Gi Pathophysiology Lecture 3: Acute And Chronic Pancreatitis

Front 1

Acute Pancreatitis

Definition.

Back 1

a sudden, generally reversible, inflammatory process of the pancreas, with variable involvement of other regional tissues or remote organ systems. Episodes are classified as severe if there is associated organ failure or local complications, such as necrosis, abscess, or pseudocyst, or as mild if there is minimal organ dysfunction and an uneventful recovery.

Front 2

Acute Pancreatitis
Epidemiology.
Maximum Incidence for Men:
For women:

Back 2

or men, the maximum incidence is between the third and fifth decade, and for women, in the fifth and sixth decades.

Front 3

Acute Pancreatitis
Etiology.
In adults living in Western countries, the two most common causes of acute pancreatitis are

Back 3

alcohol abuse and gallstone disease

Front 4

Acute Pancreatitis
Etiology.
Trauma and congenital anomalies, are important etiological factors in

Back 4

children (minor role in adults)

Front 5

Early Changes in Pancreatitis.
About 95% of patients have a common pattern of tissue damage. Early stages are characterized by:

Back 5

1. Confluent peripancreatic fat necrosis extending along interstitial septa between lobules.

2. Interstitial edema develops in the gland.

3. Acinar cells abutting the fat necrosis appear flattened, depleted of zymogen granules, and lose lumenal microvilli.

4. Autophagic vacuoles form. These vacuoles contain various cell elements, including zymogen granules and lysosomes.

This process may progress to coagulation necrosis of the parenchyma and the surrounding fatty tissue.

Front 6

Environmental Causes of Pancreatitis

Back 6

Definite:
- Methanol
- Ethylene Glycol
- Organophosphorus Insecticides
- Scorpion Toxins

Probable:
- Pentachlorophenol
- Trichloroethylene

Front 7

Early Changes in Pancreatitis
2 less common necrosis patterns:

Back 7

1. Disseminated ductal and periductal necrosis with little or no fat necrosis.

2. Scattered acinar cell necrosis with an acute inflammatory infiltrate but no fat or ductal necrosis. This pattern indicates infection.

Front 8

Late Changes in Pancreatitis
pseudocyst

Back 8

Larger areas of peripancreatic fat necrosis (2-5cm) are demarcated by macrophages, generally resolve slowly, and may be replaced with fibrotic tissue. The larger necrotic areas (>5cm) may resolve spontaneously, but some persist. In those that do not resolve, granulation tissue replaces the lining macrophages within 10-20 days. The granulation tissue forms a fibrotic capsule that thickens into a grossly visible wall by 20-30 days. This structure is called a pseudocyst

Front 9

Pathogenesis of Acute Pancreatitis
4 Mechanisms:

Back 9

1. Obstruction
2. Bile Reflux
3. Ischemia
4. Premature Zymogen Activation

Front 10

Pathogenesis of Acute Pancreatitis
1. Obstruction (describe mechanism)

Back 10

Obstruction of the pancreatic duct prevents the flow of pancreatic juice leading to pancreatic hypersecretion and ductal hypertension. Small ductules rupture, secretions extravasate into the parenchyma, and the digestive enzymes are activated.

Front 11

Pathogenesis of Acute Pancreatitis
2. Bile Reflux (Mechanism)

Back 11

Impacted gallstones allow bile to reflux into the pancreatic duct where the bile damages the duct and causes the release and activation of pancreatic enzymes.

Front 12

Pathogenesis of Acute Pancreatitis
3. Ischemia (Mechanism)

Back 12

Vasoconstriction and/or thrombosis of vessels around the pancreas causes ischemia to the organ, thus exacerbating pancreatitis. In the 1960s, animal experiments showed that injection of microspheres of sufficiently small size into arteries feeding the pancreas caused pancreatitis. Alterations to the so-called pancreatic microcirculation may be a primary event or secondary to leakage of enzymes.

