Pancreatitis Facts From All Over...

 

NOTE:
Before you read from here, know that I am posting and saving this information for my own benefit; as well as for those of you that might want to know more about Casey's disease, diagnosis and prognosis. Or even for your own info.
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Stolen from Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins

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Good Morning,
Having done a million hours of searching online over the past 3 years, it has occurred to me that although I find interesting things about Chronic Pancreatitis, I have yet to find that 'magical' diagnosis/prognosis as it applies to her.

Casey has had two days of excruciating and debilitating pain.

Rough days for her...
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Please pray.
*Please do not feel as though you must read this all.

XOXO
Me

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Free Web Counter

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I hope that is large enough to read.

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Copyright Details for bottom two pictures: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.


Chronic Pancreatitis:

• Chronic Pancreatitis is an ongoing inflammation of the pancreas over a prolonged period. Most cases of chronic pancreatitis are caused by alcohol overuse.
• Complications of Chronic Pancreatitis are secondary conditions, symptoms, or other disorders that are caused by Chronic Pancreatitis. In many cases the distinction between symptoms of Chronic Pancreatitis and complications of Chronic Pancreatitis is unclear or arbitrary.
• Chronic pancreatitis is a painful condition of the pancreas.
• Some evidence suggests that chronic pancreatitis may increase the risk of pancreatic cancer.

(Source: excerpt from What You Need To Know About Cancer of the Pancreas: NCI)

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Treatment (Tx)

• I.V. fluid replacement,
• morphine,
• diazepam,
• antibiotics,
• calcium gluconate,
• insulin

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The list of complications that have been mentioned in various sources for Chronic Pancreatitis includes:

• * Abdominal pain
• * Diabetes
• * Mild hyperglycemia
  
• * Malabsorption
• * Pancreas calcification
  
• * Insulin deficiency
• * Glucagon deficiency
• * Hypoglycemia unawareness
• * IGT (Impaired Glucose Tolerance)
• * Diabetes
• * Type 1 Diabetes
• * Type 2 Diabetes
• * Pancreas cyst
• * Pancreas abscess

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Complications and sequelae of Chronic Pancreatitis from the Diseases Database include:

• * Diarrhea
• * Hyperglycemia
• * Back pain
• * Parotid gland enlargement
• * Pancreatic pseudocyst
• * Abdominal pain
• * Malabsorption syndrome

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Obstruction

• Gallstone pancreatitis
• Choledocholithiasis
• Ampullary tumors
• Pancreatic tumors
• Metastatic carcinoma to pancreas
• Periampullary diverticulum
• Choledochocele
• Choledochal cyst
• Duodenal cyst
• Pancreatic calculi
• Pancreatic duct stricture*
• Pancreatic pseudocyst
• Pancreatic abscess
• Sclerosing cholangitis
• Hypertensive sphincter of Oddi

Stenosis or fibrosis of the papilla*

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Congenital/inherited disorders

• Pancreas divisum*
• Hereditary pancreatitis*
• Cystic fibrosis*
• Annular pancreas
• Heterotopic pancreas
• Duodenal duplication
• Alpha1-antitrypsin deficiency*

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Toxins

• Alcohol*
• Methanol
• Organophosphate insecticides
• Scorpion venom
• Occupational chemicals

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Drugs

• Azathioprine
• 6-Mercaptopurine
• Thiacide diuretics
• Furosemide
• Ethacrynic acid
• Tetracycline
• Sulfonamides
• Nitrofurantoin
• Metronidazole
• Erythromycin
• Pentamidine
• Didanosine
• Sulfasalazine
• 5-Acetylsalicylic acid products
• l-Asparaginase
• Oral contraceptives
• Corticosteroids
• Estrogens
• Valproic acid
• Methyldopa
• Cimetidine
• Ranitidine
• Sulindac
• Acetaminophen
• Salicylates
• Octreotide

