Huge archive

Rudy,
Welcome Back!!!!
The door is always open for you. My friend I wish you the best. We

Dear Sally,
Sorry you have been having it so rough. I see you found out what a
bad ERCP can do to you. You also have another problem, Alabama is
ranked 43rd out of 50 in healthcare rankings. Just incase you would
like to check the rankings click here:
http://www.unitedhealthfoundation.org/shr2003/Findings.html#Table3
We will be here with you throughout this CP.
Many thoughts and prayers,
Robert
Founder "All Diabetic International"
General Manager "The Pancreatitis Place"
rehammett@...

Abby,
I hope this helped out some. I am still curious if they will face
facts or try to cover it up. Sometimes I think docs will prescibe
boulders for a drowning person.
Thoughts and prayers,
Robert
Founder "All Diabetic International"
General Manager "The Pancreatitis Place"
rehammett@...

I have never used this diet but it seems effective you can handle the
fats and carbs.
Hope this helps,
Robert
Founder "All Diabetic International"
General Manager "The Pancreatitis Place"
rehammett@...

I am wishing you Happy Birthday with many more to come. May all your
wishes come TRUE. I hope you and your family are doing fine and Joe
is improving. You have mail.
You are in our thoughts and prayers,
Robert
Robert
Founder "All Diabetic International"
General Manager "The Pancreatitis Place"
rehammett@...

Dear Michelle,
Please get him to go to the doctor or the ER. With much being said
about Reglan, I think that is what he really needs at this point. I
have had this happen to me and that is the fastest cure. He could
also may need to have some fiber and enzymes to help with this. He
does not need to keep much on his stomach at this point. Please I
urge you to get him some medical help.
He is in our thoughts and prayers,
Robert
Founder "All Diabetic International"
General Manager "The Pancreatitis Place"
rehammett@...

Have any of you tried the South Beach diet? Did it effect your flare-
ups? Did you feel better or worse when on the diet?
Thanks in advance for your input,
jang

I don't know what's going on or what to do for Darrick, but he isn't
looking very good at all. He said that he's spewing out from both
ends, it's not diarreah, but very very liquidy and he said it
contained blood. He has chronic gastritis...but I'm not a medical
person so I'm not sure if it's related or not, and I don't know what
to think of the situation at this point. Has anyone ever had or
have often times where your stomach turns sour or rots??? This is
the way he explained it to me and I just need to know what to do for
him...he won't go to the er, I don't know why...I'm just very
worried.
Thank you,
Michelle C.

Hello everybody, this a Rudy from Belgium. I had to sign out and

Hi Gary,
It seems like about everyone on this list is great.
I had labs last week and I did not do well. I may have to go into the
hospital and go on an insulin drip to get stabelized. All of my labs are
either way to high or way to low.
Robert,
I am very glad that you posted about Trazadone. I have been taking
itfor sleep for several years and it helps me slep. I literally do not
sleep for days without it. I know two indivuduals who had bad reactions,
one was fainting as her blood pressure would suddenly drop, the other while
on this had a pscycotic episode.
Helen in SD where are official flower is a sunflower

Pico de Gallo Shrimp Salad

Barbecued Oriental Flank Steak
Sodium

This recipe has only 5g of fat, but if you use fat free milk instead
of milk, low fat margarine instead of butter, it will be lower in fat
grams. I got this recipe from a dear friend of mine, and I jsut
change it around a little.
Denise
Strawberry Shortcake Muffins

Hello Sally,
I am glad to see that you are back. Sorry to hear that you have been
so sick. But glad that you are feeling better today. I do have some
more recipes. I made the cherry bomboms for Robert. He just LOVES
cherries. I hate them!!! But he loves them so much so I made them for
him. I will get some of the recipes and post them for you. Take care
girl and ALways remember, Our thoughts and Prayers are with you.
God Bless
~*~Denise~*~
Caregivers Moderator
deniseatdiabetes@...
sdhammett@...
http://www.thepancreatitisplace.org/

Hi Sally, I am so glad u post me...Im sorry that you havent been feeling well.
Same here...seem to be getting worse everyday for some reason . this disease has
a mind of it's own. You know i wish and pray everyday that i wake up and it will
go away on it's own like a cold or flu.....
But like everyone tells me there is a reason for this...just waiting to see why
i was chosen to be one to have it....Maybe it was to bring us together as a
family, make us stronger ppl , and help others with any type of illness....we
are our own guardian angels and for others also....
My prayers and thoughts are with you....oh by the way my mother did survive the
surgery, it's the therapy that's really making it painful for her. therapy
started the day after the surgery...she's a very strong woman (like all women
are). and i know she will have a full recovery....
I went to see the psycologist in regards to my pain pump they are going to put
in someday soon...It all went well....just waiting for all his paperwork to be
done then they can start the temp. pump...hoping for next weekend....
THank you again, ur friend,
Brenda

