METABOLIC DISORDER

Overview

Metabolic disorders are usually defined as inborn errors of

metabolism, encompassing deficiencies in enzymes involved
in the metabolism of carbohydrates, amino acids derived
from proteins, and fatty acids liberated from lipids
(Encyclopedia of Genetics, 2001).

OBESITY

“abnormal or excessive fat accumulation that may impair

health” (WHO, 2016).
Pathophysiology

1. Obesity is a chronic, relapsing disease characterized

Obesity Risk Factor
Behavioral (lifestyle choices, Unhealthy diet, Liquid calories,
Inactivity, etc.)
Environmental (Family members tend to share similar eating
and activity habits)
Physiologic (how your body regulates your appetite and how
your body burns calories during exercise)
Genetic factors (the amount of body fat you store, and
where that fat is distributed)
Obesity is associated with a 6- to 20-year decrease in overall
life expectancy.
Obesity is associated with morbidity and mortality from
numerous other diseases.
by an excessive accumulation of body fat and weight
gain.
- These increases in body fat cause adiposopathy.
- Dysfunctional adipose tissue cells release
biochemical mediators that cause chronic
inflammatory changes.
2. Excess of caloric consumption relative to caloric
expenditures (“thrifty gene” hypothesis).
3. The types and quantities of foods consumed affect
complex digestive and metabolic pathways
(obesogenic food – foods containing fructose corn
syrup, simple sugars, or trans fats).
- The portions of foods served in restaurants
and packaged on grocery shelves have
increased over the past 20 years.
4. Multiple hormones that control food cravings and
feelings of fullness could be affected by individual
genes (orexigenic hormones - stimulate appetite).
5. Increases in fat stores, or adipose tissue, result in
increases in the hormone leptin, which is secreted by
fat cells. Leptin signals satiety in the hypothalamus.

Assessment and Diagnostic Findings

 BMI

-Waist circumferences assessment (women – more than 35

inches; men – more than 40 inches).

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-Waist-to-hip ratio assessment (women greater than 0.80
and men greater than 0.90, “apple-shaped” or android
obesity vs “pear-shaped” body or gynoid obesity).

-Laboratory studies (cholesterol and triglycerides, fasting

blood glucose and glycosylated hemoglobin (hemoglobin
A1c), as aspartate aminotransferase (AST) and alanine
aminotransferase (ALT)).

-Diagnostic workup follows that prescribed for the primary

disease or disorder (hypothyroidism or Cushing syndrome).

Medical Management

1. Lifestyle Modification
- Setting weight-loss goals,
- Improving diet habits,
- Increasing physical activity,
- Addressing barriers to change, and,
- Self-monitoring and strategizing ongoing 3. Non-Surgical
lifestyle changes aimed at a healthy weight.  Vagal blocking therapy - placement of a pacemaker-
2. Pharmacological therapy like device into the subcutaneous tissue in the lateral
thoracic cavity

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-A pre-programmed, pulsating signal is delivered for 12 hours
daily causing intermittent “blocking” of the vagus nerve.

-Vagal blocking results in diminished gastric contraction and

emptying, limited ghrelin secretion, and diminished
pancreatic enzyme secretion.

-Causes increased satiety, decreased cravings, and

diminished absorption of calories.

 Intragastric balloon therapy - endoscopic placement

of a saline-filled balloon or a saline-filled dual
balloon into the stomach.
-increased feelings of satiety and decreased gastric emptying
-the intragastric balloon(s) remain in place for 3 to 6 months,
and are then deflated and removed
 Sleeve gastrectomy – The stomach is incised
vertically and up to 85% of the stomach is surgically
removed, leaving a “sleeve”-shaped tube that retains
intact nervous innervation and does not obstruct or
decrease the size of the gastric outlet.

-Balloons should be removed within 6 months of placement;

longer placement periods are associated with increased
likelihood of rupture and intestinal obstruction.

Surgical Management

 Bariatric surgery - involves making surgical changes

in the digestive system to help lose weight.
-Roux-en-Y gastric bypass – a horizontal row of staples across
the fundus of the stomach creates a pouch with a capacity of
20 to 30 mL. The jejunum is divided distal to the ligament of
Treitz, and the distal end is anastomosed to the new pouch.
The proximal segment is anastomosed to the jejunum.
 Biliopancreatic diversion with duodenal switch - half
of the stomach is removed, leaving a small area that
holds about 60 mL.
-The entire jejunum is excluded from the rest of the
gastrointestinal tract.

-The duodenum is disconnected and sealed off.

-The ileum is divided above the ileocecal junction, and the

distal end of the jejunum is anastomosed to the first portion
of the duodenum.

-The distal end of the biliopancreatic limb is anastomosed to

the ileum.

 Gastric banding - A prosthetic device is used to

restrict oral intake by creating a small pouch of 10 to
15 mL that empties through the narrow outlet into
the remainder of the stomach.

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Nursing Intervention
1. ENSURING DIETARY RESTRICTIONS
-clear liquids 24 to 48 hours before and after surgery
-clear liquids to full liquids to soft solids and eventually solid
foods
2. REDUCING ANXIETY
3. RELIEVING PAIN
-Patients are usually prescribed opioid agents via PCA pumps
-Done so the patient can perform pulmonary care activities
(deep breathing and coughing) and ambulate
-Positioning the patient in a low Fowlers position promotes
comfort and emptying of the stomach
4. ENSURING FLUID VOLUME BALANCE
-Patients usually receive intravenous (IV) fluids for the first
several hours postoperatively
-Once they are awake and alert, they are encouraged to
begin intake of sugar-free oral fluids.
-Patients are encouraged to slowly sip 30 mL of fluids every
15 minutes
-Antiemetic agents may be prescribed to relieve nausea and
prevent vomiting
5. PREVENTING INFECTION/ANASTOMOTIC LEAK
-Disruption at the site of anastomosis may cause leakage of
gastric contents into the peritoneal cavity.
-Nonspecific signs and symptoms include fever, abdominal
pain, tachycardia, and leukocytosis.
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-This may progress to sepsis and possibly septic shock if not
recognized and treated early.
6. ENSURING ADEQUATE NUTRITIONAL STATUS
-After bowel sounds have returned, six small feedings
consisting of a total of 600 to 800 calories per day are
provided.
-Consumption of fluids between meals is encouraged to
prevent dehydration.
-Eating too much or too fast or eating high-calorie liquids and
soft foods can result in vomiting or painful esophageal
distention.
-Gastric retention may be evidenced by abdominal
distention, nausea, and vomiting.
-Supplementation with oral or parenteral iron; monthly
vitamin B12 intramuscular injections to prevent pernicious
anemia.
7. SUPPORTING BODY IMAGE CHANGES
-acknowledging the patient’s feelings as real
8. ENSURING MAINTENANCE OF BOWEL HABITS
-Patients may complain of either diarrhea or constipation
postoperatively.
-Diarrhea is more common an occurrence post bariatric
surgery.
-Steatorrhea also may occur as a result of rapid gastric
emptying.
9. MONITORING AND MANAGING POTENTIAL
COMPLICATIONS
 Hemorrhage - bright red oral or rectal bleeding, tarry
melena, bloody output from the wound or drains
Bleeding within the first 72 hours postoperatively is most
likely caused by disruption in a staple or suture.
Bleeding 72 hours to 30 days postoperatively is most likely
from formation of a gastric or duodenal ulcer.
 Venous Thromboembolism (VTE) - prophylactic
anticoagulation with subcutaneous low molecular
weight heparin (LMWH) agents
 Bile Reflux - may occur with procedures that
manipulate or remove the pylorus.
-Reflux of bile can cause inflammation of the
stomach or esophagus.
May be managed with proton pump inhibitors.
  Dumping Syndrome - unpleasant set of vasomotor
and GI symptoms after bariatric surgery.
-Symptoms of dumping syndrome occur 15 minutes
to 2 hours after eating.
-Symptoms include tachycardia, dizziness, sweating,
nausea, vomiting, bloating, abdominal cramping, and
diarrhea.
-These symptoms typically resolve once the intestine
has been evacuated
 Dysphagia - tends to be most severe 4 to 6 weeks
postoperatively and may persist for up to 6 months
after surgery.

