NCMB 316 Cu11 Liver, Pancreas, & Gallbladder
NCMB 316 Cu11 Liver, Pancreas, & Gallbladder
NCMB 316 Cu11 Liver, Pancreas, & Gallbladder
Dr. PA Maroma
“gallstones”
FAT, FEMALE,
FORTY, FERTILE
• More common in
women after age 40
(estrogen therapy),
women taking oral
contraceptives, and in
the obese
Cholecystitis
• acute or chronic
inflammation of the
gallbladder
Theory of Stone formation:
Metabolic factors (obesity, pregnancy, DM,
hypothyroidism,stasis) MAY all lead to stagnation of bile in
the gallbladder
Diagnostic tests
• Direct bilirubin transaminase, alkaline
phosphatase, WBC, amylase, lipase: all
increased
• Oral cholecystogram (gallbladder series):
positive for gallstone
Nursing interventions
• Administer pain medications as
ordered and monitor for effects.
• Administer IV fluids as ordered.
• Provide small, frequent meals of
modified diet, low fat (if oral intake
allowed)
• Provide care to relieve pruritus
• Provide care for the client with a
cholecystectomy or
choledochostomy
Medical management
Supportive treatment: NPO with NG
• Cholecystectomy
• Choledochostomy
• Choledochotomy
Cholecystectomy
• removal of the gallbladder with insertion of a T-tube into the
common bile duct if common bile duct exploration is
performed
Choledochotomy
• opening of common duct, removal of stone, and insertion of a
T-tube
Laparoscopic Cholecystectomy
• performed via laparoscopy for uncomplicated cases when
client has not had previous abdominal surgery
Cholecystostomy
• opening of the gallbladder to remove stones
Nursing interventions:
Provide routine pre-op care
Provide routine post-op care
Position client in semi-Fowler’s or side-lying
positions; reposition frequently.
Splint incision when turning, coughing, and deep
breathing
Maintain/monitor functioning of T-tube
• Ensure that T-tube is connected to closed
gravity drainage.
• Avoid kinks, clamping, or pulling of the tube.
Nursing interventions
cont… Maintain/monitor functioning of T-tube
• Measure and record drainage every shift
• Expect 300 – 500 ml bile-colored drainage for the 1st
24° then 200 ml/24° for 3 - 4 days
• Assess for signs of peritonitis
• Monitor color of urine and stools (stools will be light
colored if bile is flowing through T tube but normal
color should reappear as drainage diminishes)
• Assess skin around T-tube; cleanse frequently and keep
dry
Provide client teaching and discharge planning
concerning
• Adherence to dietary restrictions
• Resumption of ADL
avoid heavy lifting for at least 6 weeks
resume sexual activity as desired unless ordered
otherwise by physician
clients having laparoscopy cholecystectomy usually
resume normal activity within two weeks
• Recognition and reporting of signs of complications (fever,
jaundice, pain, dark urine, pale stools, pruritus)
• An inflammatory process with varying degrees
of pancreatic edema, fat necrosis, or hemorrhage
• Proteolytic and lipolytic pancreatic enzymes are
activated in the pancreas rather than in the
duodenum, resulting in tissue damage and
autodigestion of the pancreas
• Occurs most often in the middle aged
Causes:
• Alcoholism/ alcohol abuse
• Biliary tract disease/ biliary obstruction
• Trauma, viral infection, penetrating duodenal
ulcer, abscesses
• Drugs (antihypertensives, steroids, thiazide
diuretics, antimicrobials, immunosuppressives,
oral contraceptives)
• Metabolic disorders (hyperparathyroidism,
hyperlipidemia)
• Unknown/ autoimmune
Assessment findings
• Pain (LUQ radiating to back, flank, or substernal
area) accompanied by DOB (shallow respiration
with pain), aggravated by eating
• N&V, decreased/absent bowel sounds,
• Abdominal tenderness w/ muscle-guarding
• (+) Grey Turner’s spots (ecchymoses on flanks)
• (+) Cullen’s sign (ecchymoses of periumbilical area)
• Tachycardia
Diagnostic tests
Serum amylase (>300
somogyi units) & lipase
urinary amylase
blood sugar
lipid levels
Serum calcium
• CT scan: enlargement of
the pancreas
Nursing interventions:
• Administer analgesics, antacids, and anticholinergics as
ordered, monitor effects
• Withhold food/fluid and eliminate odor and sight of food from
environment to decrease pancreatic stimulations
• Maintain NGT and assess for drainage.
• Institute Non-pharmacologic measures to decrease pain.
Assist client to positions of comfort (knee chest, fetal
position)
Teach relaxation techniques and provide a quiet, restful
environment.
Provide client teaching and discharge planning
concerning
• Dietary regimen when oral intake permitted
High CHO, high CHON, low-fat diet
Eating small, frequent meals instead of three
large ones
Avoiding caffeine products
Eliminating alcohol consumption
Maintaining relaxed atmosphere after meals
cont… Provide client teaching & discharge planning
concerning
• Recognition/reporting of signs of complications
Continued N&V
Abdominal distension with increasing fullness
Persistent weight loss
Severe epigastric or back pain
Frothy/foul-smelling bowel movements
Irritability, confusion, persistent elevation of
temperature (2 days)
Medical management:
Drug therapy
• Diet modification
• NPO usually for a few days to promote GIT rest
• Peritoneal lavage
• Dialysis if the condition is severe
Infectious inflammation of the liver parenchyma
caused by bacteria, viruses and other
microorganisms.