http://www.pancreas.org/patients/patients_other_gentesting.html
Hereditary Pancreatitis:
Trypsinogen Gene Mutations
Frequently Asked Questions, Including Genetic Testing
download this file in PDF format
Topics:
What is hereditary pancreatitis (HP)?
Is there a cure for HP?
What causes HP?
If I have inherited any of the HP mutations, will I definitely
develop pancreatitis?
What is the risk for my child to inherit HP?
Genetic testing for HP
Who might benefit from genetic testing?
Potential benefits of genetic testing
Potential risks & limitations of genetic testing
Disclaimer
Recommended reading
What is hereditary pancreatitis (HP)?
Hereditary Pancreatitis is a rare genetic condition characterized by
recurrent episodes of acute pancreatitis attacks. In about half of
these cases the problem progresses to chronic pancreatitis, which is
severe scarring of the pancreas. Symptoms of an acute attack include
abdominal pain, nausea, and vomiting. Laboratory test during an
attack usually detect high blood levels of amylase and lipase, which
are enzymes released from the pancreas. The first attack typically
occurs within the first two decades of life, but can begin at any
age. In the United States, it is estimated that at least 1,000
individuals are affected with hereditary pancreatitis.
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Is there a cure for HP?
At this time, there is no cure for HP. Treating the symptoms
associated with HP is the choice method of medical management.
Patients may be prescribed pancreatic enzyme supplements to treat
maldigestion, insulin to treat diabetes, analgesics and narcotics to
control pain, and lifestyle changes to reduce the risk of pancreatic
cancer (for example, NO SMOKING!).
Dietary recommendations to help control pain with digestion include
the consumption of small meals throughout the day that are high in
carbohydrates and low in protein and fat. Pancreatic enzymes such as
Creon, Pancrease, and Violiase are helpful in providing improved
digestion and a reduction in diarrhea and pain for some patients with
more advanced disease.
Exposure to smoking and alcohol are known to dramatically increase
the risk for pancreatic attacks among individuals with HP. Smoking is
strongly discouraged as it doubles the risk for pancreatic cancer.
Similarly, alcohol consumption is not recommended for these patients
because alcohol is a known risk factor for both acute and chronic
pancreatitis. Therefore it is recommended that all HP patients avoid
smoking and alcohol consumption.
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What causes HP?
HP is a genetic disorder, which means that it is usually passed from
one generation to the next.
The symptoms of HP are caused by a change to a specific gene. Genes
are the packages of information that control how our bodies look and
function. A single gene appears to be involved in 60-75% of
hereditary pancreatitis families. This gene produces the "cationic
trypsinogen" enzyme, which breaks down the proteins present in the
foods we eat. (In some research papers cationic trypsinogen is called
PRSS1).
When a change to a gene occurs, the gene may no longer function
properly. These gene changes are called mutations. Currently, there
are two common, and more that 6 uncommon cationic trypsinogen gene
mutations that are associated with hereditary pancreatitis. The major
mutations are known as cationic trypsinogen "R122H", "N29I".
Families with HP might carry one of these mutations, but usually not
more than one type of mutation. It is also possible that a family
with a strong history of HP may not carry any of the currently known
mutations. For this reason, it is believed that additional genes and
mutations that cause HP are awaiting discovery. (Every concerned
person is encouraged to join on going research studies through the
University of Pittsburgh 1-888-PITT DNA, or an affiliated medical
center)
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If I have inherited any of the HP mutations, will I definitely
develop pancreatitis?
HP symptoms can develop at any age, but most patients have their
first pancreatic attack before the age of 20. In addition, there is a
great deal of variability in the frequency and severity of pancreatic
attacks. Some affected relatives may only have a few episodes of
pain, while others in the same family experience more severe
symptoms. The cause for this variation in symptoms is unknown.
Individuals who have inherited either the R122H or the N29I mutation
have an 80% risk of developing clinical symptoms of HP over the
course of their lifetime. Although the remaining 20% of these
mutation carriers do not show any symptoms, it is important to
remember that they still have a risk of having a child who inherits
their HP mutation and is affected with HP.
Much less is known about the other mutations, and it is believed that
are rare in the population. Without additional knowledge about these
mutations, it is not possible to predict how many people will
eventually develop symptoms of pancreatitis.
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What is the risk for my child to inherit HP?
All of our genes come in pairs. We inherit one set of genes from each
of our parents. Hereditary pancreatitis is inherited in a dominant
manner, which means that only one copy of the HP gene needs to have a
mutation in order for an individual to become affected with HP.
When a parent carries an HP mutation in one of their genes, then each
child has a 50% (or 1 in 2) chance of inheriting that mutation. It is
important to remember that this risk to inherit an HP mutation is 50%
for each pregnancy. The risk to have an affected child is actually
less than 50% (it is approximately 40%) since one out of five
individuals with the R122H or N29I mutation remain symptom-free over
their lifetime.
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Genetic testing for HP
Genetic testing for HP is currently available both on a research and
commercial basis.
Commercial testing is conducted through a licensed laboratory for a
specified fee that may be covered by your insurance plan. A small
blood sample is drawn at your doctorís office or hospital laboratory
and sent to the commercial laboratory for testing. Results are then
provided to your referring physician or counselor. One commercial
laboratory that provides testing for HP is Molecular Diagnostics at
the University of Pittsburgh (phone: 412-648-8519). Currently, the
fee for commercial testing through Molecular Diagnostics is $276.50
per person. Check with your insurance carrier to determine whether
genetic testing is covered by your health plan. Testing can only be
done in a laboratory licensed to perform this test. If testing is
being done at other institutions within the United States, please
call the 888- PITT DNA number to be sure that the site is approved.
Research testing is available for a reduced fee for those who qualify
to be enrolled in the HP research study at the University of
Pittsburgh. Research testing is confidential, requires the completion
of several forms and questionnaires, but may be associated with a
longer turnaround period to obtain results.
Genetic testing for any condition is a complex process. Genetic
counselors are available in your local area to help identify the
potential risks, benefits, and limitations of genetic testing for HP.
Referrals to local genetic counselors can be obtained from your
primary care physician. To find a genetic counselor near you, ask
your physician or call us for assistance at 888-PITT-DNA.
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Who might benefit from genetic testing?
ï Individuals who have a relative with a documented diagnosis of
hereditary pancreatitis.
ï Individuals with a strong history of unexplained abdominal pain
that resembles pancreatitis.
See the Genetic Consensus Statement published in Pancreatology
2001;1:405-415, through the Hereditary Pancreatitis Research Study
office 888-PITT DNA, or on www.pancreas.org
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What are some of the risks, benefits, and limitations of genetic
testing?
Before requesting HP genetic test results, we ask that each
participant consider the possible benefits and limitations of genetic
testing.
back to top
Potential benefits of genetic testing:
1. Obtaining a diagnosis of HP.
Some individuals with HP have reported difficulty in obtaining a
diagnosis or explanation of their abdominal symptoms. A positive test
result (i.e. when a person is found to carry an HP mutation) may help
validate or prove that an individual has true medical symptoms that
are hereditary in nature. In short, physicians can use genetic
testing to diagnose HP.
2. Identifying relatives at risk to develop HP.
Once an HP mutation has been found in a family, other relatives can
be tested to determine whether they inherited the same HP mutation.
This type of testing, "pre-symptomatic testing," is conducted for
individuals who have not yet developed pancreatitis but are at risk
of having inherited an HP mutation from either parent. Individuals
who test positive prior to developing symptoms of HP can then be
educated about important lifestyle recommendations to reduce the risk
of developing future pancreatic disease such as pancreatic cancer.
Although pancreatitis cannot be prevented at this time, these
individuals would be recommended to avoid the use of tobacco and
alcoholic beverages, since these exposures are risk factors for
pancreatic cancer in the general population.
3. Reducing feelings such as anxiety or uncertainty.
Test results can often help reduce feelings of anxiety and
uncertainty for individuals with a family history of HP. For example,
an unaffected relative who receives negative test results (i.e. when
a person is found NOT to carry an HP mutation) is likely to feel
relieved from the uncertainty of whether symptoms will ever develop
in the future. Note: negative test results only eliminate the risk to
develop a hereditary form of pancreatitis. It is still possible to
develop pancreatitis due to other causes later in life.
4. Prenatal Genetic Testing.
Genetic testing can provide information that is useful when making
important reproductive decisions. Prenatal diagnosis is a form of
testing that is conducted during pregnancy to determine whether a
developing baby has inherited a specific mutation or other health
problem. Currently prenatal testing is not being conducted.
If both members of the couple have tested negative for a particular
HP mutation, then the risk to pass on that HP mutation is essentially
zero. For example, if your family is known to carry the R122H*
mutation and you test negative for R122H*, then none of your children
(or future pregnancies) would be at risk to develop HP.
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Potential risks & limitations of genetic testing:
1. Genetic discrimination.
As with genetic testing for any type of condition, there is a small
but potential threat for insurance and/or employment discrimination.
We have never heard of a documented case of this type of
discrimination among our research population of over 700 individuals.
Moreover, it is reassuring to known that there are no published cases
of insurance discrimination with regard to hereditary pancreatitis.
Individuals who undergo genetic testing as part of a research study
are generally well protected because of our strict rules of
confidentiality. For instance, no information about an HP participant
is ever released to a third party without written permission from a
participant. All blood samples are identified using a code number
instead of personal information such as names or social security
numbers. Because no research organization can completely eliminate
the risk for discrimination, this potential threat should be
considered before requesting your genetic test results are confirmed
and released to you.
2. Adverse psychological emotions.
Powerful emotions such as anxiety, guilt, and depression can
accompany the process of genetic testing. In addition, genetic
information has a powerful influence on an individualís reproductive
behavior and a lifelong impact on future descendants.
3. Genetic test results cannot prevent or cure HP.
At this time, there is no cure for HP, nor is there a way to prevent
pancreatic attacks in patients who carry HP mutations. Furthermore,
there does not appear to be a difference in medical treatment for
patients who have a hereditary form of pancreatitis versus patients
who have a non-hereditary form of pancreatitis.
4. "Non-informative" test results.
Non-informative test results include any type of test result that is
not conclusive in ruling out a hereditary form of pancreatitis.
Negative test results must be interpreted very carefully, especially
for individuals undergoing pre-symptomatic testing. Pre-symptomatic
testing applied to an individual who is not clinically affected with
the disease, but has at least one parent affected with a dominant
disorder.
When test results for know trypsinogen mutaions are negative,
then . . .
If a mutaion has been identified in another family member.
Interpretation: He/she is not at risk to develop the genetic form of
pancreatitis that runs in the family. Since he/she does not carry the
mutation, his/her children are not at risk either.
Action: Stop
If a mutaion has not been identified in another family member.
Interpretation: Since we do not know what mutation runs in the
family, it is possible that this family carries a mutation that we
cannot yet recognize. Therefore it is possible that this person could
carry the unrecognizable mutation as well.
Action: Enter a research study with the extended family to search
for a new gene mutation.
This information is basen on 2001 data for the cationic trypsinogen
gene (PRSS1)
Disclaimer:This information is intended for general education of
individuals who are interested in hereditary pancreatitis and related
disorders. It in no way can substitute for the evaluation and care
provided to individuals through their trained health care providers.
For further information the following publications will be helpful.
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Recommended reading (technical)
Chronic Pancreatitis
1. Etemad B, Whitcomb DC. Chronic Pancreatitis: Diagnosis,
Classification, and New Genetic Developments. Gastroenterology
2001;120:682-707.
Trypsinogen Gene Mutations
The trypsinogen R122H and N29I mutations*
2. Whitcomb DC, Gorry MC, Preston RA, Furey W, Sossenheimer MJ,
Ulrich CD, et al. Hereditary pancreatitis is caused by a mutation in
the cationic trypsinogen gene. Nature Genetics 1996;14(2):141-5.
3. Gorry MC, Gabbaizedeh D, Furey W, Gates LK, Jr., Preston RA, Aston
CE, et al. Mutations in the cationic trypsinogen gene are associated
with recurrent acute and chronic pancreatitis. Gastroenterology
1997;113(4):1063-8.
4. Whitcomb DC. Hereditary Panceatitis: New insights into acute and
chronic pancreatitis. Gut 1999;45:317?22.
5. Whitcomb DC. Genetic Predispositions to Acute and Chronic
Pancreatitis. Medical Clinics of North America 2000;84(2):531-47.
Genetic Testing
6. Ellis I, Lerch MM, Whitcomb DC, Committee C. Genetic Testing for
Hereditary Pancreatitis: Guidelines for indications, counselling,
consent and privacy issues. Pancreatology 2001;1(5):401-11.
7. Applebaum SE, Kant JA, Whitcomb DC, Ellis IH. Genetic testing:
counseling, laboratory and regulatory issues and the EUROPAC protocol
for ethical research in multi-center studies of inherited pancreatic
diseases. Medical Clinics of North America 2000;82(2):575-88.
8. Applebaum SE, OíConnell JA, Aston CE, Whitcomb DC. Motivations and
concerns of patients with access to genetic testing for hereditary
pancreatitis. American Journal of Gastroenterology 2001;96(5):1610-7.
9. Applebaum-Shapiro SE, Finch R, Pfützer RH, Hepp LA, Gates L, Amann
S, et al. Hereditary Pancreatitis in North America: The Pittsburgh -
Midwest Multi-Center Pancreatic Study Group Study. Pancreatology
2001;1(5):439-43.
Cancer Risk
10. Lowenfels AB, Maisonneuve P, Whitcomb DC, Lerch MM, DiMagno EP.
Cigarette smoking as a risk factor for pancreatic cancer in patients
with hereditary pancreatitis. Journal of the American Medical
Association 2001;286(2):169-70.
11. Lowenfels AB, Maisonneuve P, Whitcomb DC. Risk factors for cancer
in hereditary pancreatitis. International Hereditary Pancreatitis
Study Group. Medical Clinics of North America. 2000;84(3):565-73.
12. Lowenfels A, Maisonneuve P, DiMagno E, Elitsur Y, Gates L,
Perrault J, et al. Hereditary pancreatitis and the risk of pancreatic
cancer. Journal of the National Cancer Institute 1997;89(6):442-6.
SPINK1 Mutations (not discussed in this document)
13. Witt H, Luck W, Hennies HC, Classen M, Kage A, Lass U, et al.
Mutations in the gene encoding the serine protease inhibitor, kazal
type 1 are associated with chronic pancreatitis. Nature Genetics
2000;25(2):213-6.
14. Pfützer RH, Barmada MM, Brunskil APJ, Finch R, Hart PS,
Neoptolemos J, et al. SPINK1/PSTI polymorphisms act as disease
modifiers in familial and idiopathic chronic pancreatitis.
Gastroenterology 2000;119:615-23.
15. Whitcomb DC. What to think about SPINK and pancreatitis. Am J
Gastrol 2002;(in press).
CFTR Mutations (not discussed in this document)
16. Cohn J, Friedman K, Silverman L, Noone P, Knowles M, Jowell P.
CFTR mutations predispose to chronic pancreatitis without cystic
fibrosis lung disease (abstract). Gastroenterology 1997;112(4):A434.
17. Cohn JA, Bornstein JD, Jowell PS. Cystic fibrosis mutations and
genetic predisposition to idiopathic chronic pancreatitis. Medical
Clinics of North America 2000;84(3):621-31.
18. Sharer N, Schwarz M, Malone G, Howarth A, Painter J, Super M, et
al. Mutations of the cystic fibrosis gene in patients with chronic
pancreatitis. New England Journal of Medicine 1998;339(10):645-52.
19. Noone PG, Zhou Z, Silverman LM, Jowell PS, Knowles MR, Cohn JA.
Cystic fibrosis gene mutations and pancreatitis risk: relation to
epithelial ion transport and trypsin inhibitor gene mutations.
Gastroenterology 2001;121(6):1310-9.
* Note: The trypsinogen R122H and N29I mutations were previously
numbered R117H and N21I.