-Instruct patients to eat slowly, to chew food thoroughly, and
to avoid eating tough foods.
 Bowel and Gastric Outlet Obstruction - it is
contraindicated to insert a nasogastric (NG) tube.
- Alternative treatment options may include endoscopic
procedures.
Anatomy of the Liver
-The liver is located behind the ribs in the upper right portion
of the abdominal cavity.
-It weighs between 1200 and 1500 g in the average adult and
is divided into four lobes.
-Its functional units are called lobules.

-Approximately 80% of the blood supply comes from the

HEPATIC DISODER
Anatomic and Physiologic Overview
-The liver is the largest gland of the body and is a major
organ.
--The liver can be considered a chemical factory that
manufactures, stores, alters, and excretes a large number of
substances involved in metabolism.
-The liver is especially important in the regulation of glucose
and protein metabolism.
- liver manufactures and secretes bile.
-The liver removes waste products from the bloodstream
and secretes them into the bile.
-The bile produced by the liver is stored temporarily in the
gallbladder.
portal vein and the rest from the hepatic artery.
-Phagocytic cells (Kupffer cells) are present in the liver.
Function of the Liver
1. Glucose Metabolism
-After a meal, glucose is taken up from the portal venous
blood by the liver and converted into glycogen (stored in
hepatocytes).
-The glycogen is converted back to glucose (glycogenolysis)
and released as needed into the bloodstream.
-Additional glucose can be synthesized by the liver through a
process called gluconeogenesis (the liver uses amino acids
from protein breakdown).
2. Ammonia Conversion
-Gluconeogenesis results in the formation of ammonia as a
by-product.

-The liver converts this metabolically generated ammonia

into urea (excreted in the urine).

3. Protein Metabolism

-The liver synthesizes almost all of the plasma proteins

(albumin, alpha-globulins, beta-globulins, etc.).

-Amino acids are used by the liver for protein synthesis.

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 4. Fat Metabolism -Past and current medical history.

-Fatty acids can be broken down for the production of energy
and ketone bodies.
-Fatty acids and their metabolic products are also used for
the synthesis of cholesterol, lecithin, lipoproteins, and other
complex lipids.
5. Vitamin and Iron Storage
-Vitamins A, B, and D and several of the B-complex vitamins
are stored in large amounts in the liver.
-Certain substances, such as iron and copper, are also stored
in the liver.
6. Bile Formation
-Bile is continuously formed by the hepatocytes and
collected in the canaliculi and bile ducts.
-The functions of bile are excretory (excretion of bilirubin).
-Family history
Physical Assessment
-Assess for physical signs (e.g. pallor, jaundice).
-The skin, mucosa, and sclerae are inspected for jaundice.
-The extremities are assessed for muscle atrophy, edema,
and skin excoriation secondary to scratching.
-The nurse observes the skin for petechiae or ecchymotic
areas (bruises), spider angiomas, and palmar erythema.
-The male patient is assessed for unilateral or bilateral
gynecomastia and testicular atrophy due to hormonal
changes.
-The nurse observes for general tremor, asterixis (involuntary
flapping movements of the hands), weakness, and slurred
speech.

-Bile salts are then reabsorbed, primarily in the distal ileum

into the portal blood (enterohepatic circulation).

7. Bilirubin Excretion

-Bilirubin is a pigment derived from the breakdown of

hemoglobin.

-Hepatocytes remove bilirubin from the blood and

chemically modify it through conjugation to glucuronic acid.

