CP - Liver Cirrhosis

Brokenshire College of Davao
Madapo, Davao City
A Case Study on
Liver Cirrhosis
Presented to the Faculty of

Brokenshire College:
Visminda B. Batoy RN., MN., MAN., COHN

Ronald Allan T. Ramo RN., MAN
Cresensio C. Cajigal RN., MAN
Norma J. Mendez RN., MAN
Prescila V. Estipona RN, MN
In Partial Fulfillment of the Requirements of

Inflammatory and Immunologic
Nursing Care Management 104
Related Learning Experience
Submitted by:
Dayanghirang, Elica Hilda C.

Custodio, Nicomedes III B.
De Milo, Kelly Kirstin T.
Carino, Yvonne Grace B.
Jayme, Julia Camille S.
Deliña, Merry Joy L.
Abulag, Sharmine L.
Hairulla, Noraina J.
Egar, Dolly Joy R.
Cadayona, Exil L.
Jang, Youngdon
ACKNOWLEDGEMENT
The group would like to express our heartfelt and deepest appreciation to the
people involved with making our case presentation possible. We are ever so grateful
for the guidance and encouragement offered. We would also like to thank our family,
friends and classmates for their endless support, emotionally, spiritually and
financially.
To our Dean of Nursing Mrs. Visminda B. Batoy RN, MN, MAN, COHN we
are ever so grateful for the advice, recommendations, assistance and encouragement
offered.
Special thanks to our clinical instructors: Mr. Ronald Ramo, RN, MN, MAN,
Mr. Cresencio C. Cajigal Jr., RN, MAN, Mrs. Norma Mendez, RN, MAN and RLE
coordinator Prescila V. Estipona RN, MN for their guidance and support with our
case presentation throughout our duty at the Medicine ward. We also appreciate the
patience shown even in stressful situations and mistakes were made.
To all medical personnel and staff of Brokenshire Integrated Health Ministries
Inc. Hospital, Medical Wing Ward we would like to thank you for the warm
accommodations during our clinical exposure as well as providing vital information
required for caring of the patient.
Lastly, we would like to thank our client and his family for their willingness to
share their time and medical information to aid in our learning for this case
presentation.
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Table of Contents
Title Page
Acknowledgement…………………………………………………………...……….2
Table of Contents…………………………………………………………………….3
The Problem
Introduction………………………………………………………………………….6-9
Background of the Case……………………………………………………………...10
Objectives………………………………………………………………………...11-13
Significance of the Study…………………………………………………………….14
Definition of Terms………………………………………………………………….15
Review of related Literature……………………………………………………...16-21
Evidence-based Study……………………………………………………...……..22-32
Anatomy and Physiology of System’s Involved………………………………….33-43
Disease Process
Symptomatology……………………………………………………………...…..44-48
Etiology………………………………………………………………………...…48-53
Pathophysiology…………………………………………………………………..54-59
Developmental Theories
Erik Erickson’s Stages Psychosocial Development Theory…………………..……..60
Sigmund Freud Psychoanalytical Theory……………………………………..….61-63
Jean Piaget Cognitive Development Theory……………………………………...64-65
Havighurt’s Developmental Stages……………………………………………….66-67
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Data Gathering
Collection Procedure/Method and Sources of Information…………………………..68
Health Assessment…………………………………………………………………...69
Physician’s Finding and Medical Diagnosis…………………………………………70
Nursing Assessment: Interview and PE-IPPA……………………………………71-81
Health History
Genogram…………………………………………………………………………….82
Developmental Stages…………………………………………………………...83-100
Medical Management
a. Doctors Order…………………………………………………………..101-103
b. Laboratory Examinations………………………………………………104-109
c. Drugs and Treatment…………………………………………………...110-130
d. Medical Prognosis…………………………………………………...…131-133
Nursing Care Plan/ Problem Solving
Assessment Data Interpretation…………………………………………..134
1. Identifying Nursing Problems
2. Problem List
3. Nursing Priorities
Nursing Diagnostic……………………………………………………135-148
1. Nursing Diagnosis
2. NCP
Plan
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1. Setting Goals/Objectives
2. Nursing Theory of care
3. Planned Interventions/Identifying Solutions and its Rationales
Implementation……………………………………...………………..149-156
1. Applications of Nursing Intervention
2. Applications of Standard of Nursing Practice
(11 Key Areas of Responsibility)
3. Progress Notes during the Course of Care and Nursing Interventions
4. Health Education
5. Discharge Plan
Evaluation and Modification……………………………………………157
Nursing Conclusions
Recommendation…………………………………………………...…158-160
Bibliography……………………………………………………………….161
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Chapter 1
THE PROBLEM
Introduction
The liver is one of the largest and most complex organs in the body. It stores
vital energy and nutrients, manufactures proteins and enzymes necessary for good
health, protects the body from disease, and breaks down (or metabolizes) and helps
remove harmful toxins, like alcohol, from the body. It is one of the most important
organs in the body since it has many significant functions. A lack or failure to provide
proper care of it may lead to an abnormality or disorder. One of the severe forms that
may happen is Liver Cirrhosis.
Liver Cirrhosis is derived from Greek word kirrhos, meaning "tawny" (the
orange yellow colour of the diseased liver). It is a chronic disease that causes cell
destruction and fibrosis (scarring) of hepatic tissue. Fibrosis alters normal liver
structure and vasculature, impairing blood and lymph flow and resulting in hepatic
insufficiency and hypertension in the portal vein. Cirrhosis is most commonly caused
by alcoholism, hepatitis B and C and fatty liver disease but has many other possible
causes. Some cases are idiopathic, i.e., of unknown cause. It may be classified by the
structural changes that take place or by the cause of the disorder.
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Internationally, liver cirrhosis is currently the 11th most common cause of
death globally and liver cancer is the 16th leading cause of death; combined, they
account for 3.5% of all deaths worldwide. Cirrhosis is within the top 20 causes of
disability-adjusted life years and years of life lost, accounting for 1.6% and 2.1% of
the worldwide burden. About 2 billion people consume alcohol worldwide and
upwards of 75 million are diagnosed with alcohol-use disorders and are at risk of
alcohol-associated liver disease. Approximately 2 billion adults are obese or
overweight and over 400 million have diabetes; both of which are risk factors for non-
alcoholic fatty liver disease and hepatocellular carcinoma. The global prevalence of
viral hepatitis remains high, while drug-induced liver injury continues to increase as a
major cause of acute hepatitis. Liver transplantation is the second most common solid
organ transplantation, yet less than 10% of global transplantation needs are met at
current rates. Though these numbers are sobering, they highlight an important
opportunity to improve public health given that most causes of liver diseases are
preventable.
It is most common among people ages 45 – 75, killing more than 25,000
people each year, 50% of which are alcohol related. In the Philippines and other
underdeveloped countries, however, the incidence of liver cancer is rather high. Liver
cancer is relatively common in our country primarily because many Filipinos suffer
from cirrhosis of the liver, a major risk factor for liver cancer. Cirrhosis of the liver
precedes 80 percent of all liver cancers; thus, any condition that predisposes to
cirrhosis indirectly causes liver cancer. The usual cause of liver cirrhosis among
Filipinos is chronic hepatitis B, a major public health problem in the country. Chronic
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hepatitis B afflicts between 10 and 12 percent of all Filipinos (i.e., more than 8
million Filipinos). Other less significant causes of cirrhosis are hepatitis C infection
and alcoholism. The latest DOH advisory shows that liver cancer is the third most
common form of cancer among Filipinos—in men, it is the second most common,
while in women, it is the ninth most common. Locally, liver cirrhosis is the 17 th
leading cause of death here in Davao.
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.
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
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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.
In connection with it, last February 27-28, 2020 our group was assigned on
duty at the Brokenshire Integrated Health Ministries Inc. Hospital, Medical Wing
Ward where we met our patient Mr. V who was diagnosed of Liver Cirrhosis
Secondary to Alcoholic Liver Disease, Insulin Requiring Diabetes Mellitus,
Hypertension II – Controlled. They were motivated to learn more and study the
disorder since it was their first time to encounter such case. Also, the group was more
encouraged to choose the patient for their case presentation in order to acquire better
understanding and to gain more knowledge and use it for the future.
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Background of the Case
This is a case of a 68-year-old male named Mr. V who was diagnosed with
Liver Cirrhosis Secondary to Alcoholic Liver Disease, Insulin Requiring Diabetes
Mellitus, Hypertension II – Controlled. Three weeks prior to admission, patient had
onset of epigastric pain. Pain was tolerable as patient self-medicated with Hyoscine
Butyl bromide (Buscopan) but still no relief of symptoms. One week prior to
admission, patient had drinking spree and had recurrence of epigastric pain with no
medications taken and no consultation done. Abdominal pain was intermittent, and it
had worsened five days prior to admission. Hence, patient sought consultation at
CHDC hospital and was given lactulose with no relief. Abdominal pain persisted with
pain scale 8/10 associated with nausea hence consult then admitted to Brokenshire
Integrated Health Ministries Incorporated.
Our group chose this study to obtain further knowledge and better
understanding about Liver Cirrhosis, what are its causes, complications, specific
treatments and nursing interventions for clients who are diagnosed with this said
illness.
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OBJECTIVES
To have a course of direction, organization and to recognize the essence of this
study, we have set the following objectives:
GENERAL OBJECTIVES
After rendering effective nursing care for two days at the Brokenshire
Integrated Health Ministries, MEDWING Ward, we aim:
 To provide an extensive study about Liver Cirrhosis Secondary to Alcoholic
Liver Disease for us to gain better understanding about the disease and be
equipped with competence in dealing with related situations in the future;
 To improve our skills in doing relevant interventions which promote
wellness to persons having the disease;
 Not only to understand the situation of the client and their families who
are confronted with the disease but also to empathize with them.
SPECIFIC OBJECTIVES
 Find a case in the BIHMI MED WING ward within the two-day duty;
 Establish a good interpersonal relationship with our chosen client as well as to
his significant others;
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 Acquire necessary data of our client which are relevant to our case study;
 Trace the patient’s family lineage and present remarkable familial disease;
 Trace the health history of the client and the family by collecting information
both from the past and present illnesses;
 Evaluate the client’s development guided by Erik Erikson, Robert Havighurst
and Jean Piaget’s Theory;
 Define the complete diagnosis of our client guided by three different sources;
 Perform cephalocaudal assessment to the client thoroughly;
 Discuss the systems involved in the development of the disease in the human
anatomy and physiology;
 Present the etiology and symptomatology of the disease process with each of
its rationales and identify which are present on the client’s case;
 Trace the pathophysiology of the disease as experienced by our client and
present it through a schematic diagram;
 Present and analyze the doctor’s order in chronological manner;
 Explain and interpret both actual and possible diagnostic studies including the
indication, result, and their implications;
 Discuss the different drugs taken by the patient with corresponding nursing
intervention;
 Identify different nursing theories made by Florence Nightingale, Virginia
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Henderson and Lydia Hall and relate it on the patient’s conditions;
 Formulate specific, measurable, attainable, realistic, and time-bounded nursing
care plans with corresponding rationales for each of the nursing interventions;
 Evaluate the client’s progress with our continuous care;
 Render health teachings or appropriate nursing interventions necessary to the
client and family as well;
 Present a discharge plan for the patient
 Present and justify the prognosis of our patient
 Provide recommendations for the better management of patient with the same
disease in the future endeavor;
 Accomplish our case presentation.
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Significance of the Study
This study hopes to establish a further understanding on Liver Cirrhosis. It is
also a thorough study about the patient’s condition and status on having this disease.
Furthermore, the study could also be important to the following:
To Students. The information gathered and presented in the study will give the
students thorough understanding about Liver Cirrhosis and will also serve as
reference or guide in creating our further case study. It will also help students taking
medical related courses as their reference about the said study.
To Clinical Instructors. The outcome of this study will facilitate them to formulate
efficient strategies and approaches to make learning more comprehensive and
retentive.
To Nurses. The information gathered in the study will give nurses more knowledge
about Liver Cirrhosis to help them improve their nursing care and to formulate
interventions that can facilitate a faster recovery for their patients diagnosed with the
said illness.
To Community. The information presented will give the community better
understanding and awareness about Liver Cirrhosis and will enable them to formulate
activities or strategies to prevent the said illness to increase.
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To Individuals. The information presented in the study will give the individuals
knowledge and understanding about Liver Cirrhosis that will enable them to avoid the
factors that can cause the said illness.
Definition of the terms
Liver - is an organ only found in vertebrates which detoxifies various metabolites,
synthesizes proteins and produces biochemicals necessary for digestion and growth.
Liver cirrhosis - also known as liver cirrhosis or hepatic cirrhosis is a condition in
which the liver does not function properly due to long-term damage.
Hepatitis B - is a viral infection that attacks the liver and can cause both acute and
chronic disease. The virus is most commonly transmitted from mother to child during
birth and delivery, as well as through contact with blood or other body fluids.
Hepatitis C – is a form of viral hepatitis transmitted in infected blood, causing
chronic liver disease.
Fatty liver disease - means extra fat in the liver.
Phospholipase - is an enzyme that hydrolyzes phospholipids into fatty acids and other
lipophilic substances.
Glisson's capsule - The capsule of the liver. A layer of connective tissue surrounding
the liver and unsheathing the hepatic artery, portal vein, and bile ducts within the liver
Kupffer cell - a phagocytic cell which forms the lining of the sinusoids of the liver
and is involved in the breakdown of red blood cells.
SGPT – is blood test measures an enzyme called alanine transaminase (ALT).
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Enzymes are chemicals that help the cells of your body work. It is released into the
blood when tissues are damaged.
Lipid profile - screening tool for abnormalities in lipids, depending on factors like
eating habits, diet, stress, exercise and life-style related.
Review of Related Literature
Chronic liver disease occurs throughout the world irrespective of age, sex,
region or race. Cirrhosis is an end result of a variety of liver diseases characterized by
fibrosis and architectural distortion of the liver with the formation of regenerative
nodules and can have varied clinical manifestations and complications. According to
WHO, about 46% of global diseases and 59% of the mortality is because of chronic
diseases and almost 35 million people in the world die of chronic diseases 1. Liver
disease rates are steadily increasing over the years. According to National statistics in
the UK, liver diseases have been ranked as the fifth most common cause of death 2.
Liver diseases are recognized as the second leading cause of mortality amongst all
digestive diseases in the US 3.
Global Burden of Disease (GBD) Project was formed by WHO to provide a
consistent estimate of mortality and morbidity which varies by age, sex and region 4.
To understand the burden of a certain disease, it is important to know its incidence,
prevalence, mortality and morbidity including, impairment of quality of life and the
direct or indirect cost expenditures. Knowledge of burden of a disease helps in
establishment of public health priorities and in guiding prevention programs.
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Global prevalence of cirrhosis from autopsy studies ranges from 4.5% to 9.5%
of the general population 5, 6, 7. Hence, we estimate that more than fifty million people
in the world, taking the adult population, would be affected with chronic liver disease.
Globally, alcohol, NASH and viral hepatitis currently are the most common causative
factors. Prevalence of cirrhosis is likely to be underestimated as almost a third of the
patients remain asymptomatic. With the use of non-invasive tests like transient
elastography, a more realistic picture could emerge in the near future. During 2001,
the estimated worldwide mortality from cirrhosis was 771,000 people, ranking 14th
and 10th as the leading cause of death in the world and in developed countries,
respectively 8. Deaths from cirrhosis have been estimated to increase and would make
it as the 12th leading cause of death in 2020
According to the WHO, alcohol consumption accounts for 3.8% of the global
mortality and 4.6% of DALYs. Liver disease represents 9.5% of alcohol-related
DALY’s worldwide, while individual rates vary in different regions. Alcohol is the
main cause of liver-related death in Europe with highest mortality rates reported from
France and Spain (approximately 30 deaths per 100,000 per year). There is a
possibility of underestimation of mortality due to legal issues of documenting alcohol
as primary cause of death. The lack of specificity of the national survey
questionnaires also fails to allow accurate classification of liver diseases. Today, even
in Asian countries like India, alcohol is emerging as the commonest cause of chronic
liver disease.
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The prevalence of alcoholic liver disease (ALD) is difficult to define because
it is influenced by many factors including genetic (eg, predilection to alcohol abuse,
gender) and environmental (eg, availability of alcohol, social acceptability of alcohol
use, concomitant hepatotoxic insults) factors. In the United States, it is estimated that
67.3% of the population consumes alcohol and that 7.4% of the population meets the
criteria for alcohol abuse.1 The use of alcohol varies widely throughout the world with
the highest use in the U.S. and Europe. 1 Men are more likely to develop ALD than
women because men consume more alcohol. However, women are more susceptible
to alcohol hepatotoxicity and have twice the relative risk of ALD and cirrhosis
compared with men.1 Elevated body mass index is also a risk factor in ALD as well as
nonalcoholic fatty liver disease. Ethnicity and genetics are important factors related to
ALD. Cirrhosis mortality is higher in men of Hispanic, Native Americans, and native
Alaskans origin compared with white populations.1 Genetic factors such as the
presence of the patatin-like phospholipase domain containing 3 (PNPLA3) gene
appear to be associated with a more severe phenotype and a poor prognosis. (Vozzo,
Welch, Fairbanks, 2018)
Alcoholic liver disease covers a spectrum of disorders beginning from the
fatty liver, progressing at times to alcoholic hepatitis and culminating in alcoholic
cirrhosis which is the most advanced and irreversible form of liver injury related to
the consumption of alcohol.
There are three histologic stages of alcoholic liver disease, the alcoholic fatty
liver or steatosis; At this stage, fat accumulates in the liver parenchyma. Next is the
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alcoholic hepatitis; Inflammation of liver cells takes place at this stage, and the
outcome depends on the severity of the damage. Alcohol abstinence, nutritional
support, treatment of infection, and prednisolone therapy in severe cases can help in
the treatment of alcoholic hepatitis, but more severe cases lead to liver failure. Lastly,
the alcoholic cirrhosis; Liver damage at this stage is irreversible and leads to
complications of cirrhosis and portal hypertension.
Different factors, such as metabolic, genetic, environmental, and
immunological, collectively play a role in alcoholic liver disease. The liver tolerates
mild alcohol consumption, but as the consumption of alcohol increases, it leads to the
disorders of the metabolic functioning of the liver. The initial stage involves the
accumulation of fat in the liver cells, commonly known as fatty liver or steatosis. If
the consumption of alcohol does not stop at this stage, it sometimes leads to alcoholic
hepatitis. With continued alcohol consumption, alcoholic liver disease progresses to
severe damage to liver cells known as” alcoholic cirrhosis." Alcoholic cirrhosis is the
stage described by progressive hepatic fibrosis and nodules. (Gossman, 2019)
The frequency of alcoholic cirrhosis is estimated to be 10–15% among persons
who consume over 50 g of alcohol (4 oz of 100-proof whiskey, 15 oz of wine, or four
12-oz cans of beer) daily for over 10 years (although the risk of cirrhosis may be
lower for wine than for a comparable intake of beer or spirits). The risk of cirrhosis is
lower (5%) in the absence of other cofactors such as chronic viral hepatitis and
obesity. Genetic factors, including polymorphisms of the genes encoding patatin-like
phospholipase domain-containing protein 3 (PNPLA3), tumor necrosis factor,
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cytochrome P450 2E1, glutathione S-transferase, and galectin-9 and heterozygosity of
the Z allele of the gene for alpha-1-antitrypsin deficiency may also account for
differences in susceptibility to and severity of liver disease. Women appear to be more
susceptible than men, in part because of lower gastric mucosal alcohol dehydrogenase
levels, but young men who drink excessively are at increased risk for liver disease
later in life when they are no longer drinking as much. Over 80% of patients with
alcoholic hepatitis have been drinking 5 years or more before symptoms that can be
attributed to liver disease develop; the longer the duration of drinking (10–15 or more
years) and the larger the alcoholic consumption, the greater the probability of
developing alcoholic hepatitis and cirrhosis. In individuals who drink alcohol
excessively, the rate of ethanol metabolism can be sufficiently high to permit the
consumption of large quantities without raising the blood alcohol level over 80
mg/dL. (Friedman, 2020)
Liver cirrhosis is the fourth cause of death in adults in Western countries, with
complications of portal hypertension being responsible for most casualties. In order to
reduce mortality, development of accurate diagnostic methods for early diagnosis,
effective etiologic treatment, improved pharmacological therapy for portal
hypertension, and effective therapies for end-stage liver failure are required. Early
detection of cirrhosis and portal hypertension is now possible using simple non-
invasive methods, leading to the advancement of individualized risk stratification in
clinical practice. Despite previous assumptions, cirrhosis can regress if its etiologic
cause is effectively removed. Nevertheless, while this is now possible for cirrhosis
caused by chronic hepatitis C, the incidence of cirrhosis due to non-alcoholic
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steatohepatitis has increased dramatically and effective therapies are not yet available.
New drugs acting on the dynamic component of hepatic vascular resistance are being
studied and will likely improve the future management of portal hypertension.
Cirrhosis is now seen as a dynamic disease able to progress and regress between the
compensated and decompensate stages. This opinion article aims to provide the
author’s personal view of the current major advances and challenges in this field.
(Berzigotti, BMC Medicine (2017).
In national setting, among the most common liver problems are chronic
hepatitis B infection, alcoholic liver disease, and nonalcoholic fatty liver disease. One
in five of people with these diseases and problems develop complications such as
liver cirrhosis, liver failure, and liver cancer. (Medical City, 2019) According to the
latest WHO data published in 2017 Liver Disease Deaths in Philippines reached 8,401
or 1.36% of total deaths. The age adjusted Death Rate is 11.32 per 100,000 of
population ranks Philippines #119 in the world. More Filipinos are being diagnosed
with liver diseases, possibly owing to today's increasingly unhealthy lifestyle. A
research published in 2017 reveals that deaths attributed to liver diseases reached
8,401 or 1.36% of total deaths in the country.According to the World Health
Organization, our country is still hyperendemic for Hepatitis B with an estimated
prevalence rate of 16% which translates to 16 million Filipinos who are currently
chronic carriers of Hepatitis B and a great majority of these patients belong to the
marginalized groups of the community. Fifteen to twenty-five percent (15-25%) of
patients with chronic hepatitis B infection may develop complications i.e. liver
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cirrhosis and hepatocellular carcinoma. Hepatitis B is considered to be the most
common cause of liver-related deaths in the Philippines. In 2005, Philippine Cancer
Facts and Estimates reported that 7,477 Filipinos would die of liver cancer second to
lung cancer (26.7%) with an estimated annual death of 15,881 calculated at 12.3%.
Evidence Based Practice
The 2017 Hepatology Society of the Philippines Consensus Statements on the
Management of Chronic Hepatitis B