http://newsbureau.upmc.com/tx/Pancrea.htm
FAMILY AND RESEARCH TEAM WORK TOGETHER TO FIND GENE FOR HEREDITARY
PANCREATITIS
SAN FRANCISCO, May 19, 1996 A year following a family reunion that
initiated an intensive study to identify the gene for hereditary
pancreatitis, researchers from the University of Pittsburgh Medical
Center (UPMC) say they have narrowed their search to a small area on
one chromosome. The finding was made possible in large part due to
the assistance of an extended family affected by this incurable
disease for generations. Results from the Midwest Multi-Center
Pancreatic Study Group, which also includes the University of
Kentucky at Lexington and the University of Cincinnati, will be
presented during Digestive Disease Week (DDW), a series of scientific
meetings May 19-22 being attended by 10,000 specialists in
gastrointestinal diseases.
The researchers, led by the UPMC's David Whitcomb, M.D., Ph.D., and
Garth Ehrlich, Ph.D., also plan to reveal the results to their
collaborators -- a family of more than 100 living relatives located
primarily in eastern Kentucky and western Virginia -- at a picnic
planned for Memorial Day. Thirty-six of the 103 relatives in the
study have the painful disorder, more than half since before the age
of five.
Genetic study of this family, which had been initiated by a
University of Indiana physician more than 25 years ago, has been
practical only in the last two to three years due to an emerging
technology called microsatellite-based familial genetic linkage
analysis. The technology permits tiny markers along strands of DNA to
be amplified. By pinpointing identical markers and their location on
a specific chromosome, researchers follow the inheritance of certain
diseases.
At DDW, Dr. Whitcomb will report the gene for hereditary pancreatitis
lies somewhere on chromosome 7q35, a location not before hypothesized
by researchers in the field. Details of the study are to be published
in the June issue of the medical journal Gastroenterology.
"This represents a major advancement. We are very close to
understanding the genetic basis for this disorder, which we hope will
enable us to develop strategies to prevent or control hereditary
pancreatitis in families that are affected, vastly improving their
quality of life," says Dr. Whitcomb, who is an assistant professor of
medicine in the division of gastroenterology and hepatology at the
UPMC.
"Although the gene has not yet been identified, using the genetic
markers we've located that map near the gene, we can tell with 95
percent accuracy if a person has inherited the high risk gene.
Implications for this family and others are great," adds Dr. Whitcomb.
"Inheritance of hereditary pancreatitis appears to be very complex.
Further study may take months or years to identify the gene,
depending on whether the gene has or has not been previously
identified in another guise," says Dr. Ehrlich, associate professor
of pathology and otolaryngology at the UPMC and co-investigator of
the project.
Information obtained through interviews, questionnaires, and blood
samples, which were collected with the assistance of a family member
who is a nurse, is helping researchers to piece together the genetic
puzzle. Family bibles and other family records have enabled the team
to construct a family tree of 500 relatives spanning eight
generations.
"This family has been incredibly helpful. It became very apparent at
our first picnic a year ago that these people wanted answers," says
Dr. Whitcomb.
Hereditary pancreatitis occurs in pockets throughout the world.
Hence, in some areas, like the location of the study family, it is
quite common, whereas in other geographic regions it is very rare.
The disease typically begins between the ages of five and 10 with an
acute attack of abdominal pain. The pancreas becomes inflamed as the
digestive enzymes intended for the intestine leak out of the cells
that produce them and the pancreas begins digesting itself. After
repeated attacks and scarring of the organ, a chronic condition
develops that is characterized by constant pain, nausea and vomiting,
as well as by weight loss due to malabsorption of food. It often
leads to severe complications, including diabetes and pancreatic
cancer, which occurs at a rate of more than 50 times higher than in
the general population. There is no treatment for hereditary
pancreatitis.
According to other findings to be presented at DDW by Dr. Whitcomb,
84 percent of the affected family members reported having had more
than 11 acute attacks, lasting more than five days in more than half
of them and requiring hospitalization in two thirds. Thirty percent
have developed diabetes and 33 percent have had surgery to remove
their gallbladders because of gallstones.
To further explore this finding, ultrasound studies using a portable
device will be offered to family members at this year's Memorial Day
picnic. The picnic is expected to attract additional family members
living in other states, who, like their relatives, were notified
through a newsletter published by the researchers on a regular basis
for the family. At the picnic, Dr. Whitcomb and Lawrence Gates, M.D.,
of the University of Kentucky, will present what has been learned
thus far with special emphasis on their findings' implications to
individual family members. Drs. Gates and Whitcomb will be joined by
others on the research team, including Dr. Ehrlich from the UPMC and
Charles Ulrich, M.D., and Stephen Martin, M.D., both from the
University of Cincinnati.

A 29-year-old patient from Sri Lanka who immigrated to Switzerland at
the age of 18 first developed recurrent abdominal pain and chronic
diarrhoea at age 24. The clinical, laboratory and radiological
http://www.smw.ch/oeil/1999/129-11-355-99.html
Tropical calcifying pancreatitis
(CT/ERCP) findings revealed chronic calcifying pancreatitis with
already subclinically documented endocrine and exocrine pancreatic
failure. On the basis of origin, no alcohol consumption in the
history, and radiologically pronounced, lumpy calcifications, the
condition was diagnosed as tropical calcifying pancreatitis. In the
previous 5 years two other pancreatitis episodes could be objectified
in this patient. In view of persistent pain symptoms due to
obstruction of the pancreatic duct in the head region, papillotomy of
the pancreatic sphincter and subsequent insertion of a pancreatic
endoprosthesis were performed endoscopically. The typical features of
tropical calcifying pancreatitis are country of origin, young age, no
history of alcohol consumption, and the diffuse, lumpy parenchymal
calcifications already present initially. Management of this disease
primarily involves apart from treatment of the exocrine and
endocrine pancreatic failure therapy for the poorly controllable
pain. The therapeutic strategy is medical and endoscopic in the first
place, but early partial pancreatic resection is necessary in the
event of failure. Life expectancy is reduced due to the early
exocrine and endocrine pancreatic failure and the relatively high
cancer risk.

http://www.amershamhealth.com/medcyclopaedia/medical/Volume%20IV%
201/SEROUS%20CYSTADENOMA%20PANCREATIC.ASP
Serous cystadenoma, pancreatic,
(also called microcystic adenoma and glycogen-rich adenoma), cystic
tumour of the pancreas characterized by the presence of innumerable
tiny cysts from less than 120 mm in diameter, with a tendency for
larger cysts to occur at the periphery and a central fibrous scar,
often associated with calcification. Serous cystadenoma occurs mainly
in middle aged or elderly persons with a female preponderance. They
represent a small percentage of pancreatic tumours.
The clinical symptoms include abdominal discomfort or more rarely
obstructive jaundice or vomiting due to mechanical compression of
adjacent organs, but in some patients the tumour may not cause any
symptoms.
Serous cystadenoma may arise in any portion of the pancreas but the
majority will be found in the body and tail. Grossly on cut section
serous cystadenoma has a honeycombed or spongy appearance due to the
presence of numerous cysts, containing clear fluid. Some tumours are
composed predominantly of cysts 12 cm in diameter whereas others
consist of smaller cysts that are less than 10 mm in diameter. A
central fibrous focus or "scar" that may be calcified is present in
some instances. In yet other tumours solid components may be seen.
The tumour has a polylobular contour secondary to the bulging cysts.
The cysts are lined with a layer of flat or cuboidal epithelium
containing abundant glycogen. The subepithelial fibrous layer and
stroma has a rich capillary network. It is generally accepted that
serous cystadenoma is a benign tumour.
Radiological findings
Plain films of the abdomen may reveal abnormal calcification in the
region of the pancreas. This may be curvilinear or punctate with
occasionally a "sunburst" aspect. Barium studies may be normal or may
display signs of displacement or compression of stomach or duodenum
if the lesion has a large volume.
On ultrasound serous cystadenoma varies in appearance from an
echogenic mass to a hypoechoic mass with posterior enhancement
depending on the size of the cysts. If multiple tiny cysts, smaller
than 0.2 mm, are present they produce numerous acoustic interfaces
resulting in a hyperechogenic aspect whereas larger cyst will display
a typical anechoic appearance. Calcification can be visualized on
ultrasound as a strongly hyperechoic structure with acoustic
shadowing.
On noncontrast enhanced CT serous cystadenoma appears as lobulated,
well-circumscribed mass with fluid attenuation (1015 HU) if the
cysts are more than 5 mm in diameter. If multiple tiny cysts are
present the individual cystic cavities are not visualized and the
mass displays an inhomogeneous attenuation of about 2030 HU. In
addition thin linear septa and calcifications may be depicted.
On contrast enhanced CT serous cystadenoma displays moderate to
marked contrast enhancement due to the rich vascularization of the
subepithelial layers of the cystic linings or the papillary
components of the lesion (Fig.1). The stellate configuration of the
septations within the cystic tumour is also better depicted following
contrast administration resulting in a "honeycomb" or "spongy"
appearance. The central fibrous scar may show a marked delayed
enhancement, if not calcified. The number and the size of the cysts
within a cystic lesion of the pancreas can be helpful in the
differential diagnosis between serous and mucinous cystadenoma. If
more than 6 cysts are depicted and if their diameter is greater than
2 cm the diagnosis of serous cystadenoma should be suggested.
MRI (Fig.2) best reveals the multicompartmental structure of serous
cystadenoma because of superior ability to depict fluid on T2-
weighted sequences as areas with high signal intensity. On T1-
weighted images the signal intensity of the lesion is low. MRI is now
considered to be equal or superior to CT in the diagnosis of this
neoplasm, except in its ability to demonstrate calcification within
the lesion. Angiography is not used anymore for the diagnosis
ALB