8. Drug Metabolism

-The liver metabolizes many medications, such as

barbiturates, opioids, sedatives, anesthetics, and -Assess for the presence of an abdominal fluid wave.
amphetamines.
-The abdomen is palpated to assess liver size and to detect
-Metabolism generally results in drug inactivation, although any tenderness over the liver.
activation may also occur.
-If the liver is palpable, the nurse notes and records its size,
-One of the important pathways for medication metabolism its consistency, any tenderness, and whether its outline is
involves conjugation (binding) of the medication with a regular or irregular
variety of compounds.
Diagnostic Evaluation
-Bioavailability is the fraction of the given medication that
actually reaches the systemic circulation (first-pass effect). 1. Liver Function Tests
2. Liver Biopsy
Health History 3. Other Diagnostic Tests
-If liver function test results are abnormal, the patient is Liver Function Test
evaluated for liver disease.
More than 70% of the parenchyma of the liver may be
-Previous exposure to hepatotoxic substances or infectious damaged before liver function test results become abnormal.
agents (occupational, recreational, and travel history).
1. Alanine aminotransferase (ALT) – increases primarily
-History of alcohol, drug use and medications. in liver disorders
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 2. Aspartate aminotransferase (AST) - increased if there
is damage or death of tissues
3. Gamma-glutamyl transferase (GGT) - Increased levels
are associated with cholestasis and alcoholic liver
disease.
Liver Biopsy
-Liver biopsy is the removal of a small amount of liver tissue,
usually through needle aspiration.
-It permits examination of liver cells.
-Done to evaluate diffuse disorders of the parenchyma and
to diagnose space-occupying lesions.
Other Diagnostic Test
-Ultrasonography, computed tomography (CT) scans, and
magnetic resonance imaging (MRI) are used to identify
normal structures and abnormalities of the liver and biliary
tree.
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-Laparoscopy is used to examine the liver and other pelvic
structures.
Manifestation of Hepatic Dysfunction
1. Jaundice - the sclerae and the skin become tinged
yellow or greenish-yellow.
-Jaundice becomes clinically evident when the serum
bilirubin level exceeds 2.0 mg/dL (34 mmol/L).
-The bilirubin concentration in the blood may be increased in
the presence of liver disease.
Types of jaundice:
a. Hemolytic Jaundice - result of an increased
destruction of the red blood cells.
b. Hepatocellular Jaundice - caused by the inability
of damaged liver cells to clear normal amounts
of bilirubin from the blood caused by hepatitis
viruses, chemical toxins or alcohol.
c. Obstructive Jaundice - caused by occlusion of the
bile duct from a gallstone, an inflammatory
process, a tumor, or pressure from an enlarged
organ.
d. Hereditary Hyperbilirubinemia - Increased serum
bilirubin levels (hyperbilirubinemia), resulting
from any of several inherited disorders.
2. Portal Hypertension - increased pressure throughout
the portal venous system.
- Manifests as splenomegaly (enlarged spleen), ascites and
varices.
3. Ascites - movement of fluid into the peritoneal
cavity.
- Marked by increased abdominal girth and rapid weight
gain.
-Caused by the failure of the liver to metabolize aldosterone
and decreased synthesis of albumin
-The medical management of the patient with ascites
includes dietary modifications, pharmacologic therapy, bed
rest, paracentesis (5-6L), the use of shunts (Transjugular
intrahepatic portosystemic shunt or TIPS), and other
therapies.
4. Esophageal Varices - varicosities that develop from
elevated pressure in the veins that drain into the
portal system.
-They are prone to rupture and often are the source of
massive hemorrhages from the upper GI tract and the
rectum.
-The patient may present with hematemesis, melena and
signs and symptoms of shock (cool clammy skin,
hypotension, tachycardia).
5. Hepatic Encephalopathy and Coma
-Hepatic encephalopathy, or portosystemic encephalopathy,
is a life-threatening complication of liver disease that occurs
with profound liver failure.
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-Hepatic insufficiency may result in encephalopathy because
of the inability of the liver to detoxify (increased ammonia
stimulates gamma-aminobutyric acid (GABA)
neurotransmission.
-Also portosystemic shunting in which collateral vessels
develop as a result of portal hypertension.
-The earliest symptoms include mental status changes and
motor disturbances.
-The patient tends to sleep during the day and has
restlessness and insomnia at night.
-Other management strategies include IV administration of
glucose to minimize protein breakdown.
-Antibiotics may also be added to the treatment regimen.
Neomycin, metronidazole (Flagyl), and rifaximin (Xifaxan)
have been used to reduce levels of ammonia-forming
bacteria in the colon.
6. Edema and Bleeding – caused by hypoalbuminemia
and decreased production of blood clotting factors.
7. Vitamin Deficiency - deficient absorption of vitamin K
from the GI tract.
-Absorption of fat-soluble vitamins (vitamins A, D, and E)
may also be impaired.
-Vitamin A deficiency, resulting in night blindness and eye
and skin changes.
-Thiamine deficiency, leading to beriberi, polyneuritis, and
Wernicke–Korsakoff psychosis
-Riboflavin deficiency, resulting in characteristic skin and
mucous membrane lesions
-Pyridoxine deficiency, resulting in skin and mucous
membrane lesions and neurologic changes
-Vitamin C deficiency, resulting in the hemorrhagic lesions of
scurvy
-Vitamin K deficiency, resulting in hypoprothrombinemia,
characterized by spontaneous bleeding and ecchymoses
-Folic acid deficiency, resulting in macrocytic anemia
Metabolic Abnormalities - abnormalities of glucose
metabolism.
- blood glucose level may be abnormally high shortly after a
meal.
 8. hypoglycemia may occur during fasting because of -Indigestion
decreased hepatic glycogen reserves and decreased
Assessment and Diagnostic Findings
gluconeogenesis.
-The liver and spleen are often moderately enlarged for a
-Medications must be used cautiously and in reduced
few days after onset.
dosages.
-HAV antibodies are detectable in the serum.
9. Pruritus and Other Skin Changes
Preventions
-severe pruritus develop due to retention of bile salts
-Hand hygiene, safe water supplies, and proper control of
-Patients may develop vascular (or arterial) spider angiomas
sewage disposal.
on the skin
-Effective (95% to 100% after two to three doses) and safe
-Patients may also develop reddened palms (“liver palms” or
HAV vaccines.
palmar erythema).
-Intramuscular administration of globulin during the
VIRAL HEPATITIS
incubation period.
-a systemic, viral infection in which necrosis and
-Pre-exposure prophylaxis is recommended for those
inflammation of liver cells produce a characteristic cluster of
traveling to developing countries or settings with poor or
clinical, biochemical, and cellular changes.
uncertain sanitation conditions.
-five types have been identified: hepatitis A, B, C, D, and E.
Management
-Hepatitis A and E are similar in mode of transmission (fecal–
-Bed rest during the acute stage.
oral route), whereas hepatitis B, C, and D share many other
characteristics -During the period of anorexia, the patient should receive
frequent small feedings, supplemented if necessary by IV
HEPATITIS A VIRUS
fluids with glucose
 Hepatitis A, formerly called infectious hepatitis, is
HEPATITIS B VIRUS
caused by an RNA virus of the enterovirus family.
 HAV is transmitted primarily through the fecal–oral -Bed rest during the acute stage.
route.
-During the period of anorexia, the patient should receive
 Hepatitis A can be transmitted during sexual activity
frequent small feedings, supplemented if necessary by IV
(oral–anal contact).
fluids with glucose
 Hepatitis A is not transmitted by blood transfusions.
 The incubation period is estimated to be between 2 Risk Factor
and 6 weeks.
-Close contact with carrier of hepatitis B virus
 The illness may last 4 to 8 weeks.
 The virus is present only briefly in the serum; by the -Frequent exposure to blood, blood products, or other body
time jaundice occurs, the patient is likely to be fluids
noninfectious.
 The patient may contract other forms of hepatitis. -Health care workers: hemodialysis staff, oncology and
chemotherapy nurses, personnel at risk for needlesticks,
Clinical Manifestation operating room staff, respiratory therapists, surgeons,
dentists
-Many patients are anicteric (without jaundice) and
symptomless. -Hemodialysis
-Mild, flu-like upper respiratory tract infection, with low- -IV/injection drug use
grade fever.
-Male homosexual and bisexual activity
-Anorexia, an early symptom, is often severe.
-Mother-to-child transmission
-Later, jaundice and dark urine may become apparent.
-Multiple sexual partners
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-Receipt of blood or blood products (e.g., clotting factor  Bed rest until the symptoms of hepatitis have
concentrate) subsided.
 Adequate nutrition should be maintained.
-Recent history of sexually transmitted infection
 Proteins are not restricted. Protein intake should be
-Tattooing 1.2 to 1.5 g/kg/day.
 The patient is evaluated for other bloodborne
-Travel to or residence in area with uncertain sanitary
diseases
conditions
 The nurse identifies psychosocial issues and
Clinical Manifestations concerns

-HBV closely resembles HAV, but the incubation period is
much longer (1 to 6 months).
-The patient may have loss of appetite, dyspepsia, abdominal
pain, generalized aching, malaise, and weakness.
-Jaundice may or may not be evident.
HEPATITIS C VIRUS
-The incubation period is variable and may range from 15 to
160 days.
-The clinical course of acute HCV is similar to that of HBV;
symptoms are usually mild or absent.

