Conditions of the accessory organs

PANCREATITIS

• Proteolytic and lipolytic enzymes are activated in the pancreas rather than in the
duodenum, resulting in tissue damage and autodigestion of the pancreas
• Incidence is increased in the middle aged
• ETIOLOGY: alcoholism penetrating duodenal ulcer
Biliary tract dse abscesses
Trauma drugs (steroids, thiazides, OCP)
Viral infection metabolic d/o (hyperparathy, hyperlipidemia)
• PATHOPHYSIOLOGY

Damage to pancreatic cells

↓↓
Inflammation
↓↓
Edema of the pancreas and pancreatic duct
↓↓
Obstruction of the flow of pancreatic enzyme
↓↓
Activation of pancreatic enzymes within
↓↓
AUTODIGESTION of the pancreas
↓↓
Fatty necrosis, ulceration, hemorrhage, infection

• CLINICAL MANIFESTATIONS
o Pain located in the ULQ with radiation to the back, flank of substernal area;
May be accompanied by DOB and aggravated by eating
o Vomiting, anorexia, severe dehydration,
o shallow respirations, tachycardia,
o decreased or absent bowel sounds, abdominal tenderness with muscle-guarding,
o (+) Grey Turner’s spots, (+) Cullen’s sign
o Steatorrhea

• DIAGNOSTIC FINDINGS
o Increased serum amylase (>300 Somogyi units) and lipase, urinary amylase,
blood sugar, lipid levels
o Decreased serum calcium level

• Medical MANAGEMENT
1. drug therapy
o Analgesics (Demerol) to relieve pan AVOID MORPHINE due to sphincteris
spasm which may aggravate pain
o Smooth-muscle relaxants (NTG)
o Anticholinergics to decreased pancreatic secretions
o Antacids to decrease pancreatic stimulation
o H2-antagonist, vasodilators, Ca gluconate as supportive meds
 Calcium supplement and Vit D to enhance absorption
Insulin for hyperglycemia
2. DIET modification
o Withhold food-fluid and eliminate odor and sight of food from env’t to decrease
pancreatic stimulations (NPO on acute phase) = TPN
o Maintain NGtube and assess for drainage
o Discharge planning (re:diet) HIGH CHO, HIGH CHON, LOW FAT
Small frequent meals
Avoid caffeine products
ELIMINATE ALCOHOL INTAKE (recurrence)
o Recognition and reporting of signs of complications
1. continued N/V
2. abdominal distension with increasing fullness
3. persistent weight loss
4. severe epigastric of back pain
5. frothy foul smelling stool
6. irritability, confusion, persistent elevation of temp (2 days)

CHOLECYSTITIS/ CHOLELITHIASIS

Cholecystitis: acute/chronic inflammation of the gallbladder most commonly associated

with gallstones.
Gallstone formation
↓↓
Inflammation of the bladder walls
↓↓
Edema of the tissue
↓↓
Thickening of inflamed tissue
↓↓
impaired circulation
↓↓
ischemia, necrosis

Cholelithiasis: formation of gall stones, cholesterol stones

Stone origin: Gallbladder – cholesterol stones
Common bile duct – calcium or pigmented stones

• Risk factors:
FAT obese
FEMALE ♀
FORTY post menopausal women with high intake of OCP
FERTILE
FAIR Caucasian