http://usagiedu.com/chrpanredoc.htm
Chronic pancreatitis: diagnosis, classification, and new genetic
developments
1. The first test in the evaluation of possible chronic pancreatitis
should be
a. pancreatic biopsy
b. pancreatic EUS
c. Computed tomography
d. ERP
2. CT techniques used to evaluate for possible chronic pancreatitis
include
a. an initial non-contrasted scan to detect pancreatic
calcification
b. using water as an oral contrast agent to maximize
pancreatic visualization
c. using a helical CT scan
d. obtaining thin cuts through the pancreas
3. A person who tests positive for one of the cationic trypsinogen
gene mutations should be advised that
a. smoking increases risk of pancreatitis and pancreatic
cancer
b. alcohol, emotional stress and fatty foods may
precipitate pancreatitis attacks
c. the risk of developing pancreatitis depends on the
type of mutation
d. the risk of the first attack of pancreatitis
increases with age
e. no specific treatment exists for the prevention or
treatment of chronic
pancreatitis
f. prophylactic pancreatectomy after age 50 is recommended because
of the
high risk of pancreatic cancer
4. Features of autoimmune pancreatitis include
a. a positive high-titer AMA (anti-mitochondrial
antibody)
b. hypergammaglobulinemia
c. histologic findings of duct destruction, atrophy of
acinar tissue with no
calcification, lymphocytic infiltration, plasma cells and fibrosis.
d. a normal pancreas on CT scan is required for diagnosis
e. prompt response to corticosteroids
True or False
5. Over 50% of heavy alcohol users develop pancreatitis.
6. Tissue diagnosis of chronic pancreatitis is the gold standard to
establish the diagnosis.
7. Findings on CT that suggest chronic pancreatitis include
calcifications within the pancreatic ducts or parenchyma, and/or
dilated main pancreatic ducts combined with parenchymal atrophy.
8. Testing for CFTR mutations to explain chronic pancreatitis is
difficult because many different types and combinations of CFTR
mutations must be considered and tested for, and the presence of some
of these mutations may not be associated with pancreatitis.
9. The "gold standard" for measuring pancreatic function is
the "tubed" secretin test
10. Individuals with mutations in the cationic trypsinogen gene
have a 80% likelihood of developing pancreatitis and a 40% likelihood
of developing chronic pancreatitis.
11. Endosonographic features suggestive of chronic pancreatitis
found during EUS examination of the pancreas have been correlated
with histologic findings and are accurate predictors of chronic
pancreatitis.
12. Tobacco smoking is considered an independent risk factor for
the development of chronic pancreatitis.
13. A normal carefully done helical CT with pancreatic protocol
excludes the diagnosis of chronic pancreatitis.
14. Chronic renal failure is associated with increased rates of
both acute and chronic pancreatitis, etiology may be multifactorial.
15. Most individuals with genetic mutations in the pancreatic
secretory trypsin inhibitor (SPINK1) and the cystic fibrosis
transmembrane conductance regulator (CFTR) develop clinical
pancreatitis.
16. ERP findings of chronic pancreatitis include
a. early changes consist of dilation and irregularity of
the smaller ducts and
branches of the pancreas
b. changes in the main pancreatic duct reflects more
advanced disease
c. tortuosity stricture and calcifications suggest
malignancy
d. findings in severe cases are pathognomonic, changes
seen in minimal
disease are difficult to distinguish from a normal pancreatogram
17. Mutations in the cationic trypsinogen gene (PRSS1):
a. is associated with an autosomal dominant form of
hereditary pancreatitis
b. allows premature activation of trypsinogen within the
pancreas leading to
pancreatic autodigestion and repeated episodes of acute pancreatitis.
c. the prevalence of this mutation varies from 0% to 19%
among patients
presumed to have idiopathic chronic pancreatitis
d. any mutation in this gene is associated with a high
probability of pancreatitis.
18. SPINK1 Mutations
a. are mutations of the pancreatic secretory trypsin
inhibitor
b. SPINK1 acts as the first line defense against
prematurely activated
trypsinogen
c. SPINK1 mutations causes autosomal dominant hereditary
pancreatitis
d. SPINK1 mutations are associated with idiopathic
chronic pancreatitis
e. People with SPINK1 mutations have a low probability
of developing
pancreatitis.
f. SPINK1 mutations appear to increase the likelihood
that other toxic or
environmental agents may trigger pancreatitis.

