1. Camille Okelberry Danielle Quinton Toni Brown
Pancreatitis
Camille Okelberry
Danielle Quinton
Toni Brown

2. Physiology

3. Physiology of Pancreas
Endocrine function
Insulin
Glucagon
Somatostatin

4. Physiology of the Pancreas
Made up of a series of microscopic ducts that drain into larger ducts
These eventually drain into the main pancreatic duct which joins with the common bile duct and drains into the duodenum.
There is also a smaller duct that drains directly into the duodenum from the pancreas

5. Source: SMART Imagebase(

6. Physiology of the Pancreas

7. Physiology of the Pancreas
Pancreatic Juice
About 1500ml/d
Hypertonic
Bicarbonate secreted by the duct cells via secretin
Bicarb levels depend on the rate of flow from the pancreas
If flow is slow, bicarb is exchanged for Chloride ions
If flow is fast, bicarb does not have time to exchange

8. Physiology of the Pancreas
Pancreatic enzymes

9. Physiology of the Pancreas
Pancreatic enzymes
Proteolytic
Trypsin, chymotrypsin, carboxypeptidase
Stored in acinar cells
Secreted in the inactive form and activated in the small intestine
Avoiding self-digestion
Chymotrypsin activated by trypsin
Hydrolyze peptide bonds
If these are activated before reaching the duodenum PANCREATITIS

10. Physiology of the Pancreas
Pancreatic Enzymes
Pancreatic amylase
Secreted in active form
CHO digestion begins w/ salivary amylase
Can digests cooked and uncooked starch
Lipolytic enzymes
Digests fatty chyme
Secreted in inactive form
Pancreatic lipase

11. Physiology of the Pancreas
Regulation of Pancreatic secretion
Vagus nerve
Hormones
Cephalic Phase
Smooth muscle cells of the ducts and blood vessels innervated by parasympathetic vagal efferent fibers
Gastric Phase
Gastrin: secreted in response to distension of stomach
Stomach distension also causes release of pancreatic enzymes
Intestinal Phase
Responsible for most of the secretion
Response to hormones secreted by upper intestinal mucosa
Secretin, CCK
Secretin: response to low pH and stimulate the secretion of bicarbonate from the duct cells. Increases secretion of pancreatic enyzmes.
CCK: when mucosal surface is bathed in monoglycerides, FA, peptides, and AA.

13. Acute Pancreatitis

14. Pancreatitis
Acute
Chronic
Mild
Severe

15. Acute Pancreatitis Sudden inflammation of the pancreas
Can sometimes result in a systemic inflammatory response that can damage other organs or systems
Most people require a short hospital stay
1 in 10 may require longer treatment

16. Incidence and Prevalence
The incidence of acute pancreatitis that is gallstone related is 15/100,000
Non-gallstone related is 25/100,000
300,000 hospital admissions/year for treatment of acute pancreatitis
African Americans are 2 to 3 times more likely to develop pancreatitis than Caucasians

17. Etiology Alcohol Gallstones Hypertriglyceridemia Hypercalcemia
Certain medications
Genetics/gene mutations

19. Alcohol
Oxidation of ethanol to acetaldehyde activates pancreatic stellate cells without any pre-activation which leads to oxidative stress and eventually fibrosis

20. Gallstones

21. Hypertriglyceridemia
Triglycerides are carried by chylomicrons in the blood
If there is an excess amount of triglycerides, there will be an excess amount of chylomicrons
When the chylomicrons are larger than 900 mg/dL they have the ability to block capillaries in the pancreas
This can lead to ischemia, alteration of acinar cells and increased lipase release
Increased lipolysis and free fatty acids in the blood can lead to inflammation, free radicals and necrosis

22. Hypercalcemia
Increased calcium over a prolonged period of time results in destruction of defense mechanisms
This leads to the premature activation of trypsinogen and acinar cell necrosis (pancreatitis)

23. Gene mutations
One of the mutations occurs in the cystic fibrosis transmembrane conductance regulator (CFTR)
The mutation of this regulator results in the retention of zymogens in the duct
These zymogens become active and begin digesting the pancreas, leading to acute pancreatitis

24. Medications Opiates Tetracycline Steroids Furosemide Acetaminophen
Erythromycin
Rifampin
Estrogen preparations
Drug-induced pancreatitis: an update.
Trivedi CD1, Pitchumoni CS.