-The liver may be tender and enlarged to 12 to 14 cm -However, a chronic carrier state occurs frequently.
vertically.
Risk Factor
-The spleen is enlarged and palpable in a few patients.
-Children born to women infected with hepatitis C virus
Assessment and Diagnostic Findings
-Health care and public safety workers after needlestick
HBV is a deoxyribonucleic acid (DNA) virus composed of the injuries or mucosal exposure to blood
following antigenic particles:
-Multiple contacts with a hepatitis C virus–infected person
 HBcAg—hepatitis B core antigen (antigenic material
-Multiple sex partners, history of sexually transmitted
in an inner core)
infection, unprotected sex
 HBsAg—hepatitis B surface antigen (antigenic
material on the viral surface, a marker of active -Past/current illicit IV/injection drug use
replication and infection)
-Recipient of blood products or organ transplant before 1992
 HBeAg—an independent protein circulating in the
or clotting factor concentrates before 1987
blood
 HBxAg—gene product of X gene of HBV DNA HEPATITIS D VIRUS

HBsAg appears in the circulation in 80% to 90% of infected
patients 1 to 10 weeks after exposure to HBV and 2 to 8
weeks before the onset of symptoms.
Preventions
-Preventing Transmission
-Occurs in some cases of hepatitis B.
-Only people with hepatitis B are at risk for hepatitis D.
-Common among those who use IV or injection drugs,
patients undergoing hemodialysis, and recipients of multiple
blood transfusions.

-Active Immunization: HBV (three doses) -Sexual contact with is an important mode of transmission of
hepatitis B and D.
-Passive Immunity: Hepatitis B Immune Globulin (HBIG)
-The incubation period varies between 30 and 150 days.
Management
-The symptoms of hepatitis D are similar to those of hepatitis
 alpha-interferon (5 million U daily or 10 million U
B.
three times weekly for 16 to 24 weeks)
 Monitor adverse effects to interferons: bone marrow -Treatment is similar to that of other forms of hepatitis.
suppression, thyroid dysfunction, alopecia, and
bacterial infections.
 antiviral agents (entecavir (ETV) and tenofovir (TDF))
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HEPATITIS E VIRUS
-Transmitted by the fecal–oral route.
-The incubation period is variable, estimated to range
between 15 and 65 days.
-Hepatitis E resembles hepatitis A.
-Jaundice is almost always present.
-Chronic forms do not develop.
-Avoiding contact with the virus through good hygiene,
including handwashing, is the major method of prevention.
NONVIRAL HEPATITIS
 Certain chemicals have toxic effects on the liver and
produce acute liver cell necrosis or toxic hepatitis
when inhaled, injected parenterally, or taken by
mouth.
 Some chemicals commonly implicated in this disease
include carbon tetrachloride and phosphorus.
 Many medications can induce hepatitis but are only
sensitizing rather than toxic.
 Drug-induced hepatitis is similar to acute viral
hepatitis, but parenchymal destruction tends to be
more extensive.
 Medications that can lead to hepatitis include
isoniazid (Nydrazid); halothane (Fluothane);
acetaminophen; methyldopa (Aldomet); and certain
antibiotics, antimetabolites, and anesthetic agents.
TOXIC HEPATITIS
 Toxic hepatitis resembles viral hepatitis.
 Anorexia, nausea, and vomiting are the usual
symptoms.
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 Jaundice and hepatomegaly are noted.
 Symptoms are more intense for the more severely
toxic patient.
 Recovery from acute toxic hepatitis is rapid if the
hepatotoxin is identified early and removed.
 Recovery is unlikely if there is a prolonged period
between exposure and onset of symptoms.
 There are no effective antidotes.
 Vomiting may be persistent, with the emesis
containing blood.
 Clotting abnormalities may be severe, and
hemorrhages may appear under the skin.
 Delirium, coma, and seizures develop, and within a
few days the patient may die of fulminant hepatic
failure unless they receive a liver transplant.
DRUG INDUCED HEPAPTITIS
 Manifestations of sensitivity to a medication may
occur on the first day of its use or not until several
months later.
 Usually, the onset is abrupt, with chills, fever, rash,
pruritus, arthralgia, anorexia, and nausea.
 Later, there may be jaundice, dark urine, and an
enlarged and tender liver.
 After the offending medication is withdrawn,
symptoms may gradually subside.
 If fever, rash, or pruritus occurs from any
medication, its use should be stopped immediately.
 The use of acetaminophen has been identified as the
leading cause of acute liver failure.
FULMINANT HEPATIC FAILURE
 The clinical syndrome of sudden and severely
impaired liver function in a previously healthy
person.
 Develops within 8 weeks after the first symptoms of
jaundice.
Three categories are frequently cited:
-Hyperacute (the duration of jaundice before the onset of
encephalopathy is 0 to 7 days)
-Acute (8 to 28 days)
-subacute liver failure (28 to 72 days
 Viral hepatitis is a common cause of fulminant
hepatic failure.
 Other causes include toxic medications and
chemicals, metabolic disturbances and structural
changes.
  The key to optimized treatment is rapid recognition Clinical Manifestations
of acute liver failure and intensive intervention.
1. Compensated
 The use of antidotes for certain conditions may be
indicated such as N-acetylcysteine for • Abdominal pain
acetaminophen toxicity and penicillin for mushroom
• Ankle edema
poisoning.
• Firm, enlarged liver
HEPATIC CIRRHOSIS
• Flatulent dyspepsia
 A chronic disease characterized by replacement of
normal liver tissue with diffuse fibrosis that disrupts • Intermittent mild fever
the structure and function of the liver.
 There are three types of cirrhosis or scarring of the • Compensated
liver: • Abdominal pain
1. Alcoholic cirrhosis, in which the scar tissue
characteristically surrounds the portal areas. This is • Ankle edema
most frequently caused by chronic alcoholism and is • Firm, enlarged liver
the most common type of cirrhosis.
2. Postnecrotic cirrhosis, in which there are broad • Flatulent dyspepsia
bands of scar tissue. This is a late result of a previous
• Intermittent mild fever
bout of acute viral hepatitis.
3. Biliary cirrhosis, in which scarring occurs in the liver 2. Decompensated
around the bile ducts. This type of cirrhosis usually
• Ascites
results from chronic biliary obstruction and infection
(cholangitis); it is much less common. • Clubbing of fingers
PATHOPHYSIOLOGY • Continuous mild fever
 Excessive alcohol intake is the major causative • Epistaxis
factor in fatty liver.
 Alcoholic cirrhosis is characterized by episodes of • Gonadal atrophy
necrosis involving the liver cells. • Hypotension
 The destroyed liver cells are gradually replaced
by scar tissue. • Jaundice
 The amount of scar tissue exceeds that of the • Muscle wasting
functioning liver tissue.
 Islands of residual normal tissue and • Purpura (due to decreased platelet count)
regenerating liver tissue may project from the • Sparse body hair
constricted areas, giving the cirrhotic liver its
characteristic hobnail appearance. • Spontaneous bruising
 The disease usually has an insidious onset and a
• Weakness
protracted course, occasionally proceeding over
a period of 30 or more years • Weight loss

