Immune Disorders Notes Disorders of the Immune System Three categories:Hypersensitivity reactions Autoimmune disorders Immune deficiencies Hypersensitivity Reactions Injury to the body due to an exaggerated immune response. Classified by how tissue is injured: Hypersensitivity Reactions Examples Anaphylaxis Hemolytic transfusion reactions Measles Transplant rejections Type 1 Hypersensitivity Reaction Anaphylactic reaction. Occurs immediately after exposure to an antigen. Can range from mild to severe, even life-threatening. Mechanism:First exposure: Body produces IgE antibodies that attach to mast cells. Second exposure: Antigen binds to IgE on mast cells, causing degranulation and release of histamine and other mediators (prostaglandins). Type 1 Hypersensitivity Disorders Allergic Rhinitis: Most common form of allergy. Symptoms: Sneezing, nasal itching, runny nose, itchy and red eyes. Atopic Dermatitis: Often called eczema. Inflammatory skin response. Symptoms: Pruritus, edema, extremely dry skin, blisters, crusts, scales.Nursing Action: Administer prescribed antipruritics and offer a lukewarm soak, followed by emollient topical cream. Rationale: Antipruritics reduce the itch-scratch cycle. Lukewarm soaks followed with application of emollients relieve dryness, which contributes to the itching. Anaphylaxis Severe systemic type 1 reaction. Widespread histamine release. Symptoms:Bronchial narrowing: Stridor, wheezing, respiratory arrest. Hypotension, tachycardia, cardiac arrest. Immediate treatment:Oxygen. Epinephrine. Antihistamines. Corticosteroids. Vasopressors. Mechanical ventilation. Nursing care:Early recognition. Maintain airway. Emotional support. Education. Urticaria (Hives) Release of histamine. Raised, pruritic, nontender, erythematous wheals on the skin. Therapeutic interventions:Epinephrine. Antihistamines. Corticosteroids. Histamine H2 blockers. Angioedema Swelling in submucosal/subcutaneous tissue due to increased vascular permeability. Causes: Allergic reaction, angiotensin-converting enzyme inhibitors, idiopathic, hereditary, acquired forms. Symptoms: Painless, nonpruritic swelling. Emergency if airway is involved. Treatment:Avoid allergen. Cinryze, Berinert. Antihistamines, corticosteroids. Haegarda. Ecallantide. Icatibant. Fresh frozen plasma. Type 1 Hypersensitivity Disorder Nursing Diagnoses Impaired Gas Exchange Anxiety Risk for Impaired Skin Integrity Ineffective Health Self-Maintenance Type 1 Hypersensitivity Disorder Nursing Care Monitor respiratory status. Monitor level of consciousness. Stay with the patient and keep them informed. Note and document skin and lesions. Explain the need to avoid scratching; apply pressure or rub itching skin. Explain the need for medical alert identification. Discuss methods of avoiding the allergen. Type 2 Hypersensitivity Reaction Destruction of a substance having an antigen. Beneficial for pathogens (bacteria). Examples: Blood types (A, B, O, AB; Rh−, Rh+), where O is the universal donor and AB is the universal recipient. Not beneficial when incompatible red blood cells (RBC) are sensed as foreign. Mechanism:Antibodies attach to normal self-marking cell membrane antigens. Foreign antibodies attach to the normal self-marking cell membrane antigens causing RBC membrane degradation. Hemolytic Transfusion Reaction RBCs with foreign antigens are rapidly lysed. Occlude blood vessels, leading to ischemia and necrosis. Life-threatening; prevention is key.Give RhoGAM to exposed Rho(D) negative patients. Careful blood transfusion administration. Therapeutic interventions:Antihistamines Corticosteroids Sympathomimetics Nursing care:Monitor transfusion; if reaction symptoms occur, immediately stop the blood. Monitor patient. Infuse normal saline with new tubing. Follow agency transfusion reaction policy. Return unused blood and tubing to blood bank. Educate patient. Type 3 Hypersensitivity Reaction Initial sensitization to an antigen, followed by a reaction to a later exposure. Causes red edematous lesion, bleeding, necrosis. Immune complexes formed by antigens and antibodies. Antigen–antibody complexes form within blood vessels. Enzymes lead to blood vessel damage. Mechanism:First Exposure to antigen. Second Exposure: Antigen-antibody complexes form, deposit in tissues and blood vessels leading to occlusion. Serum Sickness Antigen–antibody complexes form from exposure to nonhuman proteins. From exposure to antivenoms, rabies vaccines, immune modulating agents. Causes inflammation, tissue damage, and necrosis. Symptoms appear in 7 to 21 days. Brief and self-limiting condition when antigen exposure is removed. Treatment based on symptoms:Antipyretics Analgesics Anti-inflammatories Antihistamines Corticosteroids Nursing care:Monitoring of symptoms Evaluation