Front 13

Pathogenesis of Acute Pancreatitis
4. Premature Zymogen Activation

Back 13

Activation of the pancreatic digestive enzymes in the acinar cells or in the pancreatic duct leads to pancreatitis

Front 14

3 mechanisms for premature zymogen activation are commonly discussed:

Back 14

1. Reflux of the duodenal contents
2. Following trauma
3. Premature activation of digestive proenzymes if intracellular transport and secretion of zymogens and lysosomes is disturbed

Front 15

Describe the mechanism and steps leading to premature activation of digestive proenzymes

Back 15

Normally, digestive and lysosomal enzymes are sorted and packaged separately and maintained in those compartments in the healthy acinar cell. In several animal models of acute pancreatitis, an early event is the formation of large autophagic vacuoles where lysosomal enzymes are mixed with digestive enzymes, resulting in activation of trypsinogen and other proenzymes. These observations suggest a plausible mechanism of acute pancreatitis in a variety of etiologies, including drugs, toxins, metabolic factors, and trauma.

Front 16

Acute Pancreatitis
Common Presentation:

Back 16

- steady dull or boring pain in the epigastrium or left upper quadrant.

- pain takes 15-60 minutes to reach peak intensity and may radiate to the back, other locations in the abdomen, or to the chest wall

- supine position and eating are common aggravating factors

- Sitting forward classically relieves the pain.

Front 17

Symptoms of Acute Pancreatitis

Back 17

Abdominal pain

Anorexia

Nausea

Vomiting

Coma (rare)

Dyspnea (rare)

Front 18

Signs of Acute Pancreatitis
*none of these are specific for pancreatitis

Back 18

Epigastric tenderness
Pleural effusion
Abdominal wall rigidity
Ascites
Rebound tenderness
Oliguria, anuria
Abdominal distension
Respiratory distress
Hypotension
Gray-Turner sign
Ileus (a disruption of the normal propulsive GI motor activity from non-mechanical mechanisms)
Cullen’s sign
Fever

Front 19

Acute Pancreatitis
Diagnosis by:

Back 19

Serum Markers:
- Amylase
- Lipase
Imaging Studies
- CT Scans
- Endoscopic Retrograde Cholangiopancreatography (ECRP)

Front 20

Acute Pancreatitis
Diagnosis
Serum Amylase: Positives

Back 20

- widespread availability, simple assay, and low cost
- Serum levels rise 2 to 12 hours after the onset of symptoms and remain elevated for 3-5 days.

Front 21

Acute Pancreatitis
Diagnosis
Serum Amylase: Negatives

Back 21

- magnitude of the rise does not correlate with the severity of disease and has no prognostic value

- In patients who present several days after symptoms start, serum amylase may be normal.

- Other organs, for example the salivary glands, stomach and small intestine, secrete amylase, and diseases affecting those organs can lead to hyperamylasemia.

- Often, alcoholics have elevated salivary amylase.

- Other intraabdominal diseases, such as perforated duodenal ulcers, mesenteric infarction, and renal disease, can cause a rise in pancreatic amylase.

Front 22

Acute Pancreatitis
Diagnosis
Lipase: Positives

Back 22

1. Serum lipase levels appear within hours after symptoms begin and peak by 2-4 days. The levels may remain elevated for 14 days after the onset of symptoms.

2. Pancreatic lipase is more specific for pancreatic inflammation, but lipase can also originate from the stomach.

- Thus, as with amylase, an elevated serum lipase alone is not sufficient to make a diagnosis of acute pancreatitis. The same nonpancreatic diseases that cause a rise in pancreatic amylase cause an increase in pancreatic lipase as well.

Front 23

Acute Pancreatitis
Imaging Studies.
CT scans

Back 23

Single Most Useful test = ULTRASOUND (LECTURE = EXAM); early presentation CT won't tell you much you don't already know from history/clinical signs

Show signs of acute inflammation, such as enlargement of the pancreas or peripancreatic inflammatory changes and fluid collections, and can confirm the diagnosis of acute pancreatitis.

- Additionally, these studies can identify gallstone disease and ultrasound can identify biliary sludge that may produce microlithiasis.

- MRI yields no more information that CT scanning and it has long scan times and higher cost, that precludes its routine use.

