Hypersensitives (Final) Flashcards
Immune system
Complex system in charged of protecting our body from foreign substances
Immune system can identify these antigens to destroy these
Hypersensitivity is a normal immune response that is:
-Inappropriately trigger
or
-Excessive
or
-Produces undesirable effects on the body
Hypersensitivity: Basic trigger
-Specific antigen antibody reaction or a specific antigen lymphocyte interaction
Four types of hypersensitivity
-Type I II II = mediated by antibodies produces by B cells (specifically plasma cells)
-Type IV = Mediated by T cells
B cells
Are antibodies
T cells
Long term immunity
Type 1: IgE mediated Reaction
-How does someone develop an allergy to something this cute?
-Pet dander - Nuts - Pollen
Type 1 hypersensitivity: Key characterisitics
Immediate reaction (15-20 min)
This reaction occurs after being sensitized to an antigen
Type 1 Hyper Sensitivity: Antigens
-Environmental (bee sting - Pet dander)
-Foods (Nuts - Shellfish)
-Medications (Penicillin - Contrast Dye)
Type 1 Hypersensitivity: Etiology
-Genetic link
1 Parent = 30% chance
2 Parent = 50% chance
Key cells involved in Type 1
-B lymphocytes
-igE (antibody)
-Mast cells (granulocyte)
Type 1: Pathogenesis
-Antigen (Ragweed) attaches to B cell during the first time they are exposed
-B cell is triggered to form into a plasma cells. This plasma cells starts producing IgE antibodies
-IgE attach to mast cells and lie and wait
-Next time the person is exposed to allergen. it binds to the IgE antibodies that are attached to the mast cells. This triggers the release of chemical mediators from the mast cell
Type 1 Response
Histamines
Type 1 Mediator Activites (know these)
Potent vasodilation - Stuffy nose, lower BP, Wheals on skin
Increased vascular permeability - Edema and runny nose
Bronchial smooth muscle contraction - Breathing difficulties and wheezing
Stimulates irritant receptor - Itching (pruritus)
Type 1: Atopic reactions (Local)
-Allergic Rhinitis
-Asthma
-Urticaria (hives)
Type 1: Anaphylaxis Reaction (Systemic)
-Systemic release of chemical mediators
-Life threatening because of bronchial constriction - airway obstruction - vascular collapse
What are most common triggers of anaphylaxis?
-Medications
-Bee stings
-Foods
Type II hypersensitivity: Cytotoxic reaction
What would happen if….
A patient received the wrong blood type?
Incompatible blood
Type II: Etiology
-Exposure to antigen or foreign tissue / cells
-Antigens are located on cell surface
Type II: Key Characteristics
-Antigen stimulate antibody production
-Antibodies recognize and attach to cell surface antigens
-Direct destruction of targeted cells that contain the antigen (Cell lysis) (Phagocytosis)
-Do this or purpose with transplant patients. Give medication that slow down and decrease immune response so we don’t have this reaction
Type II Hypersensitive: Immune Cells involved
-Antibodies (IgG and IgM)
-Complement (Fixes to foreign cell and lysis it)
-WBC’s (Phagocytes)
Examples of Type II antigens
Blood
Some of your bodies own cells (auto immune conditions like diabetes)
Erythroblastosis fetalis (Hemolytic Anemia) (RH factor difference between parent and fetus)
Slide for type 2 can go here
Type II response: Example disorders
-Blood transfusion
-Rg incompatibility in pregnancy birth
-Autoimmune disorders
-Certain drug reactions
RH parents slide
RH+ father
RH- mother carrying her first RH+ fetus. RH antigens from the developing fetus can enter the mothers blood during delivery
In response to the fetal Rh antigens, the moth will produces anti-Rh antibodies
IF the woman becomes pregnant with another Rh+ fetus, her antibodies will cross the placenta and damage fetal red blood cells
Type II manifestations: transfusion Reaction
-Fever - Chills - Flushing (first sign)
-Increase HR
-Decrease BP
-Chest pain or back pain
-N/V
-Restlessness and anxiety
-Headache
Type III hypersensitivity: Immune Complex Reaction
What happens when you have rheumatoid arthritis?
Inflammation of tissue that causes the damage
Type III: Key Charactersitics
- Antigen anitbody complexes form (IgG and IgM)
- There are deposited into tissues
- Inflammatory response cause tissue damage
Type III: Etiology
-Autoimmune attack
-Low grade infection
-Inhaled antigens from molds or contaminated plants
Type III: Possible offending antigens
-Inhaled from antigens from molds or contaminated plants
-Body’s own response
-Bacteria and viruses
Type III: Key immune cells involved
-Antibodies IgG and IgM taht clump with antigens
-Complement
-Neutrophils and mast cells
Type III: Pathogenesis
antibody complex formed in blood
Deposits in tissue
Activation of complement and chemo attraction of neutrophils
Release of enzymes and free radicals
A ton of inflammation going on
Type III: Clinical Manifestations
-Manifestations depend on where the complexes are deposited in the tissue
Rheumatoid arthritis = Joints
Glomerulonephritis = Kidney Failure
Systemic lupus erythematosus = skin and organs
Type II vs Type III
Type II: Reacitons 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
Type IV: Delayed Hypersensitivity
- Have you ever had poison ivy? Postive TB skin test? Jellyfish sting? Allergic reaction to jewelry? Chron’s disease?
Type IV hypersensitivity: Key characteristics
-Delayed response
-No antibody involvement
Type IV: Key Immune cells
-T cells (NO B CELLS)
-Cytokines
-Mast cells and Macrophages
Type IV: Etiology
Delayed cellular reaction to antigen. Because it takes time for the T cells to make their journey to the site
Type IV: Possible Antigens
-Plant oil
-Cosmetics and clothings
-Nickel alloys
-Tuberculin antigen (TB test)
-Organ transplant or skin graft
-Gluten
Type IV: Pathogenesis
-Small, incomplete antigen, call a hapten penetrates the skin
-The hapten combines with human protein to form a complete antigen
-T cells become aware of antigen (antigen processing cell)
-T cells attack the antigen via:
1. Direst attack from T cells
2. Release of cytokine (inflammation)
3. Macrophages (cell destruction)
Type IV: Clincial Maifestiations
-Peak 49-72 hours
-Contact dermatitis: Redness, edema, itching, blisters
-Tuberculin hypersensitivity: Redness, induration and inflammation
Hypersinsitivity Reaction: Pharmacotherapy Options
Immunosuppressants (transplant patients) (Lower the immune response)
Antihistamines (reduces symptoms) (do not stop reaction)
Epinephrine (Important with anaphlyic reaction)
People on immune suppressants we need to watch for what?
Infections
Antihistamines
not stoping reaction just suppressing symptoms
Organ transplatn and drug therapy options (know slide)