Authors: Jade D. Jamias, M.D.; Dulcinea A. Balce-Santos, M.D. Joseph C. Bocobo,
M.D.; Madalinee Eternity D. Labio, M.D.; Ma. Antoinette DC. Lontok, M.D.;
Therese C. Macatula, M.D.; Janus P. Ong, M.D.; Arlinking K. Ong-Go, M.D.;
Stephen Wong, M.D.; Ira I. Yu, M.D.; Diana A. Payawal, M.D.
Foreword
Chronic hepatitis B virus (CHB) infection is a serious problem that affects over 300
million people worldwide and is highly prevalent in the Asia Pacific region. In the
Philippines, an estimated 7.3 million Filipinos or 16.7% of adults are chronically
infected with HBV, more than twice the average prevalence in the Western Pacific
region. In view of the above, the Hepatology Society of the Philippines (HSP)
embarked on the development of consensus statements on the management of
hepatitis B with the primary objectives of standardizing approach to management,
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empowering other physicians involved in the management of hepatitis B and
advancing treatment subsidy by the Philippine Health Insurance Corporation
(PhilHealth). The local guidelines include screening and vaccination, general
management, indications for assessment of fibrosis in those who did not meet
treatment criteria, indications for treatment, on-treatment and post-treatment
monitoring and duration of antiviral treatment. Recommendations on the management
of antiviral drug resistance, management of special populations including patients
with concurrent HIV or hepatitis C infection, women of child-bearing age (pregnancy
and breastfeeding), patients with decompensated liver disease, patients receiving
immunosuppressive medications or chemotherapy and patients in the setting of
hepatocellular carcinoma are also included. However, the guidelines did not include
management for patients with liver and other solid organ transplantation, patients on
renal replacement therapy, and children. The consensus statements will be amended
accordingly as new therapies become available.
Introduction
Chronic hepatitis B virus (HBV) infection is a serious problem that affects over 300
million people worldwide and is highly prevalent in the Asia-Pacific region.1-5 In the
Philippines, an estimated 7.3 million Filipinos or 16.7% of adults are chronically
infected with HBV, more than twice the average prevalence in the Western Pacific
region. The course of chronic infection with HBV (i.e., immune tolerant, immune
clearance, inactive and reactivation phases) varies and is unpredictable. Chronic
hepatitis B (CHB) ranges from an inactive carrier state to chronic active hepatitis that
may progress to cirrhosis and hepatocellular carcinoma (HCC) in 30% and 53% of
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cases, respectively. CHB accounts for 5% to 10% of liver transplantations and 0.5 to
one million deaths each year. The interplay of host and viral factors, superimposed
co-infections (e.g., hepatitis C virus [HCV], hepatitis D virus [HDV] or human
immunodeficiency virus [HIV]) and the presence of risk factors (e.g., alcohol abuse
and obesity) alter the natural course of HBV infection and the efficacy of and
response to treatment. HBV is transmitted through perinatal, percutaneous, sexual, or
close person-to-person contact. The risk of progression to chronic infection is around
90% in newborns of HBeAg-positive mothers, 25% to 30% in infants and children
less than five years of age, and less than 5.0% in adults. Moreover, specific groups are
especially at risk for HBV infection
Method
The applicability and feasibility of current international guidelines formulated by the
Asian Pacific Association for the Study of the Liver (APASL), the European
Association for the Study of the Liver (EASL) and the American Association for the
Study of Liver Diseases (AASLD) on the management of hepatitis B to the existing
healthcare situation in the Philippines was determined by a thorough review of the
consensus statements conducted by a core working group composed of nine members
(Jamias J, Bocobo J, Labio ME, Ong J, Wong S, Yu I, Co A, Macatula T, Go A and
Lontok M.) The members were chosen for their expertise, academic affiliations,
active clinical practice and research in hepatitis B. Literature searches were performed
in Medline, Embase, and the Cochrane Central Register of Controlled Trials. Manual
searches in bibliographies of key articles including those published in the Philippine
Journal of Internal Medicine (PJIM) and Philippine Journal of Gastroenterology were
24
likewise done. Local data gathering was also performed through a review of scientific
papers submitted by fellows-in-training from different accredited training institutions
of the Philippine Society of Gastroenterology (PSG). A Knowledge, Attitudes and
Practices (KAP) survey was also conducted among family physicians, general
internists, infectious disease specialists, gastroenterologists and hepatologists during
the Annual convention of the Hepatology Society of the Philippines (HSP) last
January 2016. A pre-consensus development conference was held where the results of
the surveys and reviews were presented and discussed. Important issues were
identified by the core working group for further deliberations. Following the modified
Delphi process, 17 recommendations were proposed by the core working group for
votation. The consensus development conference proper was held in July 2016 in
which the chairs and training officers or the representatives from all the training
institutions in gastroenterology, representatives from the Philippine College of
Physicians (PCP), the Philippine Society for Microbiology and Infectious Diseases
(PSMID) and the Philippine Academy of Family Physicians (PAFP) participated.
During the consensus development proper, voting for each statement was done as
follows: (1) Accept completely; (2) Accept with some reservation; (3) Accept with
major reservation; (4) Reject with reservation; (5) Reject completely. Liberal
discussion and debate was encouraged during the conference. Votation on every
statement was conducted anonymously using wireless keypads. If the pre-determined
agreement of 85% was not achieved, the statement is rejected and revised accordingly
and subjected to up to three rounds of votation until the pre-determined agreement has
been achieved. The level of evidence and the strength for each recommendation were
25
graded using the Grading of Recommendations Assessment, Development, and
Evaluation (GRADE) system
Evaluation
2-1 A comprehensive evaluation, patient education and counselling should be done in
all patients with chronic hepatitis B infection (High quality, Strong). 2-2 Initial
evaluation should include the following: HBeAg, anti-HBe, HBV DNA, ALT and
liver ultrasound [high quality, strong]. HBsAg quantification is recommended
(Moderate quality, Strong). 2-3 For those with risk factors, testing for HCV
(antiHCV), HIV (EIA) and screening and surveillance for HCC (AFP and ultrasound
every six months) should be done (High quality, Strong). 2-4 Immunity to hepatitis A
(anti-HAV IgG) should be determined. If negative, vaccination is strongly
recommended (High quality, Strong). Counselling of patients with HBV should be
provided during initial evaluation and on every consultation. Details on the disease,
treatment options and need for long-term follow up and monitoring should be
emphasized. Avoidance of high-risk behavior and prevention of HBV transmission
should be discussed with patients, their sexual partners and household members.
Heavy alcohol intake (>20 g/day in women and >30 g/day in men) also increases the
risk of liver disease and patients should be advised to abstain or limit alcohol
consumption. An assessment of patients with CHB should include the evaluation of
HBV risk factors and related co-infections, alcohol intake, any family history of HBV
infection or HCC, and a complete physical examination. Serological markers for
HBV, particularly HBeAg, anti-HBe and HBV DNA, in conjunction with biochemical
26
(by serum alanine aminotransferase [ALT]) and other clinical evidence of liver
disease (by liver ultrasound) are necessary for identifying the status of HBV infection
and assessing the need for and response to treatment. Because low HBsAg levels may
distinguish true inactive carriers from CHB when HBV DNA and ALT levels are low,
HBsAg quantification is also recommended. HBsAg loss before the onset of cirrhosis
has also been associated with improved outcomes with less risk of progression to
hepatic decompensation or HCC. Laboratory examinations (e.g., complete blood
counts [CBC] with platelets, hepatic panel, prothrombin time [PT]) and liver
ultrasound are used to assess liver status. Liver cirrhosis is suspected in patients who
have a reversal in the ALT to aspartate aminotransferase (AST) ratio (<1), a
progressive decline in serum albumin concentrations and/or an increase in γ-
globulins, and a prolongation in the PT (often with a decline in platelet counts).
Histopathological confirmation, including the grading and staging of liver disease by
a liver biopsy, should also be performed if suspected. Furthermore, HCC screening
and surveillance through serum α-fetoprotein (AFP) and liver ultrasound every six
months is indicated for HBV subgroups considered at higher risk for HCC
Screening for HCV (via anti-HCV) or HIV (via enzyme immunoassay [EIA]) co-
infections in at-risk patients should also be performed. HCV co-infection increases the
risk for severe hepatitis, cirrhosis and HCC. Similarly, those with HIV coinfection
have higher levels of HBV DNA, lower rates of spontaneous HBeAg seroconversion,
more severe liver disease and increased rates of liver related deaths. Patients with
CHB should also be screened for hepatitis A virus antibodies (anti-HAV IgG) and
vaccination is strongly recommended in hepatitis A virus (HAV) seronegative
27
patients. Although HBV does not increase the risk of HAV infection, patients with
chronic liver disease from HBV infection are susceptible to developing fulminant
hepatitis A.
Treatment 4-1 Treatment should be considered for those with (1) persistently elevated
ALT levels ≥2x ULN [high quality, strong] over three to six months [moderate
quality, strong] AND (2) HBV DNA level ≥20,000 IU/mL if HBeAg-positive and
≥2,000 IU/mL if HBeAg-negative [high quality, strong]. 4-2 Patients with advanced
fibrosis or at least moderate inflammation on biopsy should be treated even if the
ALT is normal [high quality, strong]. 4-3 Treatment should be initiated in cirrhotic
patients with detectable HBV DNA regardless of the level of serum ALT [high
quality, strong]. 4-4 For patients who do not meet treatment criteria, monitoring of
ALT every three to six months is recommended [high quality, strong]. The decision to
start treatment depends on the risk of disease progression and the likelihood of
treatment response. Those with high levels of viral replication (as reflected by the
serum HBV DNA level and HBeAg status) and necro inflammatory activity in the
liver (as reflected by the serum ALT levels) are at increased risk of developing
cirrhosis and HCC. Other host factors such as older age, duration of infection, family
history of HCC, heavy alcohol consumption and co-infection with hepatitis C,
hepatitis delta and HIV are also associated with an increased risk for complications.
Starting treatment is also influenced by the likelihood of achieving treatment
endpoints. An elevated serum ALT at baseline is an important predictor of response
compared to those with normal ALT. In those with normal ALT, HBeAg
seroconversion occurs in less than 10% of patients. In a trial of Asian patients with
28
normal ALT, response to treatment was poor. The urgency of initiating treatment is
largely dictated by the severity of liver disease. This is determined using clinical and
laboratory parameters. Urgent treatment is recommended for those with life-
threatening conditions such as acute liver failure, protracted severe acute hepatitis,
decompensated cirrhosis and those with severe hepatitis flares. In those with
compensated cirrhosis or significant fibrosis on biopsy or non-invasive testing,
treatment is recommended if HBV DNA is detectable regardless of the serum ALT
level. Threshold values considered as triggers for treatment are constantly being
revised. Whether a serum HBV DNA level greater than 2,000 IU/mL (European
Association for the Study of the Liver [EASL]) or 20,000 IU/ mL for HBeAg positive
(American Association for the Study of Liver Diseases [AASLD]) is associated with
better outcomes remains controversial. Similarly, the cut-off used for the serum ALT
whether greater than ULN (EASL) or twice the ULN (AASLD) as well as what
constitutes a normal ALT is a topic of debate.
Options for Treatment 5-1 Options for antiviral agents for treatment-naïve HBeAg-
positive and HBeAg-negative individuals are: Peg-IFN alpha 2a at a dose of 180
μg/wk OR pegIFN alpha 2b at a dose of 1-1.5 μg/kg/wk [high quality, strong],
conventional IFN 5-10 MU three times/ wk [high quality, conditional], entecavir
(ETV) 0.5 mg/ day, tenofovir (TDF) 300 mg/day [high quality, strong], lamivudine
(LAM) 100mg/day, adefovir (ADV) 10mg/day, telbivudine (LdT) 600mg/day [high
quality, conditional], clevudine (CLV) 30mg/day [moderate quality, conditional]. 5-2
Peg-IFN, ETV and TDF are preferred first-line agents [high quality, strong]. The
ultimate goal of antiviral treatment for CHB is to reduce the risk of HCC, liver failure,
29
liver cirrhosis and improve survival. With the availability of increasing options for
treatment and a better understanding of the natural history of CHB, the optimal choice
depends on efficacy, safety, resistance profile and durability of response.
Immunomodulatory agents (e.g., interferon [IFN], pegylated [peg]-IFN) and
nucleos(t)ide analogues (NAs) (e.g., lamivudine [LAM], adefovir [ADV], entecavir
[ETV], telbivudine [LdT], tenofovir [TDF], clevudine [CLV]) are the two main
classes of antiviral agents approved for the treatment of CHB. International guidelines
recommend peg-IFN, ETV or TDF as first-line therapies. However, there are no
specific recommendations on which to choose from among these options. The main
advantages of peg-IFN are its finite duration of treatment and higher rates of sustained
response off-therapy. However, side effects and the need for more intensive
monitoring remain a concern. NAs, on the other hand, have an excellent safety
profile, making it the agent of choice in patients with decompensated cirrhosis, under
immunosuppression and in the setting of liver transplantation. In addition, NAs are
the most potent drugs currently available for suppressing viral replication. Serum
HBV DNA levels less than 60-80 IU/mL are achieved in 94% and 98% to 99% of
patients treated with long-term ETV and TDF, respectively. The first-generation NAs
such as LAM, ADV and LdT are no longer preferred as first line agents because they
often lead to incomplete viral suppression due to the development of resistance in
20% to 75% of patients with long-term use. The choice of treatment should be
individualized and should take into account socio-demographic factors such as
affordability, patient and health provider preference, occupational requirements and
the possibility of pregnancy.
30
Patients with Decompensated Liver Disease 13-1 For patients with hepatic
decompensation, treatment should be initiated promptly with ETV or TDF [high
quality, strong]. LdT, LAM or ADV can also be used in nucelos(t)ide naive patients
[high quality, conditional]. IFN should not be used in this setting (High quality,
Strong). Referral and evaluation for liver transplantation should be done.
Decompensated liver cirrhosis that is untreated carries a high risk of progressing to
HCC and hepatic failure with an estimated five-year survival rate of only 14%. The
underlying cause of liver deterioration (HBV antiviral resistance, presence of HCC,
etc) must be determined. Child-Turcotte-Pugh (CTP) or Model for End-Stage Liver
Disease (MELD) scores are used to monitor liver function. Management includes
addressing liver complications (e.g., ascites, bleeding, hepatic encephalopathy),
administering antiviral therapy and continued HCC surveillance. Prompt assessment
and referral for liver transplantation is also warranted. Current Asian Pacific
Association for the Study of the Liver (APASL) and EASL guidelines recommend
antiviral treatment irrespective of HBV DNA level. Kidney disease is common in
these patients and should be considered when planning the choice and dosage of
antiviral treatment. ETV and TDF have demonstrated efficacy in improving or
stabilizing liver function. A 12-month course of ETV significantly improved
pretreatment CTP and MELD scores in patients with decompensated CHB. However,
patients should be monitored for ETV-associated lactic acidosis. TDF monotherapy is
comparable in efficacy to TDF plus emtricitabine or ETV monotherapy. Data showed
similar rates of reduction in HBV DNA (<400 IU/ML) and a decrease or
improvement in MELD scores across all three groups after 48 weeks of treatment.
31
Patients with Acute Hepatitis B 16-1 For patients with HCC and detectable HBV
DNA, treatment with a nucleos(t)ide analogue (preferably with ETV or TDF) should
be initiated before any therapy for HCC is considered (High quality, Strong). 16-2 For
patients with HCC and decompensated liver disease, treatment with a nucleos(t)ide
analogue (preferably with ETV or TDF) should be initiated (High quality, Strong).
HBV reactivation can occur following HCC liver resection, especially with baseline
HBV DNA >104 IU/mL. It has been shown to significantly reduce postoperative
recovery of liver function, increase liver failure rates, and worsen three-year disease
free and overall survival rates. A prospective randomized controlled trial has
demonstrated that in patients who had undergone liver resection for HBV-related
HCC, LdT reduced the incidence of perioperative HBV reactivation versus controls
(HR 0.07 [95% CI 0.01-0.65]; p=0.001). Rates o with preemptive LAM therapy than
without concomitant antiviral treatment (2.8% versus 29.7%; p=0.002). Nonetheless,
in light of limited trials on the use of antivirals in these patients, antiviral treatment
similar to patients with decompensated liver disease is currently recommended.
Concurrent evaluation and referral for liver transplantation should also be undertaken.
(2017 Hepatology Society of the Philippines Consensus Statements) hepatitis after
transarterial chemo-lipiodolization were also significantly lower.
32
Anatomy and Physiology of System’s Involved
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
33
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 consist 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 hepatic portal system begins in the capillaries of the digestive organs and
ends in the portal vein. Consequently, portal blood contains substances absorbed by
the stomach and intestines. Portal blood is passed through the hepatic lobules where
nutrients and toxins are absorbed, excreted or converted.
34
Restriction of outflow through the hepatic portal system can lead to portal
hypertension. Portal hypertension is most often associated with cirrhosis. Patients
usually present with splenomegaly, ascites, GI bleeding and/or portal systemic
encephalopathy.
The consequences of portal hypertension are due to
portal systemic anastomosis formed by the body as an
attempt to bypass the obstructed liver circulation. These
collateral vessels form along the falciform ligament,
diaphragm, spleen, stomach and peritoneum. The
collaterals find their way to the renal vein where blood
drained from the digestive organs is let into the systemic
circulation.
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
 Enzyme activation
 Storage of glycogen, vitamins, and minerals
 Synthesis of plasma proteins, such as albumin and globulin, and clotting
factors
 Blood detoxification and purification
35
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.
36
 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.
37
Biliary tract
The biliary tract (or biliary tree) is the common anatomy
term for the path by which bile is secreted by the liver on its way
to the duodenum, or small intestine, of most members of the
mammal family. It is referred to as a tree because it begins with
many small branches which end in the common bile duct,
sometimes referred to as the trunk of the biliary tree. The duct is
present along with the branches of the hepatic artery and the
portal vein forming the central axis of the portal triad. Bile flows
in opposite direction to that of the blood present in the other two channels. The liver is
usually excluded, but sometimes included.
Pressure inside in the biliary tree can give rise to
gall stone and lead to cirrhosis of the liver.
Blockage can cause jaundice.
The biliary tract can also serve as a
reservoir for intestinal tract infections. Since
biliary tract is an internal organ, it has no
somatic nerve supply, and, therefore there is
pain due to infection and inflammation of the
biliary tract is not a somatic pain but it may be caused by luminal distension which
38
causes stretching of the wall (the same mechanism of pain in intestinal colic in
intestinal obstruction in which intestine also do not have somatic nerve supply)
39
The path is as follows:
 Bile canaliculi>>Canals of Hering>> bile ductules (in portal tracts) >>
intrahepatic bile ducts >> left and right hepatic ducts >>
 merge to form >>common hepatic duct>>
 exits liver and joins >>cystic duct (from gall bladder) >>
 forming >>common bile duct>> joins with >>pancreatic duct>>
 forming >>ampulla of Vater>> enters duodenum
The anatomy of the biliary tree is a little complicated, but it is important to
understand. The liver's cells (hepatocytes) excrete bile into canaliculi, which are
intercellular spaces between the liver cells. These drain into the right and left hepatic
ducts, after which bile travels via the common hepatic and cystic ducts to the
gallbladder. The gallbladder, which has a capacity of 50 milliliters (about 5
tablespoons), concentrates the bile 10-fold by removing water and stores it until a
person eats. At this time, bile is discharged from the gallbladder via the cystic duct
into the common bile duct and then into the duodenum (the first part of the small
intestine), where it begins to dissolve the fat in ingested food.
The liver excretes approximately 500 to 1000 milliliters (50 to 100
tablespoons) of bile each day. Most (95%) of the bile that has entered the intestines is
resorbed in the last part of the small intestine (known as the terminal ileum) and
returned to the liver for reuse.
40
The many functions of bile are best understood by knowing the composition of bile:
1. Bile Salts (cholates, chenodeoxycholate, deoxycholate): these are produced by
the liver's breakdown of cholesterol. They function in bile as detergents that
dissolve dietary fat and allow it to be absorbed. Hence, disruption of bile
excretion disrupts the normal absorption of fat, a process called malabsorption.
Patients develop diarrhea because the fat is not absorbed (steatorrhea), and
develop deficiencies of the fat-soluble vitamins (A, D, E, and K).
2. Cholesterol and phospholipids-while only
4% of bile is cholesterol, the secretion of
cholesterol and its metabolites (bile salts)
into bile is the body's major route of
elimination of cholesterol. Phospholipids,
which are components of cell membranes,
enhance the cholesterol solubilizing
properties of bile salts. Inefficient excretion
of cholesterol can cause an increased serum
cholesterol. This predisposes to vascular disease (heart attacks, strokes, etc.)
3. Bilirubin-while this comprises only 0.3% of bile, it is responsible for bile's
yellow color. Bilirubin is a product of the body's metabolism of hemoglobin,
the carrier of oxygen in red blood cells. Disruption of the excretion of this
component of bile leads to a yellow discoloration of the eyes and skin
(jaundice).
41
4. Protein and miscellaneous components
Bile production and recirculation is the main excretory function of the liver. Tumors
that obstruct the flow of bile from the liver can also impair other liver functions.
Therefore, it is necessary to understand these other functions to understand the
symptoms that these tumors can cause. These include:
Metabolic functions, such as the maintenance of glucose (blood sugar) levels
Synthetic functions, such as the synthesis of serum proteins such as albumin, blood
clotting (coagulation) factors, and complement (a mediator of inflammatory
responses)
Storage functions, such as the storage of sugar (glycogen), fat (triglycerides), iron,
copper, and fat-soluble vitamins (A, D, E, and K)
Catabolic functions, such as the detoxification
of drugs
Circulation of the blood in blood vessels
There are two circulatory routes of blood
as it flows through the blood vessels: the
42
systemic and the pulmonary circulation. In systemic circulation, blood flows from the
left ventricle of the heart through blood vessels to all parts of the body (except gas
exchange tissues of lungs) and back to the atrium. In pulmonary circulation on the
other hand, venous blood moves from the right atrium to right ventricle to pulmonary
artery to lung arterioles and capillaries where gases exchanged; oxygenated blood
returns to the left atrium via pulmonary veins; from left atrium, blood enters the left
ventricle.
Hepatic Portal Circulation
The veins of the hepatic
portal circulation drain the
digestive organs, spleen, and
pancreas and deliver this blood to
the liver through the hepatic portal
vein. When you have just eaten,
the hepatic portal blood contains
large amounts of nutrients. Since
the liver is a key body organ
involve in maintaining the proper
glucose, fat and protein
concentrations in the blood, this system “takes a detour “to ensure that the liver
processes these substances before they enter the systemic circulation. As blood flows
slowly through the liver, some of the nutrients are removed to be stored or processed
43
in various ways for later release to the blood. The liver is drained by the hepatic veins
that enter the inferior vena cava. Like the portal circulation that links the
hypothalamus of the brain and the anterior pituitary gland, the hepatic portal
circulation is a unique and unusual circulation. Normally, arteries feed capillary beds,
which in turn drain into veins. Here we see veins feeding the liver circulation.
The inferior mesenteric vein, draining the terminal part of the large intestine,
drains into the splenic vein, which itself drains the spleen, pancreas and the left side
of the stomach. The splenic vein and superior mesenteric vein (which drains the
small intestine and the first part of the colon) join to form the hepatic portal vein. The
L .Gastric vein, which drains the right side of the stomach, drains directly into the
hepatic portal vein.
44
CHAPTER 2
DISEASE PROCESS
Symptomatology
SYMPTOMS Present/abse Rationale Actual

