Week 3.

COURSE TASK Acute Pancreatitis

Explain the pathophysiology of acute pancreatitis.

The pathophysiology of acute pancreatitis is characterized by a loss of intracellular

and extracellular compartmentation, by an obstruction of pancreatic secretory
transport and by an activation of pancreatic enzymes. In biliary acute pancreatitis,
outflow obstruction with pancreatic duct hypertension and a toxic effect of bile salts
contribute to disruption of pancreatic ductules, with subsequent loss of extracellular
compartmentation. Alcohol induces functional alterations of plasma membranes and
alters the balance between proteolytic enzymes and protease inhibitors, thus
triggering enzyme activation, autodigestion and cell destruction. Once the disease
has been initiated, the appearance of interstitial edema and inflammatory infiltration
are the basic features of acute pancreatitis. The accumulation of polymorphonuclear
granulocytes in pancreatic and extra pancreatic tissue, and the release of leukocyte
enzymes play an essential role in the further progression of the disease and in the
development of systemic complications. Activation of different cascade systems by
proteolytic activity, and consumption of alpha 2-macroglobulin further characterize
the severe clinical course of acute pancreatitis.
What is the most common cause of acute pancreatitis?
The two most common causes are gallbladder disease and alcohol abuse.
Gallstones and acute pancreatitis.

• Gallstones commonly form in the gallbladder. However, if a stone moves into the
bile duct (through the cystic duct), it can become impacted (stuck) at the exit
into the duodenum (papilla of Vater). This exit hole is normally shared with the
pancreatic duct, so that an impacted stone can block the pancreas and cause
pancreatitis.

• Alcohol causes acute pancreatitis by direct poisoning of the gland. Patients

(and pancreases) vary in their sensitivity to alcohol. There is no completely safe
level of consumption, and yet many people drink heavily for years without ever
developing pancreatitis (or other alcohol-related diseases such as liver and heart
disease). Once pancreatitis has occurred, alcohol should be avoided completely.
Alcohol can aggravate pancreatitis even if it has originally been caused by
something else.

After these, causes include cigarette smoking, biliary sludge, hypertriglyceridemia,

trauma, certain drugs, metabolic disorders, and vascular diseases.

How do the results of V. A’s laboratory value relate to the

pathophysiology of acute pancreatitis?

The serum and urinary amylase levels and serum lipase levels are elevated,
indicating release of these enzymes into the blood circulating through the pancreas.
The WBC count is high, indicating marked inflammation. The blood glucose level
is elevated, indicating impairment of insulin production and release by the β
-cells. The decreased calcium indicates hypocalcemia, a sign of severe pancreatitis.

What causes hypocalcemia in acute pancreatitis? How does the

nurse assess for hypocalcemia?

Pancreatitis can be associated with tetany and hypocalcemia. It is caused

primarily by precipitation of calcium soaps in the abdominal cavity, but glucagon-
stimulated calcitonin release and decreased PTH secretion may play a role. When
the pancreas is damaged, free fatty acids are generated by the action of
pancreatic lipase. Insoluble calcium salts are present in the pancreas, and the
free fatty acids avidly chelate the salts, resulting in calcium deposition in the
retroperitoneum. In addition, hypoalbuminemia may be a part of the clinical
picture, resulting in a reduction in total serum calcium. In patients with concomitant
alcohol abuse, a poor nutritional intake of calcium and vitamin D, as well as
accompanying hypomagnesemia, may predispose these patients to hypocalcemia.

Hypocalcemia occurs in part because calcium combines with fatty acids released
during fat necrosis of the pancreas. The nurse should observe for symptoms of
tetany, such as jerking, irritability, muscular twitching, and positive Chvostek’s and
Trousseau’s signs. Numbness or tingling around the lips and in the fingers is an early
indicator of hypocalcemia.

Describe the characteristics of the pain that occurs in acute pancreatitis

The cardinal symptom of acute pancreatitis is abdominal pain, which is characteristically

dull, boring, and steady. Usually, the pain is sudden in onset and gradually intensifies
in severity until reaching a constant ache.

The pain is usually located in the LUQ but may be in the mid epigastric area and
frequently radiates to the back. It has a sudden onset and is described as severe, deep,
piercing, and continuous. It is aggravated by eating and often begins when the patient
is recumbent. It is not relieved by vomiting and may be accompanied by flushing, cyanosis,
and dyspnea.

What complications can occur with acute pancreatitis?

The most common complication of acute pancreatitis (occurring in approximately 25%

of patients, especially those with alcoholic chronic pancreatitis) is the collection of
pancreatic juices outside of the normal boundaries of the ductal system called
pseudocysts. Most pseudocysts resolve spontaneously.

Hypovolemia, shock, and the local complications of pseudocysts and abscesses;

paralytic ileus with abdominal distention; and crackles in the lungs. Seepage of
bloodstained exudates may cause Grey Turner’s or Cullen’s signs.

Why VA NPO? What is the purpose of the NG tube?

NPO status and suction with an NG tube prevent gastric contents from entering
the duodenum and stimulating pancreatic secretion.
Identify the purpose of each medication prescribed for this patient.
Morphine is for pain relief. Pantoprazole (proton pump inhibitor) is to decrease
hydrochloric acid production by the stomach because hydrochloric acid stimulates
pancreatic activity. Omeprazole (Prilosec) may be taken orally when the patient is no
longer NPO.

Priority Decision: Based on the assessment data presented, what are the
priority diagnosis? Are there any collaborative problems?

Nursing diagnoses:

Priority Nursing Diagnosis:

• Acute pain related to distention of the pancreas and peritoneal irritation

Collaborative Problems:

• Deficient fluid volume related to nausea, vomiting, NG suction, and

restricted oral intake
• Impaired oral mucous membrane related to NG tube and NPO status
• Imbalanced nutrition: less than body requirements related to dietary restrictions,
nausea and vomiting, and impaired digestion Collaborative problems: Potential
complications: hypovolemia and shock, hypocalcemia, hyperglycemia, fluid, and
electrolyte imbalance