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SYSTEMIC LUPUS ERYTHEMATOSUS - Coggle Diagram
SYSTEMIC LUPUS ERYTHEMATOSUS
Pathogenesis
SLE is characterized by the multisystem inflammation with generation of autoantibodies. The specific
cause of SLE is unknown but interaction between genetics, environment, and hormones lead to immune dysregulation and breakdown of tolerance to self antigens. This leads to production of autoantibodies, inflammation, and destruction of end organs.
A longstanding proposed mechanism to the creation of autoantibodies is that there is inappropriate apoptosis and a disturbance in immune tolerance. Apoptosis leads to cell-surface display of plasma and nuclear antigens in the form of nucleosomes, which attracts intolerant lymphocytes to target them. This ultimately comes down to defective clearance of apoptotic cell debris and allows for immune complex production.
Immune complexes are formed in various tissues and may be directly correlated to clinical manifestations. For example, immune complexes form in the microvasculature. This results in complement activation and inflammation. Another example is the presence of immune complexes in the basement membranes of the skin and kidneys.
Patients with SLE have consistently shown decreased T Cell function, which makes experts believe they play a part in the development of SLE. T cells have shown to secrete less interleukin (IL)-2, CD* cytotoxicity; T-regulatory, B-cell help; migration; and adhesion.
SLE has a clear connection to genetics. Polymorphism in many genes have the chance of affecting the risk of developing SLE. Most of these genes are connected to the immune system and likely affect proper targeting of the immune system.
Lupus can be triggered by many different things such as a virus, UV light exposure, and drugs.
Risk Factors
Family history is a risk factor as relatives of people with lupus have a 5-13 percent of developing it.
African Americans, Hispanics, and Asian Americans
Diagnosis frequently occurs in childbearing age
Women compose more than 90% of SLE cases
Incidence/Prevalence
In the United States, it is estimated that there are 20 to 150 cases per 100,000 people.
In women, it varies from 164 (white) to 406 (African American) per 100,000
This disease occurs more in urban than rural areas.
The prevalence rate is much higher in African American, African Caribbeans, and Hispanic Americans.
Estimated 1.5 million cases in America
Diagnostics
SLE can be a very difficult disease to diagnose due to the varying signs and symptoms. There is not a specific test that can be used to accurately diagnose a case of lupus. Multiple tests and screenings may be used.
Complete Blood Count - A CBC will be used to determine if the patient has anemia, a very common disease process that occurs in patient with SLE
Erythrocyte Sedimentation Rate - Patients with SLE will often have a faster rate
Kidney and liver assessment - Lupus patient often have affected liver and kidney function
Urinalysis - An analysis of the urine will determine the presence of RBCs or proteins
ANA test - These antibodies are often found in Lupus patients
Chest X-Ray - This will be ordered to examine any fluid or inflammation in the lungs
Echocardiogram - This will determine if there are any valve problems in the heart
Biopsy - A biopsy of the liver/kidneys will determine if there is damage and to determine the best treatment
Clinical Manifestations
The clinical manifestations of SLE will vary throughout all cases.
Joint pain and swelling
Severe malaise
Fever
Muscle pain
Skin lesions that worsen with sun exposure
Dry eyes
Confusion
Shortness of breath
Weight loss
Lupus nephritis
Treatments
Antimalarials
Antimalarials were originally used to treat malaria but have shown to decrease manifestations of lupus. They improve lupus by decreasing autoantibody production. They can protect the patient from UV light and improve skin lesions.
eg, hydroxychloroquine, chloroquine, quinacrine
Corticosteroids
Steroids work by decreasing inflammation and deterring the activity of the immune system. Since SLE is an autoimmune disease, corticosteroids work to reduce stiffness, swelling, warmth, pain, and tenderness.
eg, prednisone, prednisolone, hydrocortisone, methylprednisolone, dexamethasone.
Nonbiologic and biologic DMARDS
Disease-modifying antirheumatic drugs are immunomodulatory agents that suppress the immune system while being cytotoxic. The specific drug that is chosen will be tailored to which organ is being affected. DMARDS are commonly prescribed to patients who are not effectively responding to glucocorticoids.
eg, cyclophosphamide, methotrexate, azathioprine, mycophenolate
NSAIDs
Non-steroidal anti-inflammatory drugs work by relieving inflammtion to decrease pain and stiffness in the muscle, joints, and other tissues. They inhibit prostaglandins which play an important part in the immune system.
eg, ibuprofen, naproxen, diclofenac
References
Christie M Bartels, M. (2021, April 03). Systemic lupus erythematosus (sle). Retrieved April 10, 2021, from
https://emedicine.medscape.com/article/332244-overview#a1
Treating lupus with anti-malarial drugs. (2019, March 27). Retrieved April 10, 2021, from
https://www.hopkinslupus.org/lupus-treatment/lupus-medications/antimalarial-drugs/
Lupus. (2021, January 27). Retrieved April 10, 2021, from
https://www.mayoclinic.org/diseases-conditions/lupus/diagnosis-treatment/drc-20365790
Christie M Bartels, M. (2021, April 03). Systemic lupus Erythematosus (SLE) MEDICATION: ANTIMALARIALS, NSAIDs, DMARDS, Immunomodulators, RHEUMATOLOGICS, Other, Corticosteroids, DMARDs, Other. Retrieved April 10, 2021, from
https://emedicine.medscape.com/article/332244-medication#1
Systemic lupus erythematosus (sle). (2018, October 17). Retrieved April 10, 2021, from
https://www.cdc.gov/lupus/facts/detailed.html