Chapter 18-19 Flashcards
immunopathology
the study of disease states associated with over-activity or under-activity of the immune response
- Allergies - Autoimmunity - Grafts and transfusions - Immunodeficiency
allergy
altered, usually exaggerated response to an allergen (antigen); manifested by inflammation
autoimmunity
antibodies or T cells sensitized to self- antigen and attack self antigens
immunodeficiency
immune response is incompletely developed, suppressed or destroyed
Hypersensitivity
allergens (antigens) cause an exaggerated immune response
Type I -allergic reactions
- Immediate hypersensitivity reactions
- Take place in less than 30 minutes
- IgE
- 10% - 30% of population suffer from allergies
- Susceptibility has strong hereditary component
Two levels of severity of type I allergies
-Atopy: localized- chronic local allergy (hay fever, asthma, etc.)
-Anaphylaxis: systemic, sometimes fatal reaction
Type 1: Atopy
- Localized
- Hay fever
- Asthma
- Eczema
- Food allergies – difficult to test for
- 8 foods account for 97% of food-related allergies:
- eggs, peanuts, tree-grown nuts, milk, soy, fish, wheat and peas
Type 1: Anaphylaxis
-Cutaneous anaphylaxis: wheal and flare inflammatory reaction to a local injection of allergen
- Systemic anaphylaxis: sudden respiratory and circulatory disruption that can be fatal
- Greatly amplified response of chemical mediators
- Death has occurred within 15 minutes
Type I: Mechanisms
First exposure
- Sensitizing dose - elicits no symptoms
- Memory B cells are produced
- Small amount of IgE antibodies are produced
- Mast cells and basophils bind the IgE
- Mast cells are located in tissue
- Basophiles circulate in blood but can enter tissue
function of mast cells and basophils
- Contain receptors that bind IgE antibodies
- Ubiquitous location (connective tissue for most organs)
- Secrete chemical mediators from cytoplasmic granules when activated
- Release contents of granules by degranulation when activated: e.g. histamine released
Type I: Second exposure
Second exposure
- Allergen binds across two IgE molecules on mast or basophil
- Allergic mediators such as histamine released
- Signs and symptoms of allergy appear
- IgE-primed mast cells can remain in the tissues for years
allergens and their portals of entry
- Proteins most common
- Proteins are more allergenic than carbohydrates, fats, or nucleic acids
- Some allergens are happens
- Typically enter through epithelial portals in the respiratory tract, gastrointestinal tract, and skin
chemical mediators released by mast cells
Responsible for allergic symptoms
- Histamine*
- Serotonin
- Leukotriene*
- Platelet-activating factor
- Prostaglandins
- Bradykinins
treatment and prevention of allergy
- avoid the allergen
- take drugs that block the action of lymphocytes, mast cells or chemical mediators
- undergo desensitization therapy
Type II- Antibody Mediated
- Antibody – mediated reactions
- Also called Cytotoxic
- Lyse foreign cells
- Interaction of antibodies, foreign cells, and complement, which then leads foreign cell lysis
- ABO blood groups
- Rh factor
- Other RBC antigens
common allergens, classified by portal of entry
inhalants, ingestants, injectants and contactants
ABO blood groups
- RBC markers (glycoproteins)
- Genetically determined
- Alleles – A, B, O
- Blood types
blood types
- Each individual will have antibodies against another antigenic type
- Type A will have anti-b antibodies
- Type B will have anti-a antibodies
- Type O will have anti-b and anti-a antibodies
- Universal donor
- Type AB will has no anti-b or anti-a antibodies
- Universal recipient
agglutination test
used to type blood
transfusion with incompatible blood
- as the type A blood flows into the veins of recipient -> Ab agglutinate the cells
- complement classic pathway-> RBC’s destroyed
Rh factor
- Another RBC antigen
- At least one dominant allele = Rh+
- Two recessive alleles = Rh-
- Placental sensitization
- Hemolytic disease
- Prevention
hemolytic disease of fetus/ newborns
-happens with Rh- mother and Rh + baby
- First pregnancy
- Little antibody against Rh produced
- Memory cells
- Second pregnancy
- Larger immune response because of memory cells
- Mother’s AB destroy baby’s RBC’s
- Hemolysis
prevention from hemolytic newborns
- Passive immunity using immunoglobin containing anti-Rh factor (RhoGAM)
- 28-38 weeks
- Immediately after delivery
- Administer for each pregnancy that involves Rh+ fetus and Rh- mother
- Ineffective if mother is already sensitized
Type III
-immune complex-mediated reactions
- soluble Ab circulating in the serum reacts with Ag
- Ab-Ag complexes are deposited in the organs and joints
- causes inflammatory response that damages tissue
Type III (similarities and differences)
- Similar to type II
- Involves production of IgG and IgM after repeated exposure to antigens and the activation of complement
- Differs from type II
- Its antigens are not attached to the surface of a cell
- Free-floating complexes that can be deposited in the tissue basement membranes
Example of Type III- Arthus reaction
- Injected antigen (eg. Vaccine, drug – usually from animal serum)
- Acute response to a second injection of antigen
- Localized dermal injury due to inflamed blood vessels
- Severe cases result in necrosis at site of injection
examples of Type III- Serum Sickness
- Injection of serum, hormones, drugs (usually from animal serum)
- Systemic injury
- Ag-Ab complexes circulate in the blood and eventually settle into membranes (kidney, heart, skin) inflammatory response
- Chronic
Type IV
- Cell-mediated (delayed) reactions
- T cell response
- Delayed-type hypersensitivity
delayed-type hypersensitivity
- Infectious allergy – e.g. TB skin test
- Contact dermatitis
- Tissue rejection
tissue rejection
- T cell mediated recognition of foreign MHC receptors
- Cytotoxic T cells
- Host rejection of graft
- Graft rejection of host
autoimmunity
- Antibodies, T cells or both, mount an immune response against self antigens
- Systemic or organ-specific
- Type II, III or IV reactions