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Metabolic disorders

• Hypertriglyceridemia
• Hypercalcemia
• Hyperparathyroidism*

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Trauma

• Blunt or penetrating trauma*
• Surgical trauma
• Endoscopic retrograde cholangiopancreatography
• Endoscopic sphincterotomy
• Sphincter of Oddi manometry

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Vascular causes

• Postoperative pancreatitis
• Atherosclerotic emboli
• Cardiopulmonary bypass surgery
• Malignant hypertension
• Ergotamine overdose
• Systemic lupus erythematosus
• Polyarteritis nodosa

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Infections

• Bacterial Mycoplasma
• Campylobacter jejuni
• M. tuberculosis
• Legionella
• Leptospirosis
• M. avium complex

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Viral

• Mumps
• Rubella
• Hepatitis A, B, C
• HIV
• CMV
• Coxsackievirus B
• Epstein-Barr
• Adenovirus
• Varicella
• Echo virus

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Fungal:
Candida albicans infection
Aspergillosis

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Parasitic

• Clonorchiasis
• Ascariasis
• Cryptosporidiosis
• Toxoplasmosis

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Miscellaneous

• Penetrating gastrointestinal ulcer
• Duodenal Crohn's disease
• Protein-calorie malnutrition
• Tropical pancreatitis*
• Reye's syndrome
• Hypothermia
• Idiopathic pancreatitis*
• Posttransplantation
• Food allergy
• Chronic renal insufficiency
• Severe burns
• Long-distance running
• Bulimia
• Eosinophilic pancreatitis

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• ❑ Acute and Chronic pancreatitis is a life-threatening emergency. Provide meticulous supportive care, and continuously monitor the patient.
• ❑ Monitor the patient vital signs and pulmonary artery pressure closely.
• ❑ Monitor the patient fluid intake and output and electrolyte levels.
• ❑ Assess the patient for crackles, rhon-chi, decreased breath sounds, or respiratory failure.
• ❑ Observe the patient for signs of calcium deficiency, such as tetany, carpopedal spasm, cramps, and seizures.

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CLINICAL TIP:
Serum calcium levels decrease in acute pancreatitis, possibly from fat necrosis, resulting in a binding of calcium with free fatty acids.

• Muscle twitching,
• tremors,
• and irritability are signs of decreased calcium levels.

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• ❑ Administer analgesics, as needed, to relieve the patient’s pain and anxiety.
• ❑ Observe the patient for adverse reactions to antibiotics: nephrotoxicity with aminoglycosides, pseudomembranous enterocolitis with clindamycin, and blood dyscrasias with chloramphenicol.
• ❑ Monitor the patient for complications due to total parenteral nutrition, such as sepsis, hypokalemia, overhydration, and metabolic acidosis.
• ❑ Observe the patient for signs of sepsis, such as fever, cardiac irregularities, changes in arterial blood gas measurements, and deep respirations.

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National Digestive Diseases Information Clearinghouse
2 Information Way
Bethesda, MD 20892-3570
E-mail: nddic@info.niddk.nih.gov

The National Digestive Diseases Information Clearinghouse (NDDIC) is a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). NIDDK is part of the National Institutes of Health under the U.S. Department of Health and Human Services. Established in 1980, the clearinghouse provides information about digestive diseases to people with digestive disorders and to their families, health care professionals, and the public. NDDIC answers inquiries; develops, reviews, and distributes publications; and works closely with professional and patient organizations and Government agencies to coordinate resources about digestive diseases.

Publications produced by the clearinghouse are reviewed carefully for scientific accuracy, content, and readability.

This e-text is not copyrighted. The clearinghouse urges users of this e-pub to duplicate and distribute as many copies as desired.

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Topic Author(s): Arnold C. Friedman, MD
Submitted by: Gastrointestinal Learning File -
© ACR -
Author Info Affiliation: ACR Learning File® Approved By: James G. Smirniotopoulos, M.D. -
Editor Info Affiliation: Uniformed Services University

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In the Western Hemisphere, Europe, and Japan the most common cause of chronic calcifying pancreatitis is alcoholism. Other etiologies include idiopathic (up to 40%), biliary tract disease (usually acute rather than chronic), hyperparathyroidism, hereditary pancreatitis, cystic fibrosis, trauma, tropical pancreatitis, and hyperlipidemia.

