Presented By

Bibi Baby
LIVER IS THE LARGEST GLAND IN THE BODY.
IT WEIGHS 1- 2.3 KG.
IT IS LOCATED IN UPPER PART OF ABDOMEN CAVITY.
IT HAS FOUR LOBES:-
LARGE RIGHT LOBES.
SMALLER WEDGE SHAPED LEFT LOBE.
CAUDATE LOBE
QUDRANT LOBE
 THE PORTAL FISSURE
 POSTERIOR SURFACE OF THE LIVER WHERE VARIOUS
STRUCTURE ENTER AND LEAVE THE GLAND.
 PORTAL VEIN
 HEPATIC ARTERY.
 NERVE FIBRES .
 RIGHT AND LEFT HEAPATIC DUCTS LEAVE , CARRYING BILE
FROM LIVERE TO GALL BLADDER.
 BLOOD SUPPLY
 HEPATIC ARTERY AND PORTAL VEIN TAKE BLOOD TO THE
LIVER
 PHYSIOLOGY OF LIVER
 CARBOHYDRATE METABOLISM.

 FAT METABOLISM

 PROTEIN METABOLISM

 BREAKDOWN OF ERYTHROCYTES.

 DETOXIFICATION OF DRUGS AND NOXIOUS SUBSTANCE.

 METABOLISM OF EATHONOL.

 INACTIVATION OF HORMONES.
PHYSIOLOGY OF LIVER (CONTD)
 SYNTHESIS OF VITAMIN A

 PRODUCTION OF HEAT.

 SECREATION OF BILE.

 STORAGE
 HEALTH HISTORY
DESCRIPTION OF CLIENTS PRESENT ILLNESS AND CHIEF COMPLAINTS.

ONSET ,COURSE,DURATION,LOCATION,AND PRECIPATATING.

 CARDINAL SIGNS AND SYMPTOMS –ALTERED HEPATIC FUNCTIONS:-

 JAUNDICE

 CHANGE IN URINE ,STOOL COLOUR.

 VAGUE TO SEVERE ABODIMAL PAIN-AFTER EATING HIGH FATTY FOODS.

 ABDOMINAL TENDERNESS AND DISTENTION.

EXPLORE CLIENTS HEALTH HISTORY
FOR RISK FACTOR.
ALCOHOL CONSUMPTION.

HIGH FAT DIET.

INFECTIOUS AGENT.

MALNUTRITION.
PHYSICAL EXAMINATION
DIAGNOSTIC TESTS
DIAGNOSTIC TESTS
 JAUNDICE
DEFINITION
JAUNDICE OR ICTERUS IS THE YELLOW PIGMENTATION OF

THE SCLERA , SKIN AND DEEPER TISSUE CAUSED BY

EXESSIVE ACCUMULATION OF BILE PIGMENTS IN THE
BLOOD.
ETIOLOGY AND RISK FACTORS
OF JAUNDICE
 BLOOD TRANSFUSION REACTIONS.

 SICKLE CELL CRISIS.

 HEMOLYTIC ANAEMIA.

 HEPATITIS.

 CIRRHOSIS.

 HEPATIC CARCINOMA.

 BILARY TRACT OBSTRUCTIONS.

TYPES OF JAUNDICE
 HEMOLYTIC JAUNDICE
IT IS DUE TO INCREASED BREAKDOWN OF THE RED CELLS WHICH

PRODUCE AN INCREASED AMOUNT OF UNCONJUGATED

BILIRUBIN IN THE BLOOD .

CAUSES:-
• BLOOD TRANSFUSION REACTIONS.

• SICKLE CELL CRISIS.

• HEMOLYTIC ANAEMIA.
 HEPATOCELLULAR JAUNDICE.
 THIS RESULTS FROM THE LIVER ALTERED ABILITY TO TAKE UP
BILIRUBIN FROM THE BLOOD OR TO CONJUGATE OR EXCREATE
IT.

CAUSES:-
HEPATITIS.

CIRRHOSIS.

HEPATIC CARCINOMA.
 OBSTRUCTIVE JAUNDICE.
IT IS DUE TO DECREASED OR OBSTRUCTED FLOW OF BILE

THROUGH THE LIVER OR BILARY DUCT SYSTEM

CAUSES:-
Intra hepatic causes.