Front 24

Acute Pancreatitis
Imaging Studies.
Endoscopic retrograde cholangiopancreatography (ERCP)

Back 24

useful to define the cause of idopathic pancreatitis once the episode has resolved. Biliary stones, periampullary tumors, microlithiasis, and anomalies of the ductal system or biliary tree can be identified by this imaging technique
(Used less for diagnostic purposes and more for therapeutic purposes now)

Front 25

Acute Pancreatitis
The Therapy.

Back 25

The mainstay of treatment for acute pancreatitis is supportive care and close observation for subsequent development of complications. Generally, treatment is:

1. Hospitalization.

2. Aggressive intravenous fluid (most important in first 24-48 hours) and electrolyte repletion.

3. Discontinuing oral intake (NPO).

4. Antiemetics and narcotic analgesics.

5. The routine use of nasogastric decompression in patients with protracted vomiting or ileus.

6. Antibiotics for pancreatic necrosis.

7. Urgent ERCP in cases of severe acute pancreatitis caused by gallstones and resulting in cholangitis with hemodynamic instability.

8. In severe acute pancreatitis requiring intubation and ICU admission, enteral feeding via an endoscopically-placed jejunal feeding tube has been shown to improve some clinical outcomes.

Front 26

Hereditary Pancreatitis (Lecture)

Back 26

- Early Onset
- Frequent Calcification
- Increased pancreatic Cancer association
- Mutations in cationic trypsinogen
- Autosomal Dominant
- Incomplete penetrance

Front 27

Acute Pancreatitis (Lecture)
Key Differential Diagnosis

Back 27

- Penetrating Duodenal Ulcer
- Penetrating Gastric Ulcer
- Gastric Outlet obstruction
- Intestinal Ischemia
- Rupture AAA
- Ruptured ectopic pregnancy

Front 28

Acute Pancreatitis
Goal of Fluid Therapy:

Back 28

30cc/hour

Goal: Basal IVF = 35cc/kg/day + 3rd space losses

(Admission HCT - Baseline HCT) / Baseline HCT x 1/3 (weight in kg) = Fluid Deficit*

* replenished over IV over 3-4 hours

Front 29

Acute Pancreatitis
Complications
(Local)

Back 29

1. Phlegmon
2. Necrosis
3. Abscess
4. Pancreatic ascites
5. Pseudocyst:
6. Gastrointestinal Hemorrhage:
7. Spreading to Adjacent organs

Front 30

Acute Pancreatitis
Complications
(Local)
1. Phlegmon

Back 30

A mass of inflamed pancreas and peripancreatic tissue resulting from the action of activated digestive enzymes and microvascular hypoperfusion.

Front 31

Acute Pancreatitis
Complications
(Local)
2. Necrosis:

Back 31

A localized area in the pancreas where pancreatic parenchyma and intralobular fatty tissue are destroyed.

Front 32

Acute Pancreatitis
Complications
(Local)
3. Abscess:

Back 32

Infected pancreatic or peripancreatic necrosis that has suppurated.

Front 33

Acute Pancreatitis
Complications
(Local)
4. Pancreatic ascites:

Back 33

Chemical peritonitis caused by pancreatic juice entering the peritoneal cavity results in fluid secretion into the peritoneum.

Front 34

Acute Pancreatitis
Complications
(Local)
5. Pseudocyst:

Back 34

The fluid in the _________ may be sterile, infected, or hemorrhagic. If the _______ is large enough, it may obstruct the stomach, the duodenum, or the biliary tree.

Front 35

Acute Pancreatitis
Complications
(Local)
6. Gastrointestinal Hemorrhage:

Back 35

Several mechanisms may cause upper GI bleeding. The Inflammation may extend to the duodenal or gastric mucosa and cause erosions or ulcers. Splenic vein obstruction, either by mass effect or thrombosis, can cause gastric varices, which may bleed even after the pancreatitis has resolved. Rupture of pancreatic vessels or erosion into the splenic artery or other contiguous vessels can produce hemorrhage, occasionally through the pancreatic duct and into the duodenum. Aneurysms of the splenic artery or other vessels can occur.