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CLINICAL FINDINGS:
Chronic pancreatitis can present with mild recurrent bouts of pain, constant abdominal or back pain, or in a small number of patients, painless exocrine and endocrine deficiency. Alcoholism is usually present for 5-10 years prior to the development of clinical pancreatitis. Initially, exocrine function is minimally impaired, but as insufficiency develops, fat and protein malabsorption occur with weight loss. Diabetes occurs in 10% of cases and impaired glucose tolerance in 14-90%. Duodenal obstruction and/or obstructive jaundice may occur in 45% of patients with moderate or advanced chronic pancreatitis.

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PATHOLOGY:
Chronic calcifying pancreatitis is characterized by a nodular, misshapen, hard gland that can be enlarged or shrunken. Calculi are present and are almost always within the ductal system. They vary in size from microscopic concretions to 1-2 cm stones.

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RADIOLOGY:
Demonstration of pancreatic lithiasis on plain films is a fast and inexpensive means of confirming a clinical diagnosis of chronic pancreatitis and effectively excluding carcinoma. In various series the frequency of plain film calcification has varied from 20 to 50% in alcoholic chronic pancreatitis. By contrast, only 2% or less of patients with chronic pancreatitis from biliary disease develop pancreatic calculi.


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SONOGRAPHY:
Due to the presence of fibrosis within the gland, there is sometimes sonographic evidence of an inhomogeneously abnormal echo texture often accompanied by calcifications.
These calcifications are in the ductal system; their distribution may be focal or diffuse, and if large enough they are associated with acoustical shadowing. The gland is often irregular in outline and there may be enlargement (focal or diffuse) or parenchymal atrophy. Pancreatic ductal dilatation is often visible due to obstructing stones or stricture.

Chronic pancreatitis can be associated with thrombosis of the portal venous system. This usually involves the splenic vein; however, extension to involve the main portal vein can also occur.

Echogenic thrombus may be identified within the involved portion of the vein accompanied by demonstration of collateral channels. In some instances, the obstructed vein itself cannot be sonographically identified.


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CT:
The gland in chronic pancreatitis can be normal in size or enlarged or it may be small, atrophic and replaced by fat. When the gland is enlarged, this enlargement may be focal or diffuse. Focal enlargement due to chronic pancreatitis (which is nearly always in the pancreatic head) is hard to distinguish on CT grounds alone from carcinoma unless punctate calcifications are present as these are almost never found in carcinoma (except sometimes following chemotherapy). The incidence of pancreatic carcinoma is low (except for familial pancreatitis) in patients with chronic pancreatitis. The calcifications that are often present in chronic pancreatitis are easily seen on CT (which is the most sensitive modality for their demonstration) and are usually multiple. They may occur in only one part of the gland or be present throughout.

Pancreatic ductal dilatation (greater than 3 mm) is often present, especially when a focal mass with calcification involves the head.
The ductal dilatation may be irregular (73%),
smooth (15%),
or beaded (12%).
Common bile duct dilatation may be associated. Occasionally in chronic pancreatitis, CT may show only a markedly dilated beaded pancreatic duct which can simulate a number of small intrapancreatic pseudocysts.

The presence of thrombosis in the portal system can be inferred when a vein fails to opacify normally following intravenous contrast injection and collateral channels are demonstrated.

Patients with chronic pancreatitis can have all the symptoms and signs of pancreatic carcinoma. If a noncalcified focal mass is found in the pancreas of such a patient, then pancreatic carcinoma has to be considered. The presence of the characteristic dense calcifications of chronic pancreatitis within a mass makes it unlikely that it represents a pancreatic cancer. If a diagnostic dilemma exists, then a percutaneous needle aspiration should be considered.

