Immune System Disorders Flashcards
innate immunity
non-specific; if surface barriers breached –> inflammatory response
adaptive immunity
specific, develops after exposure to a specific antigen
humoral immunity
antibodies produced to protect body
cell-mediated immunity
lymphocytes programmed to attack non-self cells to protect body
B and T
antibodies
produced by B-lymphocytes
occur freely in circulation
immunoglobulins
function as Abs
found on plasma membranes of B-LCs (also found on other immune cells)
IgG (most common; fights bacteria, viruses, toxins)
IgE (allergic responses)
active, natural immunity
natural exposure to antigen –> body creates antibodies to prep for second exposure
(primary and secondary response)
active, artifical
antigen purposefully introduced into body (immunization) –> simulates what would happen to a virus by our own immune cells
passive, natural
IgG transferred from mother to fetus (crossing placenta)
passive, artificial
injection of antibodies (anti-venom); short-term protection
type I hypersensitivity disorders
excessive or inappropriate activation of immune response
effects –> local (atopic); systemic (anaphylactic)
exposure to allergen can occur by:
inhalation, ingestion, skin contact
Type I HS d/o mediated by
IgE
local effects of type I HS d/o
atopic:
early phase –> inflammation
late phase: mucosal edema, mucous secretion
contained to epithelium, not bloodstream
mechanism of hypersensitivity
exposure to antigen (pollen) –> immune response: B-lymphocytes recognize as non-self –> produce antibodies (IgE)
IgE attaches to mast cells
second exposure –> IgE recognizes antigen –> sensitized mast cells release histamine –> immediate inflammatory response
anaphylaxis
systemic response to inflammatory mediators released
life-threatening
anaphylaxis: vasodilation
histamine ACh kinins leukotrienes PGs
consequence: drop in BP
anaphylaxis: bronchoconstriction
Ach
leukotrienes
PGs
kinins
consequence: impaired O2 delivery to capillary beds
signs and symptoms of anaphylaxis
generalized itching or tingling (oral cavity)
coughing
difficulty breathing
weakness
dizzy/fainting
sense of fear/panic
edema (around eyes, lips, tongue, hands feet)
hives
collapse with LOC
effects of anaphylaxis
inflammatory mediators into general circulation:
vasodilation (decreased BP)
bronchoconstriction (impairs O2 delivery)
mucous release
skin: nerve ending irritated (itchy)
***reducing availability of oxygenated blood to brain
treatment of anaphylaxis
first aid: epipen and 911
Epi: stabilizes BP (vasoconstriction)
Glucocorticoids: reduce AA (AA produces leukotrienes and PGs –> reduced vasodilation and cap permeability)
antihistamines: reduce histamine locally and systemically
O2: help with bronchoconstriction –> drive partial pressure of O2 up
autoimmune disorders
immune system attacking our own healthy cells; development of antibodies against self-cells and tissues
autoimmune process
immune system forms antibodies against self-antigens
autoantibodies attack self-antigens
inflammation and tissue damage occur (local to organ or systemically)
mechanisms of autoimmune
- genetic susceptibility
2. environmental triggers (virus, chemical)
immunodeficiency
partial or total loss of one or more immune system components
primary immunodeficiency
inherited –> basic developmental failure somewhere in system
secondary or acquired immunodeficiency
loss of immune response from specific causes
infections; splenectomy, malnutrition, liver disease, immunosuppressant drugs, radiation, chemo
