CNUR823 - Module 4 PDF

CNUR823, Module 4 - Acute pancreatitis 2014-03-27, 11:35 AM
Introduction
Acute pancreatitis is inflammation of the pancreas. This condition is rising in incidence (Skipworth & Periera, 2008)
with a yearly incidence of about 40 cases per year per 100,000 adults (Gardner, 2011). The increase in acute
pancreatitis may be due to the increase of biliary pancreatitis and obesity (van Woerkom & Adler, 2012). Mortality as
a result of complications is approximately 8% (van Woerkom & Adler, 2012).
Learning Objectives
1. Describe the anatomic location of the pancreas relative to the other organs in the upper portion of the
abdominal cavity.
2. Describe the functional anatomy of the duct system that conveys bile from the liver and digestive juice from
the pancreas to the lumen of the duodenum.
3. Briefly outline the endocrine and exocrine functions of the pancreas.
4. Describe the hormonal control of the secretion of bile and pancreatic juice during the digestive process.
5. Explain why proteases are secreted in an inactive state and describe the means by which proteases are
activated in the stomach and small intestine.
6. What is pancreatitis and what is the basic mechanism that underlies the condition?
7. List the most common causes of pancreatitis.
8. List the symptoms, signs, and laboratory fi ndings associated with pancreatitis, and state which of these
George presents with.
9. Explain what is meant by the phenomenon of referred pain. Is this phenomenon often seen in patients with
https://de.ryerson.ca/de_courses/templates/default/?c=9E82757E9A1C12CB710AD680DB11F6F1 Page 1 of 20
acute pancreatitis?
10. Describe the treatment of the condition and its prognosis.
Definition
Pancreatitis is an inflammatory process in which pancreatic enzymes autodigest the gland. Generally, the pancreas
heals without loss of function or any structural in acute pancreatitis; however, pancreatitis can remit sporadically.
Reocccurence of acute pancreatitis can result in functional and structure deterioration of the pancreas (Gardner,
2011).
Pancreas Anatomy and Functions (Hall, 2010)
The pancreas, located behind greater curvature of the stomach, is divided into the head, body, and tail. The body
lies posterior to the stomach. The head of the pancreas sits in the concave part of the duodenum and the tail
connects to the duodenum through the sphincter of Oddi. The release of bile and pancreatic juice from the pancreas
is regulated by the sphincter of Oddi, which opens in the presence of food in the duodenum.
The body and neck (the narrow part between the head and the body) drain into the splenic vein while the head
drains into the superior mesenteric and portal veins. Lymph drains by way of the splenic, celiac, and superior
mesenteric lymph nodes.
The pancreas (and the stomach) is innervated by the vagus nerve which is stimulated in anticipation of a meal.
The pancreas has both exocrine functions (acinar cells) that aid in the digestive process, and endocrine functions
(islets of Langerhans) which regulate carbohydrate metabolism.
Anatomy of the Pancreas
Original Reference: http://www.clevelandclinicmeded.com
The exocrine functions of the pancreas are primarily with the digestive system. Pancreatic secretions consist of
digestive enzymes, water, salt, and bicarbonate, which are released into the duodenum in the presence of food. One
to two liters of pancreatic juices is secreted each day.
Enzymes aid in the digestion of food and buffer the acidic stomach contents. Enzymes are produced and stored in
their inactive forms as proenzymes or zymogens where they are stored in secretory vesicles with protease
inhibitors. Zymogens granules are acidic and have a low calcium concentration. These factors prevent premature
activation until after secretion has occurred and extracellular factors have triggered the activation cascade. They
become activated in the duodenum by brush border enzymes (enterokinase) (Gardner, 2012).
Enzymes Released From the Pancreas

Source: B. Swart
Islets of Langerhans
Source: science.howstuffworks.com
The endocrine functions of the pancreas are concerned with the metabolism of carbohydrates through the
production of hormones produced by cells in the islets of Langerhans (make up approximately 1% which are
situated close to blood vessels; the hormones are secreted directly into the bloodstream.
Endocrine Functions of the Pancreas

