NUR 228 Exam 1 Flashcards
Hypersensitivity
a NORMAL immune response that is inappropriately triggered OR excessive OR produces undesirable effects on the body.
What are two basic triggers?
antigen-antibody reaction
antigen-lymphocyte interaction
What is in common between types I, II, III hypersensitivity reactions?
they are all mediated by antibodies produced by B cells
-specifically PLASMA cells
What causes type IV hypersensitivity
mediated by T cells
What kind of hypersensitivity reactions does meds typically cause?
type I and IV
What type of hypersensitivity reaction does PCN cause
all four types
What kind of mediated reaction is type I
IgE mediated reaction
Type I hypersensitivity reaction
caused by B cells
Immediate reaction
occurs after being sensitized to an antigen
what antigens cause type I hypersensitivity?
environmental(pet dander, bee stings)
Foods (nuts, seafood, eggs)
Medications (penicillin, contrast dye)
What are key immune cells involved in Type 1 reaction?
B lymphocytes
IgE (antibody)
Mast cells (granulocyte)
Etiology of Type 1
Genetic link
1 parent allergic=30%
2 parents allergic= 50%
What is the pathogenesis of type 1?
-person exposed
-IgE antibody made
-IgE antibody attaches to mast cell
-person exposed again
-allergen binds to the IgE antibodies that are attached to the mast cells
-triggers the release of chemical mediators from the mast cell
Potent vasodilation causes
stuffy nose
lower blood pressure
wheals on skin
Increased vascular permeability causes
edema
runny nose
Bronchial smooth muscle constriction causes
breathing difficulties
wheezing
Stimulates irritant receptors causes
itching
Atopic reactions
local
inherited tendency to become sensitive to allergens
Ex: allergic rhinitis, asthma, urticaria(hives)
Anaphylactic reaction
systemic
life threatening because of bronchial constriction, airway obstruction, vascular collapse.
treat quickly
Most common triggers of atopic and anaphylactic reactions?
Atopic: pollen, dust, mold, animal dander
Anaphylactic: meds, bee stings, foods
What causes the symptoms from a type 1 hypersensitivity reaction?
release of chemical mediators
What is type II caused by?
b-cells
Etiology of Type II reactions
exposure to antigen or foreign tissue/cells
antigens are located on cell surface
What are the key characteristics of a type II reaction
-antigens stimulate antibody production
-antibodies recognize and attach to cell surface antigens
-direct destruction of targeted cells that contain the antigen
——-cell lysis
——-phagocytosis
what immune cells are involved with a type II reaction?
antibodies (IgG and IgM)
complement
WBCs (phagocytes)
what are the examples of antigens of type II
blood
some of your body’s own cells (autoimmune)
erythroblastosis fetalis
What are some example disorders from type II
blood transfusion reaction
newborn/mother Rh incompatibility
autoimmune disorders
certain drug reactions
What are some examples of type II manifestations of a transfusion rx?
Fever
Chills
angina
N/V
restlessness and anxiety
headache
What kind of reaction is type III?
Immune complex reaction
Key characteristics of type III hypersensitivity
antigen-antibody COMPLEXES (attach to each other) form
deposit into tissues
inflammatory response causes tissue damage
Etiology of Type III HSRx?
autoimmune
low grade infection
inhaled antigens from molds or contaminated plants
What are possible offending antigens for type III?
bodys own tissues/dna
Inhaled antigens from mold or contaminated plants
bacteria or viruses
What are key immune cells involved in type III sensitivity?
IgG and IgM antibodies that clump with antigens
complement
neutrophils and mast cells
Type III Pathogenesis?
antigen-antibody complex formed in blood
deposits in tissue
activation of complement + chemoattraction of neutrophils
Fc Receptor
Release of enzymes and free radicals
Tissue distruction
What are clinical manifestations of Type III?
depends on where the complexes are deposited in the tissue
Rheumatoid arthritis: joints
Glomerulonephritis: kidney failure
Systemic lupus erythematosus: skin and organs
What are the primary differences between type II and type III?
type II- reactions occur on the cell surface and result in direct cell death or malfunction
type III- immune complexes are deposited into tissues and the resulting INFLAMMATION destroys the tissue
What is type IV hypersensitivity?
Delayed hypersensitivity
What are key characteristics of Type IV hypersensitivity
delayed hypersensitivity response
NO antibody involvement
What are key immune cells for type IV
T cells
Cytokines
Mast cells and macrophages
Etiology of type IV
delayed cellular reaction to an antigen
What are some antigens for type IV
plant oils
cosmetics
nickel
tuberculin
organ transplant
skin graft
Type IV pathogenesis
small incomplete antigen (hapten) penetrates the skin
Hapten combines with human protein to form the complete antigen
T cells become aware of antigen
T cells attack the antigen via:
-direct attack of t cell
-release of cytokines
-macrophages
what are clinical manifestations of type IV
generally peak 48-72 hours
contact dermatitis
tuberculin hypersensitivity
Autoimmunity
the immune system recognizes “self” cells as foreign
an immune responses is initiated
your bodies own tissues are injured
Etiology of autoimmunity
genetic factors
environmental triggers
antigenic mimicry
some viruses/bacteria look like “self”
self cells similar to these foreign cells are attacked
Risk factors of autoimmunity
over age 50
genetics
female
African american, hispanic, asian, native american
viral bacterial infections