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False Positives/Negatives

Chronic pancreatitis and pancreatic carcinoma share many CT features, and occasionally, differentiation may be impossible. Obliteration of the fat sleeve around the superior mesenteric artery has been described in both chronic pancreatitis and pancreatic carcinoma.

Pseudotumoral enlargement around focal pancreatitis with extensive fibrous tissue proliferation usually fails to enhance after the administration of contrast material. This characteristic makes the differential diagnosis of pancreatic carcinoma difficult.
So tell me, did you get this far?

http://www.emedicine.com/med/TOPIC1721.HTM
Pancreatic calcifications, often considered pathognomonic of chronic pancreatitis, are observed in approximately 30% of cases.


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PROGNOSIS

* The prognostic factors associated with chronic pancreatitis are age at diagnosis, smoking, continued use of alcohol, and the presence of liver cirrhosis.

* The overall survival rate is 70% at 10 years and 45% at 20 years. In an international study, 559 deaths occurred among patients with chronic pancreatitis, compared to an expected number of 157, which creates a standard mortality ratio of 3.6 (confidence interval 3.3-3.9). Taking the opposite view, the 10-year mortality rate is 30%, and the 20-year mortality rate is 55%.

* The risk of developing pancreatic cancer is approximately 4% at 20 years.
Source: Office of Rare Diseases


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Chronic Pancreatitis is listed as a "rare disease" by the Office of Rare Diseases (ORD) of the National Institutes of Health (NIH).
This means that Chronic Pancreatitis, or a subtype of Chronic Pancreatitis, affects less than 200,000 people in the US population.

Source - National Institutes of Health (NIH)

More links.




http://en.wikipedia.org/wiki/Chronic_pancreatitis

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1891454

http://www.touchgastroenterology.com/endoscopic-therapy-chronic-pancreatitis-a7848-1.html

http://www.angelfire.com/md/danil/nephrology.html

http://people.virginia.edu/~wmd4n/pgdt/ch3s5.html

http://www.angelfire.com/sc2/lupiebeth/digestiveterm.html

Dr. Pfau:
http://local.yahoo.com/info-30970213-pfau-patrick-r-md-adult-gastroenterology-clinic-madison

http://www.emedicine.com/med/topic1721.htm

Background
Chronic pancreatitis is commonly defined as a continuing chronic inflammatory process of the pancreas, characterized by irreversible morphological changes. This chronic inflammation can lead to chronic abdominal pain and/or impairment of endocrine and exocrine function of the pancreas. Chronic pancreatitis usually is envisioned as an atrophic fibrotic gland with dilated ducts and calcifications. However, findings on conventional diagnostic studies may be normal in the early stages of chronic pancreatitis, as the inflammatory changes can be seen only by histologic examination.


By definition, chronic pancreatitis is a completely different process from acute pancreatitis. In acute pancreatitis, the patient presents with acute and severe abdominal pain, nausea, and vomiting. The pancreas is acutely inflamed (neutrophils and edema), and the serum levels of pancreatic enzymes (amylase and lipase) are elevated. Full recovery is observed in most patients with acute pancreatitis, whereas in chronic pancreatitis, the primary process is a chronic irreversible inflammation (monocyte and lymphocyte) that leads to fibrosis with calcification. The patient with chronic pancreatitis clinically presents with chronic abdominal pain and normal or mildly elevated pancreatic enzyme levels; when the pancreas lose its endocrine and exocrine function, the patient presents with diabetes mellitus and steatorrhea.

Pathophysiology

Causes of chronic pancreatitis
The main causes of chronic pancreatitis include the following:


Alcoholism: Changes appear to develop slowly and may develop after excessive alcohol consumption for 10 years or more. Alcoholism is associated with chronic pancreatitis in 70% of patients.2

Cholelithiasis: Cholelithiasis is a common cause of acute pancreatitis, but it probably is associated with chronic pancreatitis in 20-25% of patients.3

Idiopathic: Etiology is idiopathic in 20% of patients.2

Drug use: Usually, drug-induced pancreatitis is an acute process and does not evolve into a chronic form.