25. Pathophysiology Sudden intense abdominal attacks
If mild, the patient can withhold feeding for a couple of days until pain subsides
To prevent further attacks, treat the underlying cause (gallstones, alcohol, hypertriglyceridemia, etc.)
If pain comes back after a few days, it may be severe pancreatitis and require longer hospitalization

26. Signs and Symptoms Sudden Attacks
Intense epigastric pain radiating to the back
N/V
Fever
Symptoms may be aggravated after eating

27. Diagnosis Blood amylase and lipase levels CT/MRI test Ultrasound
Ranson’s Criteria
Amylase and lipase levels are 3 times the normal amount in acute pancreatitis

28. Diagnosis – Amylase and Lipase
Evaluating amylase and lipase levels is
one of the most widely used diagnostic
tests to determine pancreatitis
Amylase and lipase levels will be 3 times
higher in a patient with pancreatitis compared
to normal
- Lipase levels rise later and stay elevated for 5 to 7 days therefore are more useful in the late diagnosis of acute pancreatitis
Pagana

29. Diagnosis - CT Scan

30. Ranson’s Criteria
The criteria that classifies the severity of pancreatitis includes:
Age >55
White blood cell >16,000 m3
Blood glucose levels >200 mg
Lactic dehydrogenase >350 units/L
Aspartate transaminase >250 units/L

31. Ranson’s Criteria During the first 48 hours:
Hematocrit decrease of >10 mg/dL
Blood urea nitrogen increase of >5 mg/dL
Arterial PO2 <60 mm Hg
Base deficit >4 mEq/L
Fluid sequestration >6000 mL
Serum calcium level <8 mg/mL

32. Treatment
Medication
Surgery (for severe acute pancreatitis)

33. Treatment - Medical therapies
H2 receptor antagonist
Proton pump inhibitors
Somatostatin
Opiods (morphine)
H2 receptor antagonists stop the release of acid from parietal cells in the stomach
One study showed there was no difference between cimetidine (H2 receptor antagonist) and a placebo considering duration of pain.
Somatostatin inhibits secretion of insulin, glucagon, gastrin

34. H2 receptor antagonists and Proton Pump Inhibitors

35. Treatment - Surgery Remove the gallbladder
Remove inflamed parts of the pancreas
Remove necrotic tissue and pseudocysts
ERCP

36. Treatment - ERCP Endoscopic Retrograde Cholangiopancreatography
Special technique designed to treat complications of pancreatitis including gallstones, narrowing of the pancreatic or bile duct, leaks and pseudocysts
An endoscope is inserted into the intestine where the problem is identified and fixed
4:08 to 6:40

37. MNT Mild Acute Pancreatitis
“Pancreatic rest”
NPO – oral feeding is withheld
Fluids given intravenously
In less severe attacks, a clear liquid diet low in fat may be given for a few days until patient can tolerate more easily digested foods.
Six, smaller meals/day
Animal and human studies show that exocrine function is decreased after pancreatitis. – it shouldn’t matter whether they are fed through NG or NJ. NJ is more expensive and requires a specialist to insert.
A study compared NPO versus NGT. NGT was well tolerated in patients with mild to moderate AP. Compared to NPO, it reduces the intensity and duration of abdominal pain, need for opiates, and risk of oral food intolerance but not overall hospital stay. Early nasogastric tube feeding versus nil per os in mild to moderate acute pancreatitis: A randomized controlled trial
Maxim S. Petrova, , , 
Kerry McIlroyb, 
Lorraine Graysona, 
Anthony R.J. Phillipsa, 
John A. Windsora

38. MNT Severe Acute Pancreatitis
Severe acute pancreatitis results in a hypermetabolic, catabolic state with demands similar to sepsis
Nutrition therapy should include adequate protein
If oral nutrition can’t be initiated in 5 to 7 days, start tube feeding
Enteral nutrition is preferred method because it stimulates GIT and reduces risk of bacterial translocation
Enteral nutrition given within 48 hours reduces MODS, mortality and pancreatic complications
Standard formula is used first and if not tolerated, switched to elemental
NG tube feeding has been found to be efficacious in AP.

