5.Immune 2 study guide

I. Distinguishing Self from Nonself

• Self-Tolerance: The absence of an immune response against a person's own antigens.

  • Maintained through several mechanisms, including:

    • Major Histocompatibility Complex (MHC) molecules on cell surfaces.

    • Role of MHC: Display antigens for T cell inspection.

      • Types of MHC Molecules:

        1. Class I MHC molecules:

           • Found on nearly all nucleated cell membranes (not phagocytic cells).

           • Present intracellular antigens:

             • Normal "self" antigens.

             • Viruses (gained access to cells).

             • Abnormal cell proteins (due to mutations).

           • Interact with cytotoxic T cells; T cells recognize antigens complexed to Class I MHC.

        2. Class II MHC molecules:

           • Found mainly on macrophages/apc (phagocytic cells).

           • Present extracellular antigens.

           • Interact with helper T cells; T cells recognize antigens complexed to Class II MHC.

           • Lack of display on Class II MHC → no activation of helper T cells.

II. Inflammation

• Description: Tissue reaction to injury, regardless of the cause.

• Purpose: Initiate healing by:

  1. Neutralizing/destroying harmful agents.

  2. Limiting their spread.

  3. Preparing damaged tissue for repair (removing dead tissue, nutrient transport).

• Signs & Symptoms (Cardinal Signs):

  • Redness

  • Heat

  • Swelling

  • Pain

  • Impaired function

• Mechanism of Action: Involves release of chemical mediators:

  • Chemical Mediators: Histamine, prostaglandins, leukotrienes, plasma proteases, platelet-activating factor, cytokines.

  • Vascular Response:

    • Initial vasoconstriction, followed by vasodilation.

    • Increased capillary permeability leads to fluid escape into tissues.

  • Cellular Response:

    • Movement of WBCs into the injured area.

  • Acute-Phase Response: Systemic effects due to cytokine release:

    • Fever.

    • Increased WBC counts.

    • Skeletal muscle catabolism.

III. Potential Problems Related to Inflammation

• Issues with Compromised Immune Function:

  • Breakdown in self-tolerance.

  • Pathological changes possible due to immune dysfunction.

  • Inflammation can cause further tissue damage.

IV. Normal Physiology of the Immune System

• Functions:

  • Provide immunity.

  • Distinguish self from nonself.

  • Mediate inflammation.

  • Cancer surveillance.

• Self-Tolerance Maintenance:

  • Mediated by suppressor T cells, elimination of self-reactive immune cells, and requirement of foreign antigens to activate T cells through MHC molecules.

V. Pathological Changes/Predisposing Factors**

• Pathological Changes:

  • Breakdown in immune self-tolerance can occur due to:

    • Abnormality in self-antigen structure.

    • Faulty T cell receptor/MHC interaction.

    • Disorders of immune surveillance.

    • Antigenic mimicry (similarities between foreign and self-antigens).

    • Release of sequestered antigens (self-antigens released post-injury).

• Predisposing Factors (PF):

  • Genetic factors.

  • Trigger events (viruses, chemicals, stressors).

  • Gender/hormones (more common in women).

VI. Example of an Autoimmune Disorder: Systemic Lupus Erythematosus

• Pathophysiology: Development of antibodies against self-antigens (e.g., nuclear antigens).

  • Cell damage releases DNA, which forms anti-DNA antibodies.

  • Antibody complexes deposit in tissues, activating the complement system.

  • Results in inflammation and further cellular damage (vicious cycle).

VII. Inflammatory Response**

• Tissue Injury: Leads to:

  • Release of chemical mediators (histamine, prostaglandins, etc.).

  • Vascular response: Vasodilation, increased capillary permeability.

  • Cellular response: Movement of WBCs and systemic effects (fever, increased WBCs).

  • Resulting in cardinal signs: Redness, heat, swelling, pain, impaired function.

VIII. Hypersensitivity Disorders**

• Pathological Response: Immune response to antigens that typically do not affect others.

• Classifications:

  1. Type I (IgE-mediated): Allergens bind to IgE → mediator release.

  2. Type II (Cytotoxic): IgG/IgM interact with cell/tissue antigens → cell damage.

  3. Type III (Immune complex-mediated): Antigen-antibody complexes cause inflammation/damage.

  4. Type IV (T cell-mediated): T cell-induced tissue damage.

• Potential Nursing Problems:

  • Examples:

    • Type I: Allergic rhinitis, asthma, anaphylaxis.

    • Type II: Blood transfusion reactions.

    • Type III: Systemic lupus erythematosus (SLE).

    • Type IV: Contact dermatitis.

IX. Assessment Findings**

• Specific to individual disorders as clinical manifestations of the various hypersensitivity reactions.