Immunity Flashcards
Differences between active and passive immunity
Active: host undergoes immune response (produces cells and factors responsible for immunity i.e. antibodies and memory cells)
Therefore, active immunity is long-lasting
Passive: host receives immune factors/Ig’s produced in another being (receives antibodies); therefore, protection is short-lived
Give an example of Natural-Active immunity
Nursing student gets the flu virus from her family - natural-active immunity occurs because she makes her own immune response, which includes T (cell-mediated) and B (humoral) cell responses
Example in coursepack: child develops measles and acquires immunity to future infection
Give an example of Natural-Passive immunity
Mother passes her immunoglobulin A to her newborn via breastmilk: passive because the baby does not create its own antibodies
Example in coursepack: fetus receives protection via placenta, breast milk
Give an example of Artificial-Active immunity
Nursing student gets the flu vaccine - her body still mounts an immune response but the exposure to the virus is artificial
Example in coursepack: injection of causative agent (polio vaccine) derived from killed microorganisms, attenuated/weakened microorganism, or inactive microbial toxins - person’s own system mounts a response to yield immunity
Give an example of Artificial-Passive immunity
Someone bitten by a dog gets a rabies vaccine - this vaccine contains antibodies (not the antigen), so the host does not mount an immune response
Example in coursepack: injection of protective material (e.g. monoclonal antibodies) developed by another individual’s immune system e.g. gamma globulin
Briefly describe the growth/development of the immune system through the life span
Maturation of lymph tissue peaks in puberty so the age groups with most vulnerable immune systems are infants and elderly Thymic involution (shrinking) occurs with age, which causes decreased T cell production and effectiveness
Describe the Antibody-mediated hypersensitivity responses
Type I (anaphylaxis) - occurs with degranulation of mast cells –> release of histamines and leukotrienes –> causes massive vasodilation and inflammation
Mediated by IgE
e.g. peanuts
Type II (Cytotoxic) - activation of complement leading to cell lysis
Mediated by IgM and IgG
e.g. hemolytic disease of the newborn due to Rh incompatibility
Type III (immune complex) - activation of complement leading to antigen-antibody complex formation and deposition in to basement membranes in the body
Mediated by IgM and IgG
e.g. RA, SLE, glomerulonephritis, allergy to penicillin
Describe the cell-mediated hypersensitivity response
Type IV (delayed hypersensitivity) - occurs because of T-cell response i.e. NO ANTIBODIES are involved
lymphokines released by T cells activate inflammatory response
e.g. contact dermatitis, TB skin testing, transplant rejection
Explain the difference between primary and secondary immunodeficiency
Primary (congenital): due to absence or decrease in T cells, B cells, or both
B cell deficiency causes no antibody production, so IgA which is present in mucus membranes is absent, causing increased risk to mucosal inflammation such as gastroenteritis
Main treatment is to provide as sterile environment as possible although bone marrow transplant may allow production of B lymphocytes
Secondary immunodeficiency occurs due to illness or treatment (iatrogenic):
- drug-induced with corticosteroids, immunosuppressants, chemotherapy drugs
- altered immune function due to stress, age, malnutrition
- surgical removal of lymphoid tissue such as the spleen, lymph nodes
- viruses, Hodgkin’s disease, systemic infections that use up all the immune resources
Treatment involves removing the cause of immunodeficiency
What is the main function of each type of Immunoglobulin (Ig A/D/E/G/M)
IgA: present in mucosal lining; passed in breastmilk
IgD: role unclear
IgE: present in allergic and parasitic infections
IgG: most predominant Ig in immune response - with subsequent exposures to antigen
IgM: most predominant Ig in immune response - initial exposure to antigen (decreases with subsequent exposures)
Explain the differences between the inflammatory and immune responses
Inflammation always occurs with infection but infection not always present with inflammation
Inflammation can occur as a result of heat, trauma, allergens vs. infection that occurs as a result of antigen
Inflammatory response is the same regardless of agent (although may be different intensity of response) i.e. always begins with vascular response, followed by cellular response (non-specific WBC e.g. neutrophils, monocytes), then exudate formation and healing phases
Briefly describe the normal humoral immune response
Body exposure to antigen –> macrophage engulfs antigen and presents to B lymphocytes –> exposure to antigen causes B cells to mature into plasma cell –> plasma cell secretes specific immunoglobulins (antibodies) for the antigen –> antibody binds to antigen –> antibody-antigen complex stimulates inflammatory response (complement system, chemotaxis, vasodilation) –> results in neutralization and elimination of antigen
Some B cells form memory cells so that subsequent exposure to antigen produces a faster response
Humoral immunity is prevalent in BACTERIAL infections
Briefly describe the normal cell-mediated immune response
Body exposure to antigen –> macrophage engulfs antigen and presents to T lymphocytes –> exposure to antigen activates T cells –> activated T cells lyse and neutralize antigen by several mechanisms
Helper T cells augment immune response by Cytotoxic T cells
Suppressor T cells suppress immune response after completed
Some T cells remain as memory cells so that subsequent exposures are more rapid
Cell-mediated response is prevalent in VIRAL INFECTIONS and MALIGNANCY
Treatment of hypersensitivity reactions
ABC’s e.g. epinephrine for anaphylaxis to open airway
Remove underlying cause if possible
Symptomatic treatment: antihistamines, corticosteroids, bronchodilators, decongestants, immunosuppressives
Briefly describe the inflammatory response
1) Vascular response: initial vasoconstriction followed by vasodilation –> increased capillary permeability, hyperemia, edema, and clot formation
2) cellular response: infiltration of WBC’s - 1st neutrophils, then monocytes and lymphocytes; release of chemical mediators such as complement system, prostaglandins, leukotrienes that cause increased blood flow, edema, and pain
3) exudate formation: fluid + WBC from circulation to the site of injury
4) healing: regeneration in which injured cells completely replaced by new cells vs. repair in which injured cells replaced with scar/connective tissue
