DES SMT. SUBHADRA K.

JINDAL COLLEGE OF NURSING

PUNE

PRACTICE TEACHING

ON

HEPATITIS

SUBMITTED TO, SUBMITTED BY,

Mrs. Shubhangi Malawade Miss. Mallika Shelar

(Lecturer) M.Sc. Nursing 1st year

DES SMT. Subhadra K. DES SMT. Subhadra K.

Jindal College of Nursing Pune Jindal College of Nursing Pune

DATE OF SUBMISSION:
NAME OF THE STUDENT - MS. MALLIKA SHELAR.

NAME OF THE GUIDE - MRS. SHUBHANGI MALAWADE.

SUBJECT - MEDICAL SURGICAL NURSING

DATE -

VENU - CLASSROOM 2nd YEAR BSc.

CLASS TAUGHT - 2ND YEAR BSc.

METHOD OF TEACHING - LECTURE CUM DISCUSSION.

AUDIO-VISUAL AIDS- - CHART, FLASH CARD, HANDOUTS, TRANSPARENT SHEET.

PREVIOUS KNOWLEDGE - THE GROUP WILL HAVE PREVIOUS KNOWLEDGE

ABOUT HEPATITIS.
 OBJECTIVES-
General Objectives- At the end of the practice teaching students will gain in depth
knowledge about the hepatitis.
Specific Objectives-
Students will be able to…
1.Discuss the anatomy and physiology of liver.
2.Define hepatitis.
3.Explain etiological factors and risk factors of hepatitis.
4. Describe the pathophysiology of hepatitis.
5.List down the types of hepatitis.
6.Identify the mode transmission of hepatitis.
7.Enlist the clinical manifestation of hepatitis.
8.Discuss the diagnostic evaluation of hepatitis.
9. Describe the complication of hepatitis.
10.Explain the management of hepatitis.

 Preventive management.
 Pharmacological management.

NO. Objectives Time Content AV Teaching Evaluation

Aids learning
activity
1. Discuss 5 Anatomy and Physiology of Liver- Chart Lecture Explain
the min The liver is located in the right upper quadrant of the cum the
anatomy abdomen, below the diaphragm. It’s in other roles in discussio anatomy
and metabolism include the regulation of glycogen n. and
physiology storage, decomposition of red blood cells, and the physiology
of liver. production of hormones. of liver.
The liver is an accessory digestive organ that produces
bile, an alkaline fluid containing cholesterol and bile
acids, which helps the breakdown of fat. The
gallbladder, a small pouch that sits just under the
liver, stores bile produced by the liver which is after
words moved to the small intestine to complete
digestion. The liver is highly specialized tissue,
consisting of mostly hepatocytes, regulates a wide
variety of high-volume biochemical reactions,
including the synthesis and breakdown of small and
complex molecules, many of which are necessary for
normal vital functions.

Structure-
The liver is a reddish-brown, wedge-shaped organ
with two lobes of unequal size and shape. A human
liver normally weighs approximately 1.5 kg and has a
width of about 15cm.
The liver is connected to two large blood vessels: the
hepatic artery and the portal vein. The hepatic artery
carries oxygen-rich blood from the aorta via the celiac
trunk, whereas the portal vein carries blood rich in
digested nutrients from the entire gastrointestinal
tract and also from the spleen and pancreas. These
blood vessels subdivide into small capillaries’ known
as liver sinusoids, which then lead to lobules.
Lobules are the functional units of the liver. Each
lobule is made up of millions of hepatic cells, Which
are the metabolic cells.
The liver is grossly divided into two parts when
viewed from the above-a right and a left lobe-and
four parts when viewed from below.

