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56 Cards in this Set
- Front
- Back
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A what age are adult levels of all immunoglobulins reached?
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1-2 years old
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What is the first immunoglobulin to be produced by maturing plasma cells?
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IgM
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Which immunoglobulin can transform into other immunoglobulins after antigen stimulus?
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IgM
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Transient Hypogammaglobulinemia of Infancy (B-cell)
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*delay in maturation process of B cells
*fewer B-cells = fewer antibodies *prolonged deficiency in IgG levels *upper respiratory and middle ear infections *usually resolves @ 2-4 years of age |
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X-Linked Agammaglobulinemia (Burton's)
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impaired ability of B-lymphocytes to produce antibodies
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DiGeorge Syndrome
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*lack of thymus development
*impaired ability of T-helper cells to orchestrate an immune response *or impaired ability of cytotoxic t-cells to mount a cytotoxic response |
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Severe Combined Immunodeficiency Syndrome
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no T or B cells
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Types of Primary Immunodeficiencies
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1) Transient Hypogammaglobulinemia of Infancy
2) X-linked Agammaglobulinemia 3) DiGeorge Syndrome 4) Severe Combined Immunodeficiency Syndrome |
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Causes of Secondary Immunodeficiency
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1) selective loss of immunoglobulins via GI &/or GI tracts (ex: nephrotic syndrome)
2) chronic or recurrent infections (Tb/AIDS) 3) CA (lymphoma); 4) iatrogenic causes (immunosuppressive therapy); 5) stress/aging; 6) drug abuse/maternal alcoholism |
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Definition of Hypersensitivity Disorder
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*exaggerated immune response to allergens
*leads to inflammation and tissue injury caused by inhalation, ingestion, skin contact, or injection |
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Factors Causing Hypersensitivity Disorders
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1) type of allergen/antigen
2) exposure 3) person's genetic make-up |
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4 Types of Hypersensitivity Disorders
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1) Type I: IgE-Mediated Hypersensitivity
2) Type II: Antibody-Mediated Hypersensitivity 3) Type III: Immune Complex Allergic Disease 4) Type IV: T-cell Mediated Hypersensitivity |
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Onset and Duration of Type I: IgE-Mediated Hypersensitivity
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*onset: few minutes
*duration: few hours |
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Minor Symptoms of Type I: IgE-Mediated Hypersensitivity
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localized, itchy skin wheal
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Severe Symptoms of Type I: IgE-Mediated Hypersensitivity
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anaphylaxis: vasodilation and bronchoconstriction
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What determines whether a Type I: IgE-Mediated Hypersensitivity is minor or severe?
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route of administration
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Type I: IgE-Mediated Hypersensitivity
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triggered by binding of allergen to mast cell or basophil with attached IgE, leading to degranulation
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Primary Phase of Type I: IgE-Mediated Hypersensitivity
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*fast acting or primary mediators released: histamine, complement
*acetylcholine = bronchoconstriction & vasodilation *eosinophilia in affected area |
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Secondary Phase of Type I: IgE-Mediated Hypersensitivity
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*slow-reacting or secondary substances of anaphylaxis
*leukotrienes: vasodilation/chemotaxis *cytokines, platelet activating factor *prostaglandins: respiratory issues |
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Atopic or Local Anaphylaxis
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*inherited: genetic & environmental component
*organ specific |
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Examples of Atopic or Local Anaphylaxis
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1) allergic rhinitis
2) atopic dermatitis (eczema) 3) certain food allergies 4) latex allergy |
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Diagnosis of Atopic or Local Anaphylaxis
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1) careful hx
2) identification of nasal eosinophilia 3) skin testing |
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Non-Atopic or Systemic Anaphylaxis
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*not organ specific
*can be lethal *non-inherited |
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Common Allergens of Non-Atopic or Systemic Anaphylaxis
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nuts, shellfish, PNC, insect stings
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Symptoms of Non-Atopic or Systemic Anaphylaxis
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*Hives, itching, bronchospasm, angioedema, contraction of GI and uterine muscles, laryngeal edema, asphyxiation and erythema
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Examples of Hypersensitivity Type II: Antibody-Mediated
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1) ABO antigens in blood transfusion reactions
2) fetal circulation does not match maternal circulation 3) drug reactions 4) autoimmune hemolytic anemia: antibodies against own RBCs 5) graft rejections; 6) parasites |
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Antibody Cytotoxicity of Hypersensitivity Type II: Antibody-Mediated
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*IgG and IgM antibodies interact with antigens on cell surfaces
*activates complement and/or antibody-dependent-cell-mediated cytotoxicity: activation of NKCs *stimulation or inhibition of cell function |
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Injuries in Hypersensitivity Type II: Antibody-Mediated
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*complex fixation leads to: inflammation, opsonization with phagocytosis, or cell lysis
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Hypersensitivity Type III: Complex Allergic Disease
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*formation of insoluble antigen-antibody complexes in blood circulation or extravascular sites
*leads to precipitate formation and complement activation |
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Factors that Contribute to Injuries in Hypersensitivity Type III: Complex Allergic Disease