Extra hepatic causes.

 CLINICAL MANIFESTATIONS
 YELLOW SCLERA.

 YELLOW ORGANE SKIN.

 CLAY COLOURED FEACES.

 TEA COLOURED URINE.

 PRURITIS.

 FATIGUE.

 ANOREXIA.
 DIAGNOSTIC TESTS
HEMOLYTIC HEPTOCELLULAR OBSTRUCTIVE
Serum Bilirubin Increase Increase Increase
Unconjugated-indirect
Conjugated-direct Normal Increase/Decrease Increase

Urine Bilirubin/ Negative Increase Increase

Urobilinogen.
Stool Increase Normal-increase. Decrease

Urine Increase Normal-increase Decrease

 MEDICAL MANAGEMENT
 DETERMINE THE CAUSE OF JAUNDICE.
 CLINICAL EVALUATION.
 PROVIDE ADEQUATE REST.
 I.V FLUIDS.
 ANTI VIRAL MEDICINES.
 STERIODS.
 REDUCE PRURITIS AND MAINTAIN SKIN INTEGRITY.
 ADMINISTER ANTIBIOTICS.
 SURGICAL MANGEMENT
 LAPROSCOPIC CHOLECYSTECTOMY.

 CHOLECYSTECTOMY.
 NURSING MANGEMENT
 ADMINISTER ANTI HISTAMINES AND ANTIBIOTICS.

 ASSESS AND DOCUMENT THE DEGREE OF JAUNDICE IN SKIN AND

SCLERA.
 KEEP THE ROOM COOL.

 ENCOURAGE THE CLIENT TO EXPRESS THE FEELINGS AND

CONCERNS OF BODY IMAGE DISTURBANCE.
 REASSURE THE CLIENT THAT DISCOLOURATION IS USUALLY
TEMPORARY.
 NURSING DIAGNOSIS
IMPAIRED SKIN INTEGRITY RELATED TO PRURITIS.

DISTURBED BODY IMAGE RELATED TO YELLOWING ,SKIN AND

SCLERAE.
INEFFECTIVE HEALTH MAINTAINANCE RELATED TO LACK OF

KNOWLEDGE OF JAUNDICE.
INFLAMATION OF LIVER CAUSED BY
VIRUS,TOXIN,MEDICATIONS.
 TYPES
VIRAL HEPATITIS

TOXIN HEPATITIS

INHERITED HEPATITIS.

AUTOIMMUNE HEPATITIS.

NON-ALCOHOLIC FATTY LIVER.

FULMINANT HEPATITIS.
 CAUSES
 HEPATITIS A.

 HEPATITIS B.

 HEPATITIS C.

 HEPATITIS D.

 HEPATITIS E.

 HEPATITIS F.

 HEPATITIS G.
 CAUSES
 CONSUMING FOOD MADE BY SOME ONE WHO TOUCHED
INFECTED FECES.
 DRINKING WATER THAT IN CONTAMINATED.

 POOR HANDWASHING.

 OUT BRESAKS OCCURS IN DAY CARE CENTERS.

 SEXUAL CONTACT.
 RISK FACTORS.
CHILDREN,TEENS AND ADULTS.

PEOPLE TRAVELLING TO ARES OR WORKING IN SOUTH

AMERICA,AFRICA,MEXICO.
PEOPLE ENGAGED IN HIGH SEXUAL ACTIVITY.

EMPLOYEES OF DAY CARE

PEOPLE WHO HANDLE PRIMATE ANIMALS.

 SYMPTOMS
 FEVER

 CHILLS

 GENERAL FEELING OF WEAKNESS

 LOSS OF APETITE

 NAUSEA

 ABDOMINAL DISCOMFORT

 JAUNDICE

 DIARRHOEA
 DIAGNOSTIC
 MEDICAL HISTORY

 PHYSICAL EXAMINATION

 BLOOD TEST
 Ig M
 anti - HAV
 PREVENTION
 VACCINE-HEPATITIS A

 TRAVELLORS

 ILLEGAL DRUG USERS.