http://www2.us.elsevierhealth.com/scripts/om.dll/serveaction=searchDB&
searchDBfor=iss&id=jsg983501&target=
Management of Complications of Pancreatitis
Keith D. Lillemoe, MD, Charles J. Yeo, MD
The clinical presentation of acute pancreatitis can vary, ranging
from mild self-limited episodes of abdominal discomfort to severe
systemic illness associated with fluid sequestration, metabolic
derangements, hypotension, sepsis, and death. Approximately 10% of
patients have a severe illness that may be life-threatening,
associated with pancreatic hemorrhage or necrosis, and often attended
by significant morbidity and mortality despite maximal supportive
care. Predictive indicators have been developed, of which Ranson's
criteria are the most commonly used, which allow one to predict
significant morbidity and mortality. For mild or self-limited
pancreatitis conditions, the mortality rate should approach zero. In
severe presentations, the mortality rate may approach 100%. Early in
the course of acute pancreatitis, death is most likely caused by
pulmonary complications, whereas in patients who die after the first
week of hospitalization, infection and associated multisystem organ
failure contribute to most deaths. Recognition of the cause of
pancreatitis is useful in both management and predicting
complications. By far, alcohol and biliary tract disease are the most
common causes. Complications can develop from acute pancreatitis of
any cause. Pancreatitis developing in a patient after operation,
however, appears to be associated with the highest morbidity and
mortality. The diagnosis of pancreatitis is made on the basis of the
clinical presentation and combined laboratory and radiographic
findings. The dynamic contrast-enhanced abdominal computed tomography
(CT) is the most sensitive noninvasive imaging test available to
confirm the diagnosis and is also useful in predicting complications
of the disease. Complications of acute pancreatitis can be divided
into three phases of the disease. Early complications develop within
the first hours to the first week of the disease. These complications
include shock, which is associated with massive fluid sequestration.
If not treated promptly with generous fluid resuscitation with the
use of crystalloid solutions, the patient can have severe acidosis,
fluid and electrolyte abnormalities, and renal failure. Nutritional
deficits develop in those patients with prolonged courses after bouts
of acute pancreatitis. Although not indicated routinely in patients
with acute pancreatitis, in the subset of patients with severe
disease, total parenteral nutrition can improve the nitrogen balance
and overall outcome. Pulmonary complications are the leading cause of
death within the first 7 days of acute pancreatitis. Impaired
diffusion capacity, decreased compliance, increased airway
resistance, and decreased vital capacity are the common abnormalities
of respiratory physiology. All patients with severe pancreatitis
should receive supplemental oxygen and careful monitoring of the
oxygen saturation. Endotracheal intubation and positive end
expiratory pressure ventilation are required in the face of
progressive pulmonary insufficiency. Complications of acute
pancreatitis developing in the mid-course of the disease are almost
exclusively related to secondary pancreatic infection. Although
retrospective and prospective studies suggest that antibiotics are
not indicated in the routine treatment of mild to moderate
pancreatitis, prophylactic antibiotics can reduce the frequency of
infectious complications in patients with severe pancreatitis.
Pancreatic infections can be classified as a pancreatic abscess,
defined as (1) a circumscribed intraabdominal collection of purulent
material containing little or no pancreatic necrosis or (2) infected
pancreatic necrosis, which refers to diffuse or focal areas of
infected nonviable pancreatic parenchyma, typically associated with
peripancreatic fat necrosis. Secondary pancreatic infections are
responsible for more than 80% of late deaths in patients with acute
pancreatitis. These infections occur with increasing frequency in
direct proportion to the severity of acute pancreatitis as judged by
the Ranson criteria. In patients with suspected secondary pancreatic
infections based on clinical criteria (i.e., clinical deterioration,
persistent fever, and documented bacteremia), radiographic
investigation is necessary to make the diagnosis. At present, CT
scanning is the most accurate method for evaluating the potential for
infectious complications. The classic finding of air bubbles in a
peripancreatic fluid collection is diagnostic for a secondary
pancreatic infection. Percutaneous needle aspiration for Gram's stain
and culture has also been shown to be highly sensitive in the
detection of these infections. The optimal method for surgical
management is either laparotomy with debridement and wide sump
drainage or laparotomy with debridement and open packing. The
predominant late complication of acute pancreatitis is the
development of a pancreatic pseudocyst. A pancreatic pseudocyst is a
localized collection of pancreatic juice enclosed by a wall of
fibrous or granulation tissue. Persistent upper abdominal pain for a
period of time longer than expected with uncomplicated pancreatitis
is the predominant symptom. Other symptoms include gastric outlet
obstruction with resultant nausea and vomiting, weight loss, and
jaundice. CT is the favored diagnostic study for demonstrating a
pancreatic pseudocyst. The appropriate management of a pancreatic
pseudocyst requires a knowledge of the natural history. Recent
reports suggest that asymptomatic pseudocysts, regardless of size,
can be managed with expectant nonoperative management. The preferred
surgical approach for an uncomplicated pseudocyst is internal
drainage. Options include cyst-jejunostomy, Roux-en-Y jejunal limb,
cyst-gastrostomy, or cyst-duodenostomy. Excisional treatment is
appropriate for those pseudocysts located in the distal body and tail
of the pancreas. External drainage is appropriate when gross
infection of the pseudocyst develops or when a pseudocyst with a thin
nonfibrous wall not suitable for anastomosis is identified at
surgery. Nonoperative approaches for the management of pancreatic
pseudocysts include percutaneous drainage or endoscopic procedures to
drain the pseudocyst into the adjacent stomach or duodenum with an
endoprosthesis or an endoscopically created fistula. Although short-
term results with these techniques appear to be favorable, long-term
results are still lacking. Complications of pancreatic pseudocysts
include infection and the development of a pancreatic abscess. In
this condition, percutaneous aspiration and drainage may be an
appropriate technique. Hemorrhage is the most severe complication and
may be life-threatening. Angiographic embolotherapy has gained
increased acceptance and utility in the management of this condition.
Obstruction of the adjacent gastrointestinal tract or biliary tree
can occur. Finally, rupture of a pseudocyst is an infrequent
complication occurring in less than 3% of patients. Few patients with
chronic pancreatitis actually die as a direct result of their
disease. Instead, the ravages of chronic alcoholism and its related
illnesses primarily account for the high mortality rate seen in
follow-up of patients with alcoholic pancreatitis. Alcoholism is the
most common cause of chronic pancreatitis in the United States and
other developed countries. Biliary tract disease is an extremely rare
cause. Other causes may include congenital or posttraumatic
strictures of the pancreatic duct, pancreatic divisum, and hereditary
or familial pancreatitis. Regardless of the cause, abdominal pain is
the presenting symptom in up to 95% of patients with chronic
pancreatitis. The pain may be disabling and often is associated with
the development of addiction to narcotics. Diarrhea and steatorrhea
are the hallmarks of significant pancreatic exocrine insufficiency
but usually do not appear until 90% of the secretory capacity of the
pancreas is gone. Abnormal glucose tolerance will occur in 70% of
patients with chronic pancreatitis, and one half of these patients
will have frank diabetes. The diagnosis of chronic pancreatitis is
based primarily on the clinical presentation with no routine
laboratory studies of significant benefit. Radiographic findings
include evidence of pancreatic calcifications on abdominal
radiographs or CT scans. Endoscopic retrograde
cholangiopancreatography (ERCP) is the radiologic procedure of choice
in the diagnosis and management of pancreatitis. Although ERCP is
diagnostic in more than 90% of patients, it should be reserved for
those patients who are being evaluated for operations or other modes
of therapy. The management of chronic pancreatitis deals with its
three major components: pain, pancreatic exocrine, and endocrine
insufficiency. Abstinence of alcohol is mandatory for nonoperative
pain relief, and that alone may be successful in some patients.
Unfortunately, many patients require narcotic pain medications, and
addiction may be common. Exogenous administration of pancreatic
enzymes and insulin is also required in a number of patients. The
nonoperative management of pancreatitis has recently included
invasive endoscopic interventions such as stenting of the pancreatic
duct. Although preliminary results are available, numbers are small
and long-term follow-up is limited. Surgical procedures for the
management of chronic pancreatitis include ampullary procedures,
ductal drainage procedures, primarily the lateral
pancreaticojejunostomy or Peustow procedure, and ablative procedures.
Ablative procedures include resection of up to 95% of the distal
gland or in patients with disease primarily of the head of the
pancreas, pancreaticoduodenectomy. Recently, operations that preserve
the duodenum and pancreatic tissue have been described with good
short-term results. Complications of chronic pancreatitis include
common bile duct obstruction caused by fibrosing stenosis of the
intrapancreatic portion of the common duct. The presentation for
common bile duct strictures caused by chronic pancreatitis is quite
variable. Some patients may have no symptoms, with the stricture
diagnosed only by abnormal liver function tests. Elevation of the
serum alkaline phosphatase appears to be the most common abnormal
laboratory finding. Serum bilirubin may be minimally to moderately
elevated and may fluctuate. Abdominal pain with or without jaundice
is another common presentation, although this pain may be difficult
to distinguish from the pain associated with uncomplicated chronic
pancreatitis. ERCP is the best diagnostic examination and offers the
advantage of demonstrating both the pancreatic ductal system and the
biliary tree. The classic finding is a long (usually 2 to 4 cm)
smooth gradual tapering of the common bile duct. The indications for
surgical management are obvious in a patient with significant pain,
jaundice, or cholangitis. The necessity of biliary decompression in
patients with asymptomatic elevations of the liver function tests is
less clear. Substantial evidence, however, suggests that in patients
with chronic biliary obstruction, the incidence of biliary cirrhosis
is increased, therefore warranting surgical management.
Choledochoduodenostomy or Roux-en-Y choledochojejunostomy are the
preferred methods of biliary bypass with excellent short-term and
long-term results. This procedure may be combined with a simultaneous
procedure to relieve the pain of pancreatitis such as a side-to-side
pancreaticojejunostomy. Finally, the differential diagnosis in this
setting must always include pancreatic carcinoma and if warranted,
based on clinical suspicion and operative findings, a
pancreaticoduodenectomy may be indicated. Duodenal obstruction is an
uncommon complication of chronic pancreatitis, occurring only in
those patients with severe pancreatitis. Overall, duodenal
obstruction complicates the course of less than 1% of patients with
chronic pancreatitis. However, in the subgroup of patients with
severe chronic pancreatitis requiring pancreatic ductal drainage, up
to 15% of patients may have evidence of duodenal obstruction.
Patients with duodenal obstruction present with classic signs of
gastric outlet obstruction including nausea, vomiting, abdominal
pain, and weight loss. Most patients are best treated with a
gastrojejunostomy. Pancreatic fistulae are the result of pancreatic
ductal disruption and present as either pancreatic ascites or
pancreatic pleural effusion. In pancreatic ascites, the ductal
disruption allows free leakage of inactivated pancreatic fluid into
the peritoneal cavity. In patients with pancreatic pleural effusions,
the disruption is located posteriorly and therefore tracks up into
the mediastinum, forming a mediastinal pseudocyst, or ruptures
through the pleura into either chest, forming a pancreatic pleural
effusion. Pancreatic ascites or pancreatic pleural effusion can
typically be diagnosed by finding amylase levels in the fluid in
excess of 1000 U/ml or fluid albumin elevations greater than 3 gm/ml.
The initial treatment of patients with internal pancreatic fistulas
should be nonoperative. To minimize pancreatic secretions, the
patient should be given nothing by mouth and total parenteral
nutrition should be instituted. The use of the somatostatin analog,
octreotide, has been suggested as an adjunct for nonoperative
management. Paracentesis or thoracentesis should be performed daily
to minimize the accumulation of fluid. With the use of this regimen,
successful management can be expected in approximately 40% to 60% of
patients. If nonoperative therapy is unsuccessful after approximately
3 weeks, ERCP should also be performed to define ductal anatomy and
to identify the site of the pancreatic leak. If the ductal leak is
located in the tail of the pancreas, a distal pancreatectomy should
be performed. If the leak occurs from the proximal gland, the site of
the leak should be drained into a Roux-en-Y loop of jejunum. Success
can be expected with operative treatment in 85% of patients.
Pancreaticoenteric fistulas are the result of drainage of a
pancreatic abscess cavity or a pseudocyst into an adjacent hollow
viscus. The transverse colon and splenic flexure of colon appear to
be the most commonly involved sites. Most of these patients will
require operative intervention with adequate drainage of the abscess
cavity being the most important factor in the management. The
location of the splenic vein directly posterior to the pancreas and
extending along its tail, body, and neck places it in close
approximation such that pancreatic inflammatory and neoplastic
conditions can contribute to thrombosis. Although traditionally
pancreatic carcinoma was considered to be the leading cause of
splenic vein thrombosis, recent reviews have suggested that 60% to
65% of patients with splenic vein thrombosis may have chronic
pancreatitis. The result of splenic vein thrombosis is the
development of "left-sided" portal hypertension and the formation of
gastric varices along the greater curvature and the fundus of the
stomach, which have the propensity to bleed. Noninvasive evaluation
of patients for splenic vein thrombosis includes ultrasonography, CT
with bolus intravenous contrast, or magnetic resonance imaging. The
diagnosis is usually confirmed by invasive celiac angiography with
venous phase studies. The management of splenic vein thrombosis in
patients with bleeding gastric varices is splenectomy. Removal of the
spleen decreases venous flow by way of the collaterals and
decompresses the associated varices, thereby preventing further
hemorrhage. Success can be accomplished in approximately 90% of
patients undergoing splenectomy. It has long been suggested that
patients with chronic pancreatitis may be at increased risk for the
development of pancreatic carcinoma. Although this relationship has
sometimes been questioned, recent data suggest that chronic
pancreatitis is a risk factor for carcinoma.

