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19 Cards in this Set

  • Front
  • Back
List features of type 1 hypersensitivity reaction.
•anaphylactic ("atopy") reactions
•IgE mediated
•allergen cross links IgE on mast cells and basophils which degranulate
•Th2 response instead of Th1 (Th2 cells activate B cells, which produce IgE instead of IgG)
•lots of eosinophils (and neutrophils)
•runs in families (chromosome 5)
•eg hay fever, asthma, hives, food allegies, eczema, allergic rhinitis
List features of type 2 hypersensitivity reaction.
•characterized by ADCC: "antibody dependent cell cytotoxicity"
•IgG or IgM (mediated), they attach to Ag on cells
•complement is activated
•target cells are destroyed
•eg blood transfusions, erythroblastosis fetalis, autoimmune hemolytic anemia
List features of the type 3 hypersensitivity reaction.
•immune complex mediated reaction
•Ag-Ab induces complement
•infiltration of neutrophils
•eg Arthus reaction, serum sickness, necrotizing vasculitis, glomerulonephritis, RA, systemic lupus ("SR SNAG" is not immune to anything, and snags all of these)
List features of type 4 hypersensitivity reaction.
•Cell mediated (delayed hypersensitivity)
•sensitized Th1, Th2, or CTLs release cytokines that activate macrophages or Tc cells, that damage cells
•eg contact dermatitis, tubercular lesions, graft rejection
What (specifically) causes degranulation of mast cells and basophils, and what aids this?
Ca+ causes degranulation.

ionophores increase membrane permeability to the extracellular Ca+.
What are the cytokines released during type 1 HS (hypersensitivity)?
IL-3
IL-4
IL-5
IL-13
TNF
GM-CSF
prostaglandin D2
leukotriene A4
(NOTE) Histamine is a neurotransmitter, not a cytokine
What recepter is crosslinked in type 1 HS?
FceRI
List the type 1 HS pathways that occur after crosslinkage.
•PLC cleaves PIP2 -> IP3 and DAG
•DAG activates PKC
•IP3 releases Ca+ from ER
•Adenylyl cyclase converts ATP to cAMP
•PLA2 (phospholipase A2) is activated, producing leukotrienes and prostaglandins
What substances increase in the cytoplasm prior to the release of histamine during type 1 HS?
cAMP and Ca+
Classify the type 1 HS (hypersensitivity) inflammatory mediators.
1.primary type 1 (histamine mainly)
2.secondary type 1 (leukotrienes, prostaglandins, cytokines)
What do the primary type 1 mediators target?
histamine receptors (H1 - H4)
What does attachment to histamine receptor H1 cause?
Anti parasite effects:

1. smooth muscle contraction (expel parasites)
2. inc mucous secretion by goblet cells
What does attachment to histamine receptor H2 cause?
1.inc vasopermeability (of caps?)
2.inc vasodilation (of caps?)
3.inc acid secretion by gastric cells (stomach)
4.suppresses degranulation (neg feed of mast and baso cells)
List properties of leukotrienes and prostaglandins, and what they cause.
•secondary type 1 HS inflammation mediators
•they're synthesized and released after primary type 1 mediators.
•more potent and longer lasting than primary type 1 med.
•their rate limiting enzyme is PLA2
•they cause bronchoconstriction, inc vascular perm, inc mucous secretion
List properties of cytokines in reference to HS reactions.
List 3 examples.
•secondary type 1 inflammation mediators
•enable local infiltration by eosinophils & neutrophils
•include IL-4 and IL-13 (stimulate Th2 response)
•include IL-5 (recruits/activates eosinophils)
Cause and result of systemic anaphylaxis?

Treatment?
CAUSE:
•allergens get into the blood
RESULT:
•systemic vasodilation → huge drop in BP
•bronchial smooth muscle contraction → difficulty breathing
TREATMENT:
•epinephrine (inc CO, relaxes SM)
List cause and symptoms of asthma.
CAUSE:
•mast cells degranulate in lower respiratory tract
SYMPTOMS:
•bronchoconstriction
•respiratory edema
•inflammation
•mucous secretion (fatal: mucous plugs)
PNEUM: asthma is "BRIMing" with symptoms
What occurs during phase 1 of asthma, and what is responsible?
•vasodilation, bronchconstriction, some mucous
•histamine, leukotrienes, prostaglandins are responsible
What occurs during phase 2 of asthma, and what is responsible?
•recruitment of eosinophils and neutrophils
•damage to ECs, more mucous
•cytokines are responsible