of medication effects Education Type 4 Hypersensitivity Reaction Delayed reaction. Sensitized T lymphocyte contacts antigen. Cell-mediated immune response. Causes necrosis. Mechanism:Antigens are encountered. Sensitized T cells are activated and release cytokines. Leading to destruction of target cells. Chemical comes in contact with the skin. On second exposure, T cells secrete chemicals. Examples: Poison ivy, poison oak, latex. Reddened, pruritic, fragile vesicles. Therapeutic interventions:Antihistamines, topical drying agents, corticosteroids, topical immunomodulators. Relieve itching. Tepid baking soda baths or Aveeno baths. Wash with brown soap (Fels-Naptha). Latex allergy protocols. Nursing diagnoses:Impaired Skin Integrity Ineffective Health Self-Maintenance Transplant Rejection Transplanted living tissue sensed as foreign. Lymphocytes are sensitized immediately. Invade transplanted tissue and destroy it, leading to failure of the tissue or organ. Prevention:Immunosuppression therapy.Infection can result in death. Education: Medications, rejection signs. Autoimmune Disorders Immune system recognizes the body’s own cells as foreign. Immune response destroys these cells. Autoimmune Disorders Examples Rheumatoid arthritis Ulcerative colitis Multiple sclerosis Pernicious Anemia Antibodies against gastric parietal cells interfere with intrinsic factor. Vitamin B12 deficiency results, decreasing RBC production and causing anemia. Can be acquired through gastric or small bowel resections. Symptoms: Weakness, anorexia, glossitis, pallor, peripheral neuropathy. Therapeutic interventions:Corticosteroids Lifelong vitamin B12 supplementation. Nursing care:Vitamin B12 education Care and safety due to fatigue Idiopathic Autoimmune Hemolytic Anemia Autoantibodies attach to RBCs, causing them to lyse or agglutinate. Signs and symptoms:Mild fatigue Pallor Hypotension Dyspnea Jaundice Therapeutic interventions:Immunosuppressive medications Oxygen Corticosteroids Folic acid Transfusion Erythrocytapheresis Splenectomy Nursing care:Monitor symptoms. Plan rest periods. Educate patient. Hashimoto’s Thyroiditis Autoantibodies for thyroid-stimulating hormone form. The thyroid gland is overstimulated, leading to enlargement (hyperthyroidism). Then, different autoantibodies destroy thyroid cells, leading to hypothyroidism. Requires lifelong thyroxine. Nursing care:Rest periods Compression stockings Daily weights, intake and output Medication education Lupus Erythematosus Three types:Discoid lupus erythematosus (DLE): Skin lesions.Drug-induced systemic lupus erythematosus (DILE): After certain medication use.Systemic lupus erythematosus (SLE): Chronic, inflammatory, multisystem disorder. Lupus Erythematosus: Signs and Symptoms DLE: Patchy, crusty, sharply defined skin plaques. Occur on face and sun-exposed areas. DILE: Pleuropericardial inflammation. Fever Rash Arthritis Systemic Lupus Erythematosus (SLE) EtiologyYoung women of childbearing years First-degree relatives of lupus patients Black, Asian, Hispanic, American Indian population more likely to develop. Signs and SymptomsEarly symptoms vague: Fatigue, fever Dermatological: Butterfly rash, bruising photosensitivity, alopecia, pain, pruritis Musculoskeletal: Arthralgia, arthritis Hematological: Anemia, leukocytopenia, thrombocytopenia Cardiopulmonary: Pericarditis, myocarditis, myocardial infarction, vasculitis, pleurisy, valvular disease Renal: Kidney disease, urinary tract infections, fluid and electrolyte imbalances Central nervous system: Cranial neuropathies, seizures, cognitive impairment Gastrointestinal: Anorexia, ascites, pancreatitis, intestinal vasculitis Ophthalmological: Conjunctivitis, dry eyes, glaucoma, cataracts, retinal pigmentation Therapeutic interventionsSymptomatic management NSAIDs Immunosuppressants Corticosteroids Antimalarials Immunoglobulin ComplicationsOsteonecrosis Kidney disease Thrombocytopenia Emboli Myocarditis Vasculitis Mesenteric or intestinal vasculitis Sepsis Nursing DiagnosesAcute Pain Disturbed Body Image Fatigue Ineffective Health Self-Maintenance Ankylosing Spondylitis Chronic progressive inflammatory disease of sacroiliac, costovertebral, and large peripheral joints. Signs and symptoms:Lower back stiffness Pain Lordosis, kyphosis Spasms Fatigue Anorexia, weight loss No cure, supportive care, surgery. Nursing care:Education on posture, range-of-motion, firm mattress, thin pillow Immune Deficiencies One or more components of the immune system is completely absent or deficient. Hypogammaglobulinemia Absence/deficiency of one or more of five immunoglobulins from defective B cell function. Prone to infections. Therapeutic interventions:Minimizing infections IgG injections Fresh frozen plasma Genetic counseling Knowt Play Call Kai