• White nails

Assessment and Diagnostic Findings

 Enzyme tests indicate liver cell damage: serum

alkaline phosphatase, AST, ALT, and GGT levels
increase
 Serum cholinesterase level may decrease.

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  Bilirubin tests are performed to measure bile PATHOPHYSIO
excretion or retention.
 Infection in the GI tract causes infecting organisms to
 Prothrombin time is prolonged.
reach the liver through the biliary system, portal
 Ultrasound scanning is used to measure the
venous system, or hepatic arterial or lymphatic
difference in density of parenchymal cells and scar
system.
tissue.
 The bacterial toxins destroy the neighboring liver
 Diagnosis is confirmed by liver biopsy.
cells
 Arterial blood gas analysis may reveal a ventilation–
 The resulting necrotic tissue serves as a protective
perfusion imbalance and hypoxia
wall for the organisms.
Medical Management  Leukocytes migrate into the infected area.
 The result is an abscess cavity full of a liquid
 Enzyme tests indicate liver cell damage: serum
containing living and dead leukocytes, liquefied liver
alkaline phosphatase, AST, ALT, and GGT levels
cells, and bacteria.
increase
 Serum cholinesterase level may decrease. CLINICAL MANIFESTATION
 Bilirubin tests are performed to measure bile
 Fever with chills and diaphoresis, malaise, anorexia,
excretion or retention.
nausea, vomiting, and weight loss may occur.
 Prothrombin time is prolonged.
 The patient may complain of dull abdominal pain
 Ultrasound scanning is used to measure the
and tenderness in the right upper quadrant of the
difference in density of parenchymal cells and scar
abdomen.
tissue.
 Hepatomegaly, jaundice, anemia, and pleural
 Diagnosis is confirmed by liver biopsy.
effusion may develop.
 Arterial blood gas analysis may reveal a ventilation–
 Sepsis and shock may be severe and life threatening
perfusion imbalance and hypoxia
ASSESSMENT AND DIAGNOSTIC FINDINGS
Nursing Management
 Aspiration of the liver abscess, guided by ultrasound,
 Enzyme tests indicate liver cell damage: serum
CT, or MRI, may be performed to assist in diagnosis
alkaline phosphatase, AST, ALT, and GGT levels
and to obtain cultures of the organism.
increase
 Serum cholinesterase level may decrease. MEDICAL MANAGEMENT
 Bilirubin tests are performed to measure bile
 Treatment includes IV antibiotic therapy; the specific
excretion or retention.
antibiotic used in treatment depends on the
 Prothrombin time is prolonged.
organism identified.
 Ultrasound scanning is used to measure the
 Percutaneous drainage of pyogenic abscesses is
difference in density of parenchymal cells and scar
carried out to evacuate the abscess material and
tissue.
promote healing.
 Diagnosis is confirmed by liver biopsy.
 A catheter may be left in place for continuous
 Arterial blood gas analysis may reveal a ventilation–
drainage; the patient must be instructed about its
perfusion imbalance and hypoxia
management.
 Herb milk thistle (Silybum marianum) to treat
 Open surgical drainage may be required if antibiotic
jaundice and other symptoms.
therapy and percutaneous drainage are ineffective
LIVER ABSCESS
LIVER TRANSPLANTATION
 Two categories of liver abscess have been identified:
 Used to treat life-threatening ESLD for which no
amebic and pyogenic.
other form of treatment is available.
 Amebic liver abscesses are most commonly caused
 Total removal of the diseased liver and replacement
by Entamoeba histolytica.
with a healthy liver from a cadaver donor.
 A pyogenic liver abscess is a pocket of pus that forms
 The success of liver transplantation depends on
in the liver due to a bacterial infection.
successful immunosuppression.
13 | P a g e
  Immunosuppressant agents are prescribed
(cyclosporine (Neoral), tacrolimus (Prograf),
corticosteroids etc.).
 General indications for liver transplantation include
irreversible advanced chronic liver disease, fulminant
hepatic failure, metabolic liver diseases, and some
hepatic malignancies.

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BIALIARY DISODER
THE GALL BLADDER
 a pear-shaped, hollow, saclike organ that is 7.5 to 10
cm (3 to 4 inches) long.
 lies in a shallow depression on the inferior surface of
the liver.
 The capacity of the gallbladder is 30 to 50 mL of bile.
 connected to the common bile duct by the cystic
duct.
 functions as a storage depot for bile.
 During storage, a large portion of the water in bile is
ENDOCRINE PANCREAS
absorbed through the walls of the gallbladder (5 to
10 times more concentrated).
 Cholecystokinin (CCK) is the major stimulus for
digestive enzyme secretion and acts by stimulating
the gallbladder to contract.
INSULIN
BILE
GLUCAGON
 half of the bilirubin (a pigment derived from the
breakdown of red blood cells) is a component of bile.
 Bilirubin is converted by the intestinal flora into
urobilinogen.
 Urobilinogen is either excreted in the feces or
returned to the portal circulation.
 About 5% is normally absorbed into the general
SOMATOSTATIN
circulation and then excreted by the kidneys.
 If the flow of bile is impeded bilirubin does not enter
the intestine (increased blood levels of bilirubin).
PANCREAS