Function of liver-
1.Production of bile, which helps carry away waste
and break down fast in the small intestine during
digestion.
2.Production of certain protein for blood plasma.
3.Production of cholesterol and special proteins to
help carry fats through the body.
 4.Conversion of excess glucose into glycogen for
storage and to balance and make glucose as needed.
5.Processing of haemoglobin for use of its iron
content.
6.Clearing the blood of drugs and other poisonous
substances.
7.Regulating blood clotting.
8.Resisting infections by making immune factors and
removing bacteria from the bloodstream.
9.Clearance of bilirubin, also from red blood cells.
Define 2 What is
hepatitis. min meant by
Hepatitis- Chart lecture hepatitis.
Explain 5 Hepatitis is inflammation of the liver cells and cum
etiological min damage to the liver. Chart discuss- What is
factors Etiology- ion the
and risk Virus aetiology
factors of Non-viral infection. and risk
hepatitis. Alcohol. factors of
Toxins. hepatitis.
Drugs.
Autoimmune. Lecture
Risk Factors- Chart cum
Poor sanitation. discuss-
Lack of safe water. ion
Living in a household with a infected person.
Being sexual partner of someone with acute hepatitis
A infection.
Use of recreational drugs.
Travelling to areas of high endemicity without being Explain
immunized. Lecture the
cum pathophys
Describe Trans
discuss- ilogy of
the paran
Pathophysiology- ion hepatitis.
pathophys 10 cy
Due to etiological factors
iology of min
hepatitis.
Necrosis and inflammation of hepatic cells

Decreased liver function

Circulating immune complexes and complement

system activation
 Impaired bilirubin level metabolism and obstruction
bile flow Classify
the types
HEPATITIS. of
hepatitis.
Lecture
Types of hepatitis- cum
List down 15 Flash discuss-
1.Viral hepatitis-
the types min card. ion
a. Type A hepatitis
of
b. Type B hepatitis
hepatitis. Explain
c. Type C hepatitis
the viral
d. Type D hepatitis
hepatitis,it
e. Type E hepatitis
s
2.Nonviral hepatitis.
types,mod
e of
1.Viral hepatitis-
transmissi
a. Type A hepatitis-
on,risk
It is caused by RNA virus of the enterovirus family.
factors.
Hepatitis A is a liver disease caused by the hepatitis A
virus. The virus is primarily spread when an uninfected
(and vaccinated) person ingests food or water that is
contaminated with the faeces of an infected person.
The disease is closely associated with a lack of safe
water, inadequate sanitation and poor personal
hygiene.
Unlike hepatitis B, C, A infection does not cause
chronic liver disease and is rarely fatal, but it can
cause debilitating symptoms and fulminant hepatitis
(acute liver failure), which is associated with high
Identify Lecture
mortality.
the mode cum
Mode of Transmission- Chart
of discuss-
1.It is primarily fecal-oral, usually through ingestion of
transmissi ion
food or liquid contaminated with virus.
on of
2.The virus has been found in the stool of infected
hepatitis.
patient.
3.Children acquire the infection at school by poor
hygiene, hand-to-mouth contact.
Risk factors-
1.As in overcrowding and poor sanitation and infected
food handlers.
2.Poor sanitation.
3.Lack of safe water.
4.Injecting drugs.
5.Living in a household with an infected person.
6.Being a sexual partner of someone with acute
hepatitis A infection.
7.Travelling to areas of high endemicity without being
immunized.
Aetiology-
1.Prevalent in underdeveloped countries or
overcrowding and poor sanitation.
2.Infected food handlers, people can contract it by
consuming water or shellfish from contaminated
water.
3.Commonly spread by person to person and rarely by
blood transmission.
Clinical manifestation-
1.Prodromal symptoms, fatigue, anorexia, malaise,
headache, low-grade fever, nausea and vomiting,
jaundice.
2.Icteric phase-jaundice, tea coloured urine, clay-
coloured stool and right upper quadrant tenderness.
b. Hepatitis B-
It is double-shelled particle containing DNA. This
particle is composed of hepatitis B core antigen,
hepatitis B surface antigen and independent protein
circulating in the blood. Hepatitis B is an infection of
liver caused by the hepatitis B virus(HBV).
Risk factors-
1.Hemodialysis, male homosexual and bisexual
activity.
2.Close contact with carrier of HBV, multiple sexual
partners.
3.Receipt of blood or blood products, recent history of
sexual transmitted disease.
4.Frequent exposure to blood or blood products.
Mode of Transmission-
1.It is primarily through blood. Oral route through
saliva or through breastfeeding.
2.Sexual activity through blood. Semen saliva or
vaginal secretions.
3.Gay men are high at risk.
4.In rare cases, it may progress to fulminant hepatitis
of hepatic failure.
5.May become chronic active or chronic persistent
hepatitis.
c. Type C hepatitis-
It was formerly called non-A, non-B hepatitis, an RNS
virus.
Risk factors-
1.Recipt of blood products, health care and safety
workers after needle stick injury.
2.Children born to women infected with hepatitis C
virus.
3.Past treatment with chronic haemodialysis, sex with
infected partner, history of STD.
4.Throgh piercing and tattooing and ink.

