Patho_notes_2d_immunity_disorders_II

Immune Disorders

Hypersensitivity

• Definition: Abnormal immune response to allergens or antigens.

• Types of Hypersensitivity:

  • Type I: Immediate hypersensitivity (e.g., Hay fever,Anaphylaxis)

    • Mechanism:

      • 1st Exposure: Immune response results in increased IgE & mast cell loading.

      • 2nd Exposure: Mast cell-IgE-antigen complex triggers mast cell degranulation. (making IgE way faster, loading mast cells causing it to degranulate, causing release of histamine, causing swelling.)

    • Phases:

      • Early Phase: Systemic histamine release.

      • Late Phase: Chemotaxis to eosinophils/neutrophils; release of leukotrienes, prostaglandins, and platelet activating factors.

    • Symptoms: Mild asthma, severe anaphylaxis, hives, rash, conjunctivitis, blocked airway, wheezing, rhinitis, shock, vomiting, diarrhea.

  • Type II: Antibody-mediated cytotoxicity.

    • Mechanism:

      • Antibodies bind to surface of cells (e.g., RBCs, basement membranes-glomeruli).

      • Causing autoimmune diseases

      • Trigger cell destruction through:

        • K cells,

        • Complement activation (MAC),

        • Phagocytic cells.

  • Type III: Immune complex mediated hypersensitivity.

    • Definition: Aggregation of antibodies and antigens forming emboli-like immune complexes.

    • Consequences: Deposits in blood vessels lead to microthrombi and inflammation; can cause arthritis and pneumoconiosis.

  • Type IV: Cell-mediated, delayed type hypersensitivity.

    • Mechanism: Helper T-cells stimulate cytotoxic T cells, macrophages, and K/NK cells. (T-cells can kill a cell)

    • Related Conditions: Chronic infections like tuberculosis (from microbacterium) and leprosy; includes tuberculin test as a diagnostic tool.

      • Things that take awhile to see exposure and response

Immune Deficiencies

• Types:

  • Primary Immune Deficiencies:

    • Genetic disorders affecting the immune system.

    • B-cell deficiencies: Hypogammaglobinemia (B-cells aren’t producing antibodies), often sex-linked.

      • Associated with “bubble boy” individuals must live in a sterile environment to avoid infections. (most likely in girls)

    • T-cell deficiencies:

      • DiGeorge syndrome (thymus dysfunction).

      • SCID (Severe Combined Immunodeficiency), both T and B cells deficient leading to opportunistic infections (similar to AIDs).

  • Secondary Immune Deficiencies:

    • Results from environmental factors:

      • Age (thymus atrophy leads to less T cell activation).

      • Poor diet (low protein, zinc deficiency).

      • Diabetes.

      • Stress and immunosuppressive drugs.

Acquired Immune Deficiency Syndrome (AIDs)

• Pathogen: HIV (HIV-I & HIV-II).

• Transmission: Through fluids with high lymphocyte counts. (how many T-cells in that fluid)

• Course of Disease:

  • Acute Phase: Antibody response, swollen lymph nodes, fatigue, diarrhea.

  • Full-blown AIDs: T-cell count drops below 200/mm3 leading to opportunistic infections (e.g., Kaposi's sarcoma, lymphoma, pneumocystis pneumonia, cryptosporidium, toxoplasmosis).

Autoimmune Diseases

• Characteristics:

  • Affect multiple organs or single organs.

  • Multifactorial origin; more prevalent in women than men.

• Example: Systemic Lupus Erythematosus (SLE).

  • Prevalence: 1 in 700 women.

  • Diagnosis: Requires 4 out of 11 criteria; primarily targets multiple organ systems and presents positive anti-nuclear antibodies directed against nuclear components.

  • Involves loss of self-tolerance resulting in B-cell dysfunction; mainly Type III immune complex-mediated hypersensitivity and secondary Type II antibody-mediated cytotoxicity.

  • look at SLE?? SLIDE 21