39. NG vs. NJ – Which is better?
NG tube will stimulate pancreatic secretion while bypassing the duodenum with an NJ tube can limit pancreatic secretion

40. Prognosis The higher the prognosis score, the poorer the outcome
Patients with mild acute pancreatitis have a low mortality rate while those with severe acute pancreatitis are more likely to have complications and therefore have a higher death rate
Mortality for mild acute pancreatitis is <1% while the death rate for severe acute pancreatitis can be 10% to 30 % depending on sterile versus infected necrosis 

41. Alcohol

42. Prevalence

43. Prevalence Prevalence of Drinking: (In 2012)
87.6 percent of people ages 18 or older reported that they drank alcohol at some point in their lifetime
71 percent reported that they drank in the past year
56.3 percent reported that they drank in the past month  
Prevalence of Binge Drinking and Heavy Drinking: (In 2012)
24.6 percent of people ages 18 or older reported that they engaged in binge drinking in the past month
7.1 percent reported that they engaged in heavy drinking in the past month

44. Drug Time Period 8th Graders 10th Graders 12th Graders
Monitoring the Future Study: Trends in Prevalence of Alcohol for 8th Graders, 10th Graders, and 12th Graders; 2014 (in percent)*
Drug
Time Period
8th Graders
10th Graders
12th Graders
Alcohol
Lifetime
26.80
[49.30]
[66.00]
Past Year
20.80
[44.00]
60.20
Past Month
9.00
[23.50]
37.40
National Survey on Drug Use and Health: Trends in Prevalence of Alcohol for Ages 12 or Older, Ages 12 to 17, Ages 18 to 25, and Ages 26 or Older; 2013 (in percent)*
Drug
Time Period
Ages 12 or Older
Ages 12 to 17
Ages 18 to 25
Ages 26 or Older
Alcohol
Lifetime
[81.50]
30.80
83.80
87.30
Past Year
66.30
[24.60]
76.80
69.60
Past Month
52.20
[11.60]
59.60
55.90

45. Prevalence: Young Adult/Teenagers
Prevalence of Drinking: 2 out of 5 15-year-olds report that they have had at least 1 drink in their lives
In 2012, about 9.3 million people ages 12–20 (24.3 percent of this age group) reported drinking alcohol in the past month (24.7 percent of males and 24 percent of females)  
Prevalence of Binge Drinking: Approximately 5.9 million people (about 15 percent) ages 12–20 were binge drinkers (16.5 percent of males and 14 percent of females)  
Prevalence of Heavy Drinking: Approximately 1.7 million people (about 4.3 percent) ages 12–20 were heavy drinkers (5.2 percent of males and 3.4 percent of females).

46. What is a drink? A standard drink equals 0.6 ounces of pure ethanol
12 ounces of beer
8 ounces of malt liquor
5 ounces of wine
or 1.5 ounces (a "shot") of 80-proof distilled spirits or liquor (e.g., gin, rum, vodka, or whiskey)

47. Drinking Terms
Moderate Drinking: Up to 1 drink per day for women and up to 2 drinks per day for men
Binge Drinking: Drinking 5 or more alcoholic drinks on the same occasion on at least 1 day in the past 30 days
Heavy Drinking: Drinking 5 or more drinks on the same occasion on each of 5 or more days in the past 30 days
Alcoholism: Alcoholism or alcohol dependence is a diagnosable disease characterized by a strong craving for alcohol, and/or continued use despite harm or personal injury
Alcohol Abuse: Alcohol abuse, which can lead to alcoholism, is a pattern of drinking that results in harm to one's health, interpersonal relationships, or ability to work