ENDOCRINE CONTROL OD CARBOHYDRATES METABOLISM
located in the upper abdomen.
has both exocrine (pancreatic enzymes) and
endocrine functions (insulin, glucagon, and
somatostatin).
EXOCRINE PANCREAS
15 | P a g e
 The secretions of the exocrine pancreas are digestive
enzymes high in protein content and an electrolyte-
rich fluid.
 The secretions are very alkaline.
 Enzymes include amylase, trypsin and lipase.
 The hormone secretin is the major stimulus for
increased bicarbonate secretion from the pancreas.
 The major stimulus for digestive enzyme secretion is
the hormone CCK.
 The vagus nerve also influences exocrine pancreatic
secretion.
 The islets of Langerhans are collections of cells
embedded in the pancreatic tissue.
 They are composed of alpha (produces glucagon),
beta (produces insulin), and delta cells (produces
somatostatin).
 A major action of insulin is to lower blood glucose by
permitting entry of glucose into the cells of the liver,
muscle, and other tissues.
 Insulin also promotes the storage of fat in adipose
tissue and the synthesis of proteins in various body
tissues.
 In the absence of insulin, glucose cannot enter the
cells and is excreted in the urine (diabetes.)
 The effect of glucagon is chiefly to raise the blood
glucose by converting glycogen to glucose in the
liver.
 Secreted by the pancreas in response to a decrease
in the level of blood glucose.
 Inhibits the secretion of other hormones.
 Exerts a hypoglycemic effect by interfering with
release of growth hormone from the pituitary and
glucagon from the pancreas
 Glucose is derived by metabolism by the process of
gluconeogenesis.
 Glucose can be stored temporarily in the form of
glycogen in the liver, muscles, and other tissues.
  Through the action of hormones, blood glucose is
normally maintained at less than 100 mg/dL (5.6
mmol/L).
 Insulin is the primary hormone that lowers the blood
glucose level.
 Hormones that raise the blood glucose level are
ACALCULOS CHOLECYSTITIS
glucagon, epinephrine, adrenocorticosteroids,
growth hormone, and thyroid hormone.
DISODER OF GALLBLADDER
1. Cholecystitis
2. Cholelithiasis
CHOLESISTITIS
 inflammation of the gallbladder which can be acute
or chronic.
 causes pain, tenderness, and rigidity of the upper
CHOLELITHIASIS
right abdomen that may radiate to the midsternal
area or right shoulder.
 associated with nausea, vomiting, and the usual
signs of an acute inflammation.
 empyema of the gallbladder develops if the
gallbladder becomes filled with purulent fluid.
PATHOPHYSIOLOGY
 Calculous cholecystitis is the cause of more than 90%
of cases of acute cholecystitis.
 Acalculous cholecystitis describes acute gallbladder
inflammation in the absence of obstruction by
gallstones.
 Secondary infection of bile occurs in approximately
50% of cases.
 The organisms involved are generally enteric and
include Escherichia coli, Klebsiella species, and
Streptococcus.
 acute gallbladder inflammation in the absence of
obstruction by gallstones.
 occurs after major surgical procedures, orthopedic
procedures, severe trauma, or burns.
 can be caused by alterations in fluids and
electrolytes and alterations in regional blood flow in
the visceral circulation.
 Can also be caused by bile stasis and increased
viscosity of the bile.
 hard deposits (gallstones, calculi) that may form in
the gallbladder.
 gallstones usually form from the solid constituents of
bile
 There are two major types of gallstones: (1)
composed of pigment and (2) composed of
cholesterol.
1. Pigment stones - form when unconjugated pigments
in the bile precipitate to form stones.

The risk is increased in patients with cirrhosis, hemolysis, and

infections of the biliary tract.

cannot be dissolved and must be removed surgically.

2. Cholesterol stones – caused by decreased bile acid

synthesis and increased cholesterol synthesis in the
liver.

- resulting in bile supersaturated with cholesterol, which

precipitates out of the bile to form stones.

CALCULOS CHOLESYSTITIS

 a gallbladder stone obstructs bile outflow.

 Bile remaining in the gallbladder causes:
1. autolysis and edema
2. the blood vessels in the gallbladder to be
compressed
3. gangrene of the gallbladder (with possible
perforation).

16 | P a g e
  Stone formation is more frequent in people who use
oral contraceptives, estrogens, or clofibrate
(increased biliary cholesterol saturation).
 increased risk in patients with GI disease or T-tube
fistula and in those who have undergone ileal
resection or bypass.
 The incidence is also greater in people with diabetes.
CLINICAL MANEFESTATION
1. Pain and Biliary Colic - excruciating RUQ pain that
radiates to the back or right shoulder.
usually associated with nausea and vomiting.
noticeable several hours after a heavy meal.
In some patients, the pain is constant rather than colicky
2. Jaundice - frequently accompanied by marked
pruritus of the skin.
3. Changes in Urine and Stool Color – dark-colored
urine and grayish or clay-colored feces.
4. Vitamin Deficiency - vitamins A, D, E, and K
deficiency.
ASSESSMENT AND DIAGNOSTIC FINDINGS
1. Abdominal X-Ray - may be obtained to exclude other
causes of symptoms.
- However, only 10% to 15% of gallstones are calcified
sufficiently to be visible on such x-ray studies.
2. Ultrasonography - the diagnostic procedure of choice
because it is rapid and accurate.
most accurate if the patient fasts overnight so that the
gallbladder is distended.
can detect calculi in the gallbladder or a dilated common bile
duct with 90% accuracy.
17 | P a g e
3. Radionuclide Imaging or Cholescintigraphy
used successfully in the diagnosis of acute cholecystitis or
blockage of a bile duct.
a radioactive agent is administered IV which is taken up by
the hepatocytes and excreted rapidly through the biliary
tract.
The biliary tract is then scanned, and images of the
gallbladder and biliary tract are obtained.
often used when ultrasonography is not conclusive, such as
in acalculous cholecystitis.
4. Oral Cholecystography - used if ultrasound
equipment is not available or if the ultrasound
results are inconclusive.
an iodide-containing contrast agent that is excreted by the
liver and concentrated in the gallbladder is given 10 to 12
hours before the x-ray study.
If gallstones are present, they appear as shadows on the x-
ray image.
5. Endoscopic Retrograde Cholangiopancreatography –
permits direct visualization of structures.
examines the hepatobiliary system via a side-viewing flexible
fiberoptic endoscope inserted through the esophagus to the
descending duodenum.
Fluoroscopy and multiple x-rays are used during ERCP to
evaluate the presence and location of ductal stones.
The patient is NPO for several hours before the procedure.
Moderate sedation is used.
During ERCP, the nurse monitors IV fluids, administers
medications, and positions the patient.
After the procedure, the nurse monitors the patient’s
condition, observing vital signs and assessing for signs of
perforation or infection.
 6. Percutaneous Transhepatic Cholangiography (PTC) -
involves the injection of dye directly into the biliary
tract.
- reserved for patients whom an ERCP may be unsafe due to
previous surgery.
- used for patients who may not be candidates for
laparoscopic cholecystectomy.
b. Stone Removal by Instrumentation - a catheter and
instrument with a basket attached are threaded through the
T-tube tract or fistula formed at the time of T-tube insertion.

The fluoroscopy table is tilted and the patient is repositioned the basket is used to retrieve and remove the stones lodged
to allow x-rays to be taken in multiple projections. in the common bile duct.

It is useful for:

 distinguishing jaundice caused by liver disease

(hepatocellular jaundice) from that caused by biliary
obstruction,
 investigating the GI symptoms of a patient whose
gallbladder has been removed,
 locating stones within the bile ducts, and diagnosing
cancer involving the biliary system.

