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

robot