Clinical manifestation-
Symptoms usually occurs 6to7weeks after transfusion
but may be attributed to another viral infection and
not diagnosed as hepatitis.
d. Type D hepatitis-
Hepatitis D virus is a defective RNA agent that appears
to replicate only with the hepatitis B virus. It requires
HBsAG to replicate.
Occurs along with HBV, or may superinfect a chronic
HBV carrier.
Cannot outlast a hepatitis B infection.
May acute or chronic.
Risk factors-
1.Chronic HBV carriers are at risk for infection with
HDV.
2.Individual who are not infected with HBV, and have
not been immunized against HBV, are at risk of
infection with HBV with simultaneous or subsequent
infection with HDV.
3.Since HDV absolutely requires the support of a
hepadnaviral for its own replication, inoculation with
HDV in the absence of HBV will not cause hepatitis D.
Alone, the viral genome indeed replicates in a hyper-
independent manner, but virus particles are not
released.
Mode of Transmission-
1.Blood born and sexual.
2.Percutaneous (injecting drug use)
3.Permucosal(sexual)
4.Perinatal.
Clinical manifestation-
Similar to HBV but more sever.
 With superinfection of chronic HBV carriers, it cause
sudden worsening of condition and rapid progression
of cirrhosis.
e. Type E hepatitis-
A single identified nonenveloped single-stranded RNA
virus.