MEDICAL MANAGEMENT
c. Intracorporeal Lithotripsy - Stones are fragmented by
1. Nutritional and Supportive Therapy - rest, IV fluids,
means of laser pulse technology.
nasogastric suction, analgesia, and antibiotic agents.
A laser pulse is directed under fluoroscopic guidance with
acute symptoms subside usually within a few days.
the use of devices that can distinguish between stones and
The diet immediately after an episode is low-fat liquids tissue.
(powdered supplements high in protein and carbohydrate
The laser pulse produces rapid expansion and disintegration
stirred into skim milk).
of plasma on the stone surface, resulting in a mechanical
The patient should avoid eggs, cream, pork, fried foods, shock wave.
cheese, rich dressings, gas-forming vegetables, and alcohol.
used percutaneously with a basket or balloon catheter
It is important to remind the patient that fatty foods may system or by direct visualization through an endoscope.
induce an episode of cholecystitis.

2. Pharmacologic Therapy

Ursodeoxycholic acid and chenodeoxycholic acid - acts by

inhibiting the synthesis and secretion of cholesterol.

can reduce the size of existing stones, dissolve small stones,

and prevent new stones from forming.

Six to 12 months of therapy is required in many patients to d. Extracorporeal Shock Wave Lithotripsy (lithotripsy or
dissolve stones. ESWL) - nonsurgical fragmentation of gallstones.

Side effects include GI symptoms, pruritus, headache. uses repeated shock waves directed at the gallstones in the
gallbladder or common bile duct to fragment the stones.The
The success rate of this therapy is low as the recurrence
waves are transmitted to the body through a fluid-filled bag
following it is high.
or by immersing the patient in a water bath.
3. Nonsurgical Removal of Gallstones

a. Dissolving Gallstones - infusion of a solvent (mono-

octanoin or methyl tertiary butyl ether [MTBE]) into the
gallbladder.

18 | P a g e
 4. Surgical Management
a. Preoperative Measures
Vitamin K may be given if the prothrombin level is low.
Provide IV glucose with protein supplements to aid wound
healing.
b. Laparoscopic Cholecystectomy
the standard of therapy for symptomatic gallstones.
performed through a small incision or puncture made
through the abdominal wall at the umbilicus.
The abdominal cavity is insufflated with carbon dioxide
(pneumoperitoneum).
The fiberoptic scope is inserted through the small umbilical
incision.
Several additional punctures or small incisions are made in
the abdominal wall to introduce other surgical instruments.
Camera attached to the laparoscope permits the surgeon to
view the intraabdominal field on a television monitor.
The cystic artery is dissected free and clipped.
The gallbladder is separated from the hepatic bed and
removed from the abdominal cavity after bile and small
stones are aspirated.
With the laparoscopic procedure, the patient does not
experience paralytic ileus.
The patient is often discharged from the hospital on the
same day of surgery or within 1 or 2 days.
The most serious complication after laparoscopic
cholecystectomy is a bile duct injury (can be repaired
immediately during the procedure).
19 | P a g e
c. Cholecystectomy
the gallbladder is removed through an abdominal incision.
performed for acute and chronic cholecystitis.
In some patients, a drain is placed close to the gallbladder
bed and brought out through a puncture wound if there is a
bile leak.
only a small amount of serosanguineous fluid drains in the
initial 24 hours after surgery; afterward, the drain is
removed.
The drain is maintained if there is excess oozing or bile
leakage.
d. Small-Incision Cholecystectomy
a surgical procedure in which the gallbladder is removed
through a small abdominal incision.
Drains may or may not be used.
e. Choledochostomy
reserved for the patient with acute cholecystitis who may be
too ill to undergo a surgical procedure.
Involves making an incision in the common duct.
a tube is usually inserted into the duct for drainage of bile
until edema subsides.
A laparoscopic cholecystectomy is planned for a future date
after acute inflammation has resolved.
f. Surgical Cholecystostomy
performed when the patient’s condition precludes more
extensive surgery or when an acute inflammatory reaction is
severe.
The gallbladder is surgically opened, stones and the bile or
the purulent drainage are removed, and a drainage tube is
secured with a purse-string suture.
A drainage tube is connected to a drainage system.
After recovery from the acute episode, the patient may
return for laparoscopic cholecystectomy
NURSING INTERVENTON  Gallstones enter the common bile duct and
lodge at the ampulla of Vater, obstructing
1. RELIEVING PAIN
the flow of pancreatic juice.
2. IMPROVING RESPIRATORY STATUS
 Reflux of bile from the common bile duct
3. MAINTAINING SKIN INTEGRITY AND PROMOTING
into the pancreatic duct activates the
BILIARY DRAINAGE
powerful enzymes within the pancreas
4. IMPROVING NUTRITIONAL STATUS
 Activation of the enzymes can lead to
5. MONITORING AND MANAGING POTENTIAL
vasodilation, increased vascular
COMPLICATIONS (Bleeding, GI symptoms,
permeability, necrosis, erosion, and
Infection)
hemorrhage.
DISORDER OF THE PANCREAS

1. Acute Pancreatitis
2. Chronic Pancreatitis
3. Pancreatic Cysts
4. Hyperinsulinism

ACUTE PANCREATITIS

 sudden inflammation of the pancreas.

 There are two main types: (1)mild (interstitial
edematous pancreatitis and (2)severe (necrotizing
pancreatitis).
1. Interstitial pancreatitis - affects the majority of
patients.
- Characterized by a lack of pancreatic or OTHER CAUSE OF ACUTE PANCREATITIS
peripancreatic parenchymal necrosis with
 Bacterial or viral infection
diffuse enlargement of the gland due to
 Spasm and edema of the ampulla of Vater, caused by
inflammatory edema.
duodenitis
- The edema and inflammation is confined to
 Blunt abdominal trauma
the pancreas itself.
 Peptic ulcer disease
- return to normal function usually occurs
 Ischemic vascular disease
within 6 months
2. Necrotizing pancreatitis - presence of tissue  Hyperlipidemia
necrosis in either the pancreatic parenchyma or  Hypercalcemia
in the tissue surrounding the gland.  Medications (corticosteroids, thiazide diuretics, oral
- Enzymes damage the local blood vessels, and contraceptives)
bleeding and thrombosis can occur. CLINICAL MANIFESTATION
- Local complications include pancreatic cysts
or abscesses and acute fluid collections in or  Severe abdominal pain in midepigastrium (major
near the pancreas. symptom)
- Also, patients who develop systemic  Pain is frequently acute in onset, occurring 24 to 48
complications with organ failure, such as hours after a very heavy meal or alcohol ingestion
pulmonary insufficiency with hypoxia, shock, (unrelieved by antacids)
kidney disease, and GI bleeding are  Abdominal tenderness and back pain
categorized as severe  Abdominal distention
 Decreased peristalsis
PATHOPYSIOLOGY
 Nausea and vomiting (bile stained)
 Self-digestion of the pancreas by its own  Abdominal guarding (a rigid or boardlike abdomen
proteolytic enzymes, principally trypsin, may indicate peritonitis)
causes acute pancreatitis.