http://faculty.washington.edu/pmrainey/pancreas03.doc
Pancreas: Anatomy, Functions and Testing
Acute and Chronic Pancreatitis
Anatomy and Physiology (Overview)
The pancreas is a large, flat, finely lobulated gland associated with
the duodenum. The pancreas is located in the upper part of the
abdomen, hidden by many organs; it is not accessible by physical
examination. It has both exocrine and endocrine glands.
The pancreas consists of a head, neck, body, and tail:
 The head fits snugly into the curve of the duodenum.
 The neck is constricted by the superior mesenteric vessels.
 The body lies above the duodenojejunal flexure, over which it
tapers into the tail and extends close to the spleen.
 The main pancreatic duct runs the length of the pancreas
collecting from branches from the entire tail and body and part of
the head.
 An accessory pancreatic duct drains the anterosuperior part
of the head, and it may join the main duct, or empty independently
into the second part of the duodenum.
Exocrine glands secrete products through a duct either outside of the
body, or into another compartment.
The exocrine portion of the pancreas secretes important enzymes for
digestion into the duodenum.
Endocrine glands secrete hormones directly into the bloodstream
The endocrine portion discharges into the venous system, and secretes
important hormones essential for the regulation of carbohydrate
metabolism.
The cells of the exocrine pancreas cluster into large acini that are
further grouped into lobules. Acinar cells are drained by ductules
that converge into large ducts which terminate in the main pancreatic
duct. Pancreatic juice ultimately drains through the sphincter of
Oddi and Ampulla of Vater, where the pancreatic duct joins the common
bile duct, and drains into the second portion of the duodenum.
 The pancreatic fluid is rich in bicarbonate, which
neutralizes hydrochloric acid that is present in the duodenum from
the stomach.
 This alkaline fluid raises the pH (basic) creating an
alkaline environment for the enzymes in the pancreatic juice to
become active.
 Many of the enzymes that are from the pancreas degrade
proteins.
 They are packaged as inactive forms so that they don't harm
the pancreas (the term would be autolytic - self-destruction, or auto-
digestion), and they become active only in the appropriate setting.
Exocrine Pancreas Secretions
Sodium Bicarbonate: Neutralizes acid entering duodenum from
the stomach, raises pH to 7.5-8, to permit activation of digestive
enzymes.
Amylase: (released in active form) breaks down starches into
simple carbohydrates.
Lipase: (released in active form) breaks down large fat
(lipid) particles into into smaller lipid.
Proteolytic enzyme precursors: Trypsinogen + chymotrypsinogen
(and many others) are proenzymes that, get activated by proteolytic
cleavage after secretion into duodenum (into trypsin and
chymotrypsin), and break down proteins into amino acids.
Released on stimulation by CCK, gastrin, secretin
Endocrine Pancreas Secretions
Insulin: Promotes uptake of glucose by cells (lowers blood
glucose).
Glucagon: Promotes breakdown of liver glycogen stores to
glucose (raises blood glucose).
Q. 1 If the pancreas makes and stores protein-digesting enzymes, then
how come it doesn't just digest itself?
A. 1. The pancreas has several levels of regulation to prevent auto-
digestion from proteolytic enzymes.
1. Proteolytic enzymes are made as inactive precursors "zymogens".
2. They are stored in membrane-bound granules (like in plastic bags).
3. They get activated in a "cascade" fashion, only after being
secreted into the duodenum.
(they can only be activated by the active form of trypsin (made from
trypsinogen, one of the precurssors), and trypsinogen itself can only
be activated after being secreted into the duodenum, because it gets
activated by a duodenal enzyme.)
4. Premature activation of trypsin in the pancreas is prevented by
inhibitors.
5. "Accidental" intrapancreatic release of active trypsin causes
activation of enzymes that destroy the other inactive enzymes, and
lysozyme enzymes can also degrade the proteolytic enzymes.
Q. 2. If the pancreas is so well protected against "accidental"
proteolytic enzyme release, then how does anyone ever get
pancreatitis in the first place?
A. 2. The answer to how trypsinogen gets activated to trypsin is not
clear. However, factors that cause a person to get pancreatitis are
clear. They major factors are duct obstruction, and alcohol (causes
secretion of protein-rich secretions that plug-up small and large
ducts, may also be directly toxic to pancreatic cells.)
Acute Pancreatitis
 Inflammatory disease of the pancreas may be acute or
chronic.
 There are approximately 5000 new cases per year in the US,
with a mortality of about 10%.
 The relative inaccessibility of the pancreas to direct exam
and the nonspecificity of the abdominal pain associated with
pancreatitis make the diagnosis of acute pancreatitis difficult
 And usually dependent on elevation of blood amylase or lipase
levels.
Acute pancreatitis (sudden onset) is inflammation of the pancreas
associated with edema, various amounts of autodigestion, necrosis,
and in some cases, hemorrhage. Acute pancreatitis is thought to
result from inappropriate intrapancreatic activation of proteases,
which causes autodigestion of the gland.
In the United States the two most common causes of the disease
alcoholism (acute alcoholic pancreatitis)
 direct toxin to pancreas
 mechanism not clear
common bile duct stone disease (biliary pancreatitis)
 a stone lodges in the ampulla of Vater, causing an
intermittent obstruction.
Obesity is a major risk factor for severe pancreatitis, likely due to
the increased deposits of peripancreatic fat, which may lead to more
extensive pancreatic and peripancreatic necrosis.
The clinical symptoms are typically an abdominal pain that is usually
constant, moderate to severe, and located in the epigastrium (around
the stomach) radiating to the back. Nausea and vomiting are usually
present, and the abdomen is usually tender.
In most patients (80-90%), acute pancreatitis is self-limited and
subsides spontaneously within 3-7 days after treatment. Treatment
remains largely supportive. Antibiotics are also used to prevent
secondary infection of pancreatic abscesses and pseudocysts.
Complications include
phlegmon which is an inflammatory pancreatic mass that
usually occurs with a severe attack and subsides spontaneously
pseudocyst is a liquefied collection of necrotic debris and
pancreatic enzymes that is surrounded by either a rim of pancreatic
tissue or some adjacent tissues( it has no true epithelial lining
pancreatic abscess is a localized infection of the pancreas
that usually occurs late in the course of a severe attack and may
result in death unless surgical debridement is performed
infection of dead tissue, called infected pancreatic
necrosis, may also occur
pancreatic ascites is due to the disruption of the main
pancreatic duct, often by an internal fistula (abnormal connection)
between the duct and the peritoneal cavity or a leaking pseudocyst,
causing leakage of irritating pancreatic juices into the peritoneum.
Laboratory tests
increased serum amylase usually diagnostic with suggestive
clinical symptoms
need to distinguish between salivary and pancreatic amylase
may measure urine amylase elevation is more prolonged, but
the test is less sensitive
increased serum lipase specific to pancreas
fecal lipase test has low sensitivity but high specificity
for chronic pancreatitis
Macroamylase - rare; false dx of pancreatitis
Ig and amylase complex -
Results: elevated serum amylase x 6-8 times and normal urine
amylase
Other lab data that may help
elevated white blood cell count (WBC)
hyperglycemia (due to decreased insulin release, increased
glucagon release)
hypocalcemia (pathogenesis incompletely understood)
Sonography may reveal edema, dilated ducts, calcification,
and pseudocysts; CT scans and ERCP (cholangiography) are also
helpful. X-rays are primarily used to exclude other diagnoses such
as perforated viscus (a hole in the GI tract).
Chronic Pancreatitis
Chronic pancreatitis is a slowly progressive destruction of the
pancreatic acini with varying amounts of inflammation, fibrosis and
dilation and distortion of the pancreatic ducts. "Chronic relapsing
pancreatitis" is defined as superimposed acute attacks that occur in
the setting of chronic pancreatitis. There is varying degrees of
pancreatic destruction and exocrine/endocrine insufficiency results.
Many of the same conditions associated with acute pancreatitis are
associated with chronic pancreatitis:
 ethanol abuse
 abdominal trauma
 drugs,
 In general, biliary tract disease is not associated with
chronic pancreatitis
In the US the most common cause of chronic pancreatitis:
alcoholism in adults
cystic fibrosis in children
In countries with chronic malnutrition, people with protein-deficient
diets from infancy on, may develop a type of chronic pancreatitis
with extensive calcification. The mechanism is unknown, and it may
have a genetic component. In some cases of chronic pancreatitis the
etiology is unknown.
Clinical manifestations are generally:
moderate to severe intractable abdominal pain which may
persist for a number of years
pancreatic calcifications
diabetes or malabsorption
Weight loss may result from anorexia or associated fat
malabsorption (steatorrhea, like with Olestra potato chips).
Progressive inflammatory disease may result in encasement of
the common bile duct with fibrosis leading to obstructive jaundice
GI bleeding may result from splenic vein thrombosis with
formation of gastric varices and subsequent hemorrhage
When there is greater than 90% destruction of the gland,
malabsorption and endocrine insufficiency with diabetes mellitus
result.
The diagnosis of chronic pancreatitis is considered in the patient
with:
chronic abdominal pain and an associated risk factors for
chronic pancreatitis
pancreatic calcifications, fat malabsorbtion (exocrine
failure)
and diabetes mellitus (endocrine failure)
However, the spectrum is broad; some patients present with diabetes
and others are found incidentally to have pancreatic calcifications
in the absence of any specific symptoms or signs. In the patient
with abdominal pain and weight loss, the differential diagnosis
includes abdominal malignancies, especially carcinoma of the
pancreas, stomach or colon. Other causes of persistent epigastric
abdominal pain include peptic ulcer disease, mesenteric ischemic
disease and even "functional" (psychosomatic) abdominal complaints
when the pain is mild.
Chronic pancreatitis does not cause an elevated serum amylase level
unless associated with a distinct attack. Thus the diagnosis is
often established by the clinical presentation in combination with
imaging studies of the pancreas. Imaging studies (US and CT) may
show pancreatic calcifications or dilated pancreatic ducts.
Cystic Fibrosis (CF)
Inherited disease (autosomal recessive) affecting lungs and
many exocrine glands, including pancreas, salivary, and sweat
Defect is in chloride transport protein in cells, including
ducts of pancreas and salivary glands, resulting in thick mucus, then
duct impaction, obstruction, and destruction
Classic test (now used for screening) sweat chloride test
(greatly elevated in patient with CF)
Confirmatory test DNA genetic testing
Lipid maldigestion (result of pancreatic exocrine lipase failure)
Steatorrhea greasy, foul-smelling, floating stool
Diagnostic test 72 hr (three days!) stool collection for
total fecal fat (grams of fat/day)
Fecal Fat screen random sample - # fat droplets seen in
microscope
Serum carotene (vit.A derivative, fat-soluble)
Treatment of chronic pancreatitis is directed toward prevention of
further pancreatic injury, pain relief and replacement of lost
endocrine/exocrine function.
Complications are usually local and related primarily to the
destruction of the gland itself and associated peripancreatic
diseases rather than systemic processes that occur in acute
pancreatitis
pseudocyst formation
pancreatic ascites
common bile duct obstruction
diabetes,
splenic vein thrombosis
exocrine insufficiency and peptic ulcer.
Endocrine tumors of the pancreas
The endocrine hormonal products of the pancreas are made by clusters
of endocrine cells - "Islets of Langerhans" - distributed throughout
the pancreatic tissue. Each mature islet is composed of four major
classes of secretory cells:
A cells, which secrete glucagon (raises blood glucose level),
B cells (also called beta cells) secrete insulin (lowers blood
glucose levels)
D cells secrete somatostatin (slows many bodily functions "somato-
body, stati-static)
PP cells secrete pancreatic polypeptide (function, if any, unknown)
Pancreatic islet cell tumors can arise from any of these cell
populations. They may secrete one or more biologically active
peptide hormones giving rise to a number of associated symptoms that
can be recognizable as part of a syndrome. The unregulated release
of hormones by endocrine tumors causes severe symptoms.
Gastrinoma
most common hormone-secreting islet cell tumor of the
pancreas
secretes gastrin, a hormone that stimulates gastric acid-
secretion in the stomach
most people with gastrinomas develop severe peptic and
duodenal ulcers due to oversecretion of stomach acid
may be benign or malignant
blood tests for elevated gastrin (
in patients with severe ulcer disease suggests the presence of a
gastrinoma
confirmatory test provocation with secretin when serum
level of gastrin increases promptly by more than 200 ng/L