nt
Anorexia Present Increased brain tryptophan This is present
(TRP) availability for serotonin with the patient.
synthesis play a role in the He stated that he
pathogenesis of anorexia. Since has no appetite to
in chronic liver failure, increased eat.
plasma and cerebrospinal fluid
TRP concentrations are
characteristically reported, that
also in liver cirrhosis, increased
brain TRP availability constitute
the pathogenic mechanism of
anorexia.
45
http://www3.interscience.wiley.c
om/journal/49716/abstract?
CRETRV=1&SRETRY=0
Nausea and Present The malabsorption of fats may Patient hasn’t
vomiting lead to deficit of fatsoluble vomited but was
vitamins, hemorrhoids, feeling nauseous
intolerance to fatty foods, nausea prior to
and vomiting attacks, and admission.
abdominal bloating. Since the
liver has already decreased in
function, its function to produce
bile which emulsifies fats is also
decreased, thus these symptoms
persist.
www.enwikipedia.org/wiki/Live
r_disease#Symptoms_of_a_dise
ased_liver
Body malaise Present This is due to the decreased in The patient
liver function of the liver experienced body
because of the hepatic fibrosis. malaise and was
Therefore, the patient has also one of his chief
decreased erythropoietin which complaint that
then results to the decrease of resulted to his
red blood cells circulating in the admission.
blood, and there will be
decreased hemoglobin. All of
this in return will cause the
patient to have body malaise.
Bleeding Absent Bleeding tendencies such as The patient had
tendencies nosebleeds, easy bruising, and no bleeding
bleeding gums may result from during our
46
thrombocytopenia secondary to rotation.
splenomegaly, decreased
vitamin K absorption and
decreased production of
coagulation factors and
regurgitation of blood to the
spleen and gastrointestinal tract.
Suddarth, Doris Smith. The

Lippincott Manual of Nursing
Practice. 5th edition. 1991. Pages
514-515.
Portal Present Portal hypertension occurs The patient has

hypertension because of the obstruction of ascites which is a
portal circulation brought about complication of
by the portal obstruction caused portal
by the hepatic scarring. hypertension.
http://www.emedicinehealth.co This is an
m/cirrhosis/page2_em.htm#Cirr
evidence that he
hosis%20Causes
indeed has portal
hypertension. In
addition, the
patient was
diagnosed to have
hypertension on
the year 2000.
Ascites Present This happened because of the The patient has
decrease of albumin in the blood ascites as
plasma. Albumin is responsible evidenced by his
for maintaining the oncotic distended
47
pressure in the blood volume. A abdominal cavity.
decrease in albumin will mean a
decrease in oncotic pressure,
which will result to a more
permeable membrane which
results to fluid leaking through
the vasculature into the
abdominal cavity.
Suddarth, Doris Smith. The

514-515.
Jaundice Present Jaundice is the buildup of bile The patient was
pigment that is passed by the noted to have
liver into the intestine. Due to yellowish skin
the portal obstruction, the bile color on all four
going to the GI tract will have a extremities
backflow to the liver. The bile including the
then goes to the blood stream, palms. The
and this causes the yellowing of patient also had
the skin, due to the presence of icteric sclera
bi when inspected.
Patient’s total
(http://www.healthscout.com/en
bilirubin level is
cy/68/292/main.html)
100.7 umol/L and
the normal range
is 3.0-17.0
umol/L
edema on the Absent Plasma albumin is reduced, Patient has no
extremities leading to edema. edema on the
48
lower and upper
Suddarth, Doris Smith. The extremities.
514-515.
Caput medusae Present Portal hypertension results from The patient was
the abnormal blood flow pattern noted to have
in liver created by cirrhosis. The large, dilated, and
increased pressure is transmitted distended veins
to collateral venous channels. on the abdomen
Sometimes these venous area when
collaterals are dilated. Caput inspected
medusa consists of dilated veins
seen on the abdomen of a patient
with cirrhosis of the liver.
Coma Absent This is a progressive symptom, The patient is not

secondary to the loss of on a comatose
ammonia to urea conversion and state.
consequent delivery of toxic
ammonia to the brain.
Deterioration of mental function
from lethargy to coma and
eventual death
Etiology
Basic Etiology Present/ Rationale Actual

Absent
Predisposing
49
Factors
Male  Liver Cirrhosis occurs The patient is male.
mostly in men.
http://www.cancer.org/docr
oot/cri/content/cri_2_2_2x_
what_causes_liver_cancer_
25.asp
Ages 45-75  Liver Cirrhosis is most The patient is 68 years old.
common among people ages
45-75 years old.
Race: Asian  In Asia and Africa, cirrhosis The patient is an Asian since
is also common but more he was born from Filipino
likely to be associated with parents, and he was born in
hepatitis. Davao City.
http://esynopsis.uchc.edu/e
Atlas/GI/1210.htm
Biliary atresia X Infants can be born without The patient has no record or
bile ducts (biliary atresia) history of Biliary atresia.
and ultimately develop
cirrhosis. The bile ducts
carry bile formed in the
liver to the intestines, where
the bile helps in the
digestion of fat. So, when
the bile ducts are blocked,
bile is trapped in the liver,
http://www.medicinenet.co
m/cirrhosis/page3.htm
50
Basic Etiology Present/ Rationale Actual
Absent
Precipitating
Factors
Chronic  Chronic high levels of alcohol As stated by the patient,
alcoholism consumption injure liver cells. the patient at his young
Alcohol seems to injure the liver age was able to drink 1
by blocking the normal long neck (750 ml) of
metabolism of protein, fats, and Tanduay and Fundador
carbohydrates. Alcohol can by his own. He started
poison all living cells, causing drinking at the age of
liver cells to become inflamed 23. Patient admitted that
and die. Thirty percent of he is alcoholic. When he
individuals who drink daily at reached his adulthood,
least eight to sixteen ounces of he continues to drink
hard liquor or the equivalent for and smoke 5 packs
fifteen or more years will develop every day.
cirrhosis.
http://www.emedicinehealth.com/
cirrhosis/page2_em.htm#Cirrhosi
s%20Causes
Chronic viral X Condition where hepatitis B or The patient had no

hepatitis (types hepatitis C virus infects the liver medical record of
B, C, and D). for years. some patients infected acquiring hepatitis B, C,
with hepatitis B virus and most or D.
patients infected with hepatitis C
51
virus develop chronic hepatitis,
which, in turn, causes progressive
liver damage and leads to
cirrhosis, and, sometimes, liver
cancers.
Hepatitis B causes liver

inflammation and injury that over
several decades can lead to
cirrhosis. Hepatitis D is
dependant on the presence of
hepatitis B, but accelerates
cirrhosis in co-infection
The hepatitis C virus ranks with

alcohol as a major cause of
chronic liver disease and
cirrhosis. Infection with this virus
causes inflammation of and low-
grade damage to the liver that
over several decades can lead to
cirrhosis.
http://www.spiritus-
temporis.com/cirrhosis/causes.ht
ml
Smoking  Research reveals that smoking The patient smokes 5
damages the liver. Smoking packs of cigarette a day,
activates chemical materials and he started smoking
within the body. These chemicals when he was a teenager.
that are manufactured by smoking
52
also provoke oxidative stress
which is linked with lipid
peroxidation. When this occurs,
the condition fibrosis is
developed.
Smoking increases the
manufacturing of pro-
inflammatory cytokines which is
related to liver cell damage.
Smoking also contributes the
continued succession of chronic
alcoholic hepatitis as well as to
the progression of cirrhosis.
Http://www.ehow.com/how-
does_4577854_effects-smoking-
drinking-liver.html
Malnutrition,  Fat builds up in the liver and Patient has an increase
especially high eventually causes cirrhosis. fat in the blood or
fat intake increased level of
Fat (triglycerides) accumulates
cholesterol in the blood
throughout the hepatocytes for the
(LDL-bad cholesterol)
following reasons:
according to his
laboratory results.
 Export of fat from the
Patient’s cholesterol
liver is decreased because
level is 6.1, Patient’s
hepatic fatty acid
LDL level is 5.2.
oxidation and lipoprotein
production decrease.
 Input of fat is increased
because the decrease in
53
hepatic fat export
increases peripheral
lipolysis and triglyceride
synthesis, resulting in
hyperlipidemia.
http://digestive.niddk.nih.gov/ddi
seases/pubs/cirrhosis/
54
Pathophysiology
Predisposing Factors: Precipitating Factors:

 Age (68 years old)  Chronic Alcoholism
 Gender (Male)  Smoking
 Race (Asian)  Lifestyle
 Diet
55
LIVER CIRRHOSIS PATHOPHYSIOLOGY (DETAILED)
chronic alcoholism
toxins from alcohol:

release of acetyldehyde
↑ AST, ALT,
damage hepatocytes
alkaline,
phophatase, GGT
necrosis of hepatocytes
fibrosis obstruction in
56 blood flow
↓ liver function liver cells regenerate PORTAL

in abnormal pattern HYPERTENSION
liver cells loaded with fat

Alcohol (ethanol) is readily absorbed from the stomach, but most is absorbed
from the small intestine. Alcohol cannot be stored. A small amount is degraded in
transit through the gastric mucosa, but most is catabolized in the liver, primarily by
alcohol dehydrogenase (ADH) but also by cytochrome P-450 2E1 (CYP2E1) and
the microsomal enzyme oxidation system (MEOS).
Metabolism via the ADH pathway involves the following:
 ADH, a cytoplasmic enzyme, oxidizes alcohol into acetaldehyde. Genetic
polymorphisms in ADH account for some individual differences in blood
alcohol levels after the same alcohol intake but not in susceptibility to
alcoholic liver disease.
 Acetaldehyde dehydrogenase (ALDH), a mitochondrial enzyme, then
oxidizes acetaldehyde into acetate. Chronic alcohol consumption enhances
acetate formation. Asians, who have lower levels of ALDH, are more
susceptible to toxic acetaldehyde effects (eg, flushing); the effects are similar
to those of disulfiram, which inhibits ALDH.
 These oxidative reactions generate hydrogen, which converts nicotinamide-
adenine dinucleotide (NAD) to its reduced form (NADH), increasing the
redox potential (NADH/NAD) in the liver.
 The increased redox potential inhibits fatty acid oxidation and
gluconeogenesis, promoting fat accumulation in the liver.
Chronic alcoholism induces the MEOS (mainly in endoplasmic reticulum),
increasing its activity. The main enzyme involved is CYP2E1. When induced, the
MEOS pathway can account for 20% of alcohol metabolism. This pathway
57
generates harmful reactive oxygen species, increasing oxidative stress and formation
of oxygen-free radicals.
Hepatic fat accumulation
Fat (triglycerides) accumulates throughout the hepatocytes for the following
reasons:
 Export of fat from the liver is decreased because hepatic fatty acid oxidation
and lipoprotein production decrease.
 Input of fat is increased because the decrease in hepatic fat export increases
peripheral lipolysis and triglyceride synthesis, resulting in hyperlipidemia .
Hepatic fat accumulation may predispose to subsequent oxidative damage.
Endotoxins in the gut
Alcohol changes gut permeability, increasing absorption of endotoxins
released by bacteria in the gut. In response to the endotoxins (which the impaired
liver can no longer detoxify), liver macrophages (Kupffer cells) release free
radicals, increasing oxidative damage.
Oxidative stress is increased by
 Liver hypermetabolism, caused by alcohol consumption
 Free radical–induced lipid peroxidative damage
 Reduction in protective antioxidants (eg, glutathione, vitamins A and E),
caused by alcohol-related undernutrition
 Binding of alcohol oxidation products, such as acetaldehyde, to liver cell
proteins, forming neoantigens and resulting in inflammation
58
 Accumulation of neutrophils and other white blood cells (WBCs), which are
attracted by lipid peroxidative damage and neoantigens
 Inflammatory cytokines secreted by WBCs
Accumulation of hepatic iron, if present, aggravates oxidative damage. Iron can
accumulate in alcoholic liver disease through ingestion of iron-containing fortified
wines; most often, the iron accumulation is modest. This condition must be
differentiated from hereditary hemochromatosis .
Resultant inflammation, cell death, and fibrosis
A vicious circle of worsening inflammation occurs: Cell necrosis and
apoptosis result in hepatocyte loss, and subsequent attempts at regeneration result
in fibrosis. Stellate (Ito) cells, which line blood channels (sinusoids) in the liver,
proliferate and transform into myofibroblasts, producing an excess of type I
collagen and extracellular matrix. As a result, the sinusoids narrow, limiting blood
flow. Fibrosis narrows the terminal hepatic venules, compromising hepatic
perfusion and thus contributing to portal hypertension . Extensive fibrosis is
associated with an attempt at regeneration, resulting in liver nodules. This process
culminates in cirrhosis. (Orfanidis MD, 2019)
CHAPTER 3
59
DEVELOPMENTAL THEORIES
This portion of Review of Related Literature will discuss the different developmental
theories.
Erickson’s Psychosocial Developmental Theory
Erikson’s (1959) theory of psychosocial development has eight distinct stages,
taking in five stages up to the age 18 years and three further stages beyond, well into
adulthood. Erickson suggests that there are still plenty of room for continued growth
and development throughout one’s life. Erikson puts a great deal of emphasis on
adolescent period, feeling it was a crucial stage for developing a person’s identity.
Erikson maintained that personality develops in a predetermined order through eight
stages of psychosocial development, from infancy to adulthood. During each stage,
the person experiences a psychosocial crisis which could have a positive or negative
outcome for personality development.
For Erikson (1958, 1963), these crises are of a psychosocial nature because
they involve psychological needs of the individual (i.e., psycho) conflicting with the
needs of society (i.e., social).
According to the theory, successful completion of each stage results in a
healthy personality and the acquisition of basic virtues. Basic virtues are characteristic
strengths which the ego can use to resolve subsequent crises.
Failure to successfully complete a stage can result in a reduced ability to
complete further stages and therefore an unhealthier personality and sense of self.
These stages, however, can be resolved successfully at a later time.
(https://www.simplypscyology.org/Erik-Erikson.html)
Sigmund Freud Psychoanalytical Theory
60
Sigmund Freud’s psychoanalytic theory of personality argues that human
behavior is the result of the interactions among three component parts of the
mind: the id, ego, and superego. This theory, known as Freud’s structural theory of
personality, places great emphasis on the role of unconscious psychological conflicts
in shaping behavior and personality. Dynamic interactions among these fundamental
parts of the mind are thought to progress through five distinct psychosexual stages of
development. Over the last century, however, Freud’s ideas have since been met with
criticism, in part because of his singular focus on sexuality as the main driver of
human personality development.
Freud’s Structure of the Human Mind
According to Freud, our personality develops from the interactions among
what he proposed as the three fundamental structures of the human mind: the id, ego,
and superego. Conflicts among these three structures, and our efforts to find balance
among what each of them “desires,” determines how we behave and approach the
world. What balance we strike in any given situation determines how we will resolve
the conflict between two overarching behavioral tendencies: our biological aggressive
and pleasure-seeking drives vs. our socialized internal control over those drives.
The id, the most primitive of the three structures, is concerned with instant
gratification of basic physical needs and urges. It operates entirely unconsciously
(outside of conscious thought). For example, if your id walked past a stranger eating
ice cream, it would most likely take the ice cream for itself. It doesn’t know, or care,
that it is rude to take something belonging to someone else; it would care only that
you wanted the ice cream.
61
The superego is concerned with social rules and morals—similar to what
many people call their” conscience” or their “moral compass.” It develops as a child
learns what their culture considers right and wrong. If your superego walked past the
same stranger, it would not take their ice cream because it would know that that
would be rude. However, if both your id and your superego were involved, and your
id was strong enough to override your superego’s concern, you would still take the ice
cream, but afterward you would most likely feel guilt and shame over your actions.
In contrast to the instinctual id and the moral superego, the ego is the rational,
pragmatic part of our personality. It is less primitive than the id and is partly
conscious and partly unconscious. It’s what Freud considered to be the “self,” and its
job is to balance the demands of the id and superego in the practical context of reality.
So, if you walked past the stranger with ice cream one more time, your ego would
mediate the conflict between your id (“I want that ice cream right now”) and superego
(“It’s wrong to take someone else’s ice cream”) and decide to go buy your own ice
cream. While this may mean you have to wait 10 more minutes, which would frustrate
your id, your ego decides to make that sacrifice as part of the compromise– satisfying
your desire for ice cream while also avoiding an unpleasant social situation and
potential feelings of shame.
Freud believed that the id, ego, and superego are in constant conflict and that adult
personality and behavior are rooted in the results of these internal struggles
throughout childhood. He believed that a person who has a strong ego has a healthy
personality and that imbalances in this system can lead to neurosis (what we now
think of as anxiety and depression) and unhealthy behaviors.
(https://positivepsychology.com/psychoanalysis/
62
Finally, one of the most enduring concepts associated with Freud is his
psychosexual stages. Freud proposed that children develop in five distinct stages, each
focused on a different source of pleasure:
1. First Stage: Oral—the child seeks pleasure from the mouth (e.g., sucking);
2. Second Stage: Anal—the child seeks pleasure from the anus (e.g., withholding
and expelling feces);
3. Third Stage: Phallic—the child seeks pleasure from the penis or clitoris (e.g.,
masturbation);
4. Fourth Stage: Latent—the child has little or no sexual motivation;
5. Fifth Stage: Genital—the child seeks pleasure from the penis or vagina (e.g.,
sexual intercourse; McLeod, 2013).
Freud hypothesized that an individual must successfully complete each stage to
become a psychologically healthy adult with a fully formed ego and superego.
Otherwise, individuals may become stuck or “fixated” in a particular stage, causing
emotional and behavioral problems in adulthood (McLeod, 2013).
Jean Piaget Cognitive Development Theory
63
Piaget's (1936) theory of cognitive development explains how a child
constructs a mental model of the world. He disagreed with the idea that intelligence
was a fixed trait and regarded cognitive development as a process which occurs due to
biological maturation and interaction with the environment.
Piaget was employed at the Binet Institute in the 1920s, where his job was to
develop French versions of questions on English intelligence tests. He became
intrigued with the reason’s children gave for their wrong answers to the questions that
required logical thinking. He believed that these incorrect answers revealed important
differences between the thinking of adults and children.
Piaget's 4 Stages of Cognitive Development
Piaget proposed four stages of cognitive development which reflect the increasing
sophistication of children's thought:
1. Sensorimotor stage (birth to age 2)
2. Preoperational stage (from age 2 to age 7)
3. Concrete operational stage (from age 7 to age 11)
4. Formal operational stage (age 11+ - adolescence and adulthood).
Each child goes through the stages in the same order, and child development is
determined by biological maturation and interaction with the environment.
Although no stage can be missed out, there are individual differences in the
rate at which children progress through stages, and some individuals may never attain
the later stages.
64
Piaget did not claim that a particular stage was reached at a certain age -
although descriptions of the stages often include an indication of the age at which the
average child would reach each stage.
Sensorimotor Stage (Birth-2 years)
The main achievement during this stage is Object Permanence - knowing that
an object still exists, even if it is hidden. It requires the ability to form a mental
representation (i.e., a schema) of the object.
Preoperational Stage (2-7 years)
During this stage, young children can think about things symbolically. This is
the ability to make one thing - a word or an object - stand for something other than
itself. Thinking is still egocentric, and the infant has difficulty taking the viewpoint of
others.
Concrete Operational Stage (7-11 years)
Piaget considered the concrete stage a major turning point in the child's
cognitive development because it marks the beginning of logical or operational
thought. This means the child can work things out internally in their head (rather than
physically try things out in the real world). Children can conserve number (age 6),
mass (age 7), and weight (age 9). Conservation is the understanding that something
stays the same in quantity even though its appearance changes.
Formal Operational Stage (11 years and over)
The formal operational stage begins at approximately age eleven and lasts into
adulthood. During this time, people develop the ability to think about abstract
concepts, and logically test hypotheses.
65
Havighurt’s Developmental Stages
According to Havighurst’s theory, when people successfully accomplish the
developmental tasks at a stage, they feel pride and satisfaction. They also earn the
approval of their community or society. This success provides a sound foundation that
allows these people to accomplish the developmental tasks that they will encounter at
later Havighurst developmental stages.
The main assertion of Robert Havighurst’s theory is that development is
continuous throughout an individual’s entire lifespan, occurring in stages. An
individual moves from one stage to the next by means of successful resolution of
problems or performance of certain developmental tasks. These tasks are typically
encountered by most people in the culture where the individual belongs.
Conversely, when people fail to accomplish a developmental task, they’re
often unhappy and are not accorded the desired approval by society. This results in
the subsequent experience of difficulty when faced with succeeding developmental
tasks at later Havighurst developmental stages.
The applications of Havighurst’s Developmental Tasks Theory extend to the
field of education and have asserted influences over educators and psychologists
worldwide. Although the theory has its roots in the 1930s, it continues to stimulate the
insights of contemporary psychologists, prompting the publication of new
manuscripts and books based on the concepts of the developmental task theory.
66
Over the years, the reception and interpretation of Havighurst’s developmental
tasks have evolved with the upsurge of new findings. Nevertheless, this theory has
remained robust in its testimony that development is continuous throughout the entire
lifespan of an individual. (Psychologynotes, 2019)
67
DATA GATHERING
PATIENT PROFILE
Patient Name: Mr. V
Date of Birth: May 21, 1951
Age: 68
Sex: Male
Civil Status: Married
Address: #169 Block 3, Phase 1, S. I.R. New Matina Davao City
Birthplace: Himamaylan, Negros
Occupation: Retired Soldier
Nationality: Filipino
Father: Deceased
Mother: Deceased
Religion: Roman Catholic
Spouse: Mrs. V
Admission Date and Time: February 26,2020 & 11:35AM
68
HEALTH ASSESSMENT
PHYSICIAN’S FINDINGS
DATE: February 26, 2020
General Appearance:
Awake, Alert, Afebrile, Not in respiratory distress, Ambulatory
Vital signs:
Blood pressure: 140/100
Pulse rate: 95 bpm
Respiratory rate: 17 cpm
Temperature: 36 ‘C
Skin: Jaundice
HEENT: Normocephalic, icterus sclera, pars plana lensectomy
Neck: Mass on left side, movable, soft, non-tender
Chest and Lungs: Equal chest expansion, with crackles on both lung fields
Heart: Lower S1 & S2, no adventitious sound noted
Abdomen: Tenderness on epigastric area on deep palpation, Ascites noted
Extremities: Full Pulses, no edema noted
Genitalia: Not assessed
Neurological exam: Not assessed
CHIEF COMPLAINT:
Patient complains of epigastric pain
69
MEDICAL DIAGNOSIS
Admitting Diagnosis:
To consider liver cirrhosis secondary to alcoholic liver disease, Insulin requiring
Diabetes Mellitus, Hypertension II – controlled.
Final Diagnosis:
Liver Cirrhosis secondary to alcoholic liver disease.
70
NURSING ASSESSMENT TOOL
DATE: February 28, 2020
PHYSICAL EXAMINATION
I. General Appearance and Mental Status
Patient was awake, coherent and responsive. Patient had an IVF D5NaCl at 80cc/hour
infusing well at left metacarpal vein. Well groomed. He is very cooperative in
answering question related to his life and health issues.
II. Vital signs/ measurement
Latest vital signs recorded as follows: BP – 130/90, Temp.- 36.2’C, Pulse rate: 82
bpm, Respiratory rate:19 cpm, and Pain scale of 3 out of 10.
III. Integument
A. Skin
The patient had jaundice, uniformly brown in color except areas exposed to sun. With
reddish palm of hands and feet His skin folds and axillae were moist. Skin
temperature is within normal limits in all extremities.
B. Hair.
Hair is short with white streaks in color. His hair is thick and evenly distributed as
evidenced by absence of alopecia along the scalp. No infestations were noted upon
inspection and palpation of the patient’s hairline and scalp. Small amount of dandruff
was noted on patient’s scalp however there were no lesions, lumps or masses upon
palpation.
C. Nails
Nails short with slightly clubbing of nails noted on patient. Toenail clean, surface
was slightly curved and rough. Upon palpation, nail base was firm, fingernails had a
rough texture. Epidermis surrounding the nails was intact and no lesions were noted.
71
IV. Head
A. Skull
Skull was rounded and normocephalic. No bumps, masses or nodules upon inspection
and palpation.
B. Face
Appeared dry and symmetrical, no sign of any muscle weakness on face.
V. Eye structures & visual acuity
A. External eye structures
External eye structures are symmetrical. Icteric sclera was noted and visible Pars
Plana lensectomy (PPL). Eyelids was intact and no unusual discharged and secretion.
A. Visual fields
Appear normal, peripheral vision and eye movement is in normal range, able to
distinguish objects in the peripheries.
B. Extraocular muscle
Twitching of right extra ocular muscle present.
C. Visual acuity
Pars Plana Lensectomy (PPL) noted. Patient does not wear glasses and able to
determine objects and read within 14 inches distance.
VI. Ears and hearing
A. Auricles
Symmetrical in shape with the same color of facial skin. They are aligned with the
outer cantus of the eye. No palpable masses upon palpation. Skin intact, mobile, firm
and non-tender.
B. External ear canal and tympanic membrane
72
External ear canal clean and intact without signs of redness, unusual discharge or
secretion. Both tympanic membranes are pearly gray in color with light reflex.
C. Gross hearing and acuity
Able to hear sounds projected to client, able to hear different types of sounds
conveyed.
VII. Nose and sinuses
A. Nose
Upon inspections external nose was symmetrical. No abnormal discharges or flaring
were noted. Was uniform in color with facia skin. Nasal septum was intact and in
midline.
B. Facial sinuses
Facial sinuses isnot inflamed and not palpable noted.
VIII. Mouth and oropharynx
A. Lips and buccal mucosa
Lips are dry in nature, but intact, buccal mucosa appears slightly pink, moist, soft and
has elastic texture.
C. Teeth and gums
Teeth enamel were shiny with yellow discolorations. No retraction of gums noted,
pinkish in color.
D. Tongue / floor of the mouth
Centrally positioned, pinkish with white taste bud on surface. Gag reflex present, able
to move tongue freely with strength. Tongue surface rough.
E. Salivary glands
Intact, without swelling of salivary glands noted.
F. Palates and uvula
73
Smooth palates are light pink and smooth while the hard palate has more irregular
texture. The uvula is positioned in the midline of the soft palate.
G. Oropharynx and tonsils
Tonsils appeared pink, symmetrical without lesions and exudate noted. Oropharynx is
pink and appeared smooth.
IX. Neck
A. Neck muscles
Mass noted on left side of the neck. Muscle has no deviation during ROM.
H. Lymph nodes
Non palpable, non-tender noted.
I. Trachea
Midline, palpable and no unusualities noted.
J. Thyroid gland
Not visible upon inspection and the gland ascend during swallowing but not visible.
X. Thorax and lungs
A. Posterior thorax
a. Inspection
The skin over the posterior thorax was intact and uniform in color with the rest of the
body. With equal chest expansion.
b. Palpation
Chest wall is intact no tenderness and masses noted.
c. Percussion
Resonant sound present when percussed.
d. Auscultation
No crackles sound on both lung fields.
74
B. Anterior thorax
a. Inspection
The client has a quiet, rhythmic and effortless respirations.
b. Palpation
No unusual masses or lesions noted.
c. Percussion
Dull sound present.
d.Auscultation
No crackles sound on both lung fields.
XI. Heart and central vessels
A. Precordium, aortic and pulmonic areas, tricuspid area, apical area, epigastric area
No visible pulsations on the aortic and pulmonic areas of the heart. No presence of
heaves or lifts noted.
K. Carotid arteries
Non palpable.
L. Jugular veins
Jugular vein is slightly distended due to HPN.
XII. Peripheral vascular system
A. Peripheral pulses
Regular and present on all four extremities.
M. Peripheral veins
No peripheral vein distention noted upon inspection
N. Peripheral perfusion
Slow capillary refill time of 4-5 seconds indicates poor peripheral perfusion
XIII. Breast and axillae
75
a. Inspection
No noticeable changes on breast and axillae noted
b. Palpation
No tenderness, swelling or any discomfort noted upon palpation.
XIV. Abdomen
a. Inspection
Distended and ascites was noted. Size of the abdomen was observed to be not
appropriate for patient’s body. Caput medusae noted on the skin of the abdomen.
Abdominal girth of 39 inches was taken.
Auscultation
Bowel sound present at left lower quadrant of the abdomen.
Percussion (including liver)
Left lobe enlargement of liver upon percussed with shifting dullness sound noted.
Palpation (including liver and bladder)
Tenderness on epigastric area on deep palpation.
XV. Musculoskeletal system
A. Muscles
Firm and appeared slightly dry with coordinated movements. No presence of tremor
noted.
B. Bones
No swelling and tenderness noted.
C. Joints
No swelling and tenderness noted.
XVI. Neurological system
A. Language
76
Able to speak spontaneously
D. Orientation
Well oriented to place, time, person.
E. Memory
Intact to remote, recent, past and immediate memory.
F. Attention span and calculation
Able to concentrate and maintain it as evidenced by politely answering the questions
being asked.
G. Level of consciousness
Alert and awake in the whole duration of the assessment. He is responsive and able to
answer the questions being asked.
H. Cranial nerves
Cranial nerve I- olfactory
Able to distinguish types of smell.
Cranial nerve II- optic
Able to read within 14 inches distance.
Cranial nerve III- oculomotor
Equally round and reactive to light.
Cranial nerve IV- trochlear
Able to follow index finger when doing six cardinal signs without double vision.
Cranial nerve V - trigeminal
With positive corneal reflex, able to respond light and deep sensation and able to
differentiate hot from cold.
Cranial nerve VI- abducens
Both are eyes are coordinated and move in unison with parallel alignment.
77
Cranial nerve VII- facial
Able to smile, raise eyebrows and puff out cheeks and close eyes without any
difficulties.
Cranial nerve VIII- auditory
Able to hear whisper within 14 inches distance.
Cranial nerve IX- glossopharyngeal
Able to elicit gag reflex and swallow without difficulty
Cranial nerve X- vagus
Able to swallow without difficulty and speak audibly.
Cranial nerve XI- accessory
Able to shrug shoulders and turn head from side to side.
Cranial nerve XII- hypoglossal
Able to move tongue without difficulty.
G. Reflexes
Biceps reflex
Reflex is present with strong character with a score of 2+.
Triceps reflex
Brachioradialis reflex
Reflex present with strong character with a score of 2+.
Patellar reflex
Achilles reflex
Plantar (Babinski’s) reflex
78
H. Motor function
Gross motor and balance
Upright with steady gait with opposing arm swing unaided. Patient cannot tolerate
long standing.
Fine motor (Upper Extremities)
Able to discriminate between sharp and dull sensation when touch with ball pen tip.
XVII. Genitals and inguinal area
Patient verbalizes that inguinal and genital area are free of swelling and abnormal
discharge.
XVIII. Rectum and anus
Able to defecate and void with no difficulty and without hemorrhoids noted.
XIX. Other observations / findings
Patient is ambulatory and able to move freely but felt fatigue and weakness of the
body. He verbalized he felt discomfort of his abdomen specially during lying flat on
bed.
79
HEALTH HISTORY
HISTORY OF PRESENT ILLNESS
For the past few years the patient showed no symptoms of any serious illnesses
related to his current condition but experience epigastric pain for three weeks prior to
being admitted. The patient and his wife assumed that the pain was a result of the
ongoing CONDITION so did not take it seriously self-treating with OTC (over the
counter drugs) medication like Buscopan. After a day the discomfort occur again and
thought it was just a 'Panuhot and Kabuhi'.
A week prior to admission the patient experience severe epigastric pain due to alcohol
over consumption. He took no medication and got no medical advice. His abdominal
pain was intermittent, but his wife noticed his abdomen distended and said, “Dili man
kayo na dako iya tiyan sauna. Murag nikalit raman.”
After admission his abdominal pain worsened after five days so consultation was
sought at the Community Health Development Cooperative Hospital (CHDC) and
was given lactulose with no relief. Although the client had these symptoms and was
discharged. On 2/26/2020 the patient experienced abdominal pain at the level of 8/10
as well as nausea so was admitted to Bronkenshire Hospital.
PAST ILLNESS/ HOSPITALIZATION
The Patient had no serious illnesses other than conditions treatable by OTC
medications and had no consultations. This was his only medical issues diagnosed
until he started aging and developed typical age-related conditions such as
hypertension (diagnosed in 2000), dizziness, nausea and pain on his nape. His other
diagnosis's included Diabetes Mellitus in 2016 and a procedure for Thoracentesis
from December 2017 to January 12. He was prescribed medications for his treatment.
80
PERSONAL HISTORY
Patient was born and raised in Himamaylan, Negros Occidental and had 6 siblings.
Two passed away from Diabetes Mellitus and one of hypertension. His father died at
the age of 45 due to liver cirrhosis probably as a result of too much alcohol
consumption.
He married a neighbor in his town and had 3 daughters and 1 son with her. His eldest
son was also diagnosed with Diabetes Mellitus at the age of 43. Patient is a retired
Philippine Military Army who was known to be a heavy drinker even with
Hypertension and Diabetes Mellitus. Although his wife has urged him to change his
lifestyle, he has not even with all the medical conditions mentioned here.
81
Genogram
Paternal Maternal
84 yrs old 88 yrs old 87 yrs old 90 yrs old 91 yrs old
89 yrs old 86 yrs old
84 yrs old 83 yrs old
58 yrs old 65 yrs old 60 yrs old 68 yrs old 54 yrs old 51 yrs old 49 yrs old
Patient Cancer Alcoholic
Hypertension Deceased
Diabetes Liver Cirrhosis
82
Legend
83
Erikson’s Stages of Psychosocial Development
Erikson’s theory proposes that life is a sequence of developmental stages or levels
of achievement. Each stage signals a task that must be accomplished. The resolution of
the task can be complete, partial, or unsuccessful. Erikson believed that the more success
an individual has at each developmental stage, the healthier the personality of the
individual. Failure to complete any developmental stage influences the person’s ability to
progress to the next level. These developmental stages can be viewed as series of crises.
Successful resolution of these crises supports healthy ego development. Failure to resolve
the crises damages the ego.
Erikson proposed that at each stage of development, special psychological tasks
need to be achieved in order to overcome developmental challenges and allow
development to proceed successfully. Successful accomplishment of these task results in
adaptation and failure in maladaptation.
Stage Description Result Justification

Trust versus Trust Vs. Mistrust is the first of Mr. V was born in
Mistrust Erik Erikson's eight stages of ACHIEVED Himamaylan
personality. Erikson's theory negros. Mr. v was
Infancy argues that following a life of breastfed by his
(Birth to 18 warmth and regularity and mother until Mr. v
months) protection from the outside world was 2 years old. He
while in the mother's womb, the has completed his
infant is faced with a less secure immunizations.
world. According to Erikson, Mother immediately
infants learn to trust when they responds to Mr. V
are cared for in a "consistent and cry and cuddles him
84
warm manner". If the infant is not every time she
cared for and not fed in such a breastfeeds. After 2
manner, the infant is more likely years, Mr. V started
to develop a sense of mistrust. eating cerelac
If an infant's physical and prepared by her
emotional needs are met in a mother. Mr. v was
consistent and caring way, he also toilet trained by
learns that his mother or her mother at the
caregiver can be counted on and age of 2 years old.
he develops an attitude of trust in At 3-year-old, she
people. If his needs are not met, started to mumble
an infant may become fearful and simple words like
learns not to trust the people “mama” and started
around him. to learn how to
walk.
Autonomy Autonomy vs. shame and doubt ACHIEVED Mr. V was potty
versus (1-3 yrs.) refers to the 2nd stage trained at the age of
Shame and of Erik Erikson's theory of 2; he began talking
Doubt Psychosocial development where at the age of 3; he
the child begins to act on his or started to walk at
Early her own, often in ways that go the age of 3.
Childhood against the parents' wishes. The Mr. V was potty
(18 months child can resolve trained by his
to 3 years) this conflict either by establishing mother. Every time
self-control (autonomy) or by her mother went to
punishing himself or herself with the comfort room,
feelings of shame, doubt, and Mr. V was brought
inadequacy. The toddler realizes along to expel his
that he is a separate person with wastes as well. She
his own desires and abilities. He also does not scold
wants to do things for himself the child when he
85
without help or hindrance from expels her waste.
other people. The toddler's She just tells him
favorite word "No" is a where to go if he
declaration of independence and a wants to urinate or
bid for increased autonomy. defecate. As a
result, Mr. V is able
to cultivate control
of himself by not
being overly
controlled and by
being told what is
right to do.
Initiative In this third stage of ACHIEVED Mr. V only
versus Guilt development, Erikson believes playmate was his
the preschooler is entering a neighbor. He also
Late wider range of social interaction preferred to be a
Childhood and is developing a more follower whenever
(3-5 years) purposeful behavior in order to they played. He
deal with challenging plays with toy cars
responsibilities. This is a time and walks outside
where children may begin to with his neighbor.
develop feelings of guilt and
begin to feel anxious.
During this stage, the healthily
developing child learns: (1) to
imagine, to broaden his skills
through active play of all sorts,
including fantasy (2) to cooperate
with others (3) to lead as well as
to follow. Immobilized by guilt,
he is: (1) fearful (2) hangs on the
86
fringes of groups (3) continues to
depend unduly on adults and (4)
is restricted both in the
development of play skills and in
imagination.
Increased muscular, mental and
language abilities set the stage for
more activities and questions.
There is a great curiosity and
openness to learning. The favorite
word of preschoolers is "why."
Parents who take time to answer
their preschoolers' questions
reinforce their intellectual
initiative. But parents who see
their children's questions as a
nuisance may stifle their initiative
and cause them to be too
dependent on others and to be
ashamed of themselves.
Imaginative play is the basic
activity of this stage. The
preschooler explores and reenacts
the different roles and activities
of people, both real (home life)
and fictional (often based on
television).
Industry Industry vs. inferiority (5-12 ACHIEVED Mr. V started to go
versus yrs.) refers to the 4th stage of to school at the age
Inferiority Erik Erikson's theory of of 6. Mr. V is an
Psychosocial development when achiever and loves
87
School Age the child become increasingly to participate at
(6-12 years) involved in situations where long, school. At 12 years
patient work is demanded of old, Mr. V already
them. Those that rise to this graduated.
challenge gain a sense of
industry; those that do not feel
inferior.
Here the child learns to master
the more formal skills of life: (1)
relating with peers according to
rules (2) progressing from free
play to play that may be
elaborately structured by rules
and may demand formal
teamwork, such as baseball and
(3) mastering social studies,
reading, arithmetic. Homework is
a necessity, and the need for self-
discipline increases yearly. The
child who, because of his
successive and successful
resolutions of earlier
psychosocial crisis, is trusting,
autonomous, and full of initiative
will learn easily enough to be
industrious. However, the
mistrusting child will doubt the
future. The shame - and guilt-
filled child will experience defeat
and inferiority.
At the school-going stage, the
88
child's world extends beyond the
home to the school. The emphasis
is on academic performance.
There is a movement from play to
work. Earlier the child could play
at activities with little or no
attention given to the quality of
results. Now, he needs to perform
and produce good results!
The child soon learns that he can
win recognition from parents,
teachers and peers by being
proficient in his schoolwork. The
attitudes and opinions of others
become important. The school
plays a major role in the
resolution of the developmental
crisis of initiative versus
inferiority.
If children are praised for doing
their best and encouraged to
finish tasks then work enjoyment
and industry may result.
Children's efforts to master
schoolwork help them to grow
and form a positive self-
concept ... a sense of who they
are.
Children who cannot master their
schoolwork may consider
themselves a failure and feelings
89
of inferiority may arise.
A child may also feel a sense of
shame if his parents unthinkingly
share his "failures" with others.
Shame stems from a sense of self-
exposure, a feeling that one's
deficiencies are exposed to
others.
Adolescence Central Task: Identity vs. Role ACHIEVED At this stage, Mr. V
(12-21 years Confusion started to be
old) The adolescent is newly alcoholic at the age
concerned with how they appear of 21 and always
to others. going out with his
The sense of central identity friends to drink. He
appears through sexual, also tried smoking
emotional, educational, ethnic, at this age for about
cultural, and vocational 2 cigarettes per day.
discovery. The adolescent person
also develops coherent sense of
self and plans to actualize one’s
abilities. The sense of self can be
confused if a core identity does
not solidify. Feelings of
confusion, hesitancy, and
possible antisocial behavior may
also emerge.
Early Central Task: Intimacy vs. ACHIEVED At this stage, he

Adulthood Isolation trained as a military.
(21 to 40 Once people have established At the age of 22
years) their identities, they are ready to years old, he then
90
make long-term commitments to met his late wife at
others. They become capable of the age of 28, he
forming intimate, reciprocal then married the
relationships and willingly make woman of his life.
the sacrifices and compromises They had 3 children.
that such relationships require. If
people cannot form these intimate
relationships--a sense of isolation
may result.
Generativity Generativity versus stagnation is ACHIEVED At the age of 58y.o,

vs. the seventh of eight stages of Erik the patient decided
Stagnation Erikson's theory of psychosocial to retire as an
40-65 years development. Generativity refers agriculturist and
old to "making your mark" on the tend to their own
world through creating or land as a farmer
nurturing things that will outlast since he successfully
an individual. made his own mark.
Freud’s Psychosexual Theories
Sigmund Freud developed a theory of how our sexuality starts from a very young
ages and develops through various fixations. If these stages are not psychologically
completed and released, we can be trapped by them and they may lead to various defense
mechanisms to avoid the anxiety produced from the conflict in and leaving of the stage.

Oral The center of pleasure is the ACHIEVED The patient recalls that
91
Stage mouth; it is the major source when he was breast fed and
Birth to 1 of pleasure and satisfaction was fond of biting the
year and exploration. The child’s plastic nipple of his bottled
primary need is security or milk.
safety.
Major conflict: weaning
Feeding produces pleasure,
a sense of comfort or ease
and safety. Feeding should
be pleasurable; it should be
provided when necessary.
Anal The sources of pleasure are ACHIEVED Mr. V reports that when
Stage the anus and the bladder he’s still young, he was
1 ½ to 3 (sensual satisfaction, self- taught by his parents to use
years control). the toilet. He often asked
Major conflict: toilet for help if he cannot lift the
training. bucket to flush the toilet.
Controlling and expelling
feces give pleasure and
sense of comfort. Toilet
training should be a
pleasurable experience.
Phallic The genitals are the center Mr. V was known to be
Stage of gratification. ACHIEVED closer with his father, but
4 to 6 Masturbation offer pleasure he also had a good
years to the child. Other actions relationship with his mother
include fantasy, when he was younger.
experimentation with peers,
and questioning of adults
about sexual issues or
sexual matter.
Major conflicts: the Oedipus
92
Complex (refers to the male
child's attraction for his
mother and unfriendly
attitudes towards his father)
and Electra Complex (refers
to the female's attraction for
her father and sees her
mother as her rival), which
resolves when the child
identifies when the child
identifies with parent of
same sex.
The child determines
together with the parent of
the opposite sex and later
takes on a love relationship
outside the family.
Latency Energy is heading for ACHIEVED Mr. V was active at school
Stage physical and intellectual activities such as sports and
6 years to activities. Sexual impulses was able to expand his
Puberty tend to be repressed. group of friends mostly
Develop relationships composed of same sex.
between peers of the same
sex.
Encourage child with
physical and intellectual
pursuits. Encourage sports
and other activities with
same-sex peers.
93
LIFE CHARACTERISTIC IMPLICATION ASSESSMEN JUSTIFICATIO
STAG S S T N
E
Genital Energy is directed Encourage ACHIEVED At the age of 18
(pubert toward full sexual separation from years old, the
y and maturity and parents, being patient reports
after) function and independent and that he began to
development of skills able to make experiment and
needed to cope with right and good explore his
the environment. decisions curiosity about
sex. Mr. V also
develops
empathy and
sympathy as he
grew up.
94
Jean Piaget’s Stages of Cognitive Development
Jean Piaget's stages of cognitive development describe the intellectual
development of children from infancy to early adulthood. Piaget believed that children
are not less intelligent than adults, they simply think differently. He also proposed a
number of concepts to explain how children process information.

Sensorimotor  In this stage, infants Mr. V, being breastfed
Thought build an understanding ACHIEVED by her mother, is able to
(birth-2years) of the world by adequately elicit a
coordinating sensory sucking reflex. She
experiences (such as moves his mouth to suck
seeing and hearing) where the breast is, as
with physical, motoric verbalized by his mother.
actions. Infants gain She also grasps an object
knowledge of the placed on her palm.
world from the
physical actions they
perform on it. An
infant progress from
reflexive, instinctual
action at birth to the
beginning of symbolic
thought toward the end
of the stage.
 Thought derives from
sensation and
movement.
 The child learns that he
is separated from his
environment and that
95
aspects of his
environment continues
to exist even they may
be outside the reach of
his senses.
Preoperationa  Thinking is still Mr. V is able to talk at
l Thought (2- egocentric: has ACHIEVED the age of 3 and has not
7 years) difficulty taking the manifested any
point of view of others. abnormalities or
 The children begin to difficulties in speech. He
represent the world tells his mother what he
with images and wants. Mr. V reports that
words. Symbolic he used to give
thought goes further nicknames of things he
than connections of cannot name and define
sensory information the images to his mother
and physical action. which he cannot directly
 Objects are classified say.
in simple ways,
especially by
significant feature; the
child isn’t able to
conceptualize
abstractly.
Concrete  The child starts to Mr. V knows the
Operational think abstractly and ACHIEVED difference between a girl
Thought (7-12 conceptualize, forming and a boy. He also
years) logical structures that knows what death is. He
explains his or her knows how to count
physical experiences. from high to low and is
 Children can execute able to read and write.
96
operations and logical
reasoning replaces
intuitive thought as
long as reasoning can
be applied to specific
or concrete examples.
 Children show
thinking is decentered
-they consider multiple
aspects of the problem
(e.g. understanding the
significance of height
and width). They focus
on the dynamic change
in the problem. And,
most importantly, they
show the reversibility
of true mental
operation.
Formal  The person is capable At the early age of 10,
Operational of deductive and ACHIEVED Mr. V recalls that was
Thought (12 hypothetical reasoning. able to reason out why
years and  The logical quality of he was still playing
above) the adolescent's outside or why he was
thought is when late to come home.
children are more
likely to solve
problems in a trial-and-
error fashion.
 During this stage the
young adult is able to
97
understand such things
as love, "shades of
gray", logical proofs
and values.
 During this stage the
young adult begins to
entertain possibilities
for the future and is
fascinated with what
they can be.
98
Havighurst’s Developmental Tasks Theory
Age Range Developmental Task Result Justification

Infancy and Early  Learn to walk ACHIEVED Mr. V recalls that he
childhood  Learn to use the started walking when
0-5 years old toilet he was 3 years old.
 Learn to talk Learned to talk at 2
 Learn to form years old and toilet
relationship with trained by his mother
others when he was young.

Middle Childhood  Learn school ACHIEVED Mr. V recalls when
6-12 years old related skills such he was 7 he is
as reading actively
 Learn about participating at
conscience and school and everytime
values he goes home he
 Learn to be blessed respectedly
independent when he saw his
parent and helping
them doing house
chores.
Adolescence  Establish ACHIEVED Mr. V recalls at the

13-17 years old emotional age of 16, he had
99
independence groups of friends and
 Learn skills hang with them after
needed for class.
productive
occupation
 Achieve gender
based social role
 Establish mature
relationships with
peers
Early Adulthood  Choose a life ACHIEVED At the age of 21 he
18-35 years old partner found his wife, got 3
 Establish a family kids and has a stable
 Take care of a work as a military.
home
 Establish a career
Middle Age  Maintain a ACHIEVED Mr. V recalls he had
36-60 years old standard of living a good relationship
 Perform civic and with his wife. At this
social stage he has retired
responsibilities being a military so he
 Maintain a always stayed at
relationship with home and drink with
spouse his friends at night.
 Adjust to
psychological
changes
Later Maturity  Adjust to ACHIEVED MR. V has adjusted
Over 80 years old deteriorating to his retirement. He
health is living with his
 Adjust to wife and 3 kids. But
having problem with
100
retirement his present health
 Meet social and status.
civil obligations
 Adjust to loss of
spouse
Doctor’s Order
PROGRESS NOTES DATE ORDERS

AND
101
TIME
2/26/20  Please admit patient under Dr.
Alcasid
 Secure consent to care
 I & O q shift
 Diabetic diet 1800 kcal
 Pnss 1L @ 60cc/hr.
 Diagnostic
- CBC PIL
- CH
- ECG RL
- CDH(PAL)
- SGPT
- L. profile
- TB, DB, IB
- S., Na., k, crea
- Alk phol
- TPAG
- PT, IWR
- Hgt Q6
 Meds
- Humulin 70130 15.0 am
10. 0 pm
SQ
RI reseve SQ for hgt
60 = 180- 220
80 = 221- 261
100 = 261
Amlodipine 10mg 1tab
OD
HNBB 10mg PRN now
102
then Q8 for ABD pain
Liverpromide capsule 1
cap TID
RI 60 IVTT now

AND
TIME
2/26/20  Will inform Dr. Alcasid
2:30 am  Call Dr. Pedima / leezyl
reculeto
 Retrieve UTZ of c/o
Review notes 2/26/20 watcher
HPI: 3 weeks PTA crampy 2:50 pm
perinulial abdominal pain Rounds with DR. Alcasid
1-week worsening of abdominal  For FOBT
pain with drinking spree no  S4 continue ceftriaxone 2gm
medication taken and consultation IVTT OD (NST)
Wt.: 63.18kg - 3 days PTA  For sputum GSCS
constipation with persistence of  Start atorvastatin 40mg 1-tab
DOD pain > A OD HS
PMHx: + DM insulin  Plan to start on
+ HPN -clopidogrel 75mg 1tabl OD
PSHx: + alcoholic drinker once duodenal pain resolved
+ smoker Refer.
Awake not in distress GCS 15
# S1 PC, P6
DHS – murmur
103
SCE
Soft abdomen + tenderness epig
area

AND
TIME
2/27/20  Azithromycin
7AM  Continue present
management
 Refer
+ abdominal pain
+ abdominal distention
Awake nird (not in respiratory
distress)
As (anicteric sclera, PPC (pink
palpebral conjunctiva))
CBS (clear breath sound) ECE
(equal chest expansion)
DHS (distinct heart sound) no
murmurs
+tympanitic
+distended abdomen
Assessment: liver cirrhosis,

secondary to decompensated liver
disease DM, HPN II
LABORATORY FINDINGS
Date Performed: March 26, 2020 3:38 PM

Test Indication Normal Actual Implication
Values Result
104
Alkaline High 46.00- 464 Problem with the liver
Phosphate 116.00 U/L or gallbladder
(ALKPO4)
CREATININE Normal 62.00- 75.7 Normal
115.00 U/L
Date Performed: March 26, 2020 6:23

Values Result
White Blood High 4.0-10.0 15.8 Increased in count of
Cells WBC it means it has
infection in the body
Red Blood Low 4.5-6.2 4.4 A decreased number of
cells RBCs result from the
decreased
erythropoietin
production of the liver
Haemoglobin Normal 13.0-18.0 14.4 Within normal range
Haematocrit Normal 0.40-0.50 0.41 Within normal range
Platelet Count Normal 150-400 323 Within normal range
Mean plt Normal 8.0-12.0 10.8 Within normal range
Volume
MCV Normal 79.0-100.0 93.8 Within normal range
MCH Normal 27.0-34.0 32.8 Within normal range
MCHC Normal 320-360 350 Within normal range
Differential
count
Neutrophil High 0.55-0.65 0.85 A high result of
neutrophil is a sign that
the body has an
infection
Lymphocytes Low 0.35-0.55 0.08 A low level of
lymphocytes is a
condition
lymphocytopenia it
105
also occurs when there
is an infection in the
body
Monocytes Normal 0.02-0.09 0.07 Within in normal range
Eosinophil Low 0.02-0.04 0.00 A low level of
eosinophil is the result
of intoxication from
alcohol or excessive
production of cortisol.
Basophil Normal 0.00-0.02 0.00 Within in normal rage

Values Result
Direct High 0-3 umol/L 79.7 High levels of direct
Bilirubin bilirubin may indicate
on a liver damaged or
disease
Indirect High 2.00-12.00 21.0 High levels of indirect
Bilirubin umol/L bilirubin mean the
body is getting rid of
too many red blood
cells
Total High 3.00-17.00 100.7 Increase in total
Bilirubin bilirubin may progress
into liver damage
Date Performed: March 26, 2020 9:56 pm

values Result
WBC Normal 0-2 /hpf 1 Within normal range
RBC High 0-2 /hpf 4 Increased of RBCs
106
indicate for infection,
trauma, tumors, or
kidney stones
Epithelial High 0-2 / hpf 19 Increased in epithelial
cells cells may indicate to
urinary tract infection
Cast Normal 0-3 /hpf 1 Within normal range
Bacteria Normal 0-20 /hpf 19 Within normal range
PHYSICAL EXAMINATION
Color Amber
Character Hazy
Reaction 5.0
Specific Gravity 1.030
CHEMICAL EXAMINATION
Sugar ++
Protein +

Values Result
APTT 28.9 secs
Control 27.1 secs
Protime 13.2 secs
INR 1.13
% Activity - %
Control 12.5 secs
Date Performed: March 27, 2020 5:49 am

Values Result
SGPT High 16.00-63.00 149 An increased in SGPT
(ALT) U/L level is decreased in
107
kidney function caused
by liver cirrhosis
caused by hepatic
inflammation.
Date Performed: March 27, 2020 6:24 AM

Values Result
TOTAL Normal 66.00-87.00 72.67
PROTEIN g/L
Albumin Low 39.70-49.50 24.55 A low albumin level
g/L the body can’t keep
fluid from leaking out
of your blood vessel.
Globulin High 15.00-35.00 48.1 An increased in
g/L globulin may indicate
in infection,
inflammatory disease
or immune disorder
A/G Low 1.50-2.20 0.5 A decreased in A/G
may reflect in
overproduction of
globulins, such as seen
in autoimmune disease,
or underproduction of
albumin, such as may
occur with cirrhosis or
selective loss of
albumin from the
circulation, as may
occur with kidney
disease.
108
Date Performed: March 27, 2020 9:47 am
Values Result
Cholesterol High 0.00-5.20 6.1 A high level of
mmol/L cholesterol can
increase your risk of
heart disease, and you
can also develop fatty
deposits in your blood
vessels.
HDL Low 1.04-1.55 0.37 a low HDL level can
mmol/L have a healthy heart,
though, people who
have low HDL will
have greater risk of
developing heart
disease than people
with high HDL.
LDL High 0.00-2.60 5.2 A high LDL can build
mmol/L up of cholesterol in
your arteries
Triglycerides Normal 0.00-1.70 1.13 Within normal range
mmol/ L
109
110
BROKENSHIRE COLLEGE
MADAPO, DAVAO CITY
DRUG STUDY
Date given February 26, 2020
Generic Brand General Mechanism of Route of Indication Contraindication Adverse Nursing
Name Name Classification Action Dosage Reaction Responsibility
H B Antispasmodic Is a quaternary 20mg 1 Relief smooth Hypersensitivity Dryness of the Be alert for
Y ammonium muscle spasm to hyoscine mouth, with adverse
U amp IV
O antimuscarnic of the butylbromide difficulty in reaction and
S T agent. Hyoscine gastrointestina Porphyria swallowing, drug
C butylbromide l and Myasthenia thirst, dilation interactions
Y
I does not really genitourinary gravis of the pupils
N L pass the blood- system. Prostatic with loss of Assess for eye
E brain barrier. It’s enlargement, accommodatio pain
B
a competitive paralytic ileus or n and
R antagonist of the pyloric stenosis photophobia, Assess for
actions of and fever. increased intra- urinary
O
acetylcholine Closed angle ocular pressure, hesitancy
M and other glaucoma, or flushing and
muscarinic narrow angle dryness of the Assess for
I
agonist. The between the iris skin, constipation
D receptors and cornea, as bradycardia
affected are hyoscine followed by Monitor urine
E
those peripheral increase tachycardia, output
structure that are intraocular with palpations
either stimulated pressure and Encourage
111
or inhibited by Pregnant and arrhythmias, patient to void
muscarine, i.e. lactating urinary urgency
Exocrine glands, mothers with the Monitor BP
smooth and inability to do for possible
cardiac muscle. so, as well as hypertension
reduction in the
tone and For pregnant
motility of the women,
gastro- monitor
intestinal tract, cervical
leading to effacement
constipation, and dilatation
occasionally
vomiting
giddiness and
staggering may
occur,
retrosternal
pain may occur
due to
increased
gastric reflux
112
BROKENSHIRE COLLEGE
MADAPO, DAVAO CITY
DRUG STUDY
Generic Brand General Mechanism of Route of Indication Contraindicatio Adverse Nursing
Name Name Classification Action Dosage n Reaction Responsibility
R H Insulin Treatment of Contraindicated Hypersensitivity: Assessment
E U regular (human) is type 1(insulin with allergy to rash, History: allergy
G M a short-acting, dependent) pork products anaphylaxis or to pork
U A man-made insulin diabetes (varies with angioedema products;
L N that's similar to Treatment for preparations; pregnancy;
A the insulin made type 2(non- human insulin Local: allergy lactation
R by your pancreas. independent) not local reaction at
It copies your diabetes that contraindicated injection site Physical: skin
I body's insulin in cannot be with pork redness, color, pulse,
N response to food. controlled by allergy) swelling, BP,
S This diet oral Use cautiously itching, usually adventitious
U extra insulin helps agents with pregnancy resolve in a few sound,
L to control your Regular (keep patients days to a few urinalysis,
I blood sugar and insulin under close weeks; a change blood glucose
N prevent injection: supervision; in type or Interventions
complications of treatment of rigid control is species source of
diabetes severe desired; insulin may be Ensure uniform
ketoacidosis following tried; dispersion of
or diabetic delivery, lipodystrophy; insulin
coma requirements pruritus suspension by
113
Treatment for may drop for rolling the vial
hyperkalemia 24-72hr, rising Metabolic: gently between
with infusion to normal levels hypoglycaemia; hands; avoid
of glucose to during next 6 ketoacidosis vigorous
produce shift wks.); lactation shaking.
of potassium (monitor mother
into the cells carefully; Give
insulin maintenance
Highly requirements doses
purified and may decrease subcutaneously,
human during rotating
insulin lactations) injection sites
promoted for regularly to
shirt courses decrease
of therapy incidence of
(surgery, lipodystrophy;
intercurrent give regular
disease), insulin IV or
newly IM in severe
diagnosed ketoacidosis or
patients, diabetic coma
patient with
poor Monitor patient
metabolic receiving
gestational insulin IV
diabetes carefully:
plastic IV
infusion sets
have been
reported to
114
remove 20%-
80% of the
insulin; dosage
delivered to the
patient will
vary
115
BROKENSHIRE COLLEGE
MADAPO, DAVAO CITY
DRUG STUDY
Generic Brand General Mechanism of Route of Indication Contraindicatio Adverse Reaction Nursing
Name Name Classification Action Dosage n Responsibility
A K calcium Amlodipine is 10 mg 1- is indicated is indicated for  Difficult or Emphasize the
M A channel an tab OD for the the treatment of labored importance of
L T blockers angioselective treatment of hypertension, to breathing continuing to
O E calcium channel hypertension, lower blood  dizziness
take as
D R blocker and to lower blood pressure.  fast,
I Z inhibits the pressure. Lowering blood irregular, directed, even
P I movement of Lowering pressure reduces pounding, or if feeling well.
I A calcium ions blood pressure the risk of fatal racing Take missed
N into vascular reduces the and nonfatal heartbeat or doses as soon
E N smooth muscle risk of fatal cardiovascular pulse as
O cells and and nonfatal events,  feeling of remembered if
R cardiac muscle cardiovascular primarily warmth not almost
V cells which events, strokes and  redness of
before next
A inhibits the primarily myocardial the face,
S contraction of strokes and infarctions neck, arms, dose; do not
C cardiac muscle myocardial and double doses.
and vascular infarctions occasionally, Medication
smooth muscle upper chest controls but
cells.  tightness in does not cure
the chest hypertension.
116
Instruct
patient to take
medication at
the same time
each day.
Warn patient
not to
discontinue
therapy unless
directed by
health care
professional.
Caution patient
to avoid salt
substitutes
containing
potassium or
foods
containing
high levels of
potassium or
sodium unless
directed by
health care
professional.
117
See food
sources for
specific
nutrients.
Encourage
patient to
comply with
additional
interventions
for
hypertension
(weight
reduction,
low-sodium
diet, smoking
cessation,
moderation of
alcohol
consumption,
regular
exercise, and
stress
management).
Medication
controls but
118
does not cure
hypertension.
Instruct patient
and family on
proper
technique for
monitoring
BP. Advise
them to check
BP at least
weekly and to
report
significant
changes.
BROKENSHIRE COLLEGE
119
MADAPO, DAVAO CITY
DRUG STUDY
Generic Brand General Mechanism of Route of Indication Contraindication Adverse Nursing
Name Name Classification Action Dosage Reaction Responsibility
A Z anti-infectives prevents bacteria Mild-to- contraindicated w Stomach may
Z I from growing by moderate ith this drug. upset, lead to
I T interfering with susceptible infec ... diarrhea/loose pseudomembr
T H their protein tions including Conditions: stools, anous colitis,
H R synthesis. It binds acute bacterial diarrhea nausea, pain, diarrhea,
R O to the 50S subunit exacerbations of from an infection vomiting, or nausea,
O M of the bacterial COPD, acute with Clostridium abdominal Stevens-
M A ribosome, thus bacterial difficile bacteria. pain may Johnson
Y X inhibiting sinusitis, acute low occur. If any syndrome,
C translation of otitis media, amount of of angioedema
I mRNA. Nucleic community- magnesium in the these effects p
may
N acid synthesis is not acquired blood. ersist or
increase risks
affected. pneumonia, worsen, tell
low for warfarin
pharyngitis/tonsi your doctor or
amount of toxicity
llitis, pharmacist
potassium in the
uncomplicated promptly monito
blood.
skin and skin r patient for
structure, myastheni signs of
urethritis, a gravis. anaphylaxis
cervicitis, a skeletal
chancroid in muscle disorders. instruc
men. t patient to
hearing
notify
loss.
physician for
torsade’s diarrhea, or
120
de pointes.
blood or pus
a type of in stool
abnormal heart
rhythm. instruc
t patient to
take
medication
exactly as
prescribed
BROKENSHIRE COLLEGE
121
MADAPO, DAVAO CITY
DRUG STUDY
Generic Brand General Mechanism of Route of Indication Contraindicati Adverse Nursing
Name Name Classification Action Dosage on Reaction Responsibility
C R cephalosporin selectively and 2-amp ivtt Susceptible diarrhe rash, Instruct patient to
E irreversibly bacterial infections of a from an diarr
O notify physician
F inhibits bacterial the lower respiratory infection with hea,
T C cell wall tract, skin and skin Clostridium immediately of signs
naus
R synthesis by structure, bone and difficile of superinfection,
E ea,
I binding to joint, acute otitis bacteria.
vom including black,
A P transpeptidases, media, UTIs, a type
X also called septicemia, pelvic iting, furry overgrowth on
H of blood
O transamidases, inflammatory disease disorder where upse tongue, vaginal
N I which are (PID), the red blood t stomach,
itching or discharge,
E penicillin- intraabdominal infecti cells burst bloo
N and loose or foul-
binding proteins ons, meningitis, called d clots,
(PBPs) that uncomplicated hemolytic dizzi smelling stools.
catalyze the gonorrhea. Surgical anemia. ness,
cross-linking of prophylaxis Instruct patient and
liver head
the problems. ache, family/caregivers to
peptidoglycan
polymers disease report other
forming the of the
gallbladder. troublesome side
bacterial cell
wall. severe effects such as
renal severe or prolonged
impairment. fever, skin problems
yellowi (rash, hives),
122
ng of the skin diarrhea, or signs of
in a newborn
child. gallstones (sudden
intense pain in the
abdomen or right
side, jaundice, chills,
fever).
BROKENSHIRE COLLEGE
MADAPO, DAVAO CITY
DRUG STUDY
Date given February 26,2020
123
Generic Brand General Mechanism of Route of Indication Contraindicati Adverse Nursing
Name Name Classification Action Dosage on Reaction Responsibility
A L reductase competitively 40 mg OD It is used to contrai Gastrointest  Take this
R inhibitors inhibits 3- lower bad cholesterol ndicated in inal drug once a
I @ HS
T (statins) hydroxy-3- and raise good patients with symptoms day, at about
O P methylglutaryl- cholesterol (HDL). active hepatic such as the same time
V coenzyme A It is used to disease diarrhea. each day,
I
A (HMG-CoA) lower triglycerides. (including preferably in
S T reductase. By cholestasis, he the evening;
It is used in Cold
T preventing the patic encephal may be taken
O some people to lower symptoms
A conversion of opathy, with food. Do
the chance of heart such as a
T R HMG-CoA to hepatitis, and not drink
attack, stroke, and runny or
I mevalonate, jaundice) or grapefruit juice
certain heart stuffy nose.
N statin unexplained while taking
procedures. Joint pain.
medications persistent this drug.
decrease It is used to elevations in  Institute
cholesterol slow the progress of serum appropriate
Insomnia.
production in the heart disease. aminotransfera dietary changes.
liver se  Arrange to
Urinary
concentrations. have periodic
tract
blood tests
infection
while you are
taking this drug.
Nausea.  Alert any
health care
Loss of provider that
appetite. you are on this
drug; it will
need to be
124
Indigestion discontinued if
symptoms acute injury or
such as illness occurs.
stomach  Do not
discomfort become
or pain. pregnant while
you are on this
drug; use
barrier
contraceptives.
If you wish to
become
pregnant or
think you are
pregnant,
consult your
health care
provider.
 You may
experience
these side
effects: Nausea
(eat frequent
small meals);
headache,
muscle and
joint aches and
pains (may
lessen over
time).
125
 Report
muscle pain,
weakness,
tenderness;
malaise; fever;
changes in color
of urine or
stool; swelling.
126
BROKENSHIRE COLLEGE
MADAPO, DAVAO CITY
DRUG STUDY
Generic Brand General Mechanism of Route of Indication Contraindicati Adverse Reaction Nursing
Name Name Classification Action Dosage on Responsibility
Insulin Humulin class of Insulin lowers 15 units Humuli During low blood sugar Ensure that patient
medications blood glucose by n R (insulin episodes (hypoglycemia). has dietary and
70/30 subcutaneou
called stimulating (human of hypoglycem Symptoms of low exercise regimen
hormones peripheral s recombinant)) ia [see blood sugar may and using good
glucose uptake U-100 is WARNINGS include headache, hygiene practices to
primarily by indicated as an AND nausea, hunger, improve the
skeletal muscle adjunct to diet PRECAUTIO confusion, effectiveness of the
cells and fat, and and exercise to NS], and. drowsiness, insulin and decrease
by inhibiting improve In patients who weakness, adverse effects of
glucose glycemic have dizziness, blurred the disease.
production and control in had hypersensi vision, fast
release by the adults and tivity reactions heartbeat, Monitor nutritional
liver. children with to HUMULIN sweating, tremor, status to provide
type 1 and type N or any of its trouble nutritional
2 diabetes excipients [see concentrating, consultation as
mellitus WARNINGS confusion, or needed.
AND seizure
PRECAUTIO (convulsions) Gently rotate the
NS]. vial containing the
agent and avoid
vigorous shaking to
ensure uniform
suspension of
127
insulin.
Rotate injection
sites to avoid
damage to muscles
and to prevent
subcutaneous
atrophy.
Monitor response
carefully to avoid
adverse effects.
Always verify the

name of the insulin
being given because
each insulin has a
different peak and
duration, and the
names can be
confused.
Use caution when
mixing types of
insulin; administer
mixtures of regular
and NPH insulins
within 15 minutes
after combining
128
them to ensure
appropriate
suspension and
therapeutic effect
129
Ideal
Treatment:
 Cirrhosis isn't curable, but it’s treatable. Doctors have two main goals in
treating this disease: Stop more damage to your liver and prevent
complications. As for the patient who have ascites, therapy should be tailored
to the patient's needs. Some patients with mild ascites respond to sodium
restriction or diuretics taken once or twice per week. Other patients require
aggressive diuretic therapy, careful monitoring of electrolytes, and occasional
hospitalization to facilitate even more intensive diuresis. The patient already
developed massive ascites that is refractory to medical therapy has dire
prognostic implications, with only 50% of patients surviving 6 months.
Medication:
 Conservative management of liver cirrhosis that will provide asymptomatic
relief measures such as pain medications. Paracetamol is safe in patients with
chronic liver disease but a reduced dose of 2-3 g/d is recommended for long-
term use. Non-steroidal anti-inﬂammatory drugs (NSAIDs) are best avoided
because of risk of renal impairment, hepatorenal syndrome, and
gastrointestinal hemorrhage.
 Sodium restriction (20-30 mEq/d) and diuretic therapy constitute the standard
medical management for ascites and are effective in approximately 95% of
patients.
 Diuretic therapy, frequently with spironolactone, a potassium-sparing diuretic
that inhibits the action of aldosterone on the kidneys
 I. V albumin to maintain osmotic pressure and reduce ascites.
130
 Administration of lactulose or neomycin through a nasogastric tube or
retention enema to reduce ammonia levels during periods of hepatic
encephalopathy.
Surgical Interventions:
 Transjugular intrahepatic portosystemic shunt may be performed in patients
whose ascites prove resistant. This percutaneous procedure creates a shunt
from the portal to systemic circulation to reduce portal pressure and relieve
ascites.
 Liver transplantation. Patients with massive ascites have 1-year survival rate
of less than 50%. Liver transplantation should be considered as a potential
means of salvaging the patient prior to the onset of intractable liver failure or
hepatorenal syndrome.
131
MEDICAL PROGNOSIS
Criteria Poor Fair Good Justification

Onset of X 3 Weeks prior to his
Illness admission, the patient
experienced headache,
chest pain, dull abdominal
pain, felt nauseated and
dizzy. We rated it poor
because it has been three
weeks since the patient
felt abdominal pain and
symptoms of liver
cirrhosis.
Duration of X Occurrence of
Illness manifestations related to
liver cirrhosis has been
observed to start 3 weeks
prior to admission. It is
fair since liver cirrhosis is
a chronic disease.
Attitude and X Ever since patient was
willingness to admitted he is committed
take in taking his medications.
medications
Age X The patient is 68 years old
132
and we rated it as poor
since geriatric patients
have deteriorating body
systems that hinder
recovery. The wear and
tear theory suggest that as
a person ages, he or she is
more prone to illness and
resistance and the ability
to heal is getting weaker.

Precipitating X We rated it poor since his
and age and race predisposes
predisposing him in developing the
factors disease. Moreover, his
chronic alcoholism
precipitates the
development of the
disease. Longtime alcohol
beverage drinking is the
most common factor that
triggers liver cirrhosis.

Environment X The ward has poor
ventilation, crowded and
noisy. With this, it is not
favorable for recovery.

Family Support X Family support is good.
They give time in giving
133
care to the patient and in
providing all the needs.
Qualitative Evaluation:
Good 1/7= 0.28 x 100%= 14%
Fair 2/7= 0.28 x 100% = 29%
Poor 4/7= .42 x 100% = 57%
100%
Qualitative Analysis:
In determining the prognosis of patient Mr. V. We have evaluated 7 criteria’s
which include Onset of illness, Duration of illness, Precipitating factors, Attitude and
willingness to take medication and treatment/ surgery, Age, Environment and family
support. 14% good prognosis, 29% fair prognosis ad 57% poor prognosis which
means that Mr. V’s condition is poor in the possibility of getting better if the said
criteria are not met accordingly. Mr. V’s age and chronic alcoholism lead him to have
advanced liver cirrhosis with a main complication of ascites. The mean time period to
its development is approximately 10 years. Ascites is a landmark in the progression
into the decompensated phase of cirrhosis and is associated with a poor prognosis and
quality of life; mortality is estimated to be 50% in 2 years. Refractory ascites carries a
poor prognosis, with a 1-year survival rate of less than 50%. Liver transplantation
should be considered to extend the patient’s life.
PROBLEM LIST
ACTUAL AND RISK
134
NURSING CARE PLAN
Name of Patients: Mr. VAge: 68 Sex: Male Civil Status: Married Religion: Catholic
Address: Davao City Informant: Self Medical Diagnosis: Liver cirrhosis secondary to alcoholic disease, DM 1, HPN controlled
Date Problem Assessment Nursing Planning Implementation EVALUATIO
List (cues & Diagnosis (objectives- N
(according evidences/o long & short Nursing Rationale/Justifications Reference
to bjective term) Interventions
priority) subjective)
F Security Subjective: Risk for Within 8 hrs. INDEPENDENT: N After the
E and Safety “dili siya injury of nursing  Establish rapport This could reduce A effective
B needs: mahimutang related to intervention, patient’s anxiety and N nursing
R Risk for ”, as Altered patient will be get his trust D intervention
injury verbalized Level of able to be free A patient was free
U by the consciousn from injury Assess level of Assist determining from injury and
th
A watcher. ess and modify consciousness and patient’s ability to 13 Editio modified his
R environment cognitive level protect self and comply n environment to
Y Objective: Definition: to enhance with required self- enhance safety.
restlessnes Patient safety. protective action Pages
27, s noted with liver 479-485
cirrhosis Provide calm, Promotes relaxation
2 agitated experience quiet and restful and comfort to patient
0 irritable decreased environment and reduces irritability
2 Limited level of and stimulation
135
0 attention consciousn
span ess as Provide frequent Monitoring for
manifested surveillance to the restlessness and
by patient agitation to avoid falls
restlessness or injury
and
agitation
that could
cause
injury or
fall to the
patient if
not safely
secured
136
NURSING CARE PLAN
(accordin evidences/o long & short Nursing Rationale/ Reference
g to bjective term) Interventions Justifications
priority) subjective
F Safety Subjective: Risk for After 8hrs of Independent: N After the
E and “maluya infection nursing  Monitor VS Provides baseline A effective
B Security siya related to intervention, data; abnormal findings N nursing
R needs: panagsa”, as increase patient will be may be a sign of D intervention
U Risk for verbalized White able to infection A patient was
A infection by the blood demonstrate demonstrated
th
R watcher cells interventions Assess for sign of Monitor for 13 interventions to
Y to prevent risk infection development of Edition prevent risk of
Objective: Defintion: of infection infection infection. He
27, Antibiotic Weakened and will not Pages did not develop
drug body develop signs Do hand washing  Patient is 472-479 signs and
2 (Azithromy defenses and symptoms before and after immunocompromised symptoms of
0 cin) present can make of infection. handling the patient; so he is susceptible to infection
2 on his a person instruct also infection. Hand
0 medication susceptibl significant others to washing must be
therapy e to do hand washing observed to prevent
infection before and after cross-contamination
137
handling the patient
 WBC
count:
Result: 15.8 COLLABORATIVE
Unit:
x10^9/L Administer  To prevent
antibiotic (e.g., development of
Normal Azithromycin) infection
value: 4.0-
10.0 Maintain sterile  Poor observation of
technique on sterile technique could
Vital signs: invasive procedure introduce pathogens in
Temp: 36.2 (e.g., urinary the body
°C catheter) .
PR: 82bpm  Increase white blood
RR: 19cpm Monitor white cell count could mean
BP: 130/90 blood cell count there is underlying
mmHg infection.
138
NURSING CARE PLAN
(according evidences/o long & short Nursing Rationale/ Reference
to bjective term) Interventions Justifications
F Physiologi Subjective: Nutritional At the end of INDEPENDENT: N After the
E c needs: “Gamay ra imbalance my 8 hours  Assess dietary  Identifies deficit in A effective
B Inability akong gina related to span of care, intake & nutritional nutritional intake & N nursing
R to absorb kaon” as Inability to patient will status adequacy of nutritional D intervention
U proper verbalized absorb be able to state A patient was able
A nutrients by the proper meet the . to meet the
R patient nutrients nutritional  Assist patient in  Reduces edema and 13th nutritional
Y Objective: requirements identifying low ascites formation Edition requirements
Loss of Definition: sodium foods.
27, appetite Patient a). Providing Pages
with Liver diet indicated  Offered smaller, Decrease feeling of 578-583
2 Loss of cirrhosis frequent meals. fullness
0 weight can no b). Offer
2 longer met small  Elevate the head of  Reduces discomfort
0 the frequent the bed during meals from abdominal
Diet: sufficient feeding distention & prevent
- diabetic amount of aspiration
diet nutrients
-low salt, for  Encourage patient  Encouragement is
low fats metabolic to eat meals. essential for patient
139
intake needs with gastrointestinal
discomfort
Limit OFI<
1 liter
NURSING CARE PLAN
140
Name of Patients: Mr. VAge: 68 Sex: Male Civil Status: Married Religion: Catholic Address: Davao City
Informant: Self Medical Diagnosis: Liver cirrhosis secondary to alcoholic disease, DM 1, HPN controlled
Date Proble Assessment Nursing Planning Implementation EVALUATION
m List (cues & Diagnosis (objectives-
(accordi evidences/o long & short Nursing Rationale/ Reference
ng to bjective term) Interventions Justifications
F Safe and Subjective: Deficient Within 8 Independent: N After 8hours of
E Security; "maayo pa knowledge hours of Ascertain level of To determine plan of A nursing intervention,
B deficient ba ko, related to nursing knowledge action will be given. N the patient
maam?" As insufficient intervention,  Determine the  The individual may D verbalized
R knowled
verbalized informatio the patient patient's ability, not be physically, A understanding of
U ge by the n as will verbalize readiness, and condition, disease
emotionally, or
A patient. associated understanding barriers to learning. mentally capable at 14 th
process and
R with of condition, Identify support this time. Edition treatment.
Y Objective: altered disease individuals/SO To instruct and "Undanggan na nako
agitated, level of process and requiring educate the pt.’s SO pages 505- akong sigeg inum-
28, irritable, consciousn treatment. information. about the condition. 509 inum" as verbalized
inaccurate ess  Identify motivating by the patient.
follow- factors.  To promote
2 through of Definition: Provide positive wellness to
0 instruction Absence or reinforcement. his/herself.
2 deficiency To encourage
State objectives
0 of clearly in learner's continuation of
cognitive term. efforts.
informatio To meet patient's
 Use short, simple
n related to need in learning
sentences and
specific
141
topic. concepts. Discuss one his/her condition.
topic at a time. To easily understand
the condition and
 Provide an active avoid giving too
role for the client in much information in
the learning process. one session.
 Provide feedback To promotes a sense
and evaluation of of control over the
learning. situation.
Provide information To determine the
about additional lapses and
learning resources. effectiveness of the
session.
Collaborative: Assist with further
Involve the SO to learning and promote
determine the learning at his/her
understanding of own pace.
condition and provide
reliable source of
information.
NURSING CARE PLAN
142
F Physiolo Subjective: Risk for Within 8 hrs. Independent: N After 8 hrs. of
E gical “Katol Impaired of nursing Inspect pressure To document status A nursing
B Needs: akong Skin intervention points and skin and provide visual N intervention the
R Skin kamot ug Integrity the patient surfaces closely and baseline for future D patient was able to
U Integrity tiil maam related to will be able to routinely. comparison. A maintain skin
A maong sige scratching maintain skin Recommend Enhance venous integrity and
R nako kalot”, due to itch integrity and elevating lower return and reduces 14th Edition demonstrate
Y as demonstrate extremities edema formation in behaviors/techniques
verbalized Definition: behaviors/tec extremities. Pages: to prevent skin
28, by the Risk for hniques to Keep linens dry and Moisture 783-790 breakdown such as:
patient skin being prevent skin free of wrinkles. aggravates pruritus -clipping short his
2 altered breakdown. and increase risk of nails
0 skin breakdown. -use moisturizer in
2 Objective: Suggest clipping Prevents patient the dry skin area
0 -Jaundice fingernails short. from inadvertently -drink enough fluids
eyes and injuring the skin
skin Use calamine lotion May be soothing to
-reddish and provide baking the skin and can
143
hands and soda baths. provide relief of
feet itching associated
-dry and with jaundice, bile
chapped lips salts in skin.
Increase oral fluid To prevent
intake dehydration and
moisten lips and
mouth.
144
NURSING CARE PLAN

F PHYSIO Subjective: Acute pain Within 2 INDEPENDENT: N GOAL MET
E LOGIC “nag sigeg related to hours of 1) Est6ablish 1) to facilitate A
B AL balik-balik irritation/ rendering rapport cooperation as well N After 2 hours on
ang sakit sa inflammati nursing as to gain patient s D nursing intervention
R NEEDS
akong on of intervention trust. A the patient was able
U tiyan.” as gastric the patient to:
A verbalized mucosa as will be able 2) Note for the 2) To determine the 10th
R by the evidenced to: location, scale, nursing care to be Edition 1) Verbalized that
Y patient. by intensity and given to the patient. the pain was
recurrent 1) Verbal onset of pain pp.388-392 decreased from 8/10
28, Objective: abdominal ize to 3/10.
-restlessness pain that 3) To minimize
-irritability the 3) Maintain a calm stimulus that could 2) Verbalized
2 -grimaced DEFINITI pain and quite aggravate the recognition of
0 face ON: scale environment. condition of the interpersonal/ family
145
2 -self- will patient. dynamics and
0 focusing Unpleasant decrea reactions that affect
V/s sensory se to the pain problem.
-BP: 140/ and 2-3/ 4) Provide a dim and 4) To add comfort
100mmHG 10 light but providing of the patient. 3) Demonstrate
emotional
-PR: 95 2) Verbal good ventilation behavioral
bpm experience ized 5) usually altered in modification of
-RR: 17 arising recogn 5) Monitor Vital acute pain lifestyle and
cpm from ition signs appropriate use of
-T: 36 C actual or of 6) As timely therapeutic
PAIN potential interp intervention is more interventions.
SCALE: 8/ tissue ersona 6)Instruct patient to likely to be
10 l/ report pain as soon as successful in
damage or
family it begins alleviating pain.
described dynam
in terms of ics
such and
damage reactio 7) Encourage
(internatio ns that verbalization of 8) To provide non-
nal affect feelings about the pharmacological
the pain. pain management.
association
pain
for the proble 8) Provide comfort
study of m. measures (e.g., back 9) To ease the
pain) ; Demonstrate rub, change of suffering
sudden or behavioral position use of
slow onset modification heat/cold compress.)
of any of lifestyle
9) Encourage use of 10) To ease the
intensity and relaxation exercises, suffering
146
from mild appropriate such as focused
to severe use of breathing or deep
with an therapeutic breathing exercise.
11) To provide
anticipated interventions.
10) Encourage comfort
or diversional activities
predictable (e.g., TV/radio,
end and a socialization with 12) Helps in pain
duration of others. management
less than
six 11)Suggest
significant others be 13) To prevent
months.
present during fatigue
procedures
12) Assist client to

alter drug regimen,
based on individual 1) To maintain
needs. acceptable level of
pain. Notify
13) Encourage
physician if regimen
adequate rest
periods. is inadequate to
meet pain control.
DEPENDENT
Administer
medication such as
analgesics a indicated
147
to maximal dosage as
prescribed by the
physician.
148
Key Areas of Core and Competency Indicators
Responsibility
A. Safe and Quality Core and Competency 1:  Explain to the
Nursing Care Demonstrate knowledge patient in his /her
based on the health health status /
/illness status or condition.
individuals  Explain all the
rationale of all the
intervention done
such as
administering
medications and
other procedures.
Core and Competency 2: Respecting their beliefs and
Provides sound decision culture of the patient
making in the care of especially in refusing
individuals considering medical treatment.
their beliefs and values
Core and Competency 3:  Vital signs checked
Promotes safety and and recorded every
comfort and privacy of 4 hours
clients  Bed making done;
side rails up
 Assisted in getting
up to bed and when
going to comfort
rooms
 Provided with calm,
clean and restful
environment
Core and Competency 4:

Sets priorities in Nursing Nursing Care Plan was
Care based on client’s done
needs
Core and Competency 5:  Vital signs
Ensure continuity of care rechecked and
recorded every after
4 hours
 Intravenous Fluid
regulate well
 Medications still
monitoring
 Bed side care done;
side rails up
Core and Competency 6: We administer medications
Administer medications the following 10 Rights in
and other health Medication Administration
therapeutics
Core and Competency 7:
Utilizes the nursing
process as framework for Assessment done using
nursing Nursing Assessment Tool
7.1 Performs
comprehensive and
systematic nursing
assessment
7.2 Formulates a plan Nursing care plan was done

of care in collaboration with interventions
with clients and other independently, dependently
members of the health and collaboratively.
team
7.3 Implements  Asked permission
planned nursing care to as assigned student
achieve to achieved nurse for the shift
identified outcomes  Gives rationale
every intervention
done
7.4 Evaluates progress Objectives were set and
toward expected within the span of nursing
outcomes care goal was evaluated if
met or unmet.
B. Management of Core and Competency  Administer
Resources and 1: medications on time
Environment Organizes workload to  Procedures carried
facilitate client care out and done
Core and Competency  Use available
2: resources as
Utilizes financial possible
resources to support  Observe 3 R’s
client care (reuse, recycle,
reduce)
Core and Competency  Ensuring
3: equipment’s and
Establishes mechanism paraphernalia’s
to ensure proper clean and
functioning of functioning orderly
equipment  Provide safety
measures; side rails
up
 Hand washing done
before and after
procedures
 Disinfection of
equipment’s and
paraphernalia’s
before and after
procedures
 Waste segregated
150
properly and
accordingly
Core and Competency  Observed proper
4: disposal of wastes
Maintains a safe and follow the
environment hospital protocols
C. Health Education Core and Competency 1:  Set priorities

Assess the learning accordingly
needs of the assessment done
client’s/partner’s
Core and competency 2:  Provided
Develops health conductive
education plan based on learning during
assessed and anticipated walking hours at
needs bedside
Core and Competency 3:  Provide proper
Develops learning instructions
materials for Health accordingly to
Education patient’s condition
Core and Competency 4:  Health teaching
Implements the health (exercise, proper
education plan hygiene regularly,
eat nutritious food,
and drink a lot of
water)
Core and Competency 5:  Documents data,
Evaluates the outcome of interventions and
health education outcome of care
D. Legal Core and Competency 1:
Responsibility Adheres to practices in  Ensured signed the
accordance with the consent and
nursing law and other documents data are
relevant legislation available
including contracts and
informed consent
Core and Competency 2:  Nursing care and
Adheres to intervention done
organizational policies and follow the
and procedures, local and hospital protocols
national
Core and Competency 3:  Charting done and
Documents care rendered documented all
to clients essential data
accordingly
E. Ethico-moral and Core and Competency 1:  Maintained
151
Responsibility Respects the rights of confidentiality and
individuals/groups privacy
Core and Competency 2:  Perform function
Accepts responsibility accordingly to our
and accountability for scope as a student
own decision and actions nurse
Core and Competency 3:  Ethical
Adheres to the national considerations
and international codes rendered, asked
of ethics for nurse permission
whenever
procedure is done
F. Personal and Core and Competency 1:  Accepted advices,
Professional Identifies own learning correction and
Development needs advice from the
clinical
instructions
Core and Competency  Applies learned

2: information for the
Pursues continuing improvement of care
education such as attended
seminars and class
discussions
Core and Competency  PNSA OFFICER
3:  ROTARACT
Gets involved in OFFICER
professional
organizational and civic
activities
Core and Competency  Dresses
4: appropriately
Projects a professional wearing prescribed
image of the nurse uniforms
 Demonstrates good
manner and right
conduct at all times
to equally
Core and Competency  Listens to
5: suggestions and
Possesses positive recommendations
attitudes toward change given by supervising
and criticisms Clinical Instructor
and Nurses on Duty
Core and Competency  Performed functions
6: according to
Perform functions standards as a
according to student nurse
152
professional standards
G. Quality Core and Competency  Informed and notify
Improvement 1: physicians in regard
Gathered the data for to patient conditions
quality improvement
Core and Competency  Endorsement of
2: patient’s assignment
Participate in nursing  NOD and student
audits and rounds Rounds
Core and Competency  Documents the data
3: and report it and
Identifies and report notify the physicians
variances to the appropriate
persons for any
discrepancies
Core and Competency  Provided preventive
4: measures; side rails
Recommends solution up
to identified problems
H. Research Core and Competency  Required and

1: complied journal
Gathered the data using readings and case
different methodologies analysis related to
our concept
Core and Competency  Initiates a research
2: study to identify
Analyzes and interprets researchable
data gathered problems
 Assessment using
NAT
 Interview
Core and Competency  Identifies
3: researchable
Recommends action for problems related to
implementations immediate care of
patient
Core and Competency  Maintained
4: patient’s privacy
Disseminated results of and confidentiality
research findings of the information
gathered
Core and Competency  Utilized findings of
5: research studies in
Applies research the immediate care
findings in nursing of the patient with
practice alteration in
perception and
153
coordination
I. Records Core and Competency  Copied and
Management 1: interpreted patients
Maintains accurate and record and latest
updated documentations doctor order and
of client care laboratory test
 Charting is
accurate and
avoided errors
 Plotted accurately
patient’s vital signs
and I & O
Core and Competency  Recorded patient
2: response to the
Records outcome of nursing
client care intervention being
rendered.
Core and Competency  Maintained
3: patient’s privacy
Observes legal and confidentiality
imperatives in record
keeping
J. Communication Core and Competency  Asked patient
1: name, introduced
Establishes rapport with self and ask related
client’s, significant questions
other and members of pertaining to the
the health team condition and life
of the patient
Core and Competency  Interprets and
2: validates client’s
Identifies verbal and body language and
non-verbal cues facial expressions
HEALTH EDUCATION
154
Health Teaching
 Teach the patient to do proper hygiene regularly
 Instruct the patient to avoid heavy and vigorous activities
 Promote therapeutic exercises teach the patient how to increase flexibility and
range of motion while building strength.
 Encourage patient not be fearful of physical therapy, instruct patient that even
he is experiencing pain and great difficulty in moving.
 Find ways to make your life less stressful.
Outpatient Orders
 Follow your provider's instructions for follow-up appointments.
 Keep appointments for any routine testing you may need.
 Encourage to meet regularly the physical therapies.
Diet
 Healthy foods include fruits, vegetables, whole-grain breads, low-fat dairy
products, beans, lean meats, and fish. Certain foods may cause your pain, such
as alcohol or foods that are high in fat. You may need to eat smaller meals and
to eat more often than usual.
 Drink plenty of water and avoid drinking alcohol and caffeine.
Spirituality:
 Advise the patient to ask a assistance when doing their religious rituals.
DISCHARGE PLAN
155
Medication
 Medication should be taken as prescribed by the physicians
 Educate the family member regarding to the dosage, time, and due of
medications.
 Compliance of medication is important for any further treatment and recovery.
 Check the expiry date in every drug taken.
 Follow the ordered dose and frequency. To avoid overdose and toxicity.
 Observed the adverse reaction of the medications.
Environment
 Maintain danger free environment like Ensuring the floors are dry and no
presence of materials that may risk for injury.
 Keep and maintain calm, clean and restful environment to promote wellness
and comfort.
Treatment
 Get plenty of rest while you’re recovering. Try to get at least 7 to 9 hours of
sleep each night.
 Instruct the patient to undergo rehabilitation therapy.
 Advice to use a assistive devices when in difficulty of walking occur.
156
Evaluation and Modification
In this case study the client was diagnosed with liver cirrhosis secondary to
alcoholic liver disease. He also was hypertensive but under control and had diabetes
mellitus. Both diseases ran in both sides of his family. In our initial assessment we
found that the patient did have an alcohol habit that started when he was working as a
soldier. Job and peer pressure made it easier to start drinking more frequently
He went to the hospital with a distended abdomen, but his condition was
misdiagnosed as they only focused on his existing diabetes and hypertension and for
some reason did not do any lab work to determine the cause of his condition. He was
admitted to Brokenshire Hospital due to his abdominal pain, vomiting and nausea.
We identified the risk factors and set objectives and interventions during our
interaction with him. Although we did not meet all of our objectives the client showed
significant improvement to his condition. He agreed to be more responsible for his
health and situation after our treatment and recommendations.
Because he delayed treatment his health is not optimal, but we feel that with
proper treatment and changes in lifestyle (stop drinking, eating healthier, exercising as
able) as well as following up with checkups and taking proper medication will
prolong his life. Of course, having the emotional support of those closest to him is
vital in keeping him on track and to live the best life possible.
157
CONCLUSION AND RECOMMENDATION
In this rotation, the 1st group of BSN-3 of Brokenshire College of Davao,
gained a lot of knowledge in this experience. This experience will serve as our guide
and basis for improvement. In relation with improvement, the group had come up
with recommendations, which we think, would have made the exposure a lot better.
To our client’s family:
One of the most important factors of recovery for a certain illness is the
participation of the patient himself and we are very thankful for our patient and the
patient’s family for being involved in the treatment. The family should know all the
basic facts and information about the patient’s illness because them, more than
anybody else are expected not just to care but also to accept his condition with utmost
understanding. Being aware of the illness itself and its treatment will elicit awareness
and would definitely pave the way to the prevention and alleviation of any ailment
that any of the family members may possibly have.
To the vulnerable groups
We recommended taking extra measures to live healthy life by avoiding binge
drinking of alcohol, eating less carbohydrates, being at optimal weight, eating healthy
foods and to drink coffee. Studies showed that coffee optimized the flow of bile
which protects the liver. While it is unclear how this happens, it is believed that
caffeine or the dark polyphenolic compounds found in coffee help protect the liver.
Watch out for certain medicines. Some cholesterol drugs can occasionally have a side
effect that causes liver problems. The painkiller acetaminophen (Tylenol) can hurt your
liver if you take too much. Learn how to prevent viral hepatitis. It's a serious disease that
harms your liver. There are several types. You catch hepatitis A from eating or drinking
water that's got the virus that causes the disease. Don't touch or breathe in toxins. Some
158
cleaning products, aerosol products, and insecticides have chemicals that can damage
your liver. Avoid direct contact with them. Additives in cigarettes can also damage your
liver. Be careful with herbs and dietary supplements. Some can harm your liver. A few
that have caused problems are cascara, chaparral, comfrey, kava, and ephedra.
To the Student Nurses:
In line with this case study, the group members would like to encourage all
student nurses to give their best in taking care of their patients and get more involved
in the promotion of health in our country. We must impart to those who are in need,
our knowledge regarding health and on how they could maintain a healthy lifestyle.
We must apply to them the skills that we have learned by rendering them a quality-
based service. We must also teach the patients as well as the significant others on the
alternative means of promoting health and on how to prevent the possible occurrence
of a disease. Empathy must always be shown not just to the patient but also to the
significant others. Student nurses must also be sensitive to the feelings and emotions
not just of the patient but also to the significant others especially in experiences of
death and finite separation.
To the medical world:
We would like to encourage the medical practitioners or the members of the
health care team that they should have to be more committed or compassionate in
their chosen profession. They must have to cater the health needs of the people of
different kinds without putting levels of discrimination on them. Their job is not that
easy, but they must have to be very careful because they are already dealing here with
the life of a person. They must have to extend their hands not only in the physical
means but also in a holistic way of giving or providing care to individuals, families
and the population groups especially in significant others who may have lost love
159
ones. They are tasked to render their services in order to achieve the good health
condition of the citizens of the country because the health of the nation lies in the
health of the populace.
160
Bibliography
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Handbook of Medical-Surgical Nursing. Springhouse: 2016
Leighton, S.S., et al. (2017) Perspective in Human Development.
Lindon, P.S & Reese, R.R. (2019) Psychology: approach and understanding.
Lindon, P.S & Reese, R.R. (2019) Psychology: approach and understanding. retrieved
from http://education.stateuniversity.com/pages/2032/Havighurst-Robert-J-
1900-1991.html. Retrieved on February 12, 2010.
Luckmann, K.L & Sorensen, W.A (2013): Medical-Surgical Nursing: a

Psychophysiologic Approach. Louis, Missouri: Mosby.
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Philadelphia: Lippincott Williams & Wilkins.
Peterson, M.L, Luis, B.D. & Chong, P.C. (2017) Personality development. Retrieved
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Brokenshire College of Davao

Madapo, Davao City

Presented to the Faculty of

Visminda B. Batoy RN., MN., MAN., COHN

In Partial Fulfillment of the Requirements of

Dayanghirang, Elica Hilda C.

patience shown even in stressful situations and mistakes were made.

To all medical personnel and staff of Brokenshire Integrated Health Ministries

accommodations during our clinical exposure as well as providing vital information

required for caring of the patient.

Background of the Case……………………………………………………………...10

Significance of the Study…………………………………………………………….14

Review of related Literature……………………………………………………...16-21

Anatomy and Physiology of System’s Involved………………………………….33-43

Erik Erickson’s Stages Psychosocial Development Theory…………………..……..60

Sigmund Freud Psychoanalytical Theory……………………………………..….61-63

Jean Piaget Cognitive Development Theory……………………………………...64-65

Havighurt’s Developmental Stages……………………………………………….66-67

Collection Procedure/Method and Sources of Information…………………………..68

Physician’s Finding and Medical Diagnosis…………………………………………70

Nursing Assessment: Interview and PE-IPPA……………………………………71-81

c. Drugs and Treatment…………………………………………………...110-130

Nursing Care Plan/ Problem Solving

Assessment Data Interpretation…………………………………………..134

1. Identifying Nursing Problems

2. Nursing Theory of care

3. Planned Interventions/Identifying Solutions and its Rationales

1. Applications of Nursing Intervention

2. Applications of Standard of Nursing Practice

(11 Key Areas of Responsibility)

3. Progress Notes during the Course of Care and Nursing Interventions

Evaluation and Modification……………………………………………157

may happen is Liver Cirrhosis.

structural changes that take place or by the cause of the disorder.

alcohol-associated liver disease. Approximately 2 billion adults are obese or

leading cause of death here in Davao.

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

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,

intake. Although necessary, excessive alcohol use is not sufficient to promote

hepatitis, and one in four will develop cirrhosis.

Different alcoholic beverages contain varying quantities of alcohol. Although

autopsy series of men, a threshold daily alcohol intake of 40 g was necessary to

the overall prevalence. There is a clear dose-dependent relation between alcohol

alcohol in men and 20 g in women significantly increases the risk of cirrhosis. In

Secondary to Alcoholic Liver Disease, Insulin Requiring Diabetes Mellitus,

Liver Cirrhosis Secondary to Alcoholic Liver Disease, Insulin Requiring Diabetes

Mellitus, Hypertension II – Controlled. Three weeks prior to admission, patient had

Integrated Health Ministries Incorporated.

To have a course of direction, organization and to recognize the essence of this

study, we have set the following objectives:

Integrated Health Ministries, MEDWING Ward, we aim:

 To provide an extensive study about Liver Cirrhosis Secondary to Alcoholic

equipped with competence in dealing with related situations in the future;