Mode of Transmission-
The hepatitis E main lt transmitted through the faecal-
oral route due to faecal contamination of drinking
water. Other transmission routes have been
identified, which includes:
1.Foodborne transmission from ingestion of products
derived from infected animals.
2.Zoonotic transmission from animal to humans.
3.Transfusion of infected blood products.
4.Vertical transmission from a pregnant woman to her
foetus.
Although humans are considered the natural host for
the hepatitis E virus, antibodies to the hepatitis E virus
or closely related viruses have been detected in
primates and several other animal species.
Hepatitis E is a waterborne disease, and contaminated
water or food supplies have been implicated in major What are
outbreaks. sign and
Risk Factors- symptoms
The risk factor for hepatitis E are related to poor of viral
sanitation in large areas of the world and shedding of hepatitis.
the hepatitis E virus in faeces. Lecture How is
Clinical manifestation- cum viral
Enlist the 5 Jaundice. Chart discuss- hepatitis
clinical Min Anorexia. ion Diagnosed
manifesta Hepatomegaly.
.
tion of Abdominal pain and tenderness.
hepatitis. Nausea and vomiting.
Fever. Lecture
Discuss Diagnostic Evaluation- Han--- cum
the 1.Elevated serum transferase levels (aspartate douts. discuss-
diagnostic transaminase), AST, alanine transaminase of all forms ion
evaluation of hepatitis.
of 2.Radioimmunossay to include HBsAg, anti-HBc, anti-
hepatitis. HBsAg detected in various stages of HBV.
3.Hepatitis C antibody-may not be detected for 3 to
 6months after onset of HCV illness, antibody test used
for screening purpose.
4.Polymerase chain reaction test to confirm viral
activity in HIV illness.
5.Antidelta antibodies of HBsAg for HDV or detection
of IgM in acute diseases and IgG in chronic disease.
6.Hepatitis E antigen.
7.Liver biopsy to detect chronic active disease,
progression and response to therapy.
8.X-ray and other diagnostic images are needed only
in very unusual circumstances.
9.CT scan or ultrasound-These diagnostic imaging
tests are used to detect the extend of liver damage What are
and may also detect cancer of the liver caused by complicati
chronic hepatitis B. ons of
9.Liver biopsy-A biopsy may be done to detect the viral
extent of liver damage or to evaluate how well a hepatitis.
treatment is working.
Complication-
Scarring of the liver.
Discuss Liver cancer.
the Liver failure.
complicati
on of
hepatitis. Lecture What are
Management- cum preventive
Pampl discuss- measures
Preventive measures-
ets. ion for viral
Hepatitis A-
Explain a. Wash your hands with soap after going to the toilet. hepatitis.
the b. Drink boiled water.
managem c. Get a vaccine for hepatitis A.
ent of Hepatitis B-
hepatitis. a. Tell the partner if you are a carrier or try to find out
whether he/she is a carrier.
1.Preventi
b. Practice safe sex.
ve
c. Use only clean syringe that have not been used by
measures.
anyone else.
d. Only allow well-sterilized skin perforating
2.Pharma-
equipment (tattoo, acupuncture)
cological
Hepatitis C-
managem
If you are infected, do not let others share your tooth
ent.
brush, razer equipment.
If you are infected cover the open wound.
Do not share needles.
Hepatitis D-
Use a same guideline as for Hepatitis B. Only a person
who is infected with Hepatitis B can become infected
with Hepatitis D.

Hepatitis E-
Lecture
Do the same as you would to protect yourself from
cum
Hepatitis A infection.
Pampl discuss-
Management-
ets ion
1.Rest according to patient’s level of fatigue.
2.Theraputic measures to control dyspeptic symptoms
and malaise.
3.Hopitalization for protracted nausea and vomiting.
4.Small frequent feeding of heigh calories, low-fat,
and proteins are restricted when liver cannot
metabolize protein by products.
5.Vitamin K-injected SC if PT is prolonged.
6.IV fluids and electrolyte replacement is indicated.
7.Antiemetic drugs are administered.
Active Immunization-A hepatitis B vaccine prepared
from plasma of humans chronically infected with HBV
is used only rarely and in patient who are
immunodeficient or allergic to recombinant yeast-
derived vaccines. It provides active immunity. The
need for booster does may be revisited if reports of
hepatitis B increase, prevalence of carrier state
develops, indicating the protection is declining.
Passive immunity-Hepatitis B immune globulin
provides passive immunity to hepatitis B and is
indicated for people exposed to HBV who have never
had hepatitis B and have never received Hepatitis B What is
vaccine. tereatmen
Pharmacological Intervention- t regimen
Hepatitis B medication- for viral
a. Polygated interferon alfa-2b- hepatits.
It is used alone or in combination with other
medication.
It slows the replication of virus and boosts the body’s
immune system to fight the infection.
It is usually not given to people whose liver damage
has progressed to cirrhosis, because is can make the
liver damage worse.
Liver function tests and HBV DNA tests are used to
check how well the treatment is working.
b. Nucleoside analogues-
NAs reduce the amount of virus in the body. Between
20% and 90% pf patients may have levels reduced so
far that they become undetectable.
HBV may become resistant to NAs overtime.
NAs do not cure the infection. Relapse is possible
even in patients who have had a good response to
treatment.
Explain
NON-VIRAL HEPATITIS-
the non
Certain chemicals have toxic effects on the liver and Trans
viral
produce active liver cell necrosis and toxic hepatitis is paran
hepatitis,it
inhaled, injected parenterally or are taken by mouth. cy
s
The chemicals most commonly implicated in this
types,mod
diseases carbon tetrachloride, phosphorus,
e of
chloroform and gold compounds. These substances
transmissi
are true hepatotoxins.
on,risk
1.Toxic Hepatitis-
factors.
It resembles the viral hepatitis. Obtaining the history
of exposure to hepatotoxic chemicals, medications or
other toxic agents assists in early treatment and
removal of causative agents.
Symptoms- Anorexia, nausea, vomiting are usual
symptoms. Jaundice and hepatomegaly are noted in
physical assessment, fever.
Treatment-Therapy as to maintain fluid and
electrolyte balance, blood replacement, comfort and
supportive measures.
2.Drug induced Hepatitis-
This liver disease is the most common cause of acute
liver failure.
Symptoms-Chills, fever, rash, anorexia, nausea. Later
may produce symptoms like jaundice, dark urine,
enlarged or tender liver.
Treatment-Stop the use of medication. A short course
of high-dose corticosteroids be used with patients
with sever hypersensitivity reaction.
3.Fulminant Hepatitis-
It is rare nut potentially fetal disease. Fulminant liver
failure is acute necrosis of liver cell without pre-
existing liver disease, resulting in inability of liver to
perform its many function.