http://www.medicine.northwestern.edu/residentnet/Dan's%
20stuff/Complications%20of%20Pancreatitis.doc
Complications of Pancreatitis
Acute pancreatitis is typically caused by gallstone disease or
alcohol. Clinical deterioration or failure to improve with
conservative management should prompt investigation for
complications; CT scan has a limited role in the acute setting, but
is useful to identify the presence of certain complications. These
complications include:
1. Pancreatic abscess
2. Pseudocyst: 1-4 weeks after onset of symptoms
3. Pancreatic necrosis with or without hemorrhage
Also: DIC, ARDS, hemodynamic collapse. Pancreatic ascites,
occasionally massive, may result from periotoneal inflammation,
leakage from pancreatic ducts or discharge of pseudocyst contents
into peritoneal cavity.
By contrast, chronic pancreatitis is usually the result of chronic
alcohol ingestion (not gallstone disease). Chronic inflammation and
fibrosis will eventually result in destruction of exocrine and
endocrine tissue, leading to the classic triad of chronic
pancreatitis: calcification, steatorrhea, and diabetes. This triad
is relatively uncommon, owing to the substantial exocrine and
endocrine reserve of the pancreas:
destruction is usually required for clinical relevance.
Complications of chronic pancreatitis are:
1. Steatorrhea: may result in fat-soluble vitamin deficiency
(think coagulopathy and osteoporosis)
2. Diabetes Mellitus: both insulin producing beta cells and
glucagon producing alpha cells are destroyed. Glucagon release in
response to hypoglycemia in these patients is therefore impaired,
putting pts at risk for severe hypoglycemia with insulin therapy;
aggressive glycemic control is therefore not recommended. The
presence of DM is an independent predictor of mortality in chronic
pancreatitis.
3. Pseudocyst: a localized collection of pancreatic secretions
encased in granulation and fibrous tissue (no true epithelial lining)
persisiting for
pancreatic duct with extravasation of amylase rich fluid. Accounts
for
chronic pancreatitis. Complications: pain, palpable mass,
nausea/vomiting (from stomach/duodenal compression), jaundice (from
compression of bile duct), infection, hemorrhage (termed hemosuccus
pancreaticus when blood drains into the duodenum from the pancreatic
duct), and pancreatic ascites from rupture into the peritoneal cavity
The old rule for surgical drainage was to drain cysts
for
pseudocysts as 60% will spontaneously regress and only 10% will
develop complications. Nonsurgical drainage is now the rule and
include two methods:
a. Percutaneous: possible complications of infection, fistula
formation, incomplete drainage.
b. endoscopic - A communication is established between pseudocyst and
epithelial lined viscus (stomach or duodenum). Requires cyst wall to
be<1cm from intestinal lumen.
4. Pseudoaneurysm: results from pressure/enzymatic digestion of
an artery by an adjacent pseudocyst. The pseudoanerysm may then
rupture into the pseudocyst, and adjacent viscus, or the peritoneal
cavity. The splenic artery is the most common. Treatment is with
angiographic embolization regardless of whether bleeding has yet
occurred.
5. Splenic vein thrombosis: 5X more common in chronic versus
acute pancreatitis. Results in gastric varices, which may then
bleed. Severe bleeding can be treated with splenectomy.
6. Biliary or Duodenal Obstruction: inflammation, fibrosis, or
pseudoaneurysm in the pancreatic head. Surgical bypass may be
necessary.
7. Pancreatic Fistula: these come in 2 varieties. External
(pancreaticocutaneous) pancreatic fistulas are a result of surgical
or percutaneous therapy, usually for a pseudocyst. Internal
pancreatic fistulas occur in the setting of chronic pancreatitis
following pseudocyst rupture, resulting in pancreatic ascites or
pancreatic pleural effusion.
The rationale behind therapy in both types is pancreatic rest to
diminish pancreatic secretions: NPO with TPN. Ocreotide 100 mcg SQ
q8h, as well as endoscopic stent placement across the site of PD
disruption, hastens closure of the fistula.
8. Malignancy: chronic pancreatitis is associated with a 4%
lifetime risk of pancreatic cancer. Endoscopic ultrasound is being
used with increasing frequency to image a suspicious pancreatic mass
and to obtain tissue.
Pancreatic Pleural Effusions
Pleural effusion occurs quite commonly in association with acute
pancreatitis; one study revealed a pleural effusion in 2 of 3 pts
with their 1st episode. 75% are bilateral; if unilateral, it is
twice as likely to be left sided than right sided. These pleural
effusions are typically small and are exudative. The abdominal
symptoms of acute pancreatitis dominate the patient's complaints.
Pleural effusions resulting from chronic pancreatitis occur as a
result of a draining pseudocyst into a fistulous tract. In this
setting, abdominal symptoms are often diminished as the pseudocyst
may be decompressed by the fistula tract. These effusions are
usually left sided.
The major differential for elevated amylase in pleural fluid analysis
is acute pancreatitis, chronic pancreatic pleural effusion (both of
which result in a very high pleural amylase level, e.g.
esophageal rupture, and malignancy. This is defined as pleural fluid
amylase greater than ULN of serum, or pleural:serum amylase
Pancreatic pleural effusions is associated with pancreatic
isoenzymes, while salivary isoenzymes are present with malignancy and
esophageal rupture.
2 Pearls:
1. In a patient with clinical pancreatitis who has a palpable
abdominal mass, consider pseudocyst or malignancy
2. The presence of diffuse pancreatic calcifications on plain
films is fairly specific for chronic pancreatitis
A note on post ERCP management: post ERCP amylase elevation is
common, with an incidence of 75%. However, the incidence of clinical
post ERCP pancreatitis with amylase elevation and abdominal pain is
only 5%. Management is no different than any other cause of
pancreatitis: bowel rest, intravenous fluids and pain control.

http://usagiedu.com/articles/html/pan.htm
Treatment of Pain in Chronic Pancreatitis
1. A patient with evidence of chronic pancreatitis on ERCP, no
pseudocyst, biliary stricture, duodenal stenosis, peptic ulcer
disease or pancreatic cancer suffers from chronic pain felt to be
secondary to chronic pancreatitis. The next step should be:
a. endoscopic pancreatic sphincterotomy or stenting
b. pain management with long-acting narcotic therapy
c. distal pancreatectomy with pancreato-jejunostomy
d. low fat diet, non-narcotic analgesics, assess severity of pain and
then consider 8 week trial of high dose pancreatic enzyme therapy
2. Regarding surgical therapies for relief to pancreatic pain
a. pancreatic decompression procedures produce relief of pain in 80%,
pain relief persists for
b. decompression of the pancreatic duct surgically requires a duct
diameter of at least 6mm
c. surgical decompression is associated with a operative morbidity
exceeding 20%
d. a lateral pancreatojejunostomy is usually referred to as a Peustow
procedure
e. distal pancreatectomy is an effective surgical approach for relief
of pain in patients with non-dilated pancreatic ducts
f. total pancreatectomy almost always resolves the chronic pain from
pancreatitis.
g. resection of the pancreatic head is more effective than distal
pancreatectomy in pain control
True or false
3. Celiac plexus nerve blocks have not been found to benefit most
patients with chronic pancreatitis and pain.
4. Pancreatic calcifications represent calcified areas of the
pancreatic parenchyma which have undergone auto-digestion.
5. When pancreatic stones are presents in patients with pain from
chronic pancreatitis, the stones should be removed, as pain usually
improve.
6. To improve compliance with the use of pancreatic enzyme for the
relief of pancreatic pain, enteric coated preparations should be
prescribed, as less number of capsules need to be ingested.
7. Chronic pancreatitis pain tends to "burn-out" with time, relief of
pain coincides with the appearance of pancreatic calcifications and
onset of pancreatic exocrine insufficiency.
8. The use of acid-reducing therapy to relieve pancreatic pain has
not been found to be useful.
9. Octretride given subcutaneously should be tried in all patients
who fail a trial of pancreatic enzyme supplementation.
10. In theory, pancreatic enzyme supplementation should work in
relieving pancreatic pain as:
a. the presence of pancreatic enzymes in the duodenum directly
inhibit production of additional enzymes by the diseased pancreas
b. patients with chronic pancreatitis do not secrete enough enzymes
to denature CCK-releasing peptide, resulting in continuos stimulation
of the pancreas
c. the presence of orally-administered pancreatic enzymes suppresses
the release of CCK from the small bowel
d. the orally-administered pancreatic enzymes improve steatorrhea,
leading to improvement of abdominal pain and distention.
11. Regarding the placement of pancreatic stents for the treatment of
pain due to chronic pancreatitis
a. pancreatic duct and parenchymal injury can be induced by the
placement of stents, even if the stents are left in place for a
relatively short period of time
b. stenting of the pancreatic duct results in relief of pain in most
patients
c. short-term stenting is safe, and can be used as a "trial" to
determine which patients will respond to long-term stenting
d. stenting should be done when intraductal pancreatic stones are
identified.

Hello Brenda,
I hope you are doing well. I have not been doing so good. I have been
trying to answer all the post that I have missed. I am kinda getting
tired, but I wanted to say hello to you. How is your Mom doing?
Take Care and I will talk to you soon.
Sally

I have tried to answer all the post that I missed. I sure hope that I
did not miss anybody, If I did, just post to me and I will make sure
I post back to you. BUT......I DO NOT SEE MY FRIEND KELLY....
Kelly---where are you at? I look forward to your sweet e cards and
your nice post and I do not see you.I am sorry that I have not posted
to you in awhile, but I have been sick,. I hope you are ok. Your
friend
Sally

Hello Denise,
WOW, these sound so good. I LOVE cherries. My mom said she is going
to make them for me. Thanks for the recipes. Do you have any more?
Sally

Hello Kin,
Welcome to the board. I hope you like this place as much as I do.
Sally

Hello Martin,
I would like to Welcome you to the board. Sorry I was not around when
you came in, but there are a bunch of good folks here.
Sally

Hello Dave,
It sure has been a long time since I have talked to you. Sorry about
that. I have been in the hospital alot here lately. I hope that you
are doing well. That seems Great about your invention. I wish you the
best. Take care and come on the board and talk to me .
Sally

Hello Ruthie,
I hope this finds you well today.
Sally

Hello Annette and Beauford.
I am glad you are doing good. I understand about them weeds. My mom
has been weeding her flower garden this past week. I just love
flowers.
Sally

Hello Abby,
Sorry I am late getting to say Welcome, but 'Better Late than Never '
huh? I have been in the hospital , in and out for the past 3 weeks,
that is why I am just writing to you. I hope this finds you and your
husband well.
Sally

Hello Rhonda,
I am so glad to hear that Amanda is doing better. Tell her to enjoy
her summer vacation. See you soon.
Sally

Hello Andre'
I don't think I have met you. (Nice to met you) I have been away for
the past 3 weeks, and I am just getting caught up on my post and saw
this one and wanting to wish you a VERY HAPPY BELATED BIRTHDAY!!!!!
Sally

Hey Stacey and Cecilia,
I am the most nauseated in the mornings too. I wonder why ? And I am
hungry then too. I thought I was the only one.
Sally

Hi Hellen,
I am just getting around to posting after being gone from the board
for around 3 weeks. I have been in the hospital 3 different times,
but I saw that you are New and I have never met you so I wanted to
say Hello and Welcome to the board. I just LOVE this site, there are
so many people here to help you and cheer you up. Robert is the best
for giving information. I guess you have already met him. Well, I
look forward to talking to you soon.
Sally