Front 36

Acute Pancreatitis
Complications
(Local)
7. Adjacent organs:

Back 36

Spreading peripancreatic necrosis and infection can involve the duodenum, small bowel, transverse colon, and spleen to produce necrosis and perforation of hollow viscus and infarction of solid organs.

Front 37

Acute Pancreatitis
Complications
(Systemic Complications)

Back 37

Acute Renal Failure***
Respiratory Failure***
Shock**
Coagulopathy
Hypocalcemia
Hyperglycemia
Subcutaneous Nodules

Front 38

Acute Pancreatitis
Complications
(Systemic)
1. Shock

Acute pancreatitis is frequently associated with intravascular hypovolemia and hypotension. Several factors contribute:

Back 38

a. Sequestration of retroperitoneal fluid or hemorrhage.

b. A diffuse capillary leak occurs in areas distant from the pancreas. The mechanism is not established but is probably multi-factorial. Hypoalbuminemia and vasoactive agents released into the circulation from the inflamed pancreas and from activated leukocytes have been implicated.

c. There is an inadequate cardiac response to diminished peripheral resistance that may be due to vasoactive agents like kinins or to, as yet unidentified, myocardial depressant factors.

Front 39

Acute Pancreatitis
Complications
(Systemic)
2. Coagulopathy:

Back 39

This manifestation is thought to result from the action of pancreatic and leukocyte proteases on components of the clotting cascade.

Front 40

Acute Pancreatitis
Complications
(Systemic)
3. Hypocalcemia:

Back 40

The serum calcium may be low enough to produce tetany. For the most part, the hypocalcemia is merely a reflection of hypoalbuminemia and serum ionized calcium will be normal. Occasionally, the ionized calcium will be low for reasons that are unclear. Several mechanisms have been proposed, including the loss of calcium in soaps with fatty acids in areas of fat necrosis, inadequate PTH release, decreased peripheral tissue response to PTH, and enhanced release of thyrocalcitonin. Most evidence suggests that decreased end-organ responsiveness to PTH and decreased PTH production may be the predominate mechanisms for hypocalcemia.

Front 41

Acute Pancreatitis
Complications
(Systemic)
4. Hyperglycemia:

Back 41

Tissue damage destroys pancreatic islets leading to decreased insulin production.

Front 42

Acute Pancreatitis
Complications
(Systemic)
5. Subcutaneous nodules:

Back 42

The nodules represent regions of distant fatty necrosis presumably by the action of pancreatic lipases.

Front 43

Acute Pancreatitis
Complications
(Systemic)
6. Acute renal failure:

Back 43

Acute tubular necrosis is generally secondary to shock, but a role for pancreatic enzymes or other substances from the inflamed pancreas and activated leukocytes has been postulated.

Front 44

Acute Pancreatitis
Complications
(Systemic)
7. Respiratory failure

Back 44

a. Pleural effusions are attributed to the passage of peripancreatic fluid through the diaphragmatic lymphatic.

b. Atelectasis may result from the abdominal distension, pain, and elevation of the diaphragm by retroperitoneal fluid.

c. Adult respiratory distress syndrome (ARDS) is a prominent cause of mortality. Hypotension probably plays a role in the development of ARDS. Products of activated neutrophils may mediate lung injury in acute pancreatitis. The contribution of pancreatic enzymes in the development of ARDS is not established, but phospholipase A2 can digest the major components of lung surfactant and produces ARDS when introduced into the lungs of experimental animals and elastase may damage pulmonary vessels and increase vascular leaks.

Front 45

Acute Pancreatitis
The Prognosis

Back 45

The most important factors shown to portend a poor prognosis are age > 50, obesity (BMI>30), and hemoconcentration (admission hematocrit > 44-47)

We often use the Ranson's Criteria or the Modified Glasgow Criteria to determine prognosis

Front 46

Chronic Pancreatitis
Definition.

Back 46

an irreversible, irregular scarring of the glandular parenchyma caused by ongoing inflammation. If progressive, it leads to the loss of pancreatic exocrine and endocrine function.

Front 47

Chronic Pancreatitis
Epidemiology.

