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Hypersensitivity Flashcards

1
Q

Th2 produces these cytokines which stimulates B cells to produce IgE

A

IL4,5,13

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2
Q

this cytokine stimulates eosinophils for worm killing

A

IL-5

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3
Q

synonym to allergy

A

hypersensitivity

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4
Q

define hypersensitivity

A

refers to undesirable reactions produced by a normal but overreacting immune system

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5
Q

hypersensitivity rxns requires this

A

a pre-sensitized immune system
- prior exposure to antigen augments hypsersensitivity rxns

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6
Q

how are the types of hypersensitivities distinguised?

A

based on the mechanisms involved and the time required for the rxn to occur

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7
Q

immediate hypersiytivity responses

A

antibody-mediates
I-III
5 mins to 10 hrs

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8
Q

delayed hypersensitivity

A

T cell mediated
type IV
24-48 hrs

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9
Q

common sources of allergens

A

inhaled = pollen, mold

injected = insect venom, vaccines, etc.

ingested = food, etc.

contact = plant leaves ,etc.

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10
Q

IgE-mediated hypersens response

A

imediate; type I

  • range symptoms = minor inconvenience like itching to death
  • 15-30 mins following exposure
  • mast cell or absophil
  • rxn may involve one or more areas of body = skin, eyes, nasopharynx, lungs, GI tract
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11
Q

this is a requirement for type I hypersens

A

preference in IgE production

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12
Q

this antibody has a very high affinity for Fc receptors on mast cells and basophils

A

IgE = connects with FcERI
= IgE bound to Fc receptor and awaits secondary exposure

  • IgE low half-life in circulation so binds to Fc receptor of mast and baso
  • changes the echanism of cell; optimizes it to recgonize a specific antigen
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13
Q

what happens when IgE binds to mast/baso?

A

second exposure to same antigen cross-links cell bound IgE
- triggers the release of substances from mast cells inducing them to degranulate
- includes vasoactive amines and potent inflammatory mediators

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14
Q

T or F. A single mast cell could have different targets when bound with IgE

A

T! if different isotypes of IgE are bound

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15
Q

influx of this causes mast cells to degranulate after crosslinking of IgE

A

intracellular Calcium

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16
Q

Why is IgE produced?

A
  • nature of antigen
  • history of exposure
  • heredity
  • TH2 cells and IL-4 = IgE production
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17
Q

IL-4

A

important for B cells to make memory and proliferate

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18
Q

roles of the mast cell granule mediators

A

constricts smooth muscle in lung and GI
vasodilation
increase permeability of small blood vessels = leaky, tissue swells
increases mucus secretion
prevents clotting
generally = pro-inflam mediators produced

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19
Q

mast cell granule mediators

A

histamine = preformed and short-lived

lipid mediators = synthesized and longer lasting = leukotrienes, prostaglandins

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20
Q

role of PAF

A
  • platelet activating factor
  • attracts leukocytes, amplifies production of lipid mediators, and activates neuts, macs, platelets
21
Q

these cytokines amplifies Th2 response (humoral)

22
Q

IL-5

A

promotes eos = amplifies inflam response = tissue destruction

23
Q

TNFa

A

promotes inflammation and stimulates cytokine production in many cell types

24
Q

a sudden, severe, potentially fatal, allergic rxn

A

anaphylaxis
- can involve various areas of body
- symptoms within minutes
- reaction = mild to life-threatening

25
asthma vs allergic rhinitis
asthma = lower airwys = danders, pollens, dust mite feces allergic rhin = nasal passages = pollen (ragweed, oak, etc.), dust mite feces
26
treatment of anaphylaxis
nullify effects of mast cells - anti-histamines, epinephrine
27
what does epinephrine do?
reduce perm of blood vessels diminish tissue swelling raise BP relax constricted smooth muscles stimulates heart **for more systemic/significant rxns**
28
the treatment of choice to save life of person experiencing severe systemic anaphylactic shock
epinephrine
29
T or F. Type IV hypersensitivity is rooted in the normal anti-helminth immune response
F! type I
30
Th1 vs Th2 in allergies
Th1 = healthy immune response when exposed to helminths early in life Th2 response = skewed immune response = allergies when growing in uran centrres, only child, etc.
31
Type II hypersens
- antibodies generated to antigens found on cell surfaves - antibodies are then recognized by Fc receptors of immune cells - promotes destruction by ADCC = macs, granulocytes and NK cells - can activate complement - variety of oragns; minutes to hours
32
T or F. In Type II Hypersens, Ab-Ag interact first then Fc receptors recognizes them
T!
33
drug rxns hypersens
type II - penicillin covalently bind to RBCs surface = proteins altered = targets for Abs
34
rheumatic fever
type II - antibodies formed against bacteria (GAS) but cross react with antigens found on heart valves
35
HDN
type II hypersens
36
blood transfusion rxns
type II hypersens
37
T or F. Type III hypersