Conditions of the Accessory Organs

Chronic - onset is gradual; symptoms may

3. The Pancreas: appear late - when almost 80 - 90% of the
pancreas are already destroyed.
Exocrine Dysfunction
Etiology factors and predisposing
Pancreas
Alcoholism
 A pistol-shaped organ; endocrine and /
exocrine gland Hypercalcemia
 Parts: head, body and tail /
Trauma
Ducts: /
 Wirsung's duct Hyperlipidemia
 Santorini's duct /
Biliary tract disease - cholelithiasis
As an endocrine gland, it produces the /
hormones: Bacterial disease
/
1. Insulin - beta cells PUD
2 Glucagon - alpha cells /
3. Somatostatin - delta cells Mumps
/
As an exocrine gland it produces the Acute Pancreatitis
enzymes necessary for digestion:
PATHOPHYSIOLOGY
1. Amylase - Self-digestion of the pancreas by its own
2. Lipase digestive enzymes principally TRYPSIN
3. Trypsin
PATHOPHYSIOLOGY of acute
Pancreatic Secretions pancreatitis
1. Bicarbonate- to neutralize the acidic
chyme from the stomach Spasm, edema or block in the Ampulla of
2. Pancreatic amylase- for carbohydrate Vater
digestion /
reflux of proteolytic enzymes auto digestion
Pancreatitis - Inflammation of the of the pancreas
pancreas /
inflammation
Can be acute or chronic /
Inflammation, Hemorrhage, Necrosis
ACUTE VS CHRONIC PANCREATITIS /
ACTIVATION of KININ (induce
Acute - may range from mild to severe acute vasodilation and
(a medical emergency); high risk for life - /
threatening complications; onset is sudden. contraction of smooth muscle
 12. Manage shock and other complications
increased permeability (in portal vessels and
pancreatic cells) Chronic Pancreatitis
/ Is an inflammatory condition
Loss of Protein-rich fluid into the characterized by progressive anatomic and
peritoneum functional destruction of the pancreas.
/
HYPOVOLEMIA with ASCITES Pathophysiology

ASSESSMENT findings Repeated attacks of pancreatitis

1. Abdominal pain- acute onset, attacks /
occurring after a heavy meal or alcohol Pancreatic cells are replaced by fibrous
intake tissues
2 Abdominal guarding /
3. Bruising on the flanks and umbilicus Pressure within the pancreas increases
4. N/V, jaundice /
5.Hypotension and hypovolemia Obstruction of the pancreatic and common
6.HYPERGLYCEMIA bile ducts and the duodenum
7. HYPOCALCEMIA /
8. Signs of shock Atrophy, inflammation and destruction of
the secreting cells of
DIAGNOSTIC TESTS /
1. Serum amylase and serum lipase elevated the pancreas
2. Ultrasound
3. WBC
4. Serum calcium 4 Major Causes
5. CT scan  Alcohol(70 - 80% of all cases)
6. Hemoglobin and hematocrit  Malnutrition (protein defičiency and
high fat)
NURSING INTERVENTIONS
1. Assist in pain management. Usually, Diagnostic Exams
Demerol is given. Morphine is AVOIDED  ERCP
2. Assist in correction of Fluid and Blood  CT scans, MRI, USG
loss  Glucose Tolerance Test
3. Place patient on NPO to inhibit pancreatic  Stool Exams
stimulation
 Blood exams
4. NGT insertion to decompress distention
 others
and remove gastric secretions
5. Maintain on bed rest
Management
7. Position patient in SEMI-FOWLER's
Treatment is aimed towards
decrease pressure on the diaphragm
preventing and managing acute attacks,
8. Deep breathing and coughing exercises
relieving pain and discomfort and managing
9. Provide parenteral nutrition
endocrine and docrine insufficiency.
10. Introduce oral feedings gradually HIGH
carbo, LOW FAT
11. Maintain skin integrity  Endoscopy-to remove stones
  Non opioid medication to pain Diagnostic Exams
 Meperidine (Demerol)  CT scan
 Insulin (for DM)  MRI, x- rays
 Pancreatic enzyme replacement  USG
 ERCP with biopsy and histology
Surgery:  Tissue diagnosis is made at the time
1. Pancreato jejunostomy of surgery for surgical patients

2 Pancreato - duodenostomy Management:

• Use of MULTIPLE SUMP TUBES after
surgery to drain and irrigate
CA of the Pancreas
- The tumor may develop in the head
(common), the body or the tail of the
pancreas
 Surgery
 Chemotherapy (Fluorouracil,
Leucovorin, gemcitabine)
 Radiation therapy
Trend: Famesyl transferase inhibitors
monoclonal antibodies and are under study
for pancreatic CA treatment (Choti, 2004).

- Clinical manifestations depend on the

location of the tumor

- If the beta cells are involved, then

syndrome of hyperinsulinism could develop

In most cases, diagnosis is made when 80 -

85% of the case is in the advanced stage
because symptoms arise late.

. Pancreatic carcinoma has only 4% survival

rate at 5 years regardless of the stage of the
disease or treatment (ACA, 2005).

Clinical Manifestations:

 Vague upper mid abdominal pain

 Jaundice

 Weight loss

 Vague upper abdominal discomfort

resulting to boring mid back pain
that will require opioids Ascites,
glycosuria, hyperglycemia and
glucose intolerance develop later