Professional Documents
Culture Documents
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
Nutritional status
Serum Phospholipids
- decrease in hepatocellular damage
- increase in biliary obstruction
Normal range : 150 -250 mg/dl
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)
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
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)
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
2. Diet
Maintain on NPO with IVF administered during nausea and vomiting episodes
Small frequent feeding and avoid gas forming foods
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
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