 SEXUAL WORKERS

 PEOPLE WITH CHRONIC LIVER DISEASE CLOTTING FACTOR

DISORDERS.
 TREATMENT
 NO NEED OF ANY TREATMENT

 BED REST

 MEDICATIONS
 HOW HEPATITIS B TRANSMITTED
BLOOD .

BODY FLUIDS:-
 BLOOD

 SEMEN

 VAGINAL SECRETION

 SALIVA

INFANTS BORN TO MOTHER WHO HAS THE VIRUS

 RISK FACTORS
 CHILDREN BORN TO MOTHER WHO HAVE BEEN INFECTED.

 PERSONS WHO HAVE BLOOD CLOTTING DISORDERS.

 PERSON WHO REQUIRES DIALYSIS FOR KIDNEY FAILURE

 I V DRUG USERS

 SEX WORKERS

 LABORATORY TECHNICIANS

 PERSONS WHO RECEIVE BLOOD TRANSFUSION AND BLOOD PRODUCTS

 SYMPTOMS
 LOSS OF APPETITE
 NAUSEA
 FATIGUE
 VOMITING
 JAUNDICE
 DARK URINE
 CLAY COLOURED URINE
 ABDOMINAL PAIN
 OCASSIONALLY SKIN RASHES, ARTHRALAGIA, ARTHRITIS.
 ENLARGED LIVER
 DIAGNOSIS STUDIES
 BLOOD

 URINE

 LIVER BIOPSY
 PREVENTION
 VACCINE
 TREATMENT
 BIOLOGICAL THERAPY WITH INTERFERON.

 CURRENTLY NO CURE

 ITS IS CRUCIAL
 HEPATITIS C
 IT IS LIVER DISEASE CAUSED BY RECENTLY IDENTIFIED BLOOD
BORNE VIRUS.
 DISCOVERED IN1989.

 RECOVERY FROM THIS INFECTION IS RARE ABOUT 55 TO 80 %

INFECTED BECOME CHRONIC CARRIRER OF VIRUS.
 INCIDENCE
 CHRONIC LIVER DISEASE DUE TO HEPATITIS C CAUSES 8000-
10,000 DEATHS.
 IT IS THE LEADING CAUSES OF DEATH INDICATION EACH YEAR
IN UNITED STATES .
 BY 2010 THE NO OF DEATHS IS EXPECTED TO RISE TO 38,000
EACH YEAR.
 CAUSES
 CONTACT WITH INFECTED BLOOD.

 SEXUAL CONTACT.

 INFECTED MOTHER TO BABY.

 USE OF SHARED NEEDLES.

 RISK FACTORS
CHILDREN BORN WITH MOTHERS WHO ARE INFECTED WITH

VIRUS.
TATTO ARTIST WHO DO IT WITH UNCLEAN METHODS.

 TOOLS USED FOR PIERCER OF BODY.

BLOOD CLOTTING DISORDERS.

PEOPLE WHO RECEIVE BLOOD TRANSFUSION.

DIALYSIS-KIDNEY FAILURE.
 SYMPTOMS
 LOSS OF APPETITE.

 FATIGUE.

 NAUSEA AND VOMITING.

 JAUNDICE.

 FEVER.

 DARK YELLOW URINE .

 LIGHT COLOURED STOOLS.

 MUSCLE AND JOINT PAIN.

 DIAGNOSIS
COMPLETE MEDICAL HISTORY.

PHYSICAL EXAMINATION.

BLOOD TESTS.

LIVER BIOPSY.
 TREATMENT
 NO VACCINE .

 BIOLOGICAL THERAPHY-INTERFERON.
 HEPATITIS D
 IT IS TRANSMITTED THROUGH BLOOD CONTACT

CAUSES:-
 CLIENT EXPOSED BLOOD AND BLOOD PRODUCTS.

 SUCH AS I.V DRUG USERS.

PEOPLE WITH HEMOPHILLIA.

PREVENTION:-
HEPATITIS B VACCINE CAN HELP TO PREVENT HEPATITIS D.
 HEPATITIS E
 IT IS RARE IN US.
 IT PRIMARILY AFFECTS YOUNG ADULTS .
 INCUBATION PERIOD:-
14-60 DAYS.

