CAMILLE OKELBERRY DANIELLE QUINTON TONI BROWN Pancreatitis.

CAMILLE OKELBERRYDANIELLE QUINTON

TONI BROWN

Pancreatitis

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-pancreatic-ducts/download-one?id=29583232&mt=tmp&decIDs=13778)


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


Pancreatic enzymes


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


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


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 Chronic

Mild Severe

Acute Pancreatitis

Sudden inflammation of the pancreasCan sometimes result in a systemic

inflammatory response that can damage other organs or systems

Most people require a short hospital stay1 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 25/100,000300,000 hospital admissions/year for

treatment of acute pancreatitisAfrican Americans are 2 to 3 times more

likely to develop pancreatitis than Caucasians

Etiology

AlcoholGallstonesHypertriglyceridemiaHypercalcemiaCertain medicationsGenetics/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

OpiatesTetracyclineSteroidsFurosemideAcetaminophenErythromycinRifampin Estrogen preparations

Pathophysiology

Sudden intense abdominal attacksIf mild, the patient can withhold feeding for a

couple of days until pain subsidesTo 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 AttacksIntense epigastric

pain radiating to the back

N/VFeverSymptoms may be

aggravated after eating

Diagnosis

Blood amylase and lipase levels CT/MRI testUltrasoundRanson’s Criteria

Diagnosis – Amylase and Lipase

Evaluating amylase and lipase levels is one of the most widely used diagnostic tests to determine pancreatitisAmylase and lipase levels will be 3 timeshigher 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 >55White 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

MedicationSurgery (for severe acute pancreatitis)

Treatment - Medical therapies

H2 receptor antagonistProton pump inhibitorsSomatostatin Opiods (morphine)

H2 receptor antagonists and Proton Pump Inhibitors

Treatment - Surgery

Remove the gallbladderRemove inflamed parts of the pancreasRemove necrotic tissue and pseudocystsERCP

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/understanding-ercp-animation.phtml

MNT Mild Acute Pancreatitis

“Pancreatic rest”NPO – oral feeding is withheldFluids given intravenouslyIn 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 proteinIf oral nutrition can’t be initiated in 5 to 7 days, start

tube feedingEnteral 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 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

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 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

Highly toxic and known carcinogen

CO2 and H2O

Metabolism

Interferes with the brain’s communication pathways, can change mood and behaviorCardiomyopathy

(stretching and drooping of heart muscle), arrhythmias (irregular heart beat), stroke, high blood pressure

Steatosis (fatty liver), alcoholic hepatitis, fibrosis, cirrhosis

Causes the pancreas to produce toxic substances that can eventually lead to pancreatitis

Increases risk of cancers of the mouth, esophagus, throat, liver, breast

Effects on the Body

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

Released in response to ingestion; regulates food intake

Inhibits secretions of hormones like GH, TSH, CCK, insulin

Physiology

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 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 tube2. 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 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

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, H2-

receptor 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 hxPhysical examElevated serum bilirubin and alkaline

phosphate Suggest pancreatic cancer, but not diagnostic

UltrasoundCT scansPercutaneous 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

Jejunum

GallbladderRemoved

Head of pancreas removed

Source: SMART Imagebase (http://ebsco.smartimagebase.com/anatomy-of-the-hepatic-and-pancreatic-ducts/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


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


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


Medications: Imipenen Pepcid Meperidine Ondansetron Colace - laxative MOM - laxative Ativan


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


MD progress note Day after admit, reports hypoactive bowel sounds HEENT: WNL Dx: Acute Pancreatitis

Case Study- Diagnosis

PES statement Excessive alcohol intake r/t stress and depression AEB

reported alcohol intake.

Case Study- Monitor/Evaluation

LabsWeightVitalsSymptoms

Sample diet Breakfast

Oatmeal w/ mixed berries Milk (LF)

AM Snack Toast with jam String cheese (LF) Carrots

Lunch Grilled cheese Chicken noodle soup

PM Snack Celery w/ PB Raisins Wheat thins

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.

KraussAbout Acute Pancreatitis. Available at

http://www.pancreasfoundation.org/patient-information/acute-pancreatitis/. Accessed March 4, 2015.

http://www.pancreasfoundation.org/patient-information/acute-pancreatitis/



References

http://www.pancreasfoundation.org/patient-information/chronic-pancreatitis/

http://www.drugabuse.gov/drugs-abuse/alcohol

http://www.niaaa.nih.gov/alcohol-health/overview-alcohol-consumption/alcohol-facts-and-statistics

Yadav D, Lowenfels AB. The epidemiology of pancreatitis and pancreatic cancer. Gastroenterology. 2013;144(6):1252-1261.



CAMILLE OKELBERRY DANIELLE QUINTON TONI BROWN Pancreatitis.

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