Immunity and Hypersensitivity Quiz

Hypersensitivity Systemic Lupus Erythematosus

• Systemic lupus erythematosus (SLE) is a chronic, inflammatory connective tissue disease.
• It affects almost all body systems.
• Symptoms vary widely.
• SLE is caused by the deposition of autoantibody-antigen complexes in connective tissues.
• This leads to damage of cells and tissues.

The Concept of Immunity

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

Alterations and Manifestations

• Hypersensitivity or hyper-responses can also be categorized as allergic reactions.
• There are four types of allergic reactions.
  • Type I: immediate hypersensitivity (e.g., asthma, allergic rhinitis, food allergies)
  • Type II: cytotoxic hypersensitivity (e.g., transfusion reaction, hemolytic disease of the newborn)
  • Type III: immune complex-mediated reaction (e.g., serum sickness, acute glomerulonephritis)
  • Type IV: delayed-type hypersensitivity (e.g., contact dermatitis, TB test)

Types of Hypersensitivity Reactions

• Type I reactions are localized or systemic.
  • Antibodies bind to cells, causing release of substances leading to inflammation.
    • Examples: asthma, allergic rhinitis, food allergies
• Type II tissue-specific reactions involve antibodies activating a system that causes tissue damage.
  • Examples: transfusion reaction, hemolytic disease of newborn, ABO incompatibility
• Type III immune complex-mediated reactions involve immune complexes deposited in tissues, leading to inflammation.
  • Examples: serum sickness, acute glomerulonephritis
• Type IV delayed reactions are cell-mediated immune responses.
  • Examples: contact dermatitis, TB test, GVH

Pathophysiology and Etiology of Type I Hypersensitivity

• Type I (IgE-mediated) hypersensitivity reactions are triggered when an allergen interacts with free IgE.
• IgE binds to mast cells and basophils, causing histamine release.
• Common allergens include ingested foods, injected or inhaled substances.
• Type I hypersensitivity can lead to anaphylaxis, an acute systemic response, and localized responses (e.g., Hay fever, Asthma, Atopic dermatitis, bee stings, food allergies). Reaction can occur within minutes.
• Signs/Symptoms include swelling, redness, itching of skin, runny nose, bronchospasm, wheezing/crackles

Collaborative Treatment for Type I Hypersensitivity

• Pharmacotherapy for Type I hypersensitivity includes:
  • Non-steroidal anti-inflammatory drugs
  • Antihistamines
  • Steroids to reduce inflammation
  • Theophylline OR Epinephrine to reduce mast cell activity
• Immunotherapy involves desensitization via repeated injections of allergens to reduce the allergic response (allergy injections)
• Collaboration involves referral to allergists and implementation of action plans for children.

Pathophysiology and Etiology of Type II Hypersensitivity

• Type II (cytotoxic) hypersensitivity involves the binding of IgG or IgM to antigens.
  • This activates a complex cascade, leading to the destruction of target cells.
  • Examples include blood transfusions and ABO blood types incompatibility.

Collaborative Treatment for Type II Hypersensitivity

• Prevention of transfusion reactions involves checking blood compatibility prior to administration by RNs.
  • Stopping incompatible blood transfusion to prevent hemolysis.
  • Keeping IV line with NS, and calling provider.
  • Treating mild reaction with antihistamine, and major reactions require rapid response (bloody urine/pain).

Pathophysiology and Etiology of Type III Hypersensitivity

• Type III (immune complex-mediated) hypersensitivity results from the formation of antibody-antigen complexes in the circulatory system (IgG or IgM).
  • These complexes deposit in capillaries or joints.
  • This triggers an inflammatory response leading to tissue damage.

Overview of Systemic Lupus Erythematosus

• SLE is a chronic, inflammatory connective tissue disease affecting multiple body systems.
• Signs and symptoms vary significantly.
• Autoantibodies are produced, resulting in the deposition of antibody-antigen complexes and tissue damage.

Autoantibodies

• Autoimmune diseases occur when the immune system fails to distinguish between self and non-self antigens.
  • This results in attacks against the body's own tissues and organs.
  • Examples include: SLE, rheumatoid arthritis.
  • Commonly diagnosed in teens and early adulthood.

Pathophysiology and Etiology of SLE

• SLE autoantibodies react with corresponding antigens.
  • Resulting in immune complex formation, often deposited in connective tissues.
  • This leads to inflammation damage at different sites like kidneys, musculoskeletal system, brain, heart, spleen, lungs, GI tract, skin, and peritoneum.

Risk Factors for SLE

• Women of childbearing age are more susceptible, with a high percentage of diagnoses.
• African Americans, Hispanics, and Native Americans are disproportionately affected.
• Asians may also be affected.

Clinical Manifestations of SLE

• Early symptoms may include joint pain, mimicking rheumatoid arthritis.
• Characteristic skin rashes such as red butterfly rash across cheeks and bridge of nose, and diffuse maculopapular rash on sun-exposed skin.
• Other possible manifestations include fever, depression, eye disorders, skin rashes, chest pain, renal disorders, arthritis, tendonitis, neurological impairments, and more.

Diagnostic Tests

• Anti-DNA antibody testing is a significant indicator of SLE.
• Erythrocyte sedimentation rate (ESR) is elevated due to inflammation.
• Complete blood count (CBC) may reveal anemia and/or leukopenia.
• Urinalysis can detect proteinuria, particularly during exacerbations affecting the kidneys.

Drug Therapy for SLE

• Antimalarias (like hydroxychloroquine) treat skin and arthritic manifestations.
• Corticosteroids (like prednisone) are used for severe cases. Initial doses are high, tapered as clinically possible.
• Immunosuppressants (like cyclophosphamide or azathioprine) are used in combination with corticosteroids. These increase risk for infection, malignancy, and bone marrow depression.

Teaching Points for Patients Taking Immunosuppressants

• Immunosuppressive medications require patient education on infection avoidance, reporting symptoms, pregnancy planning, vitamin/herb/supplement consultation, sun exposure avoidance, and immunizations.

Nursing Process Assessment

• A comprehensive nursing assessment includes nutritional evaluation, skin assessment, respiratory assessment, musculoskeletal assessment, neurological evaluation, assessment of the GI system, psychosocial evaluation, and pain assessment.

Diagnoses

• Possible diagnoses include risk for infection, risk for ineffective tissue perfusion, chronic pain, risk for activity intolerance, risk for disturbed body image, and compromised family coping.

Implementation of Nursing Care

• Implementation strategies for SLE include promoting adequate nutrition (keeping in mind steroid effects), ensuring skin integrity, promoting rest and comfort, and documenting weight, skin health, activity balance, medication adherence, and body image to track progress and prevent complications.

Evaluation of Nursing Care

• Evaluation of nursing care should assess patient progress in maintaining weight, healthy skin, rest/activity balance, medication compliance, and positive body image.

Pathophysiology and Etiology of Type IV Hypersensitivity

• Type IV (delayed) hypersensitivity is a cell-mediated immune response not involving antibodies.
  • It results from exaggerated antigen-T cell interactions.
• Common examples include PPD/TB skin tests.

Delayed Type IV Hypersensitivity

• Delayed response occurs 48-72 hours post-exposure, unlike other hypersensitivity types which happen within minutes.
• Macrophages cause inflammation and subsequent tissue damage.
• Continued macrophage activation can lead to chronic inflammation, scarring, and granuloma formation.