48. Metabolism CO2 and H2O Highly toxic and known carcinogen
The process of breaking alcohol down generates toxins even more harmful than alcohol itself. These by­products damage liver cells, promote inflammation, and weaken the body’s natural defenses. Eventually, these problems can disrupt the body’s metabolism and impair the function of other organs.
CO2 and H2O

49. Effects on the Body
Increases risk of cancers of the mouth, esophagus, throat, liver, breast
Interferes with the brain’s communication pathways, can change mood and behavior
Cardiomyopathy (stretching and drooping of heart muscle), arrhythmias (irregular heart beat), stroke, high blood pressure  
Causes the pancreas to produce toxic substances that can eventually lead to pancreatitis
Steatosis (fatty liver), alcoholic hepatitis, fibrosis, cirrhosis

50. Alcohol-related Mortality
Nearly 88,000 people (approximately 62,000 men and 26,000 women) die from alcohol related causes annually, making it the third leading preventable cause of death in the United States  
In 2012, alcohol-impaired-driving fatalities accounted for 10,322 deaths (31 percent of overall driving fatalities)
In 2012, 3.3 million deaths, or 5.9 percent of all global deaths (7.6 percent for men and 4 percent for women), were attributable to alcohol consumption  
Alcohol contributes to over 200 diseases and injury-related health conditions, most notably alcohol dependence, liver cirrhosis, cancers, and injuries  
Alcohol misuse is the fifth leading risk factor for premature death and disability; among people between the ages of 15 and 49, it is the first worldwide

51. Health Benefits
Decreased risk for heart disease and mortality due to heart disease
Decreased risk of ischemic stroke (in which the arteries to the brain become narrowed or blocked, resulting in reduced blood flow), and
Decreased risk of diabetes  
“In most Western countries where chronic diseases such as coronary heart disease (CHD), cancer, stroke, and diabetes are the primary causes of death, results from large epidemiological studies consistently show that alcohol reduces mortality, especially among middle-aged and older men and women—an association which is likely due to the protective effects of moderate alcohol consumption on CHD, diabetes, and ischemic stroke.”  
“It is estimated that 26,000 deaths were averted in 2005 because of reductions in heart disease, stroke, and diabetes from the benefits attributed to moderate alcohol consumption.”  
Alcohol may not benefit everyone who drinks moderately
Pg 26

52. Chronic Pancreatitis

53. Chronic inflammation of the pancreas that leads to permanent damage (necrosis)

54. Usually develops in patients between the ages of 30 and 40
people in every 100,000 will develop pancreatitis in industrialized countries
Usually develops in patients between the ages of 30 and 40
More prevalent among men than women
Numbers in parenthesis indicate approximate yearly incident rates per 100,000 persons. Arrow indicates relationship between benign and malignant disease. Recurrent AP develops predominately in patients with non-gallstone related pancreatitis, although it can develop in patients with gallstone-related pancreatitis when cholecystectomy has been delayed or refused.

55. Incidence of CP

56. Physiology Inhibits secretions of hormones like GH, TSH, CCK, insulin
Released in response to ingestion; regulates food intake

57. Causes Heavy alcohol use Elevated triglycerides Autoimmune disorders
Genetic conditions (cystic fibrosis, hereditary pancreatitis)
Blocked pancreatic duct or common bile duct
Inherited pancreatitis (2 or more immediate family members with a history of pancreatitis)

58. Signs and Symptoms Nausea Vomiting Back pain Weight loss (late stages)
Diarrhea
Oily or fatty stools (late stages)

59. Individuals with chronic pancreatitis frequently lose weight, even when their appetite and eating habits are normal

60. Diagnosis
Blood tests are NOT helpful, but sometimes test for IgG4 to assess for autoimmune pancreatitis useful
Transabdominal ultrasound
Endoscopic ultrasound
Magnetic resonance cholangiopancreatopgraphy (MRCP)
Computerized Tomography (CT)

61. Transabdominal Ultrasound
Sound waves are sent toward the pancreas via a handheld device that a technician glides over the abdomen
The sound waves bounce off the pancreas, gallbladder, liver, and other organs, and their echoes generate electrical impulses that create an image (a sonogram) on a video monitor
If gallstones are causing inflammation, the sound waves will bounce off of them, showing their location