Back 47

4/100,000
Affects predominantly men between 25 and 50 years of age
In tropical countries, ________ pancreatitis is a disease of youth often starting in the first decade of life.

Front 48

Chronic Pancreatitis
Etiology.

Back 48

in Western countries, alcohol abuse is associated with the majority of cases.

Front 49

Chronic Pancreatitis
Pathology.

Macroscopic:

Back 49

1. In early disease, the gland is unevenly enlarged and indurated. The cut surface shows areas of coarse lobulation or nodular scarring and there are often pseudocysts or foci of recent necrosis.

2. In advanced disease, the pancreas is hard and irregular. The cut surface is gray, with loss of lobulation. The ducts are dilated and distorted. Calculi and pseudocysts are commonly present.

Front 50

Chronic Pancreatitis
Pathology.

Microscopic:

Back 50

1. Interlobular fibrosis is prominent early in the disease. Inflammatory cells are present along with perilobular fibrosis. The cells in the lobules are well preserved.

2. In advanced disease the fibrosis is widespread and pronounced, still, some areas are relatively normal. The ducts are distorted and plugs are found in the lumen. The intralobular fibrosis produces a disorderly arrangement of the lobules and islets. Cell debris is common and lymphocytes are scant. The acinar cells are atrophic.

Front 51

Chronic Pancreatitis
Pathophysiology.

Back 51

1. The obstruction theory (most common = pancreatic tumor)
2. The toxic-metabolic hypothesis
3. The oxidative stress hypothesis
4. The recurrent acute pancreatitis hypothesis

Front 52

Chronic Pancreatitis
Pathophysiology.
1. The obstruction theory

Back 52

most widely accepted. The tenets of this theory are:

a. Alcohol or another etiological factor disturbs acinar and ductal cell functions altering the composition of the pancreatic secretions, promoting diffusion of active enzymes into the interstitial space, and enhancing diffusion of calcium into the ducts.
b. The calcium and protein precipitate in the alkaline duct environment forming the ductal plugs observed in alcohol related chronic pancreatitis.
c. Duct obstruction causes periductal inflammation and fibrosis.

Front 53

Chronic Pancreatitis
Pathophysiology.
2. The toxic-metabolic hypothesis

Back 53

simply states that the toxic effects of alcohol induce progressive intrapancreatic lipid deposition, fibrosis, and atrophy. The secretory changes are considered to be secondary to the morphological changes rather than their cause.

Front 54

Chronic Pancreatitis
Pathophysiology.
3. The oxidative stress hypothesis

Back 54

states that the tissue damage in chronic pancreatitis is the result of excess free radicals from increased cytochrome P450 activities of the pancreas and liver and disturbed hepatic detoxification.

Front 55

Chronic Pancreatitis
Pathophysiology.
4. The recurrent acute pancreatitis hypothesis

Back 55

holds that chronic pancreatitis result from repetitive episodes on acute pancreatitis.

Front 56

Chronic Pancreatitis
Pathophysiology

A gene may predispose to chronic pancreatitis.

Back 56

Some patients with idiopathic acute relapsing pancreatitis have abnormal sweat tests

Exocrine pancreas is affected in CF

Ductal obstruction is seen in both CP and CF

Though most people with CFTR mutations do not have pancreatitis,
people with pancreatitis show significantly increased chances of carrying a CFTR mutation

The physiological mechanism is not known. Hypotheses center on decreased flow in the pancreatic ducts leading to bile duct obstruction and recurrent episodes of acute pancreatitis. Over time fibrosis and the manifestations of chronic pancreatitis result.

Front 57

Chronic Pancreatitis
The Presentation.

Back 57

The most common symptom of _____ pancreatitis is abdominal pain.
Weight loss, malabsorption with steatorrhea, upper GI bleeding, and symptoms of diabetes mellitus can also lead to the diagnosis

Front 58

Chronic Pancreatitis
The Diagnosis
Serum markers:

Back 58

Serum amylase and lipase are not helpful because as acini are destroyed and replaced by fibrosis, less amylase and lipase is produced and leaked into the circulation. Other pancreatic enzymes such as trypsin and Trypsinogen may be low in some patients but this finding is neither specific nor sensitive.