 RISK FACTORS:-
TRAVELLING OR LIVING IN AREAS WHERE INCIDENCE IS HIGH.

 TRANSMISSION:-
• FECAL-ORAL ROUTE ,FOOD OR WATER BORNE.
 HEPATITIS F
 IT IS RARE .

 MODE OF TANSMISSION:-

 FECAL-ORAL ROUTE,FOOD AND WATER BORNE.

 DIAGNOSIS:-

 ELETRON MICROSCOPE
 HEPATITIS G
 IT IS TRANSMITTED :-
 BLOOD.
 BLOOD PRODUCTS.

 BODY FLUIDS.

 MOST CLIENTS ARE ASSYMPTOMATIC AND CHRONIC INFECTION

DEVELOP 90-100%OF INFECTED INDIVIDUALS.
 PREVENTION OF HEPATITIS E,F,G
 GENERAL HYGIENE.

 PRECAUTIONS WITH BLOOD,BLOOD PRODUCTS AND BODY

FLUIDS.
 CURRENTLY NO VACCINES FORMED..

 VACCINE FOR HEPATITIS E IS IN PROGRESS.

CLINICAL MANIFESTATION
PREICTERIC ICTERIC POST ICTERIC

ANOREXIA. JAUNDICE. MALAISE.

NAUSEA,VOMITING. PRURITIS. EASY
FATIGABILITY.
CONSTIPATION OR DARK URINE. HEPATOMEGALL
DIARRHOEA. Y.
DECREASED SENSE OF BILIRUBINURIA.
TASTE AND SMELL.
MALAISE. FATIGUE.
HEADACHE. CONTINUAL
HEPATOMEGALLY
WITH TENDERNESS.
FEVER WEIGHTLOSS.
 COMPLICATIONS
 FULMINANT VIRAL VIRAL HEPATITIS .

 CHRONIC HEPATITIS.

 CIRRHOSIS OF LIVER.
 DIAGNOSTIC STUDIES
 LIVER FUNCTION TEST.

 HEPATITIS SEROLOGY.

 HBSAg.

 Anti -HBS.

 Anti –HCV.
 MANAGEMENT
 NO SPECIFIC TREATMENT.

 HOME MANGEMENT-DIET ,REST.

 A LOW FAT HIGH ,CARHBOHYDRATE DIET.

 PROTEIN AND SODIUM RESTRICTED DIET.

 VITAMIN K IS GIVEN IF PT IS PROLONGUED.

 ANTIHISTAMINES ARE GIVEN FOR PRURITIS ASSOCIATED WITH JAUNDICE.

 ANTIEMETICS FOR JAUNDICE.

 PREVENTION
 PROPER HANDWASHING BY PATIENT AND STAFF.

 WEARNING GLOVES WHEN HANDLING FECES AND URINE.

 CLEANSING DAILY.

 PROPER CLENSING ,BAGGING AND LABELLING OF

CONTAMINATED ITEMS SUCH ASA BED LINENS AND BED PAN.
 DISCARD CONTAMINATED ITEMS SAFELY.
 TOXIC HEPATITIS
 INFLAMMATION OF LIVER.

 OCCURS WHEN LIVER IS DAMAGED BY TOXIC

CHEMICALS,DRUGS OR CERTAIN POISONOUS MUSHROOMS.
CAUSES
 SYMPTOMS
 YELLOWING OF SKIN ,EYES-SCLERA.

 FATIGUE.

 LOSS OF APPETITIE.

 NAUSEA AND VOMITING.

 WEIGHT LOSS.

 DARK OR TEA –COLOURED URINE.

 ANOREXIA.

 HEPATOMEGALLY.
 COMPLICATIONS
 JAUNDICE.

 CIRRHOSIS.

 ENLARGED VEINS.{VARICES}.

 INCREASED BLOOD PRESSURE IN PORTAL VEIN.

 TREATMENT
o SUPPORTIVE THERAPHY.

o LIVER TRANSPLANTATION.
 PREVENTION
LIMIT MEDICATION.

TAKE MEDICATIONS ONLY AS DIRECTED.

