Hypersensitivity Reactions Overview

Hypersensitivity Systemic Lupus Erythematosus

• Hypersensitivity is the body's natural or induced response to foreign agents
• Immunocompromised patients have an ineffective immune system
• Hypersensitivity is an overreaction of the immune system
• Autoimmune disorders occur when the immune system attacks the body's own tissues
• Immunodeficiency is an incompetent immune system

Types of Hypersensitivity Reactions

• Type I: Localized or systemic
  • Antibodies bind to cells, release substances, causing inflammation
  • Examples include asthma, allergic rhinitis, and food allergies
• Type II: Tissue-specific reaction
  • Antibodies activate systems causing tissue damage
  • Examples include transfusion reactions, hemolytic disease of the newborn, and ABO incompatibility
• Type III: Immune complex-mediated reaction
  • Immune complexes deposit in tissues, triggering inflammation
  • Examples include serum sickness and acute glomerulonephritis
• Type IV: Delayed reactions
  • Cell-mediated immune response where antigens stimulate T-cells
  • Examples include contact dermatitis and the TB skin test

Pathophysiology and Etiology of Type I Hypersensitivity

• IgE-mediated hypersensitivity, also known as common hypersensitivity reactions
• Triggered when allergens interact with free IgE
• IgE binds to mast cells and basophils, releasing histamines
• Common allergens include ingested foods, inhaled substances, or injected substances
• Type I (IgE-mediated) hypersensitivity reactions often cause anaphylaxis (acute systemic response)
• Histamine and other mediators are released
• Localized responses are more common than anaphylaxis

Pathophysiology and Etiology of Type I Hypersensitivity

• Sign/symptoms occur within minutes
• IgE releases histamine and other mediators causing swelling, redness, itching, skin sensitivity, runny nose, bronchospasm, and wheezing
• Treatments include pharmacotherapy via non-steroidal anti-inflammatory drugs and antihistamines
• Immunotherapy is a desensitization technique using repeated injections of allergens to reduce allergic response

Pathophysiology and Etiology of Type II Hypersensitivity

• Cytotoxic hypersensitivity
• Occurs when IgG or IgM antibodies bind to antigens, triggering a cascade hypersensitivity response leading to destruction of target cells
• Blood transfusions have to check for ABO blood types for compatibility

Pathophysiology and Etiology of Type III Hypersensitivity

• Immune complex-mediated hypersensitivity
• Results from formation of antibody-antigen immune complexes in the circulatory system (IgG or IgM)
• These immune complexes deposit in capillaries or joints, activating complement cascades, and causing inflammatory damage

Type III Hypersensitivity - Systemic

• Immune complexes are deposited in small blood vessels of organs and tissues
• Serum sickness is a response to some medications

Type III Hypersensitivity - Localized Disease

• Deposited in joints cause arthritis
• Deposited in kidneys cause glomerulonephritis
• Deposited in connective tissue causes SLE (Systemic Lupus Erythematosus).

Overview of Systemic Lupus Erythematosus (SLE)

• Chronic, inflammatory connective tissue disease
• Affects almost all body systems
• Autoantibodies are created and deposited, causing inflammation and damage to the tissues

Autoantibodies

• Immune system loses the ability to distinguish self from non-self
• Results from hyperactivity of B cells
• Often diagnosed in teen or early adult years

Pathophysiology and Etiology of SLE Autoantibodies

• Produce immune complexes that react with corresponding antigens
• Deposited into connective tissue
• This immune complex deposition triggers an inflammatory response
• Tissues are damaged due to localized response

Risk Factors of SLE

• Women of childbearing age are at higher risk (90%)
• More common in African Americans, Hispanics, Native Americans, and Asians.

Clinical Manifestations of SLE

• Early manifestations include joint pain
• Red butterfly rash across cheeks and nose bridge
• Diffuse maculopapular rash on sun-exposed skin.
• Various internal organ involvement.

Diagnostic Tests for SLE

• Anti-DNA antibody test: a specific indicator
• Erythrocyte sedimentation rate (ESR): increased due to inflammation
• CBC: may show anemia or leukopenia
• Urinalysis: presence of proteinuria during exacerbations.

Drug Therapy for SLE

• Anti-malarials (hydroxychloroquine) for skin and arthritic symptoms
• Corticosteroids (high doses of prednisone) for severe symptoms, initially at high doses that are later tapered as much as possible.
• Immunosuppressive agents (cyclophosphamide or azathioprine): for severe disease; increased risk for infection, malignancy, and bone marrow depression

Nursing Process Assessment of SLE

• Nutritional status
• Skin
• Respiratory
• Musculoskeletal
• Neurological
• GI
• Psychosocial
• Pain

Diagnoses related to SLE

• Risk for Infection
• Ineffective Tissue Perfusion
• Chronic pain
• Risk for activity intolerance

Implementation for SLE

• Promote adequate nutrition
• Promote skin integrity
• Promote rest and comfort

Evaluation of SLE

• Patient maintains healthy weight, skin, and a balance of rest and activity/exercise
• Patient takes medication as directed to prevent side effects; prevent any negative impact on health from steroid use
• Patient maintains a positive body image