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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

Lipolytic enzymes
Digests fatty chyme
Secreted in inactive form
Pancreatic lipase

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

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

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
Ransons 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

Ransons 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

Ransons 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,

catabolic state with demands similar to sepsis


Nutrition therapy should include adequate protein
If oral nutrition cant 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 1220 (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 1220 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 1220 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

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


brains 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)

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

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 patients 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 patients 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


WHOs 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

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:

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

Bacterial overgrowth in small intestine


Lactose intolerance

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

Case Study

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

Case Study- Assessment


Admit hx
Friend brings him to ER b/c he has acute abdominal pain, N/V
States he didnt 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 cant stand
it. I cant seem to quit vomiting and cannot keep anything
down.
Pt is pale and obese, in obvious distress

Case Study- Assessment


Vital Signs
Temp: 101.7F
Pulse: 108 bpm
Resp rate: 27
BP: 132/96
Ht: 511
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

Celery w/ PB
Raisins
Wheat thins

Oatmeal w/ mixed berries


Milk (LF)

AM Snack
Toast with jam
String cheese (LF)
Carrots

Lunch

Grilled cheese
Chicken noodle soup

PM Snack

Dinner
Pasta
Spinach Salad w/ LF dressing

HS Snack
Apple
Pudding

References

References
Pagana KD, Pagana TJ. Mosbys 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.

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