BE CAUTION WITH HERBS AND SUPPLEMENT.

DON’T MIX ALCHOL AND DRUGS.

TAKE PRECAUTION WITH CHEMICALS.

PROTECT CHILDREN.
INHERITED HEPATITIS
 LABORATORY TEST
 IRON TEST-SERUM IRON,TOTAL IRON BINDING
CAPACITY,FERITIN
 ALPHA-1 ANTI TRYPSIN LEVEL.

 CERUOPLASMIN AND COPPER TESTS.

 GENETIC TESTING.

 LIVER BIOPSY.
 TREATMENT
 HEMATOCHROMATOSIS.

 WILSONS DISEASE.
 AUTOIMMUNE HEPATITIS
IT IS CHRONIC FORM OF HEPATITIS.

IT LEADS TO PROGESSIVE DAMAGE OF LIVER.

 INCIDENCE
 IT IS MORE COMMON IN WOMEN THAN MEN .

 ACCORDING TO AMERICAN LIVER FOUNDATION:-

 70% OF THOSE AFFECTED ARE FEMALE,USUALLY BETWEEN
THE AGES OF 15 AND 40.
TYPES
 LABORATORY TEST
ANTI NUCLEAR ANTIBODIES.

SMOOTH MUSCLE ANTIBODIES

ANTI-LKM
 TREATMENT
 PREDNISONE.

 AZOTHIOPRINE.
NON ALCHOLIC FATTY LIVER
 CAUSES
METABOLIC PROBLEMS:-
 OBESITY.

 HYPERTENSION.

 HIGH TRIGLYCERIDIES.

 LOW HDL CHOLESTROL.

 INSULIN RESISITANCE TYPE 2 DIABETES.

 TESTS
C T.

MRI.

LFT.

ELECTROLYTES.

LIVER BIOPSY.
 TREATMENT
 NO SPECIFIC TREATMENT.

 WEIGHT LOSE IN THOSE OBESE.

 GOOD GLUCOSE CONTOL –DIABETES.

 LOWERING OF CHOLESTROL OR TRIGLYCERIDIES.

 AVOID ALCOHOL.

 DECREASE INSULIN RESISTANCE.

 FULMINANT HEPATITIS
IT IS RARE.

SEEN PRIMARILY IN HEPATITIS A,B,D,E.

CAUSES:-
 SEVERE ILLNESS.

 20% CASES OCCURING IN PREGNANT WOMEN.

 COMPLICATION
JAUNDICE .

HEPATIC ENCEPHALOPATHY.

ASICITIS.
 DEFINITION
IT IS THE CONSEQUENCE OF CHRONIC LIVER DISEASE.

IT IS CHARACTERIZED BY REPLACEMENT OF LIVER TISSUE BY

FIBROSIS, SCAR TISSUE AND REGENERATIVE NOUDLES LEADING

TO PROGRESSIVE LOSS OF LIVER FUNCTION.
 INCIDENCE
 IT IS THE 12 TH LEADING CAUSE OF DEATH,ACCOUNTING FOR
27,000 DEATH EACH YEAR.
 IT AFFECTS MEN SLIGHTLY MORE OFTEN THAN WOMEN.
 CAUSES
 ALCOHOL –RELATED LIVER DISEASE.

 CHRONIC HEPATITIS C, B.

 NON ALCOHOLIC FATTY LIVER DISEASE.

 AUTO IMMUNE HEPATITIS.

 INHERITED DISEASE.

 DRUGS ,TOXINS AND INFECTIONS.

TYPES
 CLINICAL MANIFESTATION
EARLY SYMPTOMS ARE:-
 ANOREXIA.

 DYSPEPSIA.

 FLATULENCE.

 NAUSEA.

 VOMITING.

 CHANGE IN BOWEL HABITS.

CLINICAL MANIFESTATION CONTD…..
LATER SYMPTOMS:-
 FLUID RETENSION IN THE LEGS AND ABDOMEN.

 JAUNDICE.

 INTENSE ITCHING.

 GALL STONES.

 COAGULATION DEFECTS.

 MENTAL DYSFUNCTION CHANGE.

 ESOPHAGEALVEIN BLEEDING.
 COMPLICATION
 PORTAL HYPERTENSION.

 ASICITIS.

 PERIPHERAL OEDEMA.

 HEPATIC ENCEPHALOPATHY.

 HEPATO RENAL SYNDROME.

DIAGNOSTIC STUDIES
 MEDICAL MANGEMENT
1. ADVICE STOP CONSUMING ALCHOL.

2. CORTISONE MEDICINE HELPS TO TREAT AUTO IMMUNE

HEPATITIS AND CIRRHOSIS.

3. RESTRICTING SALT- USE DIURETICS.

4. TOXINS AND INJURIOUS DRUGS MUST BE AVOIDED.

5. DECREASE DIETARY PROTEIN AND USING CERTAIN LAXATIVE

GENERALLY CAN PREVENT CHANGES IN MENTAL FUNCTION.
 MEDICAL MANGEMENT CONTD….
BLEDDING VEINS IN THE ESOPHAGUS CAN BE INJECTED WITH

SCLEROSING AGENTS .
UROSIIOL(ACTIGALL)AND OTHER DRUGS HAVE BEEN HELPFUL IN

TREATING PRIMARY BILIARY CIRRHOSIS AND PRIMARY SCLEROSING

CHOLANGITIS.
 SURGICAL MANGEMENT
 LIVER TRANSPLANT.
NURSING MANGEMENT
 HEPATIC ENCEPHALOPATHY
 ‘HEPATIC’ STANDS FOR “OF THE LIVER”.

 ‘ENCEPHALOPAHTY’ FOR “BRAIN DISORDERS”.

 HEPATIC ENCEPHALOPATHY IS BRAIN DISORDER CAUSED DUE

TO COMPLICATION OF LIVER.
CAUSES OR PRECIPITATINDG
FACTORS
 DECREASE IN HEPATOCELLULAR FUNCTIONS.

 HYPOXIA.

 INFECTION.

 DIURETICS.

 DEPRESSANTS.

 GASTRO INTESTINAL BLEEDING.

 MEDICATION CONTAINING AMMONIUM OR AMINO COMPOUNDS.

 CAUSES…
 PANCREATITIS.

 INCREASED PROTEIN.

 CONSTIPATION.

 DEHYDRATION.

 HYPOKALEMEIA.

 PROTOSYSTEMIC AND PROTACAVAL SHUNTS.

STAGE 1
CLINICAL MANIFESTATION
STAGE 2 STAGE 3 STAGE 4
FATIGUE. DETERIORATION IN SEVERE CONFUSION COMA.
HANDWRITING.

RESTLESSNESS ASTERIXIS. ABILITY TO FOLLOW UNRESPONSIVE TO

COMMANDS PAIN STIMULI.

SLEEP PATTERN REVERSAL DROWSINESS DEEP SOMNOLENCE, DECEREBRATE

BUT AROUSABLE. POSTURING.

DECREASED INTELLECTUAL CONFUSION.

PERFORMANCE

DECREASED ATTENSION LETHARGY.

SPAN
SHORT TERM MEMORY

PERSONALITY CHANGES.
 COMPLICATION
CIRCULATORY OR RESPIRATORY .

INFECTION.

DELIRIUM.

CONVULSION.
 DIAGNOSTIC STUDIES
 SERUM AMMONIA LEVELS.

 ELECTROLYTES.

 BLOOD GASES.

 HEPATIC FUNCTION TEST RESULTS.

 EEG.
 MEDICAL MANGEMNET
 IDENTIFY AND TREAT THE PRECIPITATING CAUSES.
 PROTEIN MAY BE TOTALLY ELLIMINATED FROM THE DIET.
 USE OF CNS DEPRSSANTS DRUGS TO BE
AVOIDED.HEMODIALYSIS AND EXCHANGE BLOOD
TRANSFUSION.
 MAINTAIN FLUID BALANCE.
 REDUCE NITOGENOUS WASTE IN BLOOD AND BACTERIA IN
COLON.
 SURGICAL MANGEMENT
LIVER TRANSPLANTATION.
 NURSING MANGEMENT
 ASSESS THE INTERVIEW TECHNIQUES TO EVALUATE
PSYCHOLOGICAL STATUS.
 OBSERVE THE CLIENT FEELING STATUS.

 ASSESS THE MENTAL FUNCTION,NEUROLOGICAL

ASSESSMENT.
PORTAL HYPERTENSION
It is abnormally high blood pressure in the branches
of the portal vein,the large vein that brings blood
from the intestine to the liver.
Causes
Pathophysiology
Clinical manifestation
Asicities.
Hepatic encephalopathy.
Increased risk of spontaneous bacterial peritonitis.
Spleenomegally.
Portacaval anastamosis.
GI bleeding.
Diagnostic studies.
Endoscopic examination.
X-ray studies.
Ultrasound/ C T –examine collateral vessels visible on
skin and abdominal wall or around the rectum..
ECG.
Angiogram.
Medical Management.
Endoscopic theraphy :-
 it is usually the first line of treatment for variceal
bleeding and consist of either banding or
sclerotheraphy.
Medications.
Lifestyles.
Contd…
Transjugular intrahepatic portosystemic shunt.
complications:-
Increased asicitis.
Re-bleeding.
Hepatic encephalopathy.
Distal splenorenal shunts.
Complications:-
Asicitis.
Surgical mangement.
Liver transplant
De-vascularization.
Paracentesis.
Nursing management.
Assess for the presence of hemorrhage.
Monitor vitals every 2 nd hourly.
Monitor the clients level of consciousness.
Prepare the patient for the diagnostic procedures.
Maintain I/O chart.
Administer drugs to reduce the B.P.
NURSING DIAGNOSIS

Ineffective tissue perfusion related to portal

hypertension and rupture and hemmorrhage of
esophageal varices.
Impaired gas exchange related to decreased oxygen
supply secondary to aspiration pneumonitis.
Acute confusion related to portosystemic
encephalopathy and hepatic coma
 LIVER CANCER
HEPATIC CANCER.

IT IS A MALIGNANT TUMOUR IN THE LIVER.

TYPES OF LIVER CANCER
 CAUSES
 UNKNOWN.

 CHRONIC HEPATITIS B AND C INFECTION.

 CIRRHOSIS OF LIVER.

 DIABETES MELLITUS.

 EXPOSURE TO TOXINS SUCH AS FUNGI, VINYLCHLORIDE,

ANABOLIC STEROIDS.
 SMOKING.
STAGES OF LIVER CANCER.
 CLINICAL MANIFESTATION
 ASICITIS.

 JAINDICE.

 FEVER.

 FATIGUE.

 WEAKNESS.

 NAUSEA.

 ABDOMINAL PAIN.
 CLINICAL MANIFESTATION CONTD…
 LOSS OF APETITE.

 WEIGHT LOSS.

 CONFUSION.

 PAIN IN THE BACK OR ABDOMEN OR IN THE RIGHT SHOULDER BLADE.

 A HARD LUMP BELOW RIBCAGE.

 DARK COLOURED URINE.

 CLAY COLOURED BOWEL MOVEMENTS.

 INTERNAL BLEDDING.
 DIAGNOSTIC EVALUATION
 L FT.

 U S G ABDOMEN.

 M R I ABDOMEN.

C T .

 LAPROSCOPY.

 BIOPSY.

 ANGIOGRAPHY.

 CHEST X-RAY.
 MEDICAL MANGEMENT
 CHEMOTHERAPY.

 RADIATION THERAPHY.

 OTHER APPROACHES:-
 TREATMENT OF PRIMARY HEPATIC TUMOURS.

 HEPATIC ARTERY EMBOLIZATION.

 CHEMOEMBOLIZATION.

 U S –GUIDED CRYOABLATION.
 SURGICAL MANGEMENT
 LIVER TRANSPLANTATION.
 NURSING MANGEMENT
 PREPARE THE CLIENT IN THE DIAGNOSTIC STAGE FOR THE
VARIOUS PROCEDURE.
 ASSESS CAREFULLY FOR POST-PROCEDURE COMPLICATION.

 IF PAIN ADMINISTER ANALGESIC AS ADVICED BY PHYSICIAN.