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*Change in blood flow
*vascular permeability *inflammatory response |
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Antigen-Antibody Complexes of Hypersensitivity Type III: Complex Allergic Disease
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*get deposited in blood vessels
*activates complement *causes vasculitis *leads to vessel wall damage |
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Localized Types of Hypersensitivity Type III: Complex Allergic Disease
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*vaccine injection site reaction with localized tissue necrosis due to antigen-antibody complexes that precipitate
*onset: 4-10 hours |
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Vasculitis in Localized Type of Hypersensitivity Type III: Complex Allergic Disease
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*blood vessel can burst causing hemorrhage into surrounding tissue
*or blood vessel can become occluded causing ischemia and necrosis |
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Immune Complex Pneumonitis of Hypersensitivity Type III: Complex Allergic Disease
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*allergic pneumonitis
*involves IV hypersensitivity as well *cough, malaise, fever, dyspnea, radiographic densities |
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Systemic Type of Hypersensitivity Type III: Complex Allergic Disease
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*antigen-antibody complexes precipitate in blood vessel, joints, heart, kidneys: pain & edema in these areas (ex: RA)
*usually temporary, symptoms subside |
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Symptoms of Systemic Hypersensitivity Type III: Complex Allergic Disease
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hives, edema, rash, fever
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Causes of Systemic Hypersensitivity Type III: Complex Allergic Disease
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PNC, foods, drugs, insect venoms
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Hypersensitivity: Type IV T-Cell Mediated Reactions
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*delayed: occur 24-72 hours s/p exposure
*triggered by specifically sensitized T-cells, NOT ANTIBODIES *direct attack by cytotoxic T-cells can occur *not tissue specific |
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Examples of Hypersensitivity Type IV: T-cell Mediated Reactions
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*contact dermatitis: poison ivy/latex allergy
*response to TB test (erythema & induration 8-12 hours after injection) *granulomatous inflammation with large, insoluble antigen (splinter, TB, silica) |
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Rheumatoid Arthritis
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*systemic inflammatory disease
*affects all races *women > men *unknown etiology *biarticular |
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Rheumatoid Factor
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*70%-80% of patients have rheumatoid factor
*RF = antibody against IgG found in blood, synovial fluid, & synovial membrane *RF + IgG form immune complexes which lead to synovitis & pannus development |
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Pannus
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*formation of granulation tissue from RF + IgG immune complexes
*swollen & puffy joint *differentiates RA from other arthritis |
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Pathogenesis of RA
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*cannot make cartilage
*over-proliferation of granulation tissue *cartilage & subchondral bone get destroyed *surrounding muscles, ligaments, & tendons weaken *reduced joint monition & possible fusion of joint |
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Mild RA
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lasts only few months to 1-2 years
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Moderate RA
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flares and remissions
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Severe RA
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*active most of the time for many years
*causes serious joint damage & disabilty |
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Extra-Articular/Systemic Manifestations of RA
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1) fatigue; 2) weakness; 3) weight loss; 4) aching;
5) stiffness; 6) elevated ESR; 7) anemia; 8) rheumatoid nodules & granulomatous lesions; 9) vasculitis, pleuritis, pericarditis |
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Systemic Lupus Erythematosus (SLE)
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*systemic connective tissue disorder due to anti-DNA antibodies
*onset: sudden or insidious *females; black; familial *lots of antibodies *hyper=gammaglobulinemia & hypo-complementemia) |
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Symptoms of SLE
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1) butterfly rash (sun sensitive); 2) synovitis;
3) necrotizing vasculitis (Type III reaction); 4) glomerulonephritis & possible RF (Type III reaction); 5) CNS depression; 6) pericarditis; 7) pleuritis (Type III reaction); 8) splenomegaly |
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Treatment of SLE
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*immunosuppressants
*corticosteroids (prolonged use can lead to osteoporosis) *Meds designed to deplete, destroy, or block B-cell effects |
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Mechanism of HIV Infection
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1) gp120 of virus binds to CD4 molecule
*(virus & host membranes fuse; virus enters host/sheds protein coat) 2) viral RNA produces viral DNA with reverse transcriptase 3) integration of pro-viral DNA (virus can be latent for some time) 4) productive virus synthesis-virions released-T-cell dies 5) virions invade other CD4 cells-fast amplification-initially millions of T-cells destroyed, but replaced 6) over time, T-cells cannot be replaced rapidly enough-T-cell #s crash |
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Classification of HIV
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based on CD4 cell count, not s/sx
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Window Phase
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between time of exposure to time antibodies are detectable
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Acute Phase of HIV
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*acute mono-like syndrome
*fever, myalgia, sore throat, nausea, lethargy, lymphadenopathy, rash, HA *symptoms decrease after 1-2 months *initial burst of viral replication-CD4 count decreases, but then immune system tries to control viral replication, CD4 count rebounds *both humoral and cell-mediated response involved |
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Clinical Presentation of HIV
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*generalized lymphadenopathy (>3 months)
*fatigue, weight loss, night sweats, diarrhea, fungal infections of mouth/nails |
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Full-Blown AIDS
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*CD count < 200
*risk for opportunistic infections *PCP/TB/thrush/toxoplasmosis/AIDS dementia |
