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HISTORY

Chief Complaint
abdominal pain
anorexia
nausea and vomiting
weight loss
stool changes
food intolerance
altered level of consciousness
Urine changes
Jaundice, pruritus
Ascites
Edema of the limbs
fatigue, fever
Past Medical History
Major illnesses or hospitalization
Recent skin/mucous membrane disruption
- ear piercing, tattooing, blood transfusion, dental procedures
Medications
- hepatotoxic drugs (acetaminophen, INH, sulfonamides, thiazides, diuretics,
arsenic, methotrexate)
Family history
- cancer of the liver, hepatitis, alcoholism, obesity
Psychosocial history and lifestyle
Occupation and Work environment
- close contact with hazardous waste or polluted water
- travel in hepatitis/pancreatitis endemic areas
- consumption of raw/steamed shellfish from polluted water
- contact with hepatitis infected animals or people
Habits
- food preference
- meal preparation
- use of alcohol
PHYSICAL EXAMINATION

general appearance and health status ( jaundice, obviously ill or impaired)

Nutritional status

Assess abdomen examine painful area last


Fat Metabolism
Serum Total Cholesterol and Cholesterol Esters
- decrease in hepatocellular damage
- increase in biliary obstruction
Normal range : 140 220 mg/dl

Serum Phospholipids
- decrease in hepatocellular damage
- increase in biliary obstruction
Normal range : 150 -250 mg/dl

Protein Metabolism BUN


Total Serum Protein - decrease in severe hepatocellular disease
- decrease in hepatocellular damage
Immunoglobulins Protime
IgA , IgG increase in liver cirrhosis - increase in hepatocellular damage (increase
IgG - increase in chronic active hepatitis biliary risk of bleeding)
cirrhosis Blood Ammonia levels
IgM - increase in Hepatitis A - increase in severe hepatocellular damage
(causes hepatic encephalopathy)
- NV : 75 ug/dl
Bilirubin Metabolism Serum Enzymes : increase in hepatocellular damage
Total serum bilirubin AST / SGOT
- increase in hepatocellular damage (causes
jaundice) ALT / SGPT
- NV : 0.1 -1 MG/DL
- most specific indicator of liver function
Conjugated / Direct Bilirubin
- increase in biliary obstruction LDH

Unconjugated / Indirect Bilirubin GGT (Gamma Glutamyl Transpeptidase)


- increase in hemolysis of RBC and - increase : liver cirrhosis in alcohol induced
hepatocellular damage
Alkaline Phosphatase
Urine Bilirubin (Foam test)
- sight to moderate elevation - hepatocellular
- increase conjugated bilirubin in the urine
disease
Urine Urobilinogen - severe elevation obstructive biliary disease
- decrease in obstructive biliary disease
- increase in hepatocellular damage
- NV: 0.2 -1.2 units

Fecal Urobilinogen (Stercobilin)


- increase in hemolysis of rbc
- absence of fecal urobilinogen: obstructive biliary
disease (causes acholic stool which is pale/gray/clay
colored stool)
Ultrasound of the Liver Biopsy of the Liver

Preparation: Preparation:
- NPO 8-12 hrs. - secure written consent
- Laxative before the procedure - NPO 2 4 hrs
- Adequate hydration - Vitamin K injection
- monitor ProTime ; initial VS
- position client to left side
- instruct client to exhale deeply: hold breath
5-10 seconds, during needle insertion to
prevent trauma to diaphragm
Care after Liver Biopsy
- Turn client to right side for 4 hours to apply
pressure and prevent bleeding
- Bedrest for 24 hrs
- monitor VS every 30 mins. To every hour fr
the first 24 hrs.
Paracentesis (Peritoneal Tap)

Preparation Care after Paracentesis


- Secure written consent Assess:
- check initial VS - VS
- Ask client to empty bladder to prevent - Urine output
puncture - rigidty of the abdomen
- check serum protein studies. If levels are - signs and symptoms of bleeding,
low, procedure may be postponed by peritonitis, hypovolemic
the physician shock,(potential complications)
- place client in sitting / upright position
Endoscopic Retrograde Care after ERCP
Cholangiopancreatography (ERCP) - NPO until gag reflex returns
- Direct visualization with radiographic examination of the liver, - Turn to side to prevent aspiration
gallbladder and pancreas. Contrast medium is introduced via an
upper GI endoscopy as X-rays are taken simultaneously
- Monitor VS
- Monitor signs and symptoms of sepsis,
Preparation before ERCP perforation, pancreatitis
- Secure written consent
- NPO 10 12 hrs
- Check for allergy to iodine/ seafoods
- Take initial VS
- AtSO4; valium is give as ordered
- Local anesthetic spray into the throat is given
- place IN Left side
Is a chronic progressive disease of the liver characterized by diffuse damage
to cells with fibrosis and nodular regeneration.

