Immuno - Immune Responses (Hypersensitivity & Blood Transfusion Reactions) Flashcards
Pg. 208-209 in First Aid 2014 Pg. 203-204 in First Aid 2013 Sections include: -Hypersensitivity types -Hypersensitivity disorders -Blood transfusion reactions
What are the types of hypersensitivity? In general, what mediates each?
Type I - Anaphylactic and atopic; Type II - Cytotoxic (antibody mediated); Type III - Immune complex; Type IV - Delayed (T cell-mediated) type; Think: “ACID = Anaphlylatic and Atopic (type I), Cytotoxic (antibody mediated, type II), Immune complex (type III), Delayed (cell mediated, type IV)”
Draw a visual depicting what happens in Type I hypersensitivity.
See p. 208-209 in First Aid 2014 or p. 203 in First Aid 2013 for Type I visual
What is the mechanism involved in Type I hypersensitivity? What response(s) occur(s)?
Free antigen cross-links IgE on presensitized mast cells and basophils, triggering release of vasoactive amines that act at posctcapillary venules (i.e., histamine).
What is the timing of reaction(s) in Type I hypersensitivity, and why?
Reaction develops rapidly after antigen exposure because of preformed antibody. Delayed response follows to production of arachidonic acid metabolites (e.g., leukotrienes)
Again, regarding the mechanism of Type I hypersensitivity, which cells and immunoglobulin are involved? What effect does their interaction cause?
Free antigen cross-links IgE on presensitized mast cells and basophils, triggering release of vasoactive amines that act at posctcapillary venules (i.e., histamine).
Which type(s) of hypersensitivity is/are antibody mediated?
Types I, II, and III are all antibody mediated.
What is the test for Type I hypersensitivity?
Test: skin test for specific IgE
What is the overall mechanism involved in Type II hypersensitivity? What effect does this have?
Cytotoxic (antibody mediated) - IgM, IgG bind to fixed antigen on “enemy” cell, leading to cellular destruction; Think: “Type II is cy-2-toxic”
What are 3 specific mechanisms involved in Type II hypersensitivity?
3 mechanisms: (1) Opsonization leading to phagocytosis or complement activation (2) Complement-mediated lysis (3) Antibody-dependent cell-mediated cytotoxicity (ADCC), usually due to NK cells or macrophages
What is the role of complement in Type II hypersensitivity?
Antibody and complement lead to membrane attack complex (MAC).
How is Type II hypersensitivity tested for?
Test: direct and indirect Coombs’
Draw a visual depicting the mechanism of Type II hypersensitivity.
See p. 208 in First Aid 2014 or p. 203 in First Aid 2013 for Type II visual
What do direct versus indirect Coomb’s tests detect? Give an example of each.
DIRECT: detects antibodies that HAVE adhered to patient’s RBCs (e.g., test an Rh+ infant of an Rh- mother); INDIRECT: detects antibodies that CAN adhere to other RBCs (e.g., test an Rh- woman for Rh+ antibodies)
What is the mechanism of Type III hypersensitivity? What effect(s) does it have?
Immune complex - antigen-antibody (IgG) complexes activate complement, which attracts neutrophils; Neutrophils release lysosomal enzymes
What type of hypersensitivity is serum sickness? More specifically, what is the mechanism by which serum sickness occurs? How long does it take to happen? What is the result?
An immune complex disease (type III) in which antibodies to the foreign proteins are produced (takes 5 days); Immune complexes form and are deposited in membranes, where they fix complement (leads to tissue damage).
Which is the more common Type III hypersensitivity: Serum sickness or Arthus reaction?
Serum sickness is more common than Arthus reaction.
What type of hypersensitivity is arthus reaction? More specifically, what is the mechanism by which arthus reaction occurs? What is the result?
Type III hypersensitivity; A local subacute antibody-mediated hypersensitivity (type III) reaction. Intradermal injection of antigen induces antibodies, which form antigen-antibody complexes in the skin.
What presentation characterizes Arthus reaction?