Hey Polly,
I just read this story, ( I just love reading your post) I had a ERCP
too, but I was sleep during mine, but I hurt so bad afterwards that I
had to go back to the ER. That is terrible. They must upset things
inside of you when they do the ERCP. I thought I was having a bad
time, but I can see that you have been having a Terrible time. I am
so sorry. I hope everything is fine with your son now. I look forward
to talking to you.
Sally

Robert,
Thank you for posting this. I know you posted it a while back but
since I have missed alot in the past weeks, I wanted to go back in
the post and see what i missed. Since the doctors just told me that I
have Chronic Pancreatitis, this information is very helpful. Thanks
again.
Sally

Robert,
I am so sorry that your daughter was in the hospital. I know that I
am late in saying this, but I hope she is better. I am praying for
her.
Sally

First of all, I would like to let EVERYBODY know where I have been. I
am sorry that I have been gone for so long. I have been in the
hospital 3 different times. My doctor told me that I have CRONIC
PANCREATITIS. I had a ERCP. Oh boy that was terrible. Afterwards, I
hurt sooo bad, I had to go back in the ER. I am not feeling really
great right now, but I wanted everybody to know that I have not
forgot about you. I am going to go back in the post and read and post
to you. I will sit at the computer until I can't then I will go lay
down.
Sally

The chat room is now open folks
Gary

Will be back in about 2 weeks. Have set my group preferences to "no mail."
Diane
Colorado Springs, CO
E-mail: BootsScoochnBoogie@...
Personal Web Pages: http://Tennchief.home.att.net
Business Web Site: http://SayItMyWay.home.att.net

Hi Diane & Bil
Scooch, Boogie & Shadow
Yall take care and have a wonderful time.
With Warmest Regards & God Bless
Gary Morris ~ Virginia
Customer Service Rep moderator.
Phone 434-490-7191
gary@...
http://www.thepancreatitisplace.org/

We're all packed . . . just finishing up a few last minute details, then as soon
as the groomer calls to tell us our furballs are ready, we'll be on the road.
We're going to Arkansas for our friends' wedding, then on to Purina Farms near
St. Louis for Beardie Camp. We'll be back about the 13th or 14th. If you need
to reach us urgently, please leave a voice mail on either our home phone (719)
633-1835 or our cell phone (719) 440-1818. We will not have e-mail access at
all during this trip, usually don't have any cell phone signal all the way
across Kansas, and don't expect to have a signal in the rural area of Arkansas
where we'll be staying. We will check messages whenever we can.
Diane & Bill
Scooch, Boogie & Shadow
Colorado Springs, CO
E-mail: BootsScoochnBoogie@...
Personal Web Pages: http://Tennchief.home.att.net
Business Web Site: http://SayItMyWay.home.att.net

Hi Lisa,
We have not really met yet and I have no idle what Intrathecal
Drug Delivery is myself. The last few lines in your post really touch
my heart Lisa. That is why I had to respond to your post. To often
people never learn their limitation as you have. As we get older or
even worse come down with this horrible illness. We just can't do
the things we use to. This is so hard for many of us to except.
Lisa you have found happiness in what you have and not in what
you lost. I thing that is so great and you must really be bless. I
know you love being a nurse and I'm sure you where one mighty fine
nurse. I could fell it in the words you wrote. You know those days
maybe gone and you have decided not to let this illness get the best
of you. Lisa you just keep enjoy being a House Wife and a Mom. I
think it's the best job in town.
With Warmest Regards & God Bless
Gary Morris ~ Virginia
Customer Service Rep moderator.
Phone 434-490-7191
gary@...
http://www.thepancreatitisplace.org/

Wow! Thank you, Robert, for all of this great
information. Reading this made me think of
something...
Sean's blood count was a little low today, so they're
going to give him a unit of blood. Reading about
Lexapro and how it increases the risk of bleeding and
the fact that they restarted this today and restarted
Sean on Heparin, made me wonder if that could be the
cause of his low blood count. I'm definitely going to
ask tomorrow.
Thanks!
Abby
--- robertatdiabetes

=====

This is a good recipe, if you love squash like I do. It only has 0.3g
of fat in it.
~*~Denise~*~
Caregivers Moderator
deniseatdiabetes@...
sdhammett@...
http://www.thepancreatitisplace.org/

If you are a diabetic like Robert is, you will LOVE this recipe. AND
I love them too. You can not tell they are diabetic. Please let me
know if you like them as well.
~*~Denise~*~
Caregivers Moderator
deniseatdiabetes@...
sdhammett@...
http://www.thepancreatitisplace.org/

I just love this recipe. It is not like the regular Shepherd's Pie,
But VERY good, and quick.
~*~Denise~*~
Caregivers Moderator
deniseatdiabetes@...
sdhammett@...
http://www.thepancreatitisplace.org/

This is a real good recipe that I have cooked. I hope you love it as
much as we do. This one also is from my friend Marilyn.
~*~Denise~*~
Caregivers Moderator
deniseatdiabetes@...
sdhammett@...
http://www.thepancreatitisplace.org/

Another great recipe from Marilyn,
1 or 2 of these are fine, just don't over do it !!!!
~*~Denise~*~
Caregivers Moderator
deniseatdiabetes@...
sdhammett@...
http://www.thepancreatitisplace.org/

Hello Everyone,
A Close friend of mine, Marilyn passed on some good recipes that are
low fat and good for the diabetic. I hope you enjoy.
~*~Denise~*~
Caregivers Moderator
deniseatdiabetes@...
sdhammett@...
http://www.thepancreatitisplace.org/

http://www.biomedicalabs.com/post_surgical_healing_wellness_tips.htm
Post Surgical Healing
GETTING BETTER AFTER SURGERY
The speed at which you recover following surgery and the completeness
of your recovery depends on a number of factors, most of which are
under your control. The following tips will help your body repair
itself as quickly and completely as possible:
Rest or immobilization of the affected area helps recovery. A splint
or brace maybe advisable. (Please consult your health care provider.)
Sleep as often as you can. Your body repairs itself during sleep.
Many people compromise the speed of their recovery by trying to get
up and about too soon.
Stay hydrated. Fluids are important as they help keep your tissues
hydrated. Aim for eight cups of fluid a day. Do not consume
caffeinated beverages as these are diuretics and cause the body to
lose water.
Eat well. Healthy foods are critical to the complete repair of your
body. Protein is particularly important as it contains amino acids
which will help build your tissues. Consider a protein-rich
multivitamin shake (available from pharmacies and supermarkets).
Think positive thoughts. Repeatedly visualizing your prompt and
complete recovery may well help you get better faster and will keep
depression at bay.
Take Recovery with Nutricol to support tissue repair and to help
improve quality of life*.
REDUCING YOUR RISK OF INJURY
Your doctor will inform you of the period of time you will need to
immobilize the areas affected by the surgery or injury. After this
period there are many things you can do to lessen your risk of
injury. Most of these include strengthening the area by proper
stretching and exercises, and reducing strain on your muscles and
connective tissues.
Learn to relax. Letting go of tension in the muscles surrounding the
area of trauma helps to reduce pain. Try deep breathing exercises,
listen to music or relaxation tapes, or visualize a pleasant activity
such as lying on a beach or soaking in a warm bath. Developing
relaxation skills can give you a greater feeling of control over pain
and a more positive outlook.
Avoid chronic intake of drugs that may accelerate tissue breakdown.
Certain medications, such as ASA, can contribute towards breakdown of
tissue structures including joint cartilage.
Pace yourself. Remember to pace yourself when doing heavy or
prolonged work and make sure you take frequent rests. Pacing allows
weakened muscles a chance to recuperate.
THE IMPORTANCE OF EXERCISE
Your muscles, bones and many other tissues respond to exercise by
becoming stronger. The most beneficial activity for your body is
weight-bearing exercise, which forces you to work against gravity.
Weight-bearing exercises include walking, jogging, hiking, stair-
climbing, weight training, tennis and dancing. Your muscles and bones
respond to exercise by increasing in strength and mass.
Developing muscle strength will help you maintain better balance and
become more flexible. This can help prevent falls that could cause
bone fractures and other injuries. If you are experiencing severe
pain, your choice of exercise may be limited. Swimming or other
exercise performed in water will reduce impact on your body and
likely be less painful.
While exercise is good for someone with Osteoporosis, it is important
not to put any sudden or excessive strain on your bones. Your doctor
can recommend specific exercises to strengthen and support your back,
which will help you to reduce the risk of fractures. Always consult
your doctor before beginning an exercise program. He or she may refer
you to a physical therapist who can advise you of the forms of
exercise that are likely to be helpful and those that could be
harmful.
Exercise helps reduce pain, inhibits further bone breakdown and can
help you maintain a healthy weight.
PREVENTING FALLS
Preventing falls is particularly important for people with
osteoporosis since falls increase the likelihood of fracturing a bone
in the hip, wrist, spine or other part of the body. In addition to
the environmental factors listed below, falls can also result from
impaired vision and/or balance, chronic diseases that impair mental
or physical functioning and certain medications such as sedatives and
antidepressants. If you have osteoporosis, it is important that you
be aware of any physical changes you may be experiencing that may
affect your balance or the way you move. These changes should be
discussed with your doctor or other healthcare practitioner.
Some tips to help eliminate the environmental factors that lead to
falls include:
When outdoors
Use a cane or walker to increase stability.
Wear rubber-soled shoes to improve traction.
Walk on grass when the sidewalks are slippery.
In winter, consider carrying salt or kitty litter to sprinkle on icy
sidewalks.
Use carpet runners to increase traction in slippery outdoor areas
such as patios.
When indoors
Keep rooms clutter-free, especially the floors.
Mop up floor spills. Highly polished floors can become particularly
slippery if wet.
Wear supportive, low-healed shoes.
Avoid walking in socks, stockings, or slippers. Use footwear
with "skid-proof treads."
Make sure that carpets and area rugs have skid-proof backing or are
tacked to the floor.
Make sure that stairs have handrails on both sides and that
stairwells are well lit.
Install grab bars on bathroom walls near tub, shower, and toilet.
Use a rubber bath mat or appliques in shower or tub. Clean often to
remove slippery soap-scum.
Keep a flashlight with fresh batteries beside your bed.