• widespread inflammation of the liver tissue
• liver cell damage due to hepatic cell degeneration and
necrosis
• proliferation and enlargement of the Kupffer cells
• inflammation of the periportal areas causing interruption
of bile flow
ssRNA virus
transmitted via fecal-
oral route.
Poor hygiene or
contaminated food and
shellfish increase risk
of transmission
Incubation period: 15 –
45 days
DNA virus, identified in all body fluids: blood, saliva,
synovial fluid, breast milk, ascites, cerebral spinal fluid,
etc.
Transmitted by blood and body fluids (saliva, semen,
vaginal secretions): often from contaminated needles
among IV drug abusers; intimate/sexual contact
accounts for 50% of cases of fulminant hepatitis
In an adult who develops acute hepatitis B, there is
approximately 10% chance that it will progress into chronic
hepatitis; in the neonate the chance is 90% for chronic
hepatitis.
Incubation period is very long: 1 - 6 months
ssRNA virus generally transmitted predominantly by
blood products
Currently the most common hepatitis among IV drug
abusers and in prisons
Before 1990 it accounted for 90% of transfusion
hepatitis
Incubation: 2 weeks - 6 months
high risk of progression to chronic form (70 – 80%)
associated with extrahepatic manifestations commonly:
mixed cryoglobulinemia and polyarteritis nodosa
RNA virus that infects either simultaneously with hepatitis
B or as a super-infection in a person with chronic hepatitis B
Hepatitis D infection cannot occur unless there is current
and ongoing replication of the hepatitis B virus
Overall, this infection carries the highest risk among acute
viral hepatitis for fulminant disease; the risk is even greater
in super-infection
Predominantly seen in patients exposed to blood products
(drug addicts and hemophiliacs). If anti-HBs antibodies are
present, then that person is immune to hepatitis B and D
Similar to Hepatitis A
with fecal or oral
transmission, there is
no chronic form
The risk of fulminant
disease has been
described mainly in
pregnant patients
Assessment findings
Preicteric stage (prodromal phase) = 1 week
• Anorexia (major manifestation), N&V, fatigue, constipation or
diarrhea, weight loss
• RUQ discomfort, hepatomegaly, splenomegaly, lymphadenopathy
Icteric stage
• Fatigue, weight loss, light-colored stools, dark urine
• Continued hepatomegaly with tenderness, lymphadenopathy,
splenomegaly
• Jaundice, pruritus
Posticteric stage
• Fatigue, but an increased sense of well-being, hepatomegaly
gradually decreasing
Collaborative Management
• Promotion of rest to relieve fatigue
• Maintenance of food and fluid intake
• 3,000 ml/day of fluids for fever and vomiting;
monitor I and O, weight
• Well – balanced diet; encourage fruit juices and
carbonated beverages
• Fats may need to be restricted
• Alcoholic beverages should be avoided
• Prevention of injury
cont… Collaborative Management
• Monitor PT (bleeding tendencies): plan so that
all blood samples are collected at one time to
avoid several punctures
avoid parenteral injections, if possible
apply pressure to injection sites and venipuncture sites
for 5 minutes
• Monitor Hgb/Hct, urine and stools for fresh or
old blood; the skin for petechiae
cont… Collaborative Management
• advise client to use soft toothbrush or swabs
• administer Vitamin K as ordered
• Provision of comfort measures
• Relaxing baths, backrubs, fresh linens and quiet
dark environment
cont… Collaborative Management
Relieve pruritus through the following measures:
• Use of cool, light, non-restrictive clothing
• Use of soft, dry, clean bedding, use of warm baths
• Application of emollient creams and lotions to dry
skin.
• Maintenance of a cool environment
• Administration of antihistamines as ordered
• Use of diversional activities, e.g. reading, TV and
radio
Chronic, progressive disease characterized by
inflammation, fibrosis, and degeneration of the liver
parenchymal cells
Destroyed liver cells are replaced by scar tissue,
resulting in architectural changes & malfunction of
the liver
Types
• Laênnec’s cirrhosis
associated with alcohol abuse and malnutrition;
characterized by an accumulation of fat in the
liver cells, progressing to widespread scar
formation.
• Postnecrotic cirrhosis
results in severe inflammation with massive
necrosis as a complication of viral hepatitis.
cont… Types
• Cardiac cirrhosis
occurs as a consequence of RSHF; manifested
by hepatomegaly with some fibrosis.
• Biliary cirrhosis
associated with biliary obstruction, usually in the
common bile duct; results in chronic impairment
of bile excretion
Fatty Liver
Normal Liver Liver cirrhosis caused
by alcoholism
Assessment:
• Anorexia, weakness, weight loss (liver is unable to metabolize
nutrients and store fat-soluble vitamins)
• Fever (in response to tissue injury)
• Jaundice, pruritus, tea colored urine (due to bilirubin in the
blood)
remember!!! bilirubin is conjugated initially before
excretion
• Increased Bleeding tendencies. (liver is unable to store Vit. K.
There is also impaired production of clotting factors)
• Portal HPN
Pathology:
In portal hypertension
• plasma shift into interstitial spaces within the liver due to the
increase pressure. The collection of fluids shifts out of the
Glisson’s capsule and accumulate in the peritoneal cavity
The liver is unable to metabolize protein, thereby
hypoalbuminemia occurs
• result to decreased oncotic pressure, fluids shift out of the
IVC, and accumulate in the peritoneal cavity.
Pathology:
The liver is unable to excrete adrenal cortex