Characterized by edema, necrosis, and activation of complement.
What is the most common cause of serum sickness?
Most serum sickness is now caused by drugs (not serum) acting as haptens.
What presentation characterizes serum sickness?
Fever, urticaria, arthralgias, proteinuria, lymphadenopathy 5-10 days after antigen exposure.
What causes the Arthus reaction? What is used to test for it?
Antigen-antibody complexes cause the Arthus reaction; Test: immunofluorescent staining
What is the overall mechanism of Type IV hypersensitivity? What effect does it have?
Delayed (T-cell mediated) type - sensitized T lymphocytes encounter antigen and then release lymphokines (leads to macrophage activation; no antibody involved).
How can Type IV hypersensitivity be tested?
Test: patch test, PPD
Is Type IV hypersensitivity transferable by serum? Why or why not?
Cell mediated; therefore, it is not transferable by serum.
What are the 4 T’s to associate with Type IV hypersensitivity?
Think: “4th and last”; 4 T’s = T lymphocytes, Transplant rejections, TB skin tests, Touching (contact dermititis)
What are 2 categories of Type I hypersensitivity disorders? Give at least 2 examples within each category.
(1) Anaphylaxis (e.g., bee sting, some food/drug allergies) (2) Allergic and atopic disorders (e.g., rhinitis, hay fever, eczema, hives, asthma)
Describe the presentation of type I hypersensitivity in 3 words (not necessarily symptoms).
Immediate, anaphylactic, atopic
What are 9 examples of Type II hypersensitivity?
(1) Autoimmune hemolytic anemia (2) Pernicious anemia (3) Idiopathic thrombocytopenic purpura (4) Erythroblastosis fetalis (5) Acute hemolytic transfusion reactions (6) Rheumatic fever (7) Goodpasture syndrome (8) Bullous pemphigoid (9) Pemphigus vulgaris
Describe the presentation of type II hypersensitivity.
Disease tends to be specific to tissue or site where antigen is found
What are 5 examples of Type III hypersensitivity?
(1) SLE (2) Polyarteritis nodosa (3) Poststreptococcal glomerulonephritis (4) Serum sickness (5) Arthus reaction (e.g., swelling and inflammation following tetanus vaccine)
Describe the presentation of type III hypersensitivity.
Can be associated with vasculitis and systemic manifestations
What are 5 examples of Type IV hypersensitivity?
(1) Multiple sclerosis (2) Guillain-Barre syndrome (3) Graft-versus-host disease (4) PPD (test for M. tuberculosis) (5) Contact dermatitis (e.g., poison ivy, nickel allergy)
Describe the presentation of type IV hypersensitivity.
Response is delayed and does NOT involve antibodies (vs. types I, II, and III)
What is the pathogenesis of allergic reaction? How is it treated?
Type I hypersensitivity reaction against plasma proteins in transfused blood; Treat with antihistamines
What is the clinical presentation of allergic reaction?
Urticaria, pruritus, wheezing, fever.
What is the pathogenesis of anaphylactic reaction? What is an implication/consequence of this in the context of blood transfusion?
Severe allergic reaction. IgA-deficient individuals must receive blood products that lack IgA.
What is the clinical presentation of anaphylactic reaction?
Dyspnea, bronchospasm, hypotension, respiratory arrest, shock.
What is the pathogenesis of febrile nonhemolytic transfusion reaction?
Type II hypersensitivity reaction. Host antibodies against donor HLA antigens and leukocytes.
What is the clinical presentation of febrile nonhemolytic transfusion reaction?
Fever, headaches, chills, flushing.
What is the pathogenesis of acute hemolytic transfusion reaction?
Type II hypersensitivity reaction. Intravascular hemolysis (ABO blood group incompatibility) or extravascular hemolysis (host antibody reaction against foreign antigen on donor RBCs).
What is the clinical presentation of acute hemolytic transfusion reaction?
Fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinemia (intravascular), jaundice (extravascular hemolysis).