Hereditary causes: Hereditary pancreatitis is an autosomal dominant disorder. Symptoms usually appear in the patient's first decade of life and eventually lead to both exocrine and endocrine pancreatic dysfunction.

Autoimmune disease: Autoimmune pancreatitis is a rare condition that is often seen in patients with primary sclerosing cholangitis.

Congenital causes: A congenital abnormality of fusion, pancreas divisum, can cause chronic pancreatitis

Cystic fibrosis: This disease is associated with pancreatic atrophy and chronic pancreatitis

Other conditions: Hyperlipidemia, hyperparathyroidism, and uremia can cause chronic pancreatitis.
Categories of chronic pancreatitis
Chronic pancreatitis can be classified into 3 categories: (1) chronic calcifying pancreatitis, (2) chronic obstructive pancreatitis, and (3) chronic inflammatory pancreatitis.

Chronic calcifying pancreatitis

Chronic calcifying pancreatitis is invariably related to alcoholism. The earliest finding is precipitation of proteinaceous material in the pancreatic ducts that forms protein plugs that subsequently calcify. The ducts and lobules are initially involved in a random manner, and they are surrounded by normal parenchymal tissue. However, as the disease progresses, these normal areas become more diffuse. The pancreatic ductal epithelium undergoes atrophy, hyperplasia, and metaplasia at the site of the protein plugs. Many of the small pancreatic ductules dilate, while others are obliterated by fibrosis.

The main pancreatic duct shows a chain-of-lakes appearance due to alternating stenoses and dilatation. In approximately 50% of patients with chronic calcific pancreatitis, the pancreatic parenchyma contains cysts of varying sizes (several millimeters to 5 cm). These cysts are lined by cuboidal epithelium and contain pancreatic enzymes. Peripancreatic fibrosis is usually a late finding that involves the portal and/or splenic veins. Peripancreatic fibrosis causes stenosis or occlusion of retroperitoneal lymph channels. Ascites may complicate chronic calcific pancreatitis as a result of portal hypertension or lymphatic obstruction in 1-2% patients.

Chronic obstructive pancreatitis

In chronic obstructive pancreatitis, the prominent histologic changes are periductal fibrosis and subsequent ductal dilatation. These changes are much more focal than those in the other forms, and in most patients, the changes involve only the portion of the pancreas in which ductal drainage is impaired. Diffuse changes may occur, in which the main pancreatic duct or ampulla is obstructed. Although protein inspissation may occur, histologic changes in the ductal mucosa are less common, and calcification is unusual. Moreover, the pancreatic duct is dilated, and the pancreas is normal in size, atrophic, or focally and/or globally enlarged. A variety of factors are implicated in chronic obstructive pancreatitis; these include ductal obstruction due to ampullary stenosis, inflammatory or neoplastic causes, surgical ductal ligation, and fibrosis due to a pseudocyst as a complication of an episode of acute pancreatitis.

Chronic inflammatory pancreatitis

Chronic inflammatory pancreatitis is rare and can affect elderly persons without a previous history of alcohol excess.



Autoimmune pancreatitis
Autoimmune-related chronic pancreatitis is a distinct clinical entity, which may present with signs of acute or chronic pancreatitis, sometimes associated with cholestatic jaundice. On imaging, it may appear as diffuse (duct destructive) or pseudotumoral lesions. These 2 aspects are probably different clinical forms of chronic autoimmune pancreatitis.4

Some autoimmune diseases are associated with chronic autoimmune pancreatitis, but not consistently. One such disease involves a bile disorder that is very similar to primary sclerosing cholangitis but is responsive to corticosteroid treatment. Pancreatitis may be associated with Crohn disease and ulcerative colitis and thus provides justification to investigate patients with idiopathic pancreatitis for underlying inflammatory bowel disease. Chronic autoimmune pancreatitis must always be considered in patients with a pancreatic mass that is atypical for carcinoma on imaging or clinical findings. Corticosteroid therapy for 4 weeks in patients with pancreatic adenocarcinoma is probably less harmful than pancreatectomy (or chemotherapy) in patients with chronic autoimmune pancreatitis.