Front 59

Chronic Pancreatitis
Imaging studies:

Back 59

1. Plain radiographs often reveal diffuse or focal pancreatic calcifications.

2. Ultrasonography and CT may show irregularity of the gland, dilation of the pancreatic duct and calcifications.

3. ERCP and transhepatic cholangiography show a dilated pancreatic duct, with intermittent points of obstructions, a "chain of lakes" appearance. Strictures, cysts, and ductal calculi can be seen. Often, these studies can distinguish pancreatic cancer from chronic pancreatitis.

Front 60

Chronic Pancreatitis
Name 3 tests for Exocrine Pancreatic Function:

Back 60

1. The bentiromide (chymes) test
2. Exogenous stimulation of pancreatic secretion
3. The 72-hour fecal fat collection

Front 61

Chronic Pancreatitis
Pathophysiology.

Back 61

1. The obstruction theory (most common = pancreatic tumor)
2. The toxic-metabolic hypothesis
3. The oxidative stress hypothesis
4. The recurrent acute pancreatitis hypothesis

Front 62

Chronic Pancreatitis
Pathophysiology.
1. The obstruction theory

Back 62

most widely accepted. The tenets of this theory are:

a. Alcohol or another etiological factor disturbs acinar and ductal cell functions altering the composition of the pancreatic secretions, promoting diffusion of active enzymes into the interstitial space, and enhancing diffusion of calcium into the ducts.
b. The calcium and protein precipitate in the alkaline duct environment forming the ductal plugs observed in alcohol related chronic pancreatitis.
c. Duct obstruction causes periductal inflammation and fibrosis.

Front 63

Chronic Pancreatitis
Pathophysiology.
2. The toxic-metabolic hypothesis

Back 63

simply states that the toxic effects of alcohol induce progressive intrapancreatic lipid deposition, fibrosis, and atrophy. The secretory changes are considered to be secondary to the morphological changes rather than their cause.

Front 64

Chronic Pancreatitis
Pathophysiology.
3. The oxidative stress hypothesis

Back 64

states that the tissue damage in chronic pancreatitis is the result of excess free radicals from increased cytochrome P450 activities of the pancreas and liver and disturbed hepatic detoxification.

Front 65

Chronic Pancreatitis
Pathophysiology.
4. The recurrent acute pancreatitis hypothesis

Back 65

holds that chronic pancreatitis result from repetitive episodes on acute pancreatitis.

Front 66

Chronic Pancreatitis
Pathophysiology

A gene may predispose to chronic pancreatitis.

Back 66

Some patients with idiopathic acute relapsing pancreatitis have abnormal sweat tests

Exocrine pancreas is affected in CF

Ductal obstruction is seen in both CP and CF

Though most people with CFTR mutations do not have pancreatitis,
people with pancreatitis show significantly increased chances of carrying a CFTR mutation

The physiological mechanism is not known. Hypotheses center on decreased flow in the pancreatic ducts leading to bile duct obstruction and recurrent episodes of acute pancreatitis. Over time fibrosis and the manifestations of chronic pancreatitis result.

Front 67

Chronic Pancreatitis
The Presentation.

Back 67

The most common symptom of _____ pancreatitis is abdominal pain.
Weight loss, malabsorption with steatorrhea, upper GI bleeding, and symptoms of diabetes mellitus can also lead to the diagnosis

Front 68

Chronic Pancreatitis
The Diagnosis
Serum markers:

Back 68

- Serum amylase and lipase are not helpful because as acini are destroyed and replaced by fibrosis, less amylase and lipase is produced and leaked into the circulation.

- Other pancreatic enzymes such as trypsin and Trypsinogen may be low in some patients but this finding is neither specific nor sensitive.

Front 69

Chronic Pancreatitis
Imaging studies:

Back 69

1. Plain radiographs
2. Ultrasonography and CT
3. ERCP and transhepatic cholangiography

Front 70

Chronic Pancreatitis
Plain Radiograph Finding

Back 70

often reveal diffuse or focal pancreatic calcifications.