Etiology-
Ischemia and hypoxia because of hepatic vascular
occlusion, hypovolemic shock, acute circulating
failure, septic shock ,heat stroke.
Other causes includes-Hepatic vein obstruction,
autoimmune hepatitis, partial hepatectomy.

What are
Clinical Features-
sign and
Malaise, anorexia, nausea, vomiting, fatigue, jaundice
symptoms
urine is tea-coloured and frothy when shaken.
of non-
Purities caused by bile salts are deposited in the skin.
viral
Ascites, altered LOC, ranging from irritability and
hepatitis.
confusion to stupor, coma.
Breath odour of acetone and portal systemic
How is
encephalopathy, also known as hepatic coma.
non viral
hepatitis
Diagnostic Evaluation-
Diagnosed
Decreased platelet count
.
Elevated ammonia, amino acid levels.
Hypoglycaemia or hyperglycaemia. What are
Complications- the
Encephalopathy and cerebral edema. complicati
Sepsis on of non-
Gastrointestinal bleeding. viral
Renal failure. Pampl
ets. hepatitis.
Hemodynamic complications.
Nursing management- Write the
Nursing assessment-- managem
Assess for systemic and liver-related symptoms. ent of
Obtain history, such as IV drug use, ingestion of non-viral
possible contaminated food or water to assess for any hepatitis.
mode of transmission of virus.
Assess size and shape of liver to detect enlargement
of characteristics of cirrhosis.
Obtain vital history, including temperature.
Management-
Oral or rectal administration of lactulose to minimize
formation of ammonia and other nitrogenous by
products in the bowel.
Rectal administration of neomycin to supress urea-
splitting enteric bacteria in the bowel and decrease
ammonia formation.
Low molecular weight or albumin followed by
potassium sparing diuretic to enhance fluid shift from
interstitial back to intravascular spaces.

Summary
In todays practice teaching we saw the Anatomy and
Physiology of liver, definition of hepatitis, aetiology
and risk factors, pathophysiology, types of hepatitis,
mode of transmission of hepatitis, clinical
manifestation, diagnostic evaluation, preventive
measures, management of hepatitis.

BIBLIOGRAPHY
 Deepak Sethi, Medical surgical NURSING,1st
edition, page no.-730-742.
 Brunner S.A textbook of medical surgical
nursing,10th edition Page. no-1925-1930.
 Siddharth and Brunner, Textbook of medical
surgical nursing,2020, Page. no.-1263-1271.