Hypersensitivites Flashcards
What are immunosuppressants for?
Dec immune response—Transplant pt, autoimmune conditions; suppress cell-mediated immunity, anti inflammatory
Antihistamines
Dec sx of inflammatory immune response; suppress histamine mediator activity
Epinephrine Class
Vasopressor, bronchodilator, anti asthmatic, vasoconstrictor
Epinephrine indications
Severe allergic rxn, cardiac arrest, severe asthmatic attack
Epinephrine MOA
Inhibits release of mediators from mast cells; works on alpha receptors (arteries) and beta receptors (heart, lungs and skeletal muscles)
Epinephrine Side Effects
CV: angina, arrhythmia, HTN, tachycardia
CNS: nervousness, restless, tremor
Giving EPI
All routes but PO, SQ preferred, start with lowest dose possible (wt based in peds), be careful with the dose bc they can vary a lot
Epinephrine NC
Monitor VS closely and watch for reversal sx; overdose can be FATAL bc vasoconstriction—have coworker check dose if drawing it up; use TB syringe for SQ use; for home use, teach to take as directed and contact HCP and go to ED/clinic after taking; teach epipen has expiration date
Hypersensitivity
normal immune response that is excessive or inappropriately triggered or produces undesirable effects on the body
Hypersensitivities I, II, and III
mediated antibodies produced by plasma B cells
Hypersensitivity type IV MOA
Mediated by T cells (no B cell involvement)
Triggers for hypersensitivities
specific antigen-antibody reaction or specific antigen-lymphocyte interaction; occurs on second exposure with specific antigen
Type I
IgE mediated rxn; in response to someone developing an allergy after being sensitized to an antigen (rxn is 15-20 minutes after the second exposure to antigen); often pet dandruff and and pollen, foods (eggs, nuts), meds; genetic basis
Cells involved in Type 1
B lymphocyte, IgE antibodies, mast cells (granulocytes)
Type 1 pathogenesis
allergen attaches immature B cell w/ first exposure and B cell matures, B cell turned on and matures to plasma cell that makes IgE antibodies, IgE attach to mast cells which release chemical mediators at the second exposure, causing an allergic rxn rxn
What do chemical mediators cause in Type 1?
vasodilation—dec BP, stuffy nose, wheals on skin, bronchial constriction–throat swells, wheeze, stimulates irritant receptors—itchy, inc vasc permeability–edema and nose run
What do allergy shots do?
dec sensitivity of B cells so they don’t release IgE antibodies
Atopic rxn to Type 1
Acute and localized; asthma, allergies, rhinitis, runny nose, hives; pollen, dust, dandruff
Anaphylactic rxn
systemic release of chemical mediators that cause life-threatening sx like swelling, airway obstruction, vascular collapse–shock
Most common triggers for anaphylaxis
meds, bee stings, food; only need a small amount
tx for anaphylaxis
GCC, anti-histamines; pt wear medical alert bracelets, carry EPI pen
Type II hypersensitivity
Cytotoxic rxn mediated by immunoglobulins after exposure to antigens or foreign tissue/cells located on cell surface
Type II Pathogenesis
Antigens stimulate an antibody response and form an antibody-antigen complex that attacks cells and destroys–cell lysis and phagocytes
Cell involved in Type II hypersensitivity
IgG and IgM cells, complement cells (kill foreign antigens), phagocytes
Examples of Cytotoxic antigens
blood transfusion, autoimmune disorders like DM, erythroblastosis fetalis–difference in Rh btwn mom and child, drug rxn
How does cytotoxic rxn occur with different blood types?
Donor A and recipient B trigger anti-A and anti-B which all clump together and donor cells burst–blocks small vessels and debris in veins
sx of Cytotoxic rxn
blood transfusion rxn–fever, chills, flush from chemical mediators, chest and back pain from clogged vessels, N/V, HA, anxiety, restless
What should you do before and after a blood transfuion?
Take temperature before and after
Type III hypersensitivity
Immune complex rxn; local or systemic antigen-antibody complex that attaches to tissue, causing INFLAMMATION which can cause tissue damage
rheumatoid arthritis
antigen-antibody complex that attaches to joints
Type III cause
autoimmune or low grade infx (body gets confused and attacks) or inhaled antigens from mold or contaminated plants
Cells involved in Type 3 immune complex rxn
IgG and IgM (clump with antigens), complement (destroy tissues with mast cells), neutrophils (release chemical mediators and mast cells)
Glomerulonephritis
Kidney failure from complex binding to kidneys
systemic lupus erythematosus
complexes bind to skin and many organs, causing inflammation
Type IV hypersensitivities and examples
Delayed hypersensitivity without antibody involvement; poison ivy, TB test, jellyfish sting, jewelry rxn, Crohn’s disease
Immune cells involved in type IV
T cells (no B cells), cytokines, mast cells, macrophages
Type IV etiology
delayed cell rxn to antigen from plant oils, cosmetics, nickel alloy, TB antigen, gluten, organ transplant/graft, contact dermatitis, tuberculin
Type IV pathogenesis
small particles/incomplete proteins called “Hapten” penetrate the skin and combine with human proteins to form complete antigens; antigen processing cells (T cells) recognize and attach the antigen via direct attack and release cytokines and macrophages
When does a delayed hypersensitivity peak?
48-72 hours