• Stone formation
metabolic factors (obesity, pregnancy, diabetes, hypothyroidism)
↓↓
Biliary stasis
 ↓↓
Excessive absorption of water
↓↓
Precipitation of biliary components
↓↓
Stone formation
↓↓
Inflammation of the gallbladder tissue
↓↓
Alteration in the function of issues: increased absorption of bile acids
↓↓
Reduction in solubility of cholesterol
↓↓
Further development of stones within
↓↓
Decreased fat emulsification = fat intolerance, anorexia, n/v, weight loss, steatorrhea
Gallbladder inflammation = RUQ pain, fever, leukocytosis
Decreased bile flow into the colon = gray/clay colored acholic stool, poor vitamin
(ADEK) absorption, jaundice, pruritus, tea-colored urine
~~~charcot’s triad (fever, jaundice, RUQ pain)~~~

↓↓
DIAGNOSTIC FINDINGs:
Increased WBC, amylase, lipase, liver enzymes
Oral cholecystogram (+) for gallstone

↓↓
MANAGEMENT
1. Relief of pain: Meperidine (DOC)
2. Diet: LOW FAT
3. Bile salts: Chenodeoxycholic acid (inhibit synth and secretion of cholesterol),
Ursodeoxycholic acid (dissolve small gallstones composed of cholesterol)
4. Surgery: CHOLECYSTECTOMY
Pre-op: a. IVF to replace fluid electrolyte losses
b. DBCE to prevent respiratory complications
c. Vita K injection
Post-op:
1. position on LOW or SEMI Fowler’s
2. NGT to prevent gastric distention
3. DBCE
4. LOW FAT diet (2-3months)
5. ambulation after 24hrs post-op
6. (+) CBD exploration: T-tube
Purpose: to drain bile
Drainage: ~ brownish red for the first 24hrs (bile + blood)
~ 300 to 500ml for the first 24hrs
~drainage bottle placed in bed at the level of incision
Avoid kinks, clamping, pulling of the tube
Urine and stool color: light due to excretion of bile through T0tube
Resumption of ADL (avoid heavy lifting for 6wks)
WOF signs of Cx: fever jaundice, pain, dark urine, pale stools, pruritus
LIVER CIRRHOSIS

• Chronic progressive disease characterized by inflammation, fibrosis, and degeneration

of the liver parenchymal cells
• Destroyed liver cells are replaced by scar tissue resulting in malfunction of the organ
• TYPES:
a. Laennec’s cirrhosis; associated with alcohol abuse and malnutrition; characterized by
an accumulation of fat in the liver, progressing to widespread scar formation
b. Postnecrotic cirrhosis: results in severe inflammation with massive necrosis as a
complication of viral hepatitis
c. Cardiac cirrhosis: occurs as a consequence of RSCHF ; manifested by hepatomegaly
with some fibrosis
d. Biliary cirrhosis: associated with biliary obstruction, usually in the CBD, results in
chronic impairment of bile excretion
• PATHOPHYSIOLOGY
Laenec’s Postnecrotis Biliary
Cardiac
ROH abuse Infection Obstruction RSCHF
Malnutrition Drugs
↓↓
Destruction of hepatocytes
↓↓
Inflammation
↓↓
Necrosis -- Fibrosis ; scarring
↓↓
Obstruction of blood flow
Pressure in the venous and sinusoidal channels
Fatty infiltration
↓↓
Portal hypertension
↓↓
• MANIFESTATIONs

Hepatomegaly - - - fibrosis leads to shrinkage

Splenomegaly - - - due to increased back pressure
Caput medusae (dilated veins over the abdomen)
Spider angioma (dilated capillaries over face & anterior trunk) due to increased estrogen
Palmar erythema due to elevated estrogen (even in males)
Ascites (inability to metabolize CHON thus hypoalbuminemia)
Esophageal varices secondary to back pressure

liver unable to metabolize nutrients and store fat-soluble vit =

anorexia, vomiting, weakness, weight loss, increased bleeding tendencies
tissue injury/damage = fever
increased serum bilirubin = jaundice, pruritus, tea colored urine

MALES: gynecomastia FEMALES: hirsutism

 Decreased libido acne
Impotence deepening of voice
Fall of body hair virilism
Atrophy of testicles
Hepatic encephalopathy
 condition secondary to increased ammonia level
 Liver cannot convert ammonia (by-product of CHON metabolism) into Urea
(excretable form).
 Toxic level of ammonia in the blood leads to hepatic coma (the initial manifestations
of which include behavioral and mental changes)
 Advanced stages show: asterixis Confusion/disorientation
Fetor hepaticus Delirium/hallucination
Coma

• MANAGEMENT

1. Priority: REST!!!!!!!!!!!! To reduce metabolic demands on the liver

2. Diet:
> early stage: HIGH CALORIE, HIGH CHO, LOW CHON, MODERATE FATS
> Late stage: HIGH CALORIE, HIGH CHO, LOW CHON supplemental ADEK

3. skin care and avoid trauma/injury (due to low synthesis of vitamin K and clotting factors)
4. prevent infection
5. manage ascites
Monitor weight, I&O, abdominal girth
Restrict Na and fluid intake
Diuretics as ordered
Albumin as ordered
6. manage esophageal varices
AVOID (to prevent rupture of varices)
>Shouting >lifting heavy objects
>Straining >hot, spicy foods
>Bending, stooping
If bleeding occurs:
>Place in semi-fowler’s >Suction the mouth
>Administer IVF, BT >Gastric lavage (RT)
>Sclerotherapy >Variceal band ligation
>Balloon tamponade with SENGSTAKEN-BLAKEMORE TUBE
7. decrease ammonia formation
Restrict CHON in diet
Duphalac (lactulose) to lower pH in the colon and reduce formation of alkaline
ammonia; enhances excretion by increasing peristalsis
Neomycin Sulfate to reduce ammonia-producing bacteria in the colon
Tap water or NSS enema to remove digested blood from the colon
8. avoid sedatives and all hepatotoxic drugs
9. avoid ASA. Eliminate ROH
10. gradual progression of activities with planned rest periods
11. relieve pruritus (X soaps and detergents; cool light nonrestrictive clothing; cool
compresses;
12.avoidance of persons with upper respiratory infections
13. recognition and reporting of signs of recurring illness (liver tenderness, increased
jaundice and fatigue, anorexia)

HEPATITIS