25 December 2009

Pancreatic Cancer: The Use of Endosonography



Endoscopy in Crohn’s Disease
By:Peter Darwin, MD
Director of Gastrointestinal Endoscopy
University of Maryland Hospital
Division of Gastroenterology

Outline
* Case histories
* Diagnosis
* Assessment of response
* Dysplasia and surveillance
* Bleeding
* Stricture management
* Emerging technology

Case 1
Case 2

Diagnosis

* Asymmetric patchy inflammation
* Skip lesions
* Rectal sparring
* Ulcerations
* Biopsy
o Erosions and normal mucosa
o Granulomas in 15 to 35% of specimens

Assessment of Response
* Endoscopic monitoring may have a role with biologic agents
* Subgroup of the ACCENT-1 trial
o Mucosal healing with infliximab, time to relapse is significantly prolonged
+ 9 with endoscopic healing remained in remission for a median of 20 weeks
+ 4 clinical remission only, relapse after a median of 4 weeks


Dysplasia and Surveillance
* Extensive colitis > 8 years
* Accuracy in predicting dysplasia correlates with # of biopsies
* Annual colonoscopy with multiple biopsy specimens
o 4 circumferential each 10 cm


Approach to Polypoid Lesions
Adenoma like DALM
Outside colitis
Within colitis
Polypectomy/biopsy
Non-IBD
adenoma
Polypectomy
Regular surveillance
No dysplasia
No carcinoma
Indeterminate
Flat dysplasia
carcinoma
Polypectomy
Increased surveillance
Colectomy

Chawla A, Lichtenstein G. Gastrointest Endoscopy Clin N Am 12 (2002) 525-534

Hemorrhage in Crohn’s

* Acute major hemorrhage is uncommon
* Bleeding can occur in any segment
* Massive hemorrhage is usually from an ulcer eroding into a vessel
* Resuscitation
* Endoscopy vs tagged RBC scan to localize a bleeding segment
* Avoid embolization if possible

Hemorrhage in Crohn’s
* No data to support cautery or injection therapy
* Surgical intervention
* Consider tattooing of the site


* Database review from 1989 to 1996
o 1739 patients / 31 (1.8%) due to IBD
o 3 with UC and 28 with CD / 1 UGI source
o None hematemesis
o GI hemorrhage in 0.1% UC and 1.2% CD
* Diagnostic evaluation
o Source found by colonoscopy in 25 patients (25%) and EGD in 2 patients


Pardi D, Loftus E, et al. Gastrointest Endosc 1999;49:153-7.

Acute Major GI hemorrhage in IBD

Endoscopic Therapy for Patients with CD and Focal Sites of hemorrhage
Patient Site Stigmata Endoscopic Rx Medical Rx

1 Duodenum clot Injection Corticosteroids ranitidine

2 Jejunum oozing ulcer Injection Corticosteroids ranitidine

3 Colon clot Injection with Corticosteroids

coagulation metronidazole


Clinical Course
Balloon Dilation of Strictures

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23 October 2009

Myasthenia Gravis



Myasthenia Gravis
By:
* Cathie Rohleder
* Sydnee Jacobson
* Ashley Cox

Pathology
* A chronic Autoimmune Disease
* Affects the Neuromuscular junction
* Postsynaptic acetylcholine receptors on muscle cells plasma membrane are no longer recognized as ‘self’ and elicit the generation of auto antibodies.
* IgG antibody is produced against the acetylcholine receptors and fixes to receptor sites, blocking the binding of acetylcholine.
* Diminished transmission and lack of muscular depolarization results.
* Several Types of Myasthenia Gravis
o Neonatal Myasthenia Gravis: A transient condition in 10% to 15% of infants born to mothers with MG.
o Congenital Myasthenia
o Juvenile Myasthenia: Onset is around 10 years of age.
o Ocular Myasthenia
o Generalized Autoimmune Myasthenia

Clinical Manifestations
* Insidious onset
o May first appear during pregnancy, during the postpartum period, or in combination with the administration of anesthetic agents.
* Complaints
o Most individuals complain of fatigue and progressive weakness.
o The person usually has a history of frequent respiratory tract infections.
* Muscles affected
o First muscles affected
+ Muscles of the eyes, mouth, face, throat and neck.
+ The most affected muscles are the extra ocular (eye) muscles and levator muscles.

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MYASTHENIA GRAVIS



MYASTHENIA GRAVIS
By Terra Cunningham

DEFINITION
* “A disorder of neuromuscular function thought to be due to the presence of antibodies to acetylcholine receptors at the neuromuscular junction”3

DISCOVERED IN
* First described in 1672 by Thomas Willis and later described in 1890 by German physicians, Samuel Goldflam, Wilhelm Erb, and Friedrich Jolly.

SYMPTOMS
* Drooping of the eyelids
* Double vision
* Difficulty smiling, speaking, swallowing
* Difficulty raising the arms
* Difficulty walking
* Difficulty breathing if chest muscle are affected

CAUSE
* The cause is unknown
* “Antibodies act against the acetylcholine receptor making a nerve come in contact with the muscle. The nerve cell conveys its message to tell the muscle to contract. The antibodies interfere with the message and the muscle contracts less efficiently. Resulting in the weakness of the arms or legs or of the muscles of the head.”4

PREVALENCE
* Today there are an estimated 50,000 cases in the United States
* Myasthenia Gravis can be found in anyone, but it is “most common in females around the third decade of life”1

TREATMENT
* Symptomatic treatment: medications that enhance the function of the acetylcholine system at the neuromuscular junction.
* Medications include – Prostigmin, Mestinon, Mytelase, Tensilon
* Long range treatment is thymectomy.
* Thymectomy is the surgical removal of the thymus gland that lies behind the breastbone and overlies the heart.

Lifestyles
* A person with Myasthenia Gravis can lead a normal life if the medications are taken in the correct dosages and at the right time of the day.

References
* Collier’s Encyclopedia with Bibliography and Index, 1988, volume 17.,Macmillan
* Dictionary of Medical Syndromes, 3rd edition, Magalini
* Dorland's Illustrated Medical Dictionary, 26th edition, 1985, Saunders
* Encyclopedia Americana, 1993, volume 19., Grolier
* The Medical and Health Encyclopedia, volume 1., Southwestern Company

MYASTHENIA GRAVIS.ppt

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