20 | P a g e
  Ecchymosis in the flank or around the umbilicus may
indicate severe pancreatitis
 Fever, jaundice, mental confusion, and agitation may
also occur.
 Hypotension is typical and reflects hypovolemia and
shock.
 Acute kidney injury is common.
 Respiratory distress and hypoxia are common
ASSESSMENT AND DIAGNOSTIC FINDINGS
 Serum amylase and lipase levels (elevated within 24
hours of the onset of the symptoms).
 Blood chemistry: elevated WBC count,
hypocalcemia, hyperglycemia and
hyperbilirubinemia.
 Imaging studies of the abdomen and chest (X-ray,
Ultrasound, CT, MRI).
 Hematocrit and hemoglobin levels
MEDICAL MANAGEMENT
1. Pain Management
Adequate administration of analgesia to minimize
restlessness, which may stimulate pancreatic secretion
further.
Pain relief may require parenteral opioids such as morphine,
fentanyl (Sublimaze), or hydromorphone.
Antiemetic agents may be prescribed to prevent vomiting.
2. Intensive Care
Correction of fluid and blood loss and low albumin levels.
Hemodynamic monitoring and arterial blood gas monitoring.
Antibiotic agents may be prescribed if infection is present.
Insulin may be required if hyperglycemia occurs.
3. Respiratory Care
21 | P a g e
4. Biliary Drainage
Placement of biliary drains (for external drainage) and stents
(indwelling tubes) in the pancreatic duct to reestablish
drainage of the pancreas.
5. Surgical Intervention
Diagnostic laparotomy - to establish pancreatic drainage; or
to resect or débride an infected, necrotic pancreas.
The patient may have multiple drains in place
postoperatively, as well as a surgical incision that is left open
for irrigation and repacking
6. Post acute Management
oral feedings that are low in fat and protein
Caffeine and alcohol are eliminated from the diet.
Follow-up may include ultrasound, x-ray studies, or ERCP to
determine whether the pancreatitis is resolving.
NURSING MANAGEMENT
1. Relieving Pain and Discomfort
Pharmacologic and nonpharmacologic interventions.
Oral feedings are withheld to decrease the secretion of
secretin.
Parenteral fluids and electrolytes are prescribed to restore
and maintain fluid balance.
2. Bed rest to decrease the metabolic rate.
Improving Breathing Pattern
- Semi-Fowler’s position to decrease pressure on the
diaphragm
Frequent changes of position.
Coughing and deep breathing.
Use of incentive spirometry.
3. Improving Nutritional Status
Laboratory test results and daily weights
Enteral or parenteral nutrition may be prescribed.
Between acute attacks, the patient receives a diet that is
high in protein and low in fat.
The patient should avoid heavy meals and alcoholic
beverages
4. Maintaining Skin Integrity
Assess the wound, drainage sites, and skin for signs of
infection, inflammation, and breakdown.
The patient must be turned every 2 hours.
5. Monitoring and Managing Potential Complications
Fluid and electrolyte disturbances (assess weight, skin
turgor, mucous membranes, fluid I/O, ascites).
Fluids are administered IV and may be accompanied by
infusion of blood or blood products.
Carefully monitor vital signs and other signs and symptoms
(MODS).
CHRONIC PANCRETITIS
 an inflammatory disorder characterized by
progressive destruction of the pancreas.
 cells are replaced by fibrous tissue with repeated
attacks of pancreatitis
 Increased pressure within the pancreas causes
obstruction of the pancreatic and common bile ducts
and the duodenum.
 Also, there is atrophy of the epithelium of the ducts,
inflammation, and destruction of the secreting cells
of the pancreas.
 Alcohol consumption and malnutrition are the major
causes of chronic pancreatitis.
 Long-term alcohol consumption causes
hypersecretion of protein in pancreatic secretions,
resulting in protein plugs and calculi within the
pancreatic ducts.
CLINICAL MANIFESTATION
 Recurring attacks of severe upper abdominal and
back pain, accompanied by vomiting (opioids, even
in large doses, do not provide relief).
 Opioid dependence
22 | P a g e
 Weight loss secondary to anorexia or fear
 Malabsorption (steatorrhea)
 Calcification of the gland may occur, and calcium
stones may form within the ducts.
ASSESSMENT AND DIAGNOSTIC FINDINGS
 ERCP (most useful study in the diagnosis of chronic
pancreatitis)
 Glucose tolerance test - evaluates pancreatic islet
cell function.
 Increased serum amylase levels
 Laboratory analysis of fecal fat content
MEDICAL MANAGEMENT
 Nonsurgical Management
 Endoscopy to remove pancreatic duct stones, correct
strictures with stenting, and drain cysts.
 Management of abdominal pain and discomfort
(celiac nerve block is a potential option).
 Yoga and other mindfulness-based therapies.
 Avoiding alcohol.
 Diabetes resulting from dysfunction of the
pancreatic islet cells is treated with diet, insulin, or
oral antidiabetic agents.
 Pancreatic enzyme replacement.
SURGICAL MANAGEMENT
1. Pancreatojejunostomy (Roux-en-Y) – allows drainage
of the pancreatic secretions into the jejunum.
2. Whipple resection (pancreaticoduodenectomy) - to
relieve the pain of chronic pancreatitis.
3. Sphincterotomy - dividing the sphincter of Oddi.
4. Endoscopic or laparoscopic interventions (distal
pancreatectomy, nerve denervation, longitudinal
decompression of the pancreatic duct)
PANCREATIC CYST
 collections of fluid walled off by fibrous tissue
(pancreatic pseudocysts)
 result of the local necrosis that occurs because of
acute pancreatitis
 Pseudocysts are amylase-rich fluid collections that
occur within 4 to 6 weeks after an episode of acute
pancreatitis.
 Diagnosis of pancreatic cysts and pseudocysts is
made by ultrasound, CT scan, and ERCP.
 Drainage into the GI tract or through the skin and
abdominal wall may be established
HYPERINSULINISM

 overproduction of insulin by the pancreatic islets.

 characterized by episodes of unusual hunger,
nervousness, sweating, headache, and faintness.
 In severe cases, seizures and episodes of
unconsciousness may occur.
 The findings at the time of surgery or at autopsy may
indicate hyperplasia of the islets of Langerhans.
 All of the symptoms that accompany spontaneous
hypoglycemia are relieved by the oral or parenteral
administration of glucose.
 Surgical removal of the hyperplastic or neoplastic
tissue from the pancreas is the only successful
method of treatment.

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