MMI133_Lecture11 Flashcards
Hypersensitivity
immune system goes haywire/doesn;t work properly
4 types of hypersensitivity
Type 1: Allergy
- localized or general anaphylaxix/shock
IgE mediated
Type 2: Cytotoxic
- blood attacks
Type 3: Immune complex mediated
Type 4: Delayed cell-mediated
all hypersensitivity reactions that cause tissue damage require
previous exposure to antigen/allergen
Type 1 Reactions
localized - hives/ urticaria
hay fever, allergic rhinitis
systemic or general
shock, need epi-pen, peanut allergies
Type 1 reactions phases
- sensitization - result of classical antigen presntation with T helper cell involvement + B cell activation
- activation - cross linking of at least 2 IgE molecules bound to Fc receptors on mast cell - triggers mast cell/basophil degranulation
- effector
- phase 1 primary mediators released - histamine, eosinophil, chemotactic factor, neutrophilchemotactic factor, proteases
- phase 2 secondary mediators released leukotrienes + prostaglandins
the only type of hypersensitivity with no antibodies involved is
type 4 - delayed cell-mediated
type 1 systemic reactions
immediate reaction (minutes)
life threatening impaired breathing to swelling of airways
uterine cramps, involuntary urination/defecation = due to smooth muscle contraction
edema from fluid leaking into tissue spaces
blood pressure drops leading to life-threatening anaphylactic shock bec BV’s widen and blood leaks out
mediators from primarily mast cells + basophils
histamine + other lipid moelcs + cytokines
collectively act to:
- inc permeability + dilate BV’s - lead to edema + erythema/redness
- inc mucus secretion + contract smooth muscle
treatment of anaphylaxis
antihistamines to block action of histamine
epinephrine (epi-pen) - to contrict BV’s + raise BP
dilates air passages in lunges, effects smooth muscles
Type 2 cytotoxic reactiosn
due to diff blood types having diff antigens on their surfaces, getting anoth kind of blood that has diff antigens and teh immune system sees the blood as non-self and attacks + kills RBC - leads to hemolysis of RBC’s
blood type A has
anti B antigens
compatable blood types are A + O
blood type B has
anti A antigens
compatable blood types are B + O
AB blood type has
no antibodies in plasma
compatable blood types: A, B, AB, O
universal recipient - can get anything
O blood type has
anti A + anti B antibodies and no antigens
compatable blood types are O
it is the universal donor, but can only accept O blood types
key components of type 2
complement system
cell-bound antigens
antibodies IgG + IgM
HDN = hemolytic disease of newborn = blue baby
mother Rh- baby Rh+
with first baby, mother is exposed to Rh+ blood which has D+ antigen, so mother becomes sensitized to that antigen + immune system produces D+ antibodies
next baby, more baby blood leaks into mum, mum’s antibodies are small enough to get into placenta + attack baby blood + cause hemolysis of baby’s blood, results in baby with less blood + annemia + at risk of respiratory issues + bad for baby maybe death
ne
baby blue
not enough o2 due to hemolysis
prevention of Rh sensitization as treatment to prevent hymolytic disease of newborn
rhogam administration to Rh- mothers before + after delivery
to rapidly eliminate fetal Rh+ RBC’s from maternal circulation + hide them from mothers immune system
prevents maternal B cell activation against Rh antigens
Type 3 Immune complex mediated
immune complex binds to endothelium then activates complement which generates chemoattractants for neutrophils which arrive then release their granules + enzymes to damage tissue
poststreptococcal glomerulonephritis or SLE
immune complex deposition is typically in skin, joints, + kidney (glomerular basement membrane)
immune complex AB+AG circulate in blood circulation which is called soluble
Type 4 delayed cell mediated reaction
no antibodies involved
takes several days to develop
T cells involved
poison oak + ivy
Tb tests
Th1 cells + macrophages
requires previous exposure + presence of T memory cells
principal effector cell is activated macrophages which release lytic enzymes that cause local tissue destruction
mechanisms of tissue destruction: cytotoxic T lymphocytes induced by Th1 cells to assist in tissue damage
allergic response of type 4 delayed cell mediated
contact dermatitis
triggered by poison oak + ivy
oils from plant act as haptens binding to skin proteins
complexes are presented by skin dendritic cells to Th1 cells initiating immune response
treatment with corticosteroids for contact dermatitis immunosuppressive drugs including cortisone for transplant rejection
other type 4 reactions
tuberculin test: assesses immune response to Tb
transplant rejection: immune reaction against foreign tissues
how does Tuberculin skin test work?
determines prev exposure to TB by Iding memory cells reactive to TB antigens
widesly used in NA bec not many people immunized against TB
cell mediated reaction type 4
involves infiltration of lymphocytes + macrophages due to mobilization by pre-existing memory cells
limitations of tuberculin tests
inapplicaability to certain pops
anergic individs are unresponsive to immune stimuli like AIDS
immunosuppressed patients won’t react redictably to test which can make it unreliable
lack of specificity
those vacc with BCG vax give false positives