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Sjogren's syndrome—implications for perioperative practice - Home Study Program

AORN Journal, March, 2003 by Lynn M. Petruzzi, Frederick B. Vivino

SJOGREN'S SYNDROME--IMPLICATIONS FOR PERIOPERATIVE PRACTICE

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

A minimum score of 70% on the multiple-choice examination is necessary to earn 2.3 contact hours for this independent study. Participants receive feedback on incorrect answers. Each applicant who successfully completes this study will receive a certificate of completion. The deadline for submitting this study is March 31, 2006.

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Send the completed application form, multiple-choice examination, learner evaluation, and appropriate fee to

AORN Customer Service c/o Home 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 on Sj6gren's syndrome (SS), the nurse will be able to

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

(2) describe the signs and symptoms of SS,

(3) explain the diagnostic tests used to differentially diagnose SS,

(4) identify treatment options available to patients with SS, and

(5) describe perioperative nurses' role in protecting patients with SS who are undergoing surgery.

This program meets 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 lymphocytes invade and destroy the exocrine glands, particularly the salivary and lacrimal glands, resulting in decreased saliva and tear production. Dryness also may affect the skin, sinuses, upper airway, gastrointestinal tract, and vaginal tissues. Systemic manifestations of SS include rash, Raynaud's phenomenon, fatigue, and nerve and muscle pain. (1)

Sjogren's syndrome is the second most common autoimmune rheumatic disease, surpassed only by rheumatoid arthritis, and even occurs more frequently than systemic lupus erythematosus. (2) Estimates of the prevalence of SS range from 500,000 to four million people, 90% of whom are women. (3) The typical patient is a Caucasian perimenopausal woman in her forties. Sjogren's syndrome frequently is unrecognized and untreated. The average time from onset of symptoms to diagnosis is at least three and one-half years. (4) The person often seeks the help of multiple physicians and specialists; only 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 the insidious development of symptoms during a number of years, the lack of universally accepted diagnostic criteria, and the tendency of patients and medical personnel to trivialize the initial symptoms of the disorder.

ETIOLOGY AND PATHOGENESIS

The trigger that initiates the autoimmune events of SS remains unknown. A variety of factors potentially may influence the development of the disease. Most research indicates that SS and other autoimmune diseases result from the interaction of specific, susceptible genes and environmental agents that fool the immune system into attacking a target organ. In SS, the exocrine or moisture producing glands are attacked. No single gene causes SS; however, the human leukocyte antigen 5 HLADQZ,DR3 occurs most frequently in Caucasian patients with SS. Apoptosis (ie, programmed cell death) of T lymphocytes and salivary acinar epithelial cells is a gene-regulated process that functions abnormally in patients with SS and appears to contribute to glandular destruction. Indirect evidence suggests that viruses may play a role as the environmental agent. Hormonal changes also may serve as an agent that influences the disease. (5)

An injury to the exocrine gland may initiate SS. As T lymphocytes invade the tissue, cytokines (ie, inflammatory messengers) are released locally, which perpetuates the immune inflammatory response. The cytokines may escape into the bloodstream, stimulating other parts of the body to make proteins that result in an increased erythrocyte sedimentation rate (ESR) and increased production of Creactive protein (CRP). T lymphocytes also stimulate B cells, 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 fibrosed and fatty tissue. The autonomic nerves that send signals to the moisture producing glands also may be damaged. (6)

SIGNS AND SYMPTOMS

The signs and symptoms of SS 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.

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Sjogren's syndrome—implications for perioperative practice - Home Study Program

AORN Journal, March, 2003 by Lynn M. Petruzzi, Frederick B. Vivino

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