Transcript Pancreatitis

Pancreatitis
CAMILLE OKELBERRY
DANIELLE QUINTON
TONI BROWN
Physiology
Physiology of Pancreas
 Endocrine function
 Insulin
 Glucagon
 Somatostatin
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
Source: SMART Imagebase
(http://ebsco.smartimagebase.com/anatomy-of-the-hepatic-and-pancreaticducts/download-one?id=29583232&mt=tmp&decIDs=13778)
Physiology of the Pancreas
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

Physiology of the Pancreas
 Pancreatic enzymes
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

Physiology of the Pancreas
 Pancreatic Enzymes
 Pancreatic amylase
Secreted in active form
 CHO digestion begins w/ salivary amylase
 Can digests cooked and uncooked starch
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Lipolytic enzymes
Digests fatty chyme
 Secreted in inactive form
 Pancreatic lipase
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Physiology of the Pancreas
 Regulation of Pancreatic secretion
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Vagus nerve
Hormones
Cephalic Phase
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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
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Intestinal Phase
Responsible for most of the secretion
 Response to hormones secreted by upper intestinal mucosa
 Secretin, CCK
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Acute Pancreatitis
Pancreatitis
Acute
Mild
Chronic
Severe
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
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
Etiology
 Alcohol
 Gallstones
 Hypertriglyceridemia
 Hypercalcemia
 Certain medications
 Genetics/gene mutations
Alcohol
 Oxidation of ethanol to acetaldehyde activates
pancreatic stellate cells without any pre-activation
which leads to oxidative stress and eventually
fibrosis
Gallstones
Hypertriglyceridemia
 Triglycerides are carried by chylomicrons in the
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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
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)
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
Medications
 Opiates
 Tetracycline
 Steroids
 Furosemide
 Acetaminophen
 Erythromycin
 Rifampin
 Estrogen preparations
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
Signs and Symptoms
 Sudden Attacks
 Intense epigastric pain
radiating to the back
 N/V
 Fever
 Symptoms may be
aggravated after eating
Diagnosis
 Blood amylase and lipase levels
 CT/MRI test
 Ultrasound
 Ranson’s Criteria
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
Diagnosis - CT Scan
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
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
Treatment
 Medication
 Surgery (for severe acute pancreatitis)
Treatment - Medical therapies
 H2 receptor antagonist
 Proton pump inhibitors
 Somatostatin
 Opiods (morphine)
H2 receptor antagonists and Proton Pump
Inhibitors
Treatment - Surgery
 Remove the gallbladder
 Remove inflamed parts of the pancreas
 Remove necrotic tissue and pseudocysts
 ERCP
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
 http://animatedpancreaspatient.com/en/understan
ding-ercp-animation.phtml
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
MNT Severe Acute Pancreatitis
 Severe acute pancreatitis results in a hypermetabolic,
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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 vs. NJ – Which is better?
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
Alcohol
Prevalence
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
Monitoring the Future Study: Trends in Prevalence of Alcohol for
8th Graders, 10th Graders, and 12th Graders; 2014 (in percent)*
Drug
Alcohol
Time Period 8th Graders
10th
Graders
12th
Graders
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
Alcohol
Time Period Ages 12 or
Older
Ages 12 to
17
Ages 18 to
25
Ages 26 or
Older
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
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).
What is a drink?
 A standard drink
equals 0.6 ounces of
pure ethanol
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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)
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
Metabolism
Highly toxic and
known carcinogen
CO2
and
H2O
Effects on the Body
Increases risk of cancers of the
mouth, esophagus, throat, liver,
breast
Cardiomyopathy
(stretching and drooping of
heart muscle), arrhythmias
(irregular heart beat),
stroke, high blood
pressure
Steatosis (fatty
liver), alcoholic
hepatitis, fibrosis,
cirrhosis
Interferes with the
brain’s communication
pathways, can change
mood and behavior
Causes the pancreas to
produce toxic
substances that can
eventually lead to
pancreatitis
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
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
Chronic Pancreatitis
Chronic inflammation
of the pancreas that
leads to permanent
damage (necrosis)
• 3.5-10 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
Physiology
Inhibits
secretions of
hormones like
GH, TSH,
CCK, insulin
Released in response
to ingestion; regulates
food intake
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)
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Signs and Symptoms
• Nausea
• Vomiting
• Back pain
• Weight loss (late stages)
• Diarrhea
• Oily or fatty stools (late stages)
Individuals with chronic pancreatitis frequently lose weight, even when
their appetite and eating habits are normal
Diagnosis
• Blood tests are NOT helpful, but sometimes test for
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IgG4 to assess for autoimmune pancreatitis useful
Transabdominal ultrasound
Endoscopic ultrasound
Magnetic resonance cholangiopancreatopgraphy
(MRCP)
Computerized Tomography (CT)
Transabdominal Ultrasound
1. Sound waves are sent toward
the pancreas via a handheld
device that a technician
glides over the abdomen
2. 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
3. If gallstones are causing
inflammation, the sound
waves will bounce off of
them, showing their location
Endoscopic Ultrasound
1. Spray a solution to numb
the patient’s throat
2. Doctor inserts an
endoscope down the
throat, through the
stomach, and into the
small intestine
3. They turn on an
ultrasound attachment to
the endoscope, which
produces sound waves to
create visual images of the
pancreas and bile ducts
Magnetic Resonance Cholangiopancreatography
(MRCP)
1. Patient is lightly sedated and lies in a cylinder-like tube
2. Technician injects dye into the patient’s veins, which helps show the pancreas,
gallbladder, and pancreatic and bile ducts
Computerized Tomography (CT)
• Noninvasive radiograph
(x-ray) that produces 3dimensional 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
Pancreatic Stimulation Test
• Injection of secretin to stimulate pancreas
• Used for cases where difficult to diagnose
• Expensive
• Invasive
Medical Treatment
• No cure for chronic
•
•
•
•
pancreatitis
Treat symptoms,
decrease pain
Avoid triggers
Pancreatic enzyme
replacement (PERT)
Antioxidants
Medical Treatment: Medications
 WHO’s 3-step ladder:
1. Begin with nonopioids (acetaminophen, ibuprofen,
or both)
2. If nonopioids do not relieve pain, mild opioids (like
codeine) are given
3. If mild opioids do not relieve pain, strong opioids
(like morphine) are given
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
•
MNT
• Avoid alcohol
• Quit smoking
• Avoid high-fat foods
• Vitamins and minerals
as needed
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, H2receptor antagonists, or proton pump inhibitors
• Insulin and nutrition therapy
Alternative Therapy
• Yoga
• Massage therapy
• Therapeutic Touch
• Physical Exercise
• Meditation
• Laughter
• Acupuncture
• Pomegranate seeds?
Pancreatic Cancer
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
Pancreatic Cancer
 Risk Factors
 Age
 Smoking
Most significant
 Twice as likely to get CA
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Chronic pancreatitis
Lots of associations between diseases and pancreatic CA, but
cause-and-effect relationship has not been established
Pancreatic Cancer
 S/S
 Pain
 Jaundice
 Wt loss
 Dull epigastric pain
 Back pain
 DVT

