitamin storage. High concentrations of riboflavin or
Vitamin B1 are found in the liver. 95% of the body's vitamin A stores are concentrated in the
liver. The liver also contains small amounts of Vitamin C, most of the body's Vitamin D stores,
and Vitamins E and K.
 ALCOHOLIC LIVER DISEASE

COURSE IN THE WARD

Date and Time Physician’s Order Rationale Nursing Intervention
3/6/10 * Please admit to * For confinement * Brought patient to
FMW FMW

* Secure consent * For legal purposes * Secured consent for

admission and
management

* BRAT DIET

* D5LRS 1l x 8hrs * For rehydration and * Administered as

medication purposes indicated by the
physician

* For fecalysis * For diagnostic * Instructed patient to

purposes put a little amount of
feces into a vial

* For CBC * For further exams * Explain to the

patient why he needs
to undergo for test

* Therapeutics:
Paracetamol 1 amp * To lower body * Observed the 10 R’s
I.V. q 4hrs for temp. ≥ temperature during in giving medication.
38.5ºC fever

* Monitor V/S q 4 hrs * For baseline data * Monitored V/S and

recorded

* I & O q Shift * For baseline data * Monitored intake

and output
accordingly

Date and Time Physician’s Order Rationale Nursing Intervention

3/7/10 * TF: D5LRS 1L x 8 * For rehydration and * Administered as
hrs medication purposes indicated by the
physician

* Continue meds * For medication * Continue meds as

purposes indicated by the
physician

* TF: D5LRS 1L x * For rehydration and * Continue meds as

8hrs medication purposes indicated by the
physician
* Refer * To provide
immediate * Referred any
 ALCOHOLIC LIVER DISEASE

intervention for any problem to the

complication the may physician
arise

* Clonidine 75 mg q * Helps to lower * Observed the 10 R’s

30mins x 3 doses if blood pressure in giving medication
BP ≥ 140/90

* Amlodipine 5 mg 1 * Helps to lower * Observed the 10 R’s

tab OD blood pressure in giving medication

Date and Time Physician’s Order Rationale Nursing Intervention

3/8/10 * TF: D5NSS 1L x * For rehydration and * Continue infusion as
KVO medication purposes prescribed by the
physician

* Furosemide 40 mg * To facilitate * Observed the 10 R’s

I.V. q 12h urination as the in administering
patient has massive medication
ascites

* Rpt CBC w/ APC

Date and Time Physician’s Order Rationale Nursing Intervention

3/9/10 * TF: D5NSS 1L x * For rehydration and * Continue infusion as
12h medication purposes prescribed by the
physician

* Refer UTZ of the * *

whole abdomen
 ALCOHOLIC LIVER DISEASE

NURSING CARE PLAN

Patient’s name: Patient JAUNDICE
Age: 48y.o.

Assessment Diagnosis Planning Intervention Rationale Evaluation

Subjective Data: Hyperthermia related to Within 30minutes to 1hour of -Established rapport to the -To build trust and After 1hour of nursing
“Madi nga bumabbaba ti pyrogenic effect secondary to nursing intervention the client through NPI cooperation of the patient and intervention the patient’s
gurigor ko” as verbalized by bacterial infection patient’s temperature will SO in the succeeding nursing temperature decreased from
the patient. decrease from 38.9°C to 37°C interventions. 38.9°C to 37°C

Objective Data: -Monitored temperature every -To detect any alterations -Goal met
-Weak appearance 15minutes immediately.
-Irritability
-Warm to touch -Provided TSB -Facilitates heat loss by
-Flushed skin evaporation
-Temperature:38.9°C
-Advised patient to increase -Increasing the fluid in the
oral fluid intake body boost its cooling system.

-Watched out for convulsions -Convulsion may cause

complications

-Advised S.O. to provide -Facilitates Heat loss by

loose clothing to the patient evaporation.

