Immune System Dysfunction PDF - Samuel Merritt University

Immune System Dysfunction N111 Pathopharmacology 1 Samuel Merritt University  Innate Adaptive Immunity...

Immune System Dysfunction N111 Pathopharmacology 1 Samuel Merritt University  Innate Adaptive Immunity Immunity Natural killer Cell- Neutrophils Macrophages Humoral cells mediated Target non- Target micro- Target micro- T helper Cytotoxic T Regulatory T B B memory self cells organisms organisms lymphocytes lymphocytes lymphocytes lymphocytes cells Suppress Secrete Destroy Secrete Secondary Chemotaxis other cytokines target cells antibodies response immune cells Inflammation  Immune Dysfunction Primary Secondary Hypersensitivity Autoimmunity Immune Immune Reactions Deficiency Deficiency Rheumatoid Type I Type II Type III Type IV IgA Deficiency Poor nutrition Arthritis Type 1 Contact DiGeorge Allergies Graves disease Lupus Stress Diabetes hypersensitivity Syndrome Myasthenia Tuberculin Medications/ Graves Disease Anaphylaxis SCID gravis reaction drugs Hemolytic Lupus disease of the Surgery newborn Hemolytic transfusion reaction Excessive Immune Dysfunction  Types Autoimmunity Abnormal excessive immune responses toward own tissues Hypersensitivity reactions  Autoimmunity Examples Rheumatoid arthritis Type I diabetes mellitus Graves disease Systemic lupus erythematosus  Types of Hypersensitivity Mediated by antibodies Mediated by T cells Type I Type IV Type II Type III  Type I (E/P) Risk Factor Genetic/hereditary link E: Response to antigens (allergens) P: Immediate; 15-30 min after exposure IgE attracts basophils and mast cells Principle effector cells: Mast cells & basophils Type I Hypersensitivity (cont’d)  Histamine Most important mediator ↑ vascular permeability Vasodilation Urticaria/pruritis Smooth mm constriction ↑ mucus secretion  Type I Clinical Manifestations Mild Severe Life Threatening Hives Throat constriction Anaphylaxis Seasonal allergic Localized edema rhinitis Wheezing Pruritis/urticarial Tachycardia Eczema  Type I Treatment Implications Mild → Severe Severe→ Life Threatening Antihistamines Reaction Beta-adrenergics IgE therapy Corticosteroids Epinephrine Anticholinergics Prevention IgE therapy Prevention  Type II Often immediate reaction Antibodies attack antigens on surface of specific cells Complement helps destroy cell Phagocytosis Non-attached antigen attacked by complement & neutrophil granules Cell mediated cytotoxicity Examples: Graves disease Myasthenia gravis  Transfusion reaction P: CM: Recipient antibodies attach to Dark urine the donor’s RBC antigens Difficulty breathing Kidney damage Chills TI: Fever Stop the transfusion Nausea Give Benadryl & Tylenol Lower back/chest pain Support the airway  Hemolytic disease of the newborn Erythroblastosis fetalis CM: E: Hyperbilirubinemia → Jaundice Rh- mother is sensitized to her Anemia → pallor fetus’ Rh+ red cell group antigens Mother’s exposure occurs when Low serum albumin → Hydrops fetalis fetal and maternal blood are mixed TI: Hepatosplenomegaly → ↓ platelets & ↓ clotting factors → Rhogam –prevention coagulopathies Treatment of un-prevented cases  1st Pregnancy 2nd Pregnancy Rh- mom Rh- mom Mom Rh+ fetus Rh+ fetus becomes sensitized No issue Mom’s reacts to fetal Rh+ antigen  Type III Immune complex reaction Not tissue specific Immune/phagocytic systems are unable to remove antigen-antibody immune complexes Example Systemic lupus erythematosus  Type IV Delayed hypersensitivity Principle mediators: lymphocytes Principle effector cells Lymphocytes Macrophages  Contact Hypersensitivity P: Epidermal issue Peaks 48-72 hours  Tuberculin-type hypersensitivity E/P: Individual (previously infected by tuberculosis) + exposure to tuberculin antigen → positive tuberculin test 48-72 hours CM: Redness, induration, inflammation at the injection site Which of the following terms describes the type of immunity that occurs when preformed antibodies transfer from donor to recipient? A. Active B. Passive C. Cellular D. Memory Which statement best describes the immune system? A.The phagocyte system is the first line of defense. B.T lymphocytes (T cells) develop in the tonsils which are strategically located. C.Sloughing of the skin epithelium occurs due to slow cellular production and turnover. D.Innate defenses require no previous exposure to mount an effective response against an antigen. Which of the following disorders involves a delayed response in which T- cells initiate an inflammatory response? A. Type I hypersensitivity B. Type II hypersensitivity C. Type III hypersensitivity D. Type IV hypersensitivity