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Hypersensitivity
Immunology and Serology
| Question | Answer |
|---|---|
| Hemolytic disease of the Newborn (HDN) | excessive destruction of fetal RBCs by maternal antibodies |
| Hypersensitivity | an unpleasant or damaging condition of the body tissues caused by antigenic stimulation |
| Angiodema | redness and swelling |
| Anaphylaxis | clinical response to immunologic formation and fixation between a specific antigen and a tissue-fixing antibody; mediated by IgE antibody |
| Etiology | Range from life-threatening anaphylactic reactions to mild manifestations associated with food allergies |
| Transfusion reaction | adverse consequences of incompatibility between patient and donor RBCs, platelets or plasma |
| Anaphylactic reactions | Drugs = penicillin insect stings = Hymenoptera; common hornet, yellow jacket, paper wasp, yellow hornet |
| Mast cells/tissue basophils: | receptors for IgEcommon in connective tissues, lungs and uterus, around blood vessels granules contain heparin, histamine and zinc |
| When mast cells are exposed to specific immunologic/chemical agents they | degranulate and release the heparin and histamine. |
| Atopic allergies | hay fever, asthma and food allergies mostly naturally occurring, source is not always known demonstrate a strong familial or genetic tendency |
| Anaphylactic reaction part 1: | 1.offending antigen attaches to IgE antibody fixed to surface of mast cells/basophils2.activated mast cells/basophils release various mediators |
| Anaphylactic reaction part 2: | 3.mediator release produces vascular changes, activation of platelets, eosinophils and neutrophils and activation of the coagulation cascade |
| Anaphylactoid (anaphylaxis-like) reactions 1: | Similar to anaphylaxis Caused by immunologically inert materials that activate serum and tissue proteases and alternate pathway of complement system |
| Anaphylactoid (anaphylaxis-like) reactions 1: | Not mediated by Ag/Ab interaction Offending substances act directly on the mast cells/basophils causing release of mediators or on tissues |
| Local reactions | hives and angiodema; severe but rarely fatal |
| histamine release | constriction of bronchial smooth muscle, edema of trachea and larynx, stimulation of smooth muscle in GI tract = vomiting and diarrhea |
| urticaria and angiodema | breakdown of cutaneous vascular integrity |
| vasodilation | reduction of circulating blood volume and progressive fall in blood pressure leading to shock |
| Cytotoxic Reactions (Type II Hypersensitivity Reactions) | Characterized by interaction of IgG or IgM Ab to cell-bound antigen Binding results in activation of complement and destruction of cells to which Ag is bound; may be RBCs, WBCs or platelets |
| Transfusion Reactions | Include hemolytic reactions occurring during or shortly after TX, shortened posttransfusion survival of RBCs, allergic response or disease transmission |
| Immediate hemolytic reactions part 1 | Most common cause = transfusion of ABO-group imcompatible blood Most serious and potentially lethal Signs and symptoms: fever and chills, back pain, shortness of breath, pain at infusion site, hypotension |
| Immediate hemolytic reactions part 2 | Immunologic manifestations: occur during or immediately after infusion, intravascular and/or extravascular hemolysis, rapid increase of free hemoglobin in circulation |
| Delayed hemolytic reactions part 1 | Occurs 7 to 10 days after infusion Occurs in extravascular spaces |
| Delayed hemolytic reactions part 2 | Decreased RBC survival due to coating of cells (DAT+) promoting phagocytosis and removal of cells by mononuclear phagocytic system, destruction mainly in spleenMay be due to a primary or secondary exposure |
| Old term for Hemolytic disease of the newborn | erythroblastosis fetalis |
| How is Hemolytic disease of the newborn characterized? | Characterized in newborn by anemia and jaundice Excessive breakdown of RBC into hemoglobin bilirubin = can cause elevated levels of bilirubin leading to buildup in brain tissue leading to retardation or death |
| Etiology of Hemolytic Disease of the Newborn part 1 | antigens possessed by fetus that are foreign to mother can lead to development of antibody in mother; first pregnancy = first exposure; antibodies are IgM and will not cross placenta to affect first fetus |
| Etiology of Hemolytic Disease of the Newborn part 2 | secondary exposures due to subsequent pregnancies will lead to production of IgG that will cross placenta and attach fetal RBCs |
| Example of Hemolytic Disease of the Newborn part 1 | Mother = Rh- (no D antigen) Fetus = Rh+ (D antigen)Mom will form anti-D upon exposure to fetus’ D antigen. The first exposure will not result in any harm to fetus due to IgM anti-D that does not cross the placenta |
| Example of Hemolytic Disease of the Newborn part 2 | Any subsequent pregnancies with an Rh+ fetus will result in the immediate production of IgG anti-D that will cross the placenta and attach the fetal D+ RBCs. |
| Signs and symptoms of HDN | mild to severe; anemia, increase in RBC breakdown products such as bilirubin, jaundice, retardation if levels rise to high, death, hydrops fetalis |
| Diagnostic evaluation of HDN | ABO blood grouping, Rh testing, Ab screen and subsequent Ab Id if necessary, prenatal amniocentesis, serum bilirubin of cord or infant blood, DAT of cord or infant blood, peripheral blood smear, Du rosette or Kleihauer-Betke test |
| Prevention of HDN | administration of Rh IgG to Rh- women after any pregnancy, abortion or miscarriage and at 28 weeks gestation; this IgG will bind to any antigen and prevent mother’s exposure and subsequent anti-D formation |
Created by:
Mgoodall
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