Front 71

Chronic Pancreatitis
Ultrasonography and CT Finding

Back 71

may show irregularity of the gland, dilation of the pancreatic duct and calcifications.

Front 72

Chronic Pancreatitis
ERCP and transhepatic cholangiography Finding

Back 72

show a dilated pancreatic duct, with intermittent points of obstructions, a "chain of lakes" appearance. Strictures, cysts, and ductal calculi can be seen. Often, these studies can distinguish pancreatic cancer from chronic pancreatitis.

Front 73

Chronic Pancreatitis
Exocrine pancreatic function:
1. The bentiromide (chymes) test

Back 73

is a screening test for exocrine pancreatic insufficiency. A synthetic peptide linked to paraaminobenzoic acid (PABA) is given orally. PABA is cleaved from the peptide by chymotrypsin and the liberated PABA is absorbed and excreted by the kidney. PABA is easily measured in the urine. If greater than 50% of the administered dose is present in a 5-hour urine collection, then pancreatic insufficiency is unlikely.

Front 74

Chronic Pancreatitis
Exocrine pancreatic function:
2. Exogenous stimulation of pancreatic secretion with secretin or secretin plus CCK

Back 74

is the most reliable test for pancreatic exocrine insufficiency, but is invasive requiring intubation of the duodenum to collect secretions. Once the nasoduodenal tube or endoscope is in position, the secretogogues are given IV and the secretions collected in timed aliquots. The volume and bicarbonate concentration are measured and the values compared to normal control values. The concentration of various digestive enzymes can be determined, but does not improve the accuracy of the test. False positive results are seen in celiac disease, diabetes mellitus, Billroth II gastrectomy, cirrhosis, and a variety of biliary disorders.

Front 75

Chronic Pancreatitis
Exocrine pancreatic function:
3. The 72-hour fecal fat collection

Back 75

can determine if fat malabsorption is present. Stool specimens are collected for 72 hours while the patient is on a defined diet, in adults, or a diary of meals is kept, in children. Normal individuals excreted about 5-7% of dietary fat in the stools. If the secretion of pancreatic lipase is less than 10% of normal then larger percentages of dietary fat appear in the stools. This test is not specific for pancreatic insufficiency and fat malabsorption form other causes affects the results as well.

Front 76

Chronic Pancreatitis
Complications

Back 76

-Pain
-Acidic lumen and malabsorption
-Common Bile Duct Obstruction
-Duodenal Obstruction
-Splenic Vein Thrombosis
- Pancreatic Ascites
- Pseudocyst
- Pleural Effusion
- Diabetes Mellitus
- Pancreatic Cancer

Some complications require surgical therapy.

Front 77

Chronic Pancreatitis
Therapy and Complications
Pain:

Back 77

is the most common symptom requiring treatment.

a. Nonnarcotic analgesics should be tried first. Narcotic analgesics if necessary

b. Modify Neural Transmission: destruction of the celiac plexus by percutaneous or endoscopic alcohol or steroid block are helpful in some patients.

c. Decreasing pancreatic secretions by administering pancreatic enzyme supplements or drugs

d. Relieve obstruction
1. ERCP
2. Surgery

e. Discontinue Alcohol

Front 78

Chronic Pancreatitis
Therapy and Complications
2. Malabsorption

Back 78

requires specific medical treatment only after steatorrhea is documented.

a. Pancreatic enzyme replacement therapy is the cornerstone of treatment

b. H2-receptor antagonists or proton pump inhibitors are important adjunctive therapy to the enzyme replacement.

Front 79

Chronic Pancreatitis
Therapy and Complications
3. Nutritional support,

Back 79

in addition to enzyme replacement, is often necessary in debilitated patients and those with complications that affect nutrition. Parenteral nutrition or enteral tube feedings may be required. Supplementation with fat-soluble vitamins and vitamin B12 needs to be considered. Also, supplementation with medium chain triglycerides, which are absorbed without prior digestion, can be useful.

Front 80

Chronic Pancreatitis
Therapy and Complications
Pancreatic Cancer

Back 80

8. The incidence of pancreatic cancer is about 5% overall, but is 30% in patients with hereditary pancreatitis.