CA in body or tail of pancreas
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
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
Treatment
 Surgical resection of tumor
 Most cancers have metastasized before it is diagnosed
 Radiation, chemotherapy
 Whipple Procedure
Whipple Procedure
 Pancreaticoduodenectomy (PD)
 Removal of head of pancreas, distal bile duct,
gallbladder, duodenum, small part of jejunum, distal
stomach and pylorus
 Complications:
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Delayed gastric emptying
Dumping
Weight loss
Diabetes Mellitus
Nutrient deficiencies
Malabsorption
Liver
Gallbladder
Removed
Jejunum
Head of pancreas removed
Source: SMART Imagebase
(http://ebsco.smartimagebase.com/anatomy-of-the-hepatic-and-pancreaticducts/download-one?id=29583232&mt=tmp&decIDs=13778)
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
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Bacterial overgrowth in small intestine
Lactose intolerance
Whipple Procedure
 Treatment of symptoms (similar to any gastric
surgery)
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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
Case Study
Case Study- Assessment
 Background
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JM is a 29-year-old white male
PhD student in English
School full-time
Lives w/ roommates
Jewish
 Hx
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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
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
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
Case Study- Assessment
 Medications:
 Imipenen
 Pepcid
 Meperidine
 Ondansetron
 Colace - laxative
 MOM - laxative
 Ativan
Case Study- Assessment
 Nutrition
 NPO
 Fluid: 1900-2400mL
 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
Case Study- Assessment
 MD progress note
 Day after admit, reports hypoactive bowel sounds
 HEENT: WNL
 Dx: Acute Pancreatitis
Case Study- Assessment
Case Study- Assessment
Case Study- Assessment
Case Study- Diagnosis
 PES statement
 Excessive alcohol intake r/t stress and depression AEB
reported alcohol intake.
Case Study- Monitor/Evaluation
 Labs
 Weight
 Vitals
 Symptoms
 Sample diet
 Breakfast
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Celery w/ PB
 Raisins
 Wheat thins

Oatmeal w/ mixed berries
 Milk (LF)
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AM Snack
Toast with jam
 String cheese (LF)
 Carrots
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Lunch
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Grilled cheese
 Chicken noodle soup
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PM Snack
Dinner
Pasta
 Spinach Salad w/ LF dressing

HS Snack
Apple
 Pudding

References
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
http://www.pancreasfoundation.org/patientinformation/acute-pancreatitis/. Accessed March 4,
2015.
References
http://www.pancreasfoundation.org/patient-information/chronicpancreatitis/
http://www.drugabuse.gov/drugs-abuse/alcohol
http://www.niaaa.nih.gov/alcohol-health/overview-alcoholconsumption/alcohol-facts-and-statistics
Yadav D, Lowenfels AB. The epidemiology of pancreatitis and pancreatic
cancer. Gastroenterology. 2013;144(6):1252-1261.