SJOGREN'S SYNDROME--IMPLICATIONS FO...

SJOGREN'S SYNDROME--IMPLICATIONS FOR PERIOPERATIVE PRACTICE

The article "Sjogren's syndrome--Implications for perioperative practice," is the basis for this AORN Journal independent subject of attention The behavioral objectives and examination for this program were prepared from Rebecca Holm, RN, MSN, CNOR, clinical editor, with consultation from Susan Bakewell, RN M education program professional, Center for Perioperative Education.

A minimum score of 70% forward the multiple-choice examination is necessary to earn 23 contact hours for this independent subject of attention Participants receive feedback on incorrect answers. Each applicant who prosperously completes this study will receive a certificate of completion. The deadline for submitting this close attention is March 31, 2006.

delegate the completed application form, multiple-choice examination, learner evaluation, and appropriate reward to

AORN Customer Service c/o family circle Study Program 2170 S Parker Rd Suite 300 Denver CO 80231-5711

or fax the information with a credit card number to (303) 750-3212

BEHAVIORAL OBJECTIVES After reading and studying the article onward Sj6gren's syndrome (SS), the cherish will be able to

(1) discuss the pathogenesis of the exhibition of SS,

(2) describe the signs and symptoms of SS

(3) explain the diagnostic trials used to differentially diagnose SS

(4) identify treatment options available to patients with S and

(5) describe perioperative nurses' part in protecting patients with S who are undergoing surgery

This program engages criteria for CNOR and CRNFA recertification, as well as other continuing education requirements.

Sjogren's syndrome (SS) also known as sicca syndrome is a chronic autoimmune disorder in which lymphocyte invade and ravage the exocrine glands, particularly the salivary and lacrimal glands, resulting in decreased saliva and tear production. Drynes also may affect the skin, sinuses, upper airway, gastrointestinal tract, and vaginal tissues. Systemic manifestations of S include rash, Raynaud's phenomenon, fatigue, and brace and muscle pain. (1)

Sjogren's syndrome is the next to the first most common autoimmune rheumatic disease, surpassed solely by rheumatoid arthritis, and on a level occurs more frequently than systemic lupus erythematosus. (2) Estimates of the prevalence of S range from 500000 to four million populace 90% of whom are women (3) The typical patient is a Caucasian perimenopausal woman in her forties. Sjogren's syndrome many times is unrecognized and untreated. The average time from attack of symptoms to diagnosis is at least three and one-half years. (4) The [i]role[/i] often seeks the help of multiple physicians and specialists; single to repeatedly receive an incorrect diagnosis or no diagnosis at all. The symptoms continue or worsen, leading to anger and frustration. Delays in diagnosis can be explained by way of the insidious development of symptoms during a number of years, the lack of universally accepted diagnostic criteria, and the bent of patients and medical personnel to trivialize the initial symptoms of the disorder.

ETIOLOGY AND PATHOGENESIS

The trigger that initiates the autoimmune incidents of SS remains unknown. A variety of factors potentially may influence the increase of the disease. Most research indicates that S and other autoimmune diseases conclusion from the interaction of specific, susceptible gene and environmental agents that idiot the immune system into attacking a target organ. In S the exocrine or moisture producing glands are attacked. No single gene causes SS; however, the human leukocyte antigen 5 HLADQZ,DR3 present itselfs most frequently in Caucasian patients with S Apoptosis (ie, programmed enclosed space death) of T lymphocytes and salivary acinar epithelial lonely dwellings is a gene-regulated process that functions abnormally in patients with S and appears to contribute to glandular destruction. Indirect evidence glance ats that viruses may play a part as the environmental agent. Hormonal changes also may be of use to as an agent that influences the disease. (5)

An injury to the exocrine gland may initiate S As T lymphocyte invade the tissue, cytokines (ie, inflammatory messengers) are released locally, which perpetuates the immune inflammatory reply The cytokines may escape into the bloodstream, stimulating other parts of the visible form [i]or[/i] frame to make proteins that eventuate in an increased erythrocyte sedimentation rate (ESR) and increased production of Creactive protein (CRP) T lymphocyte also stimulate B enclosed spaces causing antibody formation (eg, immunoglobulin G [IgG], immunoglobulin A [IgA], immunoglobulin M [IgM], antinuclear antibody [ANA], Sjogren's syndrome antigen A [SSA], Sjogren's syndrome antigen B [SSB]) Eventually the normal glandular tissue is replaced by dint of fibrosed and fatty tissue. The autonomic braces that send signals to the moisture producing glands also may be damaged. (6)

SIGNS AND SYMPTOMS

The signs and symptoms of S are divided into the hallmark signs and symptoms and the extraglandular signs and symptoms. The hallmark signs and symptoms also are called the sicca symptoms.