Immunity/infections/vaccines/measles Flashcards
Anergy panel
immunocompetence test by injecting common antigens intradermally
Antibody titers
lab tests that monitor IgM and IgG levels and confirm adequate immune protection against particular antigens
Allergy testing
measure IgE reaction
Type 1 immediate hypersensitivity reaction
IgE binds to a mast cell and combines with antigen to release histamine
What does histamine do
vasodilates
Type 2 cytotoxic hypersensitivity
mediated by IgS directed towards antigens present on cell surfaces, cell destruction and phagocytosis occur
Type 3 immune complex hypersensitivity
antigen combines with IgS and develop tissue complexes that are deposited in the tissue, causing organ dysfunction
Type 4 delayed hypersensitivity
initiated by T-lymphocytes, delayed T-cell attack causing dermatitis, delayed inflammatory reaction
Anaphylaxis
severe type 1 hypersensitivity reaction treated with epinephrine, antihistamines, and glucocorticoids to reduce risk of anaphylactic shock from vasodilation and low blood pressure
Hypersensitivity
immune system becomes oversensitive to foreign invaders
Immunodeficiency
immune system is weakened and can no longer fight against invaders
Autoimmunity
immune system cannot distinguish between self and non-self
Innate immunity
natural, born immunity, the body’s first round of defense
What is innate immunity made of
the body’s natural barriers: normal flora, WBC, protective barriers
Adaptive immunity
second line of defense, lymphocytes are the primary cell
Cytokines
inflammatory mediators produced by WBC that attract the rest of the inflammatory response
Macrophages
arise from monocytes, gets rid of debris through apoptosis
Natural killer cells
T-cells that don’t need to be stimulated by APCs and go directly to the antigen
GI tract defense
salvia –> gastric mucus traps –> intestinal flora
Adaptive immunity
specific, develops memory
cell-mediated and humoral mediated immunity
Cell mediated immunity
T-lymphocytes, mature in the thymus
Humoral mediated immunity
B-lymphocytes, mature in bone
slower than cell mediated immunity but long lasting
What CD4 cells do
influence other immune system cells
What do CD8 cells do
directly attack antigens
Cell mediated immunity process
T-cells are activated by APCs –> release cytokines –> adaptive immune response
Humoral mediated immunity process
Encounter antigens –> mature into plasma cells –> produce IgS –> attack antigens
IgA
found in breast milk, mucus, saliva, tears, protect against antigens
IgD
activates basophils and mast cells
IgE
responsible for allergic reactions
IgG
secreted by plasma cells, second responder to antigen, amnestic response
IgM
responsible for early stages of immunity, attached to B cells and then distributed in the blood, first responder to an antigen
Antibody-mediated response
Primary phase and then secondary phase
Primary phase of antibody-mediated response
IgM response, the host cell is exposed to an antigen and then there is creation of immunoglobulins (but there is a lag response and this takes 5-7 days)
What happens during the lag response of the primary phase of antibody-mediated response
CD4 cells attack
Secondary phase of antibody-mediated response
Immunoglobulin count increases and initiates the amnestic response
What do vaccines do
allow the body to recognize and develop defense against antigens without contracting the disease
Booster
are needed because immunity can wear off
Toxoids
vaccines produced by killed bacterial derivatives
Complications of measles
bacterial pneumonia, eye damage, and blindness
Treatment of measles
vitamin A for eyes, rest, antipyretics, oatmeal baths
How is measles transmitted
droplet
When is measles contagious
4 days after the rash and 4 days after
How long are the incubation and prodromal periods of measles
7-14 days
Clinical presentation of measles
high fever, cough, Koplick’s spots (pathognomic to measles), maculopapular rash after 5-7 days