-Provided well room -To facilitate heat loss by

ventilation convection

-Administered paracetamol -Pharmacologic management

accurately as ordered by the for hyperthermia.
physician and document
 ALCOHOLIC LIVER DISEASE
NURSING CARE PLAN
Assessment Diagnosis Planning Intervention
Subjective Data: Acute pain related to Within 1° of nursing >Established rapport to the
abdominal cramping 2° to intervention the patient will patient
“Nasakit toy tiyan ko” as hyperperistalsis manifest relaxation and no
verbalized by the patient signs of pain. >Encouraged S.O. to position
the client in supine position
Objective Data: with a warm heating pad on
the abdomen
>Guarding behavior at the
epigastric region >Instructed S.O. to avoid
>Irritability giving hot and cold oral fluids
>Reduced interaction to
people
>Pain scale: 8/10 >Fixed bed linen free from
wrinkles
>Provided calm environment
>Encouraged patient to have
divertional activities like
listening to music
>Encouraged relaxation
technique such as deep
breathing
>Watched out if pain scale
increases
>Administered buscopan
accurately as ordered by the
physician and document
Rationale Evaluation
>To build trust After 1° of nursing
intervention the patient will
manifest relaxation and no
>These measures promote GI signs of pain.
muscular relaxation and reduce
cramping -Goal met
>Cold liquid can induce
cramping and hot liquid can
stimulate peristalsis
>To provide comfort
>To promote
nonpharmacological pain
management
>Diverting attention will help
to reduce pain
>This measure promote
relaxation and helps divert pain
>Immediate increase in pain
scale can be a cause of other
complication
> Pharmacologic management
for abdominal pain.
 ALCOHOLIC LIVER DISEASE

DRUG STUDY
DRUG CLASSIFICATION ROUTE/DOSAGE ACTION INDICATION CONTRAINDICATION ADVERSE REACTION NURSING
CONSIDERATION
 Contraindicated with  CNS: Headache,  History:
allergy to dizziness, Allergy to
CIPROFLOXACIN Antibacterial 500 mg/ 1 tab BID Bactericidal; For the treatment
interferes with of infections ciprofloxacin, insomnia, fatigue, ciprofloxacin,
DNA replication in caused by somnolence,
norfloxacin or other norfloxacin or
susceptible susceptible gram-
bacteria negative bacteria, depression, blurred
fluoroquinolones, other
preventing cell including vision,
pregnancy, lactation. quinolones;
reproduction. Escherichia coli, hallucinations,
Proteus mirabilis,  Use cautiously with renal
Klebsiella ataxia, nightmares
renal impairment, impairment;
pneumoniae,  CV: Arrhythmias,
Enterobacter seizures, tendinitis seizures;
cloacae, Proteus hypotension,
or tendon rupture lactation
vulgaris, Proteus angina
rettgeri, associated with  Physical:
 EENT: Dry eye,
Morganella
morganii, fluoroquinolone use. eye pain, Skin color,
Pseudomonas keratopathy lesions; T;
aeruginosa,
Citrobacter  GI: Nausea, orientation,
freundii, vomiting, dry reflexes,
Staphylococcus
aureus, mouth, diarrhea, affect; mucous
Staphylococcus abdominal pain membranes,
epidermidis, group
 GU: Renal failure bowel sounds;
D streptococci
 Hematologic: LFTs, renal
Elevated BUN, function tests
AST, ALT, serum
creatinine and
alkaline
phosphatase;
decreased WBC,
neutrophil count,
Hct