Diagnosis depends on clinical and radiologic findings. The diagnostic value of serologic markers and, especially, autoantibodies must still be clarified.



Non-alcoholic duct destructive chronic pancreatitis
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1891454

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http://www.emedicine.com/radio/topic522.htm


Degree of Confidence
Currently, CT is regarded as the imaging modality of choice for the initial evaluation of suggested chronic pancreatitis. The diagnostic features of pancreatic enlargement, pancreatic calcifications, pancreatic ductal dilatation, thickening of the peripancreatic fascia, and bile duct involvement are depicted well on CT scans.

CT is more sensitive than plain radiography and ultrasonography in the depiction of pancreatic calcification. Moreover, CT depicts calcification in the pancreas, and confusion with nonpancreatic calcification is less likely. The accuracy of CT is 59-95%; the wide variation is due to the wide discrepancy in the criteria used for diagnosis and in the quality of CT scanners. CT helps in the diagnosis of atrophy of the pancreas, providing better results than ultrasonography.


False Positives/Negatives
Chronic pancreatitis and pancreatic carcinoma share many CT features, and occasionally, differentiation may be impossible. Obliteration of the fat sleeve around the superior mesenteric artery has been described in both chronic pancreatitis and pancreatic carcinoma.

Pseudotumoral enlargement around focal pancreatitis with extensive fibrous tissue proliferation usually fails to enhance after the administration of contrast material. This characteristic makes the differential diagnosis of pancreatic carcinoma difficult.



Findings
In most patients, a normal pancreatic duct is seen on images obtained with T2-weighted short-tau inversion recovery MRI sequences and MRCP. MRCP may depict the characteristic beaded appearance of the pancreatic duct in chronic pancreatitis. Pancreatic duct calculi are depicted as round filling defects. In chronic pancreatitis, fat-suppressed T1-weighted images usually show a loss of signal intensity. This loss is explained by the fact that pancreatic fibrosis decreases the proteinaceous fluid content of the pancreas, resulting in loss of pancreatic signal intensity. Fibrosis is associated with decreased vascularity, which causes decreased pancreatic gadolinium enhancement.

Small punctate pancreatic calcification is difficult to detect by using MRI, but larger calcifications may be seen as foci of a signal void. As a result of its ability to depict fluid, T2-weighted MRI may demonstrate pancreatic and common bile duct irregularities and pseudocysts associated with chronic pancreatitis.

Parenchymal gadolinium enhancement is a useful technique in evaluating focal areas of inflammation. Compared with normal pancreatic segments, inflamed areas have decreased enhancement in the arterial phase and increased enhancement in the equilibrium phase.

Currently, the diagnosis of early chronic pancreatitis is difficult. With future improvement in spatial resolution and with the use of secretin-enhanced pancreatography, the detection of subtle changes of the side branches may allow the earlier noninvasive diagnosis of chronic pancreatitis. Secretin-enhanced pancreatography also has the potential to depict the anatomic relationships of pancreatic ducts and pseudocysts and to aid in the evaluation of pancreatic exocrine function.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with troublemoving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.


Degree of Confidence
Because of the introduction of faster imaging sequences and phased-array coils, the accuracy of MRCP has improved considerably, although some concern remains regarding the resolution of smaller pancreatic ducts.

Secretin-enhanced MRCP improves the detection of diseased pancreatic ducts when no abnormality can be shown in physiologic conditions. It also provides additional functional information regarding pancreatic exocrine function. As experience grows, MRI imaging, particularly MRCP, may be increasingly used in assessing and screening for chronic pancreatitis.

False Positives/Negatives
Standard good-quality protocols are important with MRCP; otherwise, poor examination technique may create false lesions, which may increase the frequency of unnecessary ERCP examinations.

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Originally posted to my Y! 360, Sunday October 12, 2008 - 08:05am (CDT)