Source: B. Swart
Pathophysiology
Pancreatitis is the inflammation of the pancreas and involves autodigestion. Pancreatitis is classified into two types:
acute and chronic. Acute pancreatitis is characterized by acute inflammation with return to normal functioning when
inflammation subsides. Chronic pancreatitis is characterized by recurrence of inflammation resulting in progressive,
irreversible scarring of pancreatic tissue and gradual fibrous replacement of the normal functional tissue.
Depending on the degree of destruction, pancreatitis may result in loss of both endocrine and exocrine functions.
Pancreatic injury allows enzymes to come into contact with pancreatic tissue, causing tissue breakdown, vascular
damage, edema, hemorrhage, and necrosis. The initiating event may be anything that injures the acinar cell and
impairs the secretion of zymogen granules. For example, if a gallstone blocks the secretary duct in the pancreas,
accidental activation of zymogens can result in acute pancreatitis. However, the precise triggering mechanism that
initiates enzyme activation is unknown (Sah, Garg, & Saluja, 2012).
The current thinking is that inflammatory response of acute pancreatitis develops independently, driven by early
activation of inflammatory pathways (Sah, Garg, & Saluja, 2012). Cytokines drive the inflammatory response
(Papachristou, Clermont, Sharma, Yadav, & Whitcomb, 2007). Activated neutrophils release toxic enzymes
(cytokines interleukin (IL)-1, IL-6, and IL-8) into the bloodstream that may damage blood vessels and vital organs.
Macrophages release cytokines (tumor necrosis factor-alpha (TNF-α) that further mediate local (and, in severe
cases, systemic) inflammatory responses. Activation of endothelial cells allows leukocyte extravasation of
leukocytes and the release of additional enzymes (Frossard, Steer, & Pastor, 2008). Hypoxia results in the release
of oxygen free radicals which also contribute to the injury (Frossard, Steer, & Pastor, 2008).
These mediators of inflammation cause increased pancreatic vascular permeability, leading to hemorrhage, edema,
and eventually pancreatic necrosis (Gardner, 2011). With mediator release systemically, complications such as
bacteremia, acute respiratory distress syndrome (ARDS), pleural effusions, gastrointestinal (GI) hemorrhage, and
acute kidney injury (Gardner).
The systemic inflammatory response syndrome (SIRS) can also develop resulting in hypovolemia and shock
(Anderson, Swärd, Tingstedt, & Äkerberg, 2009). A hyperinflammatory state may result in multiple organ dysfunction
(MODS) (Anderson et al).
Local complications include pseudocysts (see http://emedicalppt.blogspot.ca/2011/04/pancreatic-pseudocyst.html
for an image) and pancreatic abscesses (see http://drbobmccool.wordpress.com/2011/10/12/pancreatitis/ for an
image) (Frossard, Steer, & Pastor, 2008).
Acute Pancreatitis
Source: Family Medicine Help
Hemorrhagic Pancreas
Source: Pathguy.com
Etiology
There are many causes that are linked to the development of pancreatitis, primarily alcohol use and biliary disease
(Lindberg, 2009).
Alcohol use over years results in intracellular accumulation of digestive enzymes and their premature activation and
release (Gardiner, 2011). Consistent alcohol use results in increased permeability of ductules which permits enzyme
damage to the parenchyma (Gardiner, 2011). Alcohol also increases the protein content of pancreatic juice and
decreases bicarbonate levels and trypsinogen concentrations. This leads to the formation of protein plugs that block
pancreatic outflow (Gardiner, 2011).
Gallstones up to 5 mm in size may obstruct the common bile duct or the pancreatic duct or both increasing pressure
in the ducts leading to activation of digestive enzymes precipitating pancreatitis (Frossard, Steer, & Pastor, 2008).
Other less common conditions associated with pancreatitis include abdominal or surgical trauma to the pancreas,
family history, obstruction of the gland by neoplastic growth, hyperlipidemia, hypercalcemia, drug effects
(intravenous tetracyclines, glucocorticoids, sulfonamides, chlorothiazide, azathioprine, propofol, and didanosine), a
variety of infectious diseases, and other chronic diseases of the gastrointestinal tract (Frossard, Steer, & Pastor,
2008).
Clinical Manifestations
Acute pancreatitis is a clinical syndrome characterized by sudden onset of sharp, twisting, deep upper abdominal
pain with radiation to the back (Brenner & Krenzer, 2010), fever, abdominal tenderness, jaundice, nausea and
vomiting (Greer & Burchand, 2009). People with pancreatitis often have rebound tenderness, hypoactive or absent
bowel sounds, hypotension, tachycardia (related to fluid sequestration), decreased breath sounds (due to pleural
effusions), abdominal distention, ascites, and steatorrhea ((Greer & Burchand, 2009).
The pain associated with acute pancreatitis results from distention of the pancreatic tissue, ductal spasm, from
obstruction of the biliary tree or duodenum, peritoneal irritation by enzyme release into the peritoneum, and/or the
accumulation of inflammatory exudate in the retroperitoneal space or pancreatic autodigestion stimulated by
increased enzyme secretion when eating.
The pain has been described as visceral, deep, and gnawing. Though typically located in the upper abdomen to the
left of the midline, this pain frequently radiates to the back and, in some people, to the lower abdomen.
Jaundice is caused by common bile duct obstruction by pancreatic edema and is usually present in patients with
biliary tree obstruction and is often a clue to early sepsis.
Nausea and vomiting exacerbate the inflammatory process by increasing ductal pressure and reflux into the
pancreatic duct.
Fever reflects entry of the tissue breakdown products into the circulation. The pancreas is not an encapsulated
organ; therefore, the inflammatory response spreads to the surrounding organs.
Acute Complications
Complications of Acute Pancreatitis