62. Endoscopic Ultrasound
Spray a solution to numb the patient’s throat
Doctor inserts an endoscope down the throat, through the stomach, and into the small intestine
They turn on an ultrasound attachment to the endoscope, which produces sound waves to create visual images of the pancreas and bile ducts

63. Magnetic Resonance Cholangiopancreatography (MRCP)
Patient is lightly sedated and lies in a cylinder-like tube
Technician injects dye into the patient’s veins, which helps show the pancreas, gallbladder, and pancreatic and bile ducts

64. Computerized Tomography (CT)
Noninvasive radiograph (x-ray) that produces 3-dimensional images of parts of the body
The patient lies on a table that slides into a donut-shaped machine
The test can show gallstones and the extent of damage to the pancreas

65. Pancreatic Stimulation Test
Injection of secretin to stimulate pancreas
Used for cases where difficult to diagnose
Expensive
Invasive

66. Medical Treatment No cure for chronic pancreatitis
Treat symptoms, decrease pain
Avoid triggers
Pancreatic enzyme replacement (PERT)
Antioxidants

67. Medical Treatment: Medications
WHO’s 3-step ladder:
Begin with nonopioids (acetaminophen, ibuprofen, or both)
If nonopioids do not relieve pain, mild opioids (like codeine) are given
If mild opioids do not relieve pain, strong opioids (like morphine) are given

68. Medical Treatment: Surgery
Lateral pancreaticojejunostomy (modified Puestow procedure): can lead to pain relief in up to 80% of patients
Whipple Procedure
Total pancreatectomy with islet auto-transplantation (TP-IAT): when pain remains incapacitating

69. MNT Avoid alcohol Quit smoking Avoid high-fat foods
Vitamins and minerals as needed

70. MNT cont.
MAIN GOALS: 1) Provide optimal nutrition support and 2) decrease pain my minimizing stimulation of the exocrine pancreas
Small frequent meals
Low-fat
Vegetable based oils
Treat vitamin B12, A, D, E, K deficiencies
Maintain acid-base balance (using antacids, H2-receptor antagonists, or proton pump inhibitors
Insulin and nutrition therapy
B12 def: pancreatic protease is necessary to cleave B12 from its carrier protein
Acid-base:pancreatic bicarbonate secretions is frequently defective
Manage blood glucose, but focus on control of symptoms rather than normoglycemia

71. Alternative Therapy Yoga Massage therapy Therapeutic Touch
Physical Exercise
Meditation
Laughter
Acupuncture
Pomegranate seeds?

72. Pancreatic Cancer

73. Pancreatic Cancer
Fourth leading cause of death from cancer in the U.S.
5 year survival rate is 4%
American Cancer Society estimates that in 2014 there will be 46,420 new cases and 39,590 deaths from pancreatic cancer.
3% of all cancer in the U.S.
Accounts for 7% of cancer deaths

74. Pancreatic Cancer Risk Factors Age Smoking Chronic pancreatitis
Most significant
Twice as likely to get CA
Chronic pancreatitis
Lots of associations between diseases and pancreatic CA, but cause-and-effect relationship has not been established

75. Pancreatic Cancer S/S Pain Jaundice Wt loss Dull epigastric pain
Back pain
DVT
CA in body or tail of pancreas

76. Pancreatic Cancer
Tumor on head of pancreas- obstructs bile flow, jaundice
Tumor on body of pancreas- impinges celiac ganglion pain
Tumor on tail of pancreas- metastasizes before symptoms appear

77. Diagnosis Pt hx Physical exam
Elevated serum bilirubin and alkaline phosphate
Suggest pancreatic cancer, but not diagnostic
Ultrasound
CT scans
Percutaneous fine-needle aspiration cytology
Misses the smaller, more curable tumors

78. Treatment Surgical resection of tumor Radiation, chemotherapy
Most cancers have metastasized before it is diagnosed
Radiation, chemotherapy
Whipple Procedure