DRUG CLASSIFICATION ROUTE/DOSAGE ACTION INDICATION CONTRAINDICATION ADVERSE REACTION NURSING

CONSIDERATION
 Contraindicated with  CNS: Dizziness,
FUROSEMIDE Loop Diurectic 40 mg/ I.V. q12 Inhibits Oral, IV: Edema
 ALCOHOLIC LIVER DISEASE
reabsorption of associated with allergy to vertigo, Profound diuresis with
sodium and heart failure,
furosemide, paresthesias, water and electrolyte
chloride from the cirrhosis, renal
proximal and disease sulfonamides; xanthopsia, depletion can occur;
distal tubules and
allergy to tartrazine weakness, careful medical
ascending limb of
the loop of Henle, (in oral solution); headache, supervision is required.
leading to a
anuria, severe renal drowsiness, fatigue,
sodium-rich
diuresis. failure; hepatic blurred vision,  Administer with
coma; pregnancy; tinnitus, food or milk to
lactation. irreversible hearing prevent GI
 Use cautiously with loss upset.
SLE, gout, diabetes  CV: Orthostatic  Reduce dosage
mellitus. hypotension, if given with
volume depletion, other
cardiac antihypertensiv
arrhythmias, es; readjust
thrombophlebitis dosage
 Dermatologic: gradually as BP
Photosensitivity, responds.
rash, pruritus,  Give early in
urticaria, purpura, the day so that
exfoliative increased
dermatitis, urination will
erythema not disturb
multiforme sleep.
 Avoid IV use if
oral use is at
all possible.

DRUG CLASSIFICATION ROUTE/DOSAGE ACTION INDICATION CONTRAINDICATION ADVERSE REACTION NURSING

CONSIDERATION
 Angina  Contraindicated with  CNS: Dizziness,
5 mg /1 tab O.D. Inhibits the
Antianginal pectoris due allergy to lightheadedness, Monitor patient
AMLODIPIN movement of
E Antihypertensive calcium ions to coronary amlodipine, impaired headache, asthenia, carefully (BP, cardiac
 ALCOHOLIC LIVER DISEASE
Calcium channel across the artery spasm hepatic or renal fatigue, lethargy rhythm, and output)
membranes of
blocker (Prinzmetal’s function, sick sinus  CV: Peripheral while adjusting drug to
cardiac and
arterial muscle variant syndrome, heart edema, arrhythmias therapeutic dose; use
cells; inhibits
angina) block (second or  Dermatologic: special caution if
transmembrane
calcium flow,  Chronic stable third degree), Flushing, rash patient has heart failure.
which results in
angina, alone lactation.  GI: Nausea,
the depression of
impulse formation or in  Use cautiously with abdominal  Monitor BP
in specialized
combination heart failure, discomfort very carefully
cardiac pacemaker
cells, slowing of with other pregnancy. if patient is
the velocity of
drugs also on nitrates.
conduction of the
cardiac impulse,  Essential  Monitor cardiac
depression of
myocardial hypertension, rhythm
contractility, and alone or in regularly
dilation of
coronary arteries combination during
and arterioles and with other stabilization of
peripheral
arterioles; these antihypertensi dosage and
effects lead to ves periodically
decreased cardiac
work, decreased during long-
cardiac oxygen term therapy.
consumption, and
in patients with  Administer drug
vasospastic without regard
(Prinzmetal’s)
angina, increased to meals.
delivery of
oxygen to cardiac
cells.
 ALCOHOLIC LIVER DISEASE

DISCHARGE CARE PLAN

 Encouraged the patient to continue medications at home as prescribed by

physician.
Medication
 Emphasized the importance of taking medication as prescribed.

 Encouraged patient to have daily exercise to reach optimum health recovery

regarding condition.
Exercise
 Encouraged patient to have an adequate sleep and rest every day.

 Emphasized the importance of adequate rest and sleep to prevent fatigue and
avoid weight loss.
Treatment
 Advised the patient to continue taking medication as ordered on a regular basis.

Hygiene/Healt
 Emphasized to the patient the importance of bathing and other hygienic
h Education procedure such as regular bathing to provide wellness and comfort.

 Encouraged patient to visit the hospital if there were problems on heath or there
Out-patient is something that alters her health condition or visit the nearest health center or
department rural health unit for check-up to monitor her health condition.

 Instructed patient to have diet as tolerated.

Diet
 Instructed patient to eat nutritious food like vegetables, fruits and the like.

 Encouraged the patient to attend Sunday mass regularly and encouraged to pray
Spiritual for the safe and wellness of their health.