DISTURBANCES IN ACCESSORY ORGANS: GALLBLADDER, LIVER AND EXOCRINE PANCREATIC

DISORDERS

by:
Prof. Marites L. Robleza

A. DISORDERS OF THE BILIARY TRACT:

1. CHOLECYSTITIS – is an acute inflammation of the gallbladder, which is the storage site for bile
production from the liver.

CAUSES: Gallstones / Surgical trauma or injury to the gallbladder / Anatomical abnormalities

PATHOPHYSIOLOGY:
= Originate from an obstruction of the cystic duct either by a stone or by a bacterial invasion. As a
result of the inflammation, the gallbladder wall becomes thickened & edematous & the diameter of the
cystic duct lumen increases in size.

= If the inflammation and edema spread to the common duct, the temporary obstruction of bile
elimination will result in jaundice.

= If the cystic duct is completely occluded, the gallbladder will become distended with inflammatory
exudate and bile. Following the acute attack, the surface mucosa heals, scarring the gallbladder wall,
affecting future gallbladder functioning.

TYPES:
1. Acute cholecystitis

a. Calculous Cholecystitis – is the cause of 90% of cases of acute cholecystitis. Gallbladder stones
obstruct s bile flow  gangrene & perforation.

b. Acalculous Cholecystitis – is the absence of obstruction by a gallstone.

ASSESSMENT FINDINGS:
 Pain in the RUQ or epigastric that last for 12 – 18 hours
 Low grade fever
 Nausea & vomiting after a High Fat Diet
 Flatulence
 Indigestion
 Abdominal tenderness
 Palpable gallbladder (Murphy’s sign)
 Clay-colored, steatorrhea stools
 Bile colored urine

COMPLICATIONS:
= Perforation, peritonitis, infection of biliary system, pancreatitis, intestinal obstruction, fistula
formation.

MEDICAL MANAGEMENT:
= Bed rest
= Fluid and electrolyte replacement
= Drug therapy – Analgesics/antibiotic
= Dietary Management – Low Fat diet
= Surgery – Cholecystostomy/Cholecystectomy
2. Chronic Cholecystitis – is a long-standing swelling and irritation of the gallbladder  thickening of the
walls  shrink.
= long term intolerance to fatty foods

Symptoms are vague, such as:

1. Chronic indigestion
2. Vague abdominal pain
3. Nausea
4. Belching

TREATMENT:
1. Surgery – Cholecystectomy
2. Diet – Low Fat
3. Weight reduction
4. Drug therapy – Acid-suppressing and Anticholenergic; Antacids.

COMPLICATIONS: Pancreatitis or Cancer of the gallbladder (rarely).

DIAGNOSTIC TEST:
 CBC – WBC is elevated

 Serum alkaline phophatase, AST

 S. Bilirubin

 S. Amylase and Lipase

 UTZ of abdomen – diagnostic test of choice

2. GALL BLADDER STONE OR (CHOLELITHIASIS) – presence of gall stones.

CAUSES: Change in bile composition, Stasis, Infection, Genetic

ETIOLOGY and RISK FACTORS : 5F’s, age, obesity, familial tendency, rapid weight loss

GROUP OF GALLSTONE includes:

 Cholesterol stones
 Pigment stones
 Mixed stones

Gallbladder with numerous stones. Their brownish and greenish colors suggest a cholesterol calculi.

ASSESSMENT FINDINGS:

 Asymptomatic for a majority of persons; Biliary colic; Jaundice in CBD obstruction; Nausea and
vomiting; Intolerance to fatty foods; vague upper abdominal discomfort.
 Positive results of diagnostic studies such as Ultrasonography; CT scan; Oral Cholecystography;
Cholangiography; ERCP.

MEDICAL MANAGEMENT:
 Nutritional and Supportive Therapy
= Complete bedrest
= NPO and NGT; Fluid and electrolyte replacement; Medications such as Demerol, Anti-emetics,
Antispasmodics, Anticholinergics, Antibiotics.

 Pharmacologic Therapy
= Ursodeoxycholic acid (UDCA/URSO, Actigall) and Chenodeoxycholic Acid (Chenodiol).
 Nonsurgical Removal of Stones
= Dissolving of stones – infusion of a solvent (Mono-octanoin or methyl tertiary butyl ether [MTBE])
into the gallbladder.

 Stone Removal by Instrumentation

a. ERCP
b. Intracorporeal Lithotripsy
c. Extracorporeal Shock Wave Lithotripsy (ESWL)
 Surgical Management
a. Laparoscopic Cholecystectomy
b. Cholecystectomy
c. Choledochostomy
d. Surgical Cholecystostomy
e. Percutaneous Cholecystostomy

POST-OPERATIVE CARE:
 Relieve pain – analgesic
 Improve respiratory status – deep breathing; use of incentive spirometer, early ambulation.
 Promote skin care/biliary drainage – signs of infection, protect from irritation of bile, measure
collected bile, never clamp T-tube, if clamped– note for color of stools.
 Improve nutritional status – low fat, high carbohydrate and protein.

Care of T-TUBE:
= Normal drain – post – op: 500 ml 1 st 24 hours post-op – decreased to 200 in 2-3 days.
= INITIALLY – GREEN
= Report excessive drainage – may indicate obstruction.
= Place in fowler’s position.
= Assess skin for bile leakage during change of dressing.
= Ensure that T-tube is properly connected to drainage (JP drain); keep it below level of surgical wound.

NURSING DIAGNOSES:
 Alteration in Comfort R/T Biliary Spasms
= NGT insertion relieves biliary spasms (contractions)
= Analgesics, except MS (causes contraction of the sphincter of Oddi); NTG – relaxes smooth muscles
thus decrease colic
= Relaxation technics, diversional activities
 Fluid Volume Deficit R/T Vomiting and NGT suctioning
 Potential for Injury R/T Endoscopic Procedure for stone removal
= Observe for S/S of bleeding & hemorrhage due to procedure.
 Knowledge deficit

B. DISORDERS OF THE LIVER

B. 1. HEPATITIS – is a systemic, viral infection in which necrosis and inflammation of liver cells produce a
characteristic cluster of clinical, biochemical and cellular changes.

TYPES:

 VIRAL such as Hepatitis A (HAV), B (HBV), C (HCV), D (HDV), E (HEV), and G (HGV).
 TOXIC/DRUG-INDUCED HEPATITIS
 CHRONIC
 ALCOHOLIC

PATHOPHYSIOLOGY:

 Basic pathophysiology of Hepatitis A, B, C, D, E & G is identical.

 During acute phase of viral inflammation of the liver  Generalized. Hepatocytes are damaged by
the body's immune response to virus  Necrosis.
 Surviving cells retain glycogen but fatty changes do not occur.
 Changes that occur in the liver interferes with normal functions  breakdown of bilirubin,
metabolism of drugs & synthesis of protein.

3.1 VIRAL HEPATITIS

ETIOLOGIC AGENTS :
 Hepatitis A, B, C, D, E and G Virus

INCUBATION PERIOD:
> A = 15 – 50 days
> B = 1 to 6 months
> C = 15 to 160 days
> D = varies between 21 and 140 days
> E = range between 15 and 65 days
> G = 14 to 145 days

MODE OF TRANSMISSION:
A) Hepatitis A Virus:
 Oral-fecal route; Airborne (droplet); Ingestion of food or liquid infected by the virus; Eating
contaminated shellfish from sewage-contaminated waters; Sexual contact & more likely with oral-
anal sex or anal intercourse & with multiple partners

2) Hepatitis B Virus
 Transmitted primarily through blood (percutaneous and permucosal routes).
 Found in blood, saliva, semen, and vaginal secretions and can be transmitted through mucous
membranes and breaks in the skin.
 Also transferred from carrier mothers to their infants.

3) Hepatitis C Virus
 Can be transmitted through blood transfusions and sexual contact; parenteral such as sharing of
contaminated needles by IV/injections.

4) Hepatitis D Virus
 Co-exist with Hepatitis B virus and with the same mode of transmission.

5) Hepatitis E Virus
 Transmitted by the fecal-oral route; through contaminated water in areas with poor sanitation. In
general, it resembles with hepatitis A.

6) Hepatitis G Virus
 Risk factors similar to Hepatitis C.

ASSESSMENT FINDINGS:

A) PRE-ICTERIC PHASE (Early Stage)

 Fatigue, Myalgia, Malaise, Arthralgia; Photophobia; Headache; Loss of appetite; Nausea &
vomiting; Altered sense of taste and smell; Fever; Pruritus; Liver and lymph node enlargement.

B) ICTERIC PHASE (lasts 1 to 2 weeks)

 Mild weight loss; Dark urine; Clay-colored stools; Yellow sclera and skin; Continued Hepatomegaly
with tenderness.

C) CONVALESCENT PHASE (lasts 2 to 12 weeks or longer)

 Fatigue; Flatulence; Abdominal pain or tenderness; Nausea; Heartburn; Indigestion.

 Children with hepatitis are usually anicteric

 Irritability and drowsiness – if it became severe assess for hepatic encephalopathy
 Anemia

 Symptoms tend to clear as soon as the jaundice reaches its peak, perhaps 10 days after its
initial appearance.

MEDICAL MANAGEMENT:
 Bed rest during the acute stage; Proper diet (Hi-caloric, High in carbohydrates, moderate amounts of
fats and protein), all alcoholic beverages are strongly forbidden; Drugs – Immunoglobulin for
HAV(post exposure prophylactic), Antiemitics for nausea and vomiting; Anti-pruritic emollients or
antihistamines for relief of pruritus; Emotional support

 The FDA has approved a combined hepatitis A and B vaccine (Twinrix) for vaccination of
people 18 years of age with indications for both hepatitis A and B vaccination. Vaccination
consists of 3 doses, on the same schedule as that used for single-antigen hepatitis B
vaccine.

NURSING MANAGEMENT:
 Teach client and family about a good personal hygiene, stressing careful hand washing (after
bowel movement and before eating) and environmental sanitation (safe food and water supply,
effective sewage disposal).
TOXIC/DRUG-INDUCED HEPATITIS – resembles with viral hepatitis at the onset of the disease. It occurs
after exposure to hepatotoxins  causes liver alterations by initiating either drug-induced hepatitis or
drug-induced cholestasis.

= Liver necrosis occurs within 2 to 3 days after acute exposure to dose-related hepatotoxins.

ASSESSMENT FINDINGS:
 Anorexia, nausea, and vomiting; jaundice and hepatomegaly.
= Recovery from an acute toxic hepatitis is rapid if the hepatotoxin is identified early and removed or if
the exposure to the agent has been limited. Recovery is unlikely if there is a prolonged period between
exposure and onset of symptoms. There are no effective antidotes, patient may die of fulminant hepatic
failure.

Fulminant Hepatic Failure – is the clinical syndrome of sudden and severely impaired liver function.

CHRONIC HEPATITIS – exists when the liver inflammation continues beyond 3-6 months, may be -
a. CHRONIC PERSISTENT HEPATITIS (CPH)– Benign or seldom progressive, more common in males with
S/S similar to Acute Viral Hepatitis.

ASSESSMENT FINDINGS:
 Slight enlargement and tenderness of liver; URQ discomfort; Nausea, anorexia and weakness.

b. CHRONIC ACTIVE HEPATITIS (CAH)– a more severe illness leading to hepatic inflammation, hepatic
necrosis and progressive fibrosis.
= It results from an idiopathic cause or from HBV, occurring more frequently in females.

ASSESSMENT FINDINGS:
 Deep jaundice (eyes); Fever; Thyroiditis; Hemolytic anemia, bleeding tendencies; Urticaria; Liver
necrosis, Hepatomegaly, Splenomegaly; Abdominal pain; Amenorrhea, ascites, severe weakness,
arthritis.

MEDICAL MANAGEMENT:
 Medications (Steroids); Supportive – Bed rest; Liver transplantation
ALCOHOLIC HEPATITIS – either an acute or chronic inflammation of the liver caused by parenchymal
necrosis resulting from heavy ingestion of alcohol.

ASSESSMENT FINDINGS:
 Anorexia, nausea; Abdominal pain; Splenomegaly; Hepatomegaly; Jaundice; Ascites; fever;
Encephalopathy; Anemia; Elevated serum bilirubin

MEDICAL MANAGEMENT:
 Bed rest; Diet – High-Caloric, Hi-Vitamin, Hi-carbohydrate; Folic acid supplements; Parenteral Fluids;
Steroids

A.2. HEPATIC CIRRHOSIS - is a chronic disease characterized by replacement of normal liver tissue with
diffuse fibrosis that disrupts the structure and function of the liver.

3 TYPES of CIRRHOSIS or SCARRING OF THE LIVER:

1. Alcoholic (Laennec’s) Cirrhosis – in which the scar tissue surrounds the portal areas; most
frequently caused by chronic alcoholism and is the most common type.

2. Postnecrotic Cirrhosis – in which there are broad bands of scar tissue; late result of a previous
bout of acute viral hepatitis.

3. Biliary Cirrhosis – scarring occurs in the liver around the bile ducts; usually results from chronic
biliary obstruction and infection (cholangitis); much less common.

PATHOPHYSIOLOGY:
= Alcohol consumption – is the major causative factor.
Other Factors: exposure to certain chemicals (carbon tetrachloride, chlorinated naphthalene, arsenic, or
phosphorus) or infectious schistosomiasis.
= Men are twice affected than women.
= Ages between 40 and 60 years old.
CLINICAL MANIFESTATIONS:
COMPENSATED:
= Intermittent mild fever; vascular spiders; palmar erythema; unexplained epistaxis; ankle edema; vague
morning indigestion; flatulent dyspepsia; abdominal pain; firm, enlarged liver; splenomegaly.

DECOMPENSATED:
= Ascitis; jaundice; weakness; muscle wasting; weight loss; continuous mild fever; clubbing of fingers;
purpura (due to decreased platelet count); spontaneous bruising; epistaxis; hypotension; sparse body
hair; white nails; gonadal hypertrophy

STAGES OF LAENNEC’S (ALCOHOLIC) CIRRHOSIS:

 1ST STAGE: accumulation of fats – fatty liver; asymptomatic & reversible.
 2nd STAGE: ALCOHOLIC HEPATITIS – inflammation & necrosis occur.
= Asymptomatic or with mild symptoms.
 3rd STAGE: END-STAGE CIRRHOSIS: fibrotic tissue replaces normal tissue.
= Early indicators: signs of portal hypertension, impaired digestion and absorption.

DIAGNOSTIC STUDIES:
= Decrease serum albumin level and increase serum globulin level – in severe parenchymal dysfunction.
= Enzyme tests: increase serum alkaline phosphatase, AST, ALT and GGT levels, and decrease serum
cholinesterase level – indicate liver cell damage.
= Bilirubin test increased with cirrhosis and other liver disease.
= Prothrombin time is prolonged.
= Ultrasound Scanning
= CT, MRI and radioisotope liver scans
= Arterial blood gas analysis
 MEDICAL MANAGEMENT:

 rug Therapy:
= Antacids or histamine-2 (H2) antagonists – to decrease gastric distress and minimize the possibility
of GI bleeding.
= Vitamins and nutritional supplements – promote healing of damaged liver cells and improve the
patient’s general nutritional status.
= Potassium-sparing diuretics such as spironolactone or triamterene (Dyrenium) – may be indicated to
decrease ascites.
 An adequate diet and avoidance of alcohol are essential.
3. For mild to moderate cirrhosis – Colchicine is prescribed which may increase survival time.
4. For clients with end-stage liver disease (ESLD) with cirrhosis – use the herb milk thistle (Silybum
marianum) – to treat jaundice and other symptoms.
5. For biliary cirrhosis – was treated with ursodeoxycholic acid (Actigall, URSO) to improve liver function.

NURSING MANAGEMENT:
= Promoting rest
= Improving nutritional status
= Providing skin care
= Reducing risk of injury
= Monitoring and managing potential complications:
> Bleeding and hemorrhage
> Hepatic encephalopathy
> Fluid volume excess

Hepatic encephalopathy – a metabolic disorder that may occur as cirrhosis progresses.

 Result from the inability of the liver to convert ammonia to urea.
 Increasing ammonia level has a neurotoxic effect on the CNS.

SIGNS OF HEPATIC ENCEPHALOPATHY:

STAGE I: Tremors, slurred speech, impaired decision making
STAGE 2: drowsiness, loss of sphincter control, asterixis
STAGE 3: dramatic confusion, somnolence
STAGE 4: Coma, unresponsiveness

Management of Variceal Hemorrhage:

 Diet: non-irritating foods/parenteral nutrition

EMERGENCY TREATMENT:
 Replacement of fluid/blood – for massive hematemesis and melena
 Administration of vasoconstrictors: Sandostatin (Ocreotide) – drug of choice; Pitressin
(Vasopressin) IV
 Balloon tamponade – Sengstaken Blakemore tube
 Gastric vein occlusion
 Sclerotherapy – injection of sclerosing agent
 Emergency surgical shunting – Porto systemic shunt – shunting to inferior vena cava

Management of Ascites and Fluid Retention:

 Bedrest
 Strict fluid/Na restriction
 Weigh OD
 Diuretics
Spironolactone (Aldactone) – diuretic of choice
 Albumin infusion
 Peritoneovenous shunt (Le Veen/Denver Shunt) / TIPS
 Therapeutic paracentesis
 Nursing Responsibilities: PARACENTESIS

 Weight before and after the procedure

 Obtain baseline VS; monitor during and after every 15 minutes until stable
 Let client void before the procedure
 Obtained signed consent
 Position client
 Drain fluid slowly; limit to 1-2L
 Apply dressing when needle is removed; record amount and characteristic

4. Management of Hepatic Encephalopathy

 Neomycin/ Lactulose p.o. – cornerstone of treatment for increased ammonia level
 No protein in the diet temporarily – until ammonia level decreases

5. Other drugs: for relief measures:

 Pain medication such as opioids, barbiturates and sedatives – used with caution.
 Antiemetics
 Antacids
 Vitamin K

C. DISORDERS OF THE PANCREAS:

PACREATITIS – IS A SERIOUS INFLAMMATION OF THE PANCREAS RESULTING IN THE OBSTRUCTION OF

THE OUTFLOW OF PANCREATIC SECRETIONS may result from edema, necrosis or hemorrhage.

ETIOLOGY:
 Biliary disease; Excessive alcohol intake; Hyperlipidemia; Gallstones; Pancreatic trauma; Certain
drugs or may be familial.

CLASSIFICATIONS (Based on pathological process):

A) ACUTE INTERSTITIAL – edema and inflammation of the interstitium – secondary to other diseases.

B) ACUTE HEMORRHAGIC – diffused areas of inflammation and hemorrhage resulting to necrosis of

some portions of the pancreas which results from fibrosis & loss of function  associated with
prolonged alcohol use.

C) CHRONIC PANCREATITIS – refers to the presence of histologic alterations of the pancreas -

progressive destructive disease of the pancreas in which normal tissues are replaced by connective
tissues.

ASSESSMENT FINDINGS:

A) IN ACUTE PANCREATITIS – Abdominal pain; Persistent vomiting; Abdominal distention; fever;

Epigastric tenderness; Hypotension & hypovolemia; Positive Chvostek’s and Trousseau’s sign;
Laboratory findings such as elevated serum and urine amylase, serum lipase, Hypocalcemia,
Hypoalbuminemia, Hyperglycemia

B) SEVERE HEMORRHAGIC
 Turner’s sign, Cullen’s sign

C) CHRONIC PANCREATITIS
 Acute bouts of abdominal pain with intervals of pain-free periods; malabsorption; severe weight
loss; frequent passage of foul fatty stools (Steatorrhea); Jaundice; Fever; Vomiting; Increased serum
and urinary amylase.
MEDICAL MANAGEMENT:
 Bed rest during acute stage
 Drugs such as Meperidine for pain; Prophylactic antibiotics
 Dietary management – NPO until pain and tenderness have improved, parenteral nutrition (TPN)
with Intralipids; Fluid and electrolyte replacement
 Surgery (Removal of gallstone through an endoscope).