Different types of liver cirrhosis:


1. Laennecs Cirrhosis is usually alcohol induced
2. Postnecrotic cirrhosis occurs after massive liver necrosis. Cirrhosis
occurs as a complication of acute viral hepatitis or exposure to hepatoxins.
3. Biliary cirrhosis develops from chronic biliary obstruction, bile statis and
inflammation resulting in severe obstructive jaundice
4. Cardiac cirrhosis is associated with severe, right sided congestive heart
failure and results in an enlarged edematous congested liver.
CAUSES :
Alcohol abuse (most common)
Malnutrition
Infection
Drugs
Biliray obstruction and right sided congestive heart
failure
Anorexia
Fever
Jaundice
Bleeding
Decreased resistance to infection
Portal hypertension
Small nodular liver
Males : (elevated estrogen ) Females: (elevated androgen)
o Gynecomastia * Hirsutism
o Decreased libido * Acne
o Impotence * Deepening of voice
o Fall f body hair * Increased virilism
o Atrophy of testicles
Asterixis ( liver flap) is a course tremor characterized by rapid, nonrythmic
extension and flexion on the wrist and fingers
Hepatic encephalopathy this is end stage hepatic failure and cirrhosis caused by
elevated serum ammonia. It is characterized by the
followings manifestations:
* confusion
* delirium
* fetor hepaticus fruity, musty breath odor of chronic liver disease
* hepatic coma irreversible

Hepatorenal syndrome progressive renal failure associated with hepatic failure.


Characterized by :
* sudden decrease in UO
* elevated blood urea nitrogen and creatinine
* decreased urine Na excretion
1. Promote rest
2. Diet
3. Skin care
4. Prevent trauma or injury
5. Protect client form infection
6. Minimize shortness of breath due to ascites by elevating HOB
7. Relieve ascites
8. Prevent rupture of esophageal varices
9. Control hemorrhage due to rupture esophageal varices
10. Reduce ammonia formation
11. Avoid medications such as narcotics , sedatives, acetaminophen
12. Avoid ASA to prevent bleeding
13. Most important client teaching: AVOID ALCOHOL
Is inflammation of the liver caused by virus, exposure to medications or
hepatotoxins

Types:
1. Hepatitis A virus (HAV) infectious hepatitis
2. Hepatitis B virus (HBV) - serum hepatitis
3. Hepatitis C virus (HCV) Non A, Non-B hepatitis or Posttransfusion
4. Hepatitis D virus (HDV) Delta agent hepatitis
5. Hepatitis E virus (HEV) Enterically transmitted or epidemic Non-A,non-B
hepatitis
6. Hepatitis G virus (HGV) Non A, non-B, non-C hepatitis
1. Preicteric phase precedes appearance of jaundice
Flu- like symptoms: malaise, fatigue
Anorexia, nausea, vomiting, diarrhea
Pain: headache,muscle aches, polyarthritis
Serum bilirubin and enzyme levels elevated