79. Whipple Procedure Pancreaticoduodenectomy (PD)
Removal of head of pancreas, distal bile duct, gallbladder, duodenum, small part of jejunum, distal stomach and pylorus
Complications:
Delayed gastric emptying
Dumping
Weight loss
Diabetes Mellitus
Nutrient deficiencies
Malabsorption

80. Liver
Gallbladder
Removed
Jejunum
Head of pancreas removed

81. Source: SMART Imagebase(

83. Whipple Procedure Post-operation symptoms
N/V, bloating, early satiety, abdominal pain
Dumping
Weight loss d/t pancreatic insufficiency
Diabetes d/t decreased insulin production
Nutrient deficiencies d/t malabsorption
Ca, Zn, Cu, Se
Vits A, E, D, K
Bacterial overgrowth in small intestine
Lactose intolerance

84. Whipple Procedure
Treatment of symptoms (similar to any gastric surgery)
Small frequent meals
Drink most of your fluids between meals
Eat slowly
Avoid simple sugars
Increase protein intake
Limit fat to <30%
Avoid sugar alcohols

85. Case Study

86. Case Study- Assessment
Background
JM is a 29-year-old white male
PhD student in English
School full-time
Lives w/ roommates
Jewish Hx
Dx of depression
s/p appendectomy age 12
No tobacco use
Family hx: Mother: breast CA; Father: HTN
Alcohol use: 6 pack beer, 4-5 shots bourbon daily; weekends: wine and other mixed drinks

87. Case Study- Assessment
Admit hx
Friend brings him to ER b/c he has acute abdominal pain, N/V
States he didn’t realize how much alcohol he had been consuming since he went off his antidepressant meds
Chief complaint: “My stomach pain is so bad- I just can’t stand it. I can’t seem to quit vomiting and cannot keep anything down.”
Pt is pale and obese, in obvious distress

88. Case Study- Assessment
Vital Signs
Temp: 101.7ºF 
Pulse: 108 bpm
Resp rate: 27 
BP: 132/96 
Ht: 5’11”
Wt: 245
HEENT: WNL, except dry mucus membranes in nose and throat
Hyperactive bowel sounds, tender abdomen

89. Case Study- Assessment
Medications:
Imipenen
Pepcid
Meperidine
Ondansetron
Colace - laxative
MOM - laxative
Ativan

90. Case Study- Assessment
Nutrition
NPO
Fluid: mL
Hx: Pt state he has gained 50lbs in the last 5 years. Eats out for most dinners. Coffee w/ toast or bagel for breakfast. Sub sandwich or pizza for lunch

91. Case Study- Assessment
MD progress note
Day after admit, reports hypoactive bowel sounds
HEENT: WNL
Dx: Acute Pancreatitis

92. Case Study- Assessment

93. Case Study- Assessment

94. Case Study- Assessment

95. Case Study- Diagnosis PES statement
Excessive alcohol intake r/t stress and depression AEB reported alcohol intake.

96. Case Study- Monitor/Evaluation
Labs
Weight
Vitals
Symptoms
Acute- probably won’t be in the hospital longer than a week. Will probably resolve itself. Manage symptoms.

97. Sample diet PM Snack Breakfast AM Snack Dinner HS Snack Lunch
Celery w/ PB
Oatmeal w/ mixed berries
Raisins
Milk (LF)
Wheat thins
AM Snack
Dinner
Toast with jam
Pasta
String cheese (LF)
Spinach Salad w/ LF dressing
Carrots
HS Snack
Lunch
Apple
Grilled cheese
Pudding
Chicken noodle soup
Elemental J-tube
Low fat
MCT
Avoid odorous foods

98. References

99. References
Pagana KD, Pagana TJ. Mosby’s Manual of Diagnostic and Laboratory Tests. 5th edition. St. Louis, MO: Mosby, Inc; 2010.
Krauss
About Acute Pancreatitis. Available at Accessed March 4, 2015.

100. References
Yadav D, Lowenfels AB. The epidemiology of pancreatitis and pancreatic cancer. Gastroenterology. 2013;144(6):