Source: B Swart (adapted from Greer & Burchand, 2009)
Serum Laboratory Diagnostics
Source: B. Swart (adapted from Bennett & Krenzer, 2010).
Source: B. Swart (content from Bennett & Krenzer, 2010)
Prognostic Indicators
Identifying patients in greatest need of aggressive medical treatment by differentiating their disease severity as mild
or severe is recommended. Numerous multifactorial clinical prognostic scoring systems are available, including the
BISAP (BUN greater than 8.93 mmol/L, impaired mental status, SIRS (more than 2 criteria), age older than 60
years, pleural effusion on CT scan) (Anand, Park, & Wu, 2012), the APACHE-II, APACHE-O (with the addition of
obesity), and the RANSON scale (Papachristou et al., 2007).
Management
Severe acute pancreatitis management involves intensive care. In general, the goals are “aggressive supportive
care, to decrease inflammation, to limit infection or superinfection, and to identify and treat complications as
appropriate” (Gardner, 2011). Surgical intervention may be indicated.
Summary
Acute pancreatitis is a significant cause of morbidity and mortality. Early and appropriate management is warranted.
References
Anand, N., Park, J. H., & Wu, B. U. (2012). Modern management of acute pancreatitis.
Gastroenterology Clinics of North America, 41(1), 1-8.
doi: 10.1016/j.gtc.2011.12.013.
Andersson, R., Swärd, A., Tingstedt, B., & Kerberg, M. (2009).Treatment of acute pancreatitis. Focus
on medical care. Drugs, 69(5), 505-514. doi: 0012-6667/09/0005-0505/$55.55/0
Bober, J., Katüchova, J, & Radoňak, J. (2012). Changes in the management of treatment in acute
pancreatitis patients. In L. Rodrigo (Ed.), Acute pancreatitis (pp. 235-258). InTech.
doi: 10.5772/27315
Brenner, Z. R. & Krenzer, M. E. (2010). Understanding pancreatitis. Nursing 2010, 40(1), 32-37.
doi: 10.1097/01.NURSE.0000365915.55641.c9
Greer, s. E. & Burchand, K. W. (2009). Acute pancreatitis and critical illness: A pancreatic tale
of hypoperfusion and inflammation. Chest, 136(5), 1413-1419.
doi: 10.1378/chest.08-2616
Frossard, J. L., Steer, M. L., & Pastor, C. M. (2008). Acute pancreatitis. Lancet, 37(9607), 143-
152. doi: 10.1016/S0140-6736(08)60107-5
Gardner, T. B. (2011). Acute pancreatitis. Retrieved from

http://emedicine.medscape.com/article/181364
Hall, R. E. (2010). Guyton and Hall Textbook of Medical Physiology (12 ed.). Toronto, ON:
Elsevier.
Lindberg, D. A. (2009). Acute pancreatitis and hyeprtriglyceridemia. Gastroenterology Nursing,
32(12), 75-82. doi: 10.1097/SGA.0b013e31819de3e0
Papachristou, G. I., Clermont, G., Sharma, A., Yadav, D., & Whitcomb, D. C. (2007). Risks and
markers of severe acute pancreatitis. Gastroenterology Clinics of North America, 6(2),
277-296. doi: 10.1016/1gtc.2007.03.003
Sah, R. P., Garg, P., Saluja, A. K. (2012).Pathogenic mechanisms of acute pancreatitis. Current
Opinion in Gastroenterology, 28(5), 507-515. doi: 10.1097/MOG.0b013e3283567f52
Van Woerkom, R. & Adler, D. G. (2012). Acute pancreatitis: Contemporary diagnosis and
management. Journal of Clinical Outcomes Management, 19(1), 13-26.
Wu, B. U. (2012). Prognosis in acute pancreatitis. Canadian Medical Association, 183(6), 673-
677. doi: 10.1503/cmaj.101433

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CNUR823, Module 4 - Acute pancreatitis 2014-03-27, 11:35 AM

Pancreas Anatomy and Functions (Hall, 2010)

Anatomy of the Pancreas

Original Reference: http://www.clevelandclinicmeded.com

Enzymes Released From the Pancreas

Endocrine Functions of the Pancreas

Source: Family Medicine Help

Complications of Acute Pancreatitis

Serum Laboratory Diagnostics

Source: B. Swart (adapted from Bennett & Krenzer, 2010).

Source: B. Swart (content from Bennett & Krenzer, 2010)

Gardner, T. B. (2011). Acute pancreatitis. Retrieved from

32(12), 75-82. doi: 10.1097/SGA.0b013e31819de3e0

677. doi: 10.1503/cmaj.101433

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