2. Icteric phase
Jaundice
Pruritus
Brown colored urine
Light colored stools

3. Posticteric phase
Increased energy levels
Subsiding pain
Minimal to absent GI symptoms
Serum bilirubin and enzyme level return to normal
High-risk groups: young children, international travelers to
developing countries, health care personnel, individuals in custodial
care institutions Incubation is 15 to 50 days ( 2 to 6 wks)
Transmission: feco-oral route, contaminated water, uncooked
shellfish, contaminated fruits and vegetables, poorly washed utensils,
person to person contact, parenteral
Associated with poor sanitation
Prevention:
a. Strict handwashing
b. Stool and needle precautions
c. Treatment of municipal water supplies
d. Hepatitis A vaccine
e. Immunoglobulin for household members and sexul contacs of individuals with
hepatitis A
Common in young adults
High risk groups: drug addicts, clients undergoing long-term hemodialysis, healthcare
personnel
Transmission: blood or bloody fluids through contaminated needles and sexual contact
Incubation period: 45 to 160 days, average of 60 to 120 days (6 to 24 weeks)
Reservoir: blood and body secretions, saliva, semen, urine, nasopharyngeal washings, feces,
pleural fluids
Prevention:
a. Strict hand washing
b. Screening blood donors
c. Testing of al pregnant women (HBsAg)
d. Needle precautions
e. Avoiding intimate sexual contact with persons who are HBsAg +
f. Hepatitis B vaccine
g. Immunoglobulin for individuals exposed to HBV thru sexual contact or through blood or
body secretions
The major cause of post transfusion hepatitis.
Common among clients on chronic hemodialysis and those with
Thalassemia, drug abusers

Incubation: 5 to 10 weeks
Prevention:
a. Strict handwashing
b. Needle precaution
c. Screening of blood donors
Co infection of hepatitis B
High risk groups: drug users. Clients receiving
hemodialysis, clients receiving frequent blood transfusions
Prevention:
a. Because hepatitis D co-exists with hepatitis B, implement
precautions that help prevent hepatitis B
Is water borne virus
Prevalent in areas where sewage disposal is
inadequate or where communal bathing in
contaminated rivers is practiced
Transmission: same as Hepatitis A
Recently discovered.
Found in blood donors & transmitted by transfusion.
Co-exists with other hepatitis viruses.
Not associated with chronic hepatitis or cirrhosis.
1. Hand washing must be strict and frequent
2. The client must not prepare food for other family members
3. Do not share bathrooms unless the client strictly adheres to personal
hygiene measures
4. Individual washcloths, towels, drinking and eating utensils and
toothbrushes and razors must be labeled and identified
5. The client should avoid alcohol and OTC drugs particularly acetaminophen
and sedatives because these medications are hepatotoxic
6. The client should increase activity gradually to prevent fatigue
7. The client should consume small, frequent high-carbohydrate, low-fat foods
1. The client should not donate blood
2. Close personal contact such as kissing should be discouraged until
hepatitis B surface antigen test results are negative
3. The client is to avoid sexual activity until hepatitis B surface antigen
results are negative
4. The client needs to carry a medic-alert card noting the date of
hepatitis onset
5. The client needs to inform other health professionals such as
medical or dental personnel of the onset of hepatitis
6. The client must maintain proper personal hygiene
7. The client needs to keep follow up appointments with the
healthcare provider
Cholelithiasis is the presence of gallstones. Acute cholecystitis is an
inflammation of the gallbladder that may occur with cholelithiasis

4 theories that attempts to explain gallstone formation:


1. Bile may undergo a change in composition.
2. Gallbladder statis may lead to bile statis
3. Infection
4. Genetics and demography

3 types:
1. Cholesterol stones
2. Pigment stones
3. Mixed stones
Cholesterol stones
the primary event in the formation of cholesterol stones is supersaturation of bile with
cholesterol.
Supersaturation almost always is caused by cholesterol hypersecretion rather than by a
reduced secretion of phospholipid or bile salts

Pigment stone
Pigment stones contain <20% cholesterol and are dark because of the presence of calcium
bilirubinate
black and brown pigment stones have little in common and should be considered as separate
entities
Black pigment stones are usually small, brittle, black, and sometimes speculated, formed by
supersaturation of calcium bilirubinate, carbonate, and phosphate, most often secondary to hemolytic
disorders, and in those with cirrhosis. Like cholesterol stones, they almost always form in the
gallbladder.
Brown stones : They may form either in the gallbladder or in the bile ducts, usually secondary to
bacterial infection (such as Escherichia coli)caused by bile stasis. calcium bilirubinate and bacterial
cell bodies compose the major part of the stone.
Predisposing factors:
5 Fs
- female
- fat
- fair (Caucasian)
- forty
- fertile (multigravida and those who use contraceptive pills)

Bile statis leads to the following:


1. Decreased fat emulsification
Manifestations:
- fat intolerance
- anorexia
- nausea and vomiting
- weight loss
- gaseous eructation (belching)
- flatulence, bloating
- steatorrhea (greasy, bulky, foul smelling stool due to undigested fats)
2. Inflammation of the gallbladder
Pain epigastric pain that radiates to the scapula 2 to 4 hours after eating
fatty foods and may persist for 4 to 6 hours then pain becomes localized in
RUQ with guarding and rigidity
Fever, leukocytosis
Murphys sign the client cannot take a deep breath when the examiners
fingers are passed below the hepatic margin

3. Biliary Obstruction
Decreased bile flow to the colon
a. Acholic stool (pale/gray/clay colored stool)
b. Decreased vitamin K absorption in the colon ( leads to bleeding
tendencies
c. Increased serum bilirubin leads to jaundice, pruritus, tea-colored urine

4. Infection cholecystitis and pancreatitis may occur


Collaborative Management
1. Relief of pain
administer analgesic (Demerol drug of choice)
Avoid morphine sulfate causes spasm of sphincter of Oddi and may increase pain

2. Diet
Maintain on NPO with IVF administered during nausea and vomiting episodes
Small frequent feeding and avoid gas forming foods

3. Administer antiemetic for nausea and vomiting


4. Administer medications for cholelithiasis
5. Extracorporeal shockwave lithotripsy to disintegrate stones in the biliary system
6. Surgical interventions
1. Cholecystectomy removal of gallbladder
2. Choledochotomy removal of stone from common bile duct
3. Laparoscopic cholecystectomy involves 3 to 4 small
incisions. Gas insufflation ( with CO2) of the abdomen is
done to lift the abdominal wall. This facilitates visualizations
of the gallbladder
4. Incisional or open cholecystectomy involves right subcostal
incision (below the diaphragm)
Is an acute or chronic inflammation of the pancreas with associated escape of pancreatic enzyme
into surrounding tissue

Precipitating factors:
1. Alcohol intake
2. Cholelithiasis
3. Drugs
4. Abdominal and pancreatic trauma
5. Viral or bacterial disease
6. Hypercalcemia
7. Hyperlipidemia
8. Peptic ulcer disease
9. Pancreatic ischemia
1. Pain normally begins in the midepigastrium or LUQ with radiation to the back.
2. Nausea and vomiting
3. Abdominal distention and tenderness with fever due to paralytic ileus that follows peritonitis
4. Anorexia and wt loss due to inadequate metabolism of nutrients
5. Severe dehydration
6. Steatorrhea due to inadequate fat digestion
7. Hypocalcemia calcium is deposited in areas of fatty necrosis and undigested intestinal fat traps
calcium in feces
8. Laboratory findings:
9. Hypeglycemia pancreatic functions may be disrupted due to tissue damage in islets of
Langerhans where DM may develop secondary to pancreatitis
10. Jaundice
11. Hemorrhagic pancreatitis produces post hemorrhagic necrosis which causes purplish
discoloration.
Grey Turners sign (left flank)
Cullens sign (periumbilical area)
1. Relieve pain - Meperidine is the drug of choice
- may also be obtained by sitting in bed with the lnees flexed and pressing a
pillow over the abdomen. The client generally experience more pain when in supine.
2. Diet NPO during acute phase
- as pain subsides , clear liquids then gradual advancement to bland, low fat diet
- TPN may be necessary for severe nutritional depletion
3. IVF therapy
4. Nasogastric tube insertion as prescribed - to remove gastrin from the stomach and secretin
from the duodenum which reduces stimulation of the pancreas
5. Digestive enzymes e.g. pancreatin or pancrelipse as prescribed.
6. Administer fat soluble vitamins (ADEK)
7. Administer antacids to neutralize gastric secretions
8. Administer histamine H2 receptor antagonist as prescribed to decreased HCl production and
prevent activation of pancreatic enzymes
9. Administer anticholinergics as prescribed to decrease vagal stimulation, decrease
gastrointestinal motility and inhibit pancreatic enzyme secretion

10. Administer antibiotics as prescribed

11. Administer calcium supplement and Vitamin D as prescribed to manage hypocalcemia.


Vitamin D enhances absorption of calcium

12. Instruct client on the importance of avoiding alcohol

13. Instruct client on the importance of follow up visits with the physician

14. Instruct client to notify the physician if acute abdominal pain, jaundice, clay-colored stools
or dark urine develops which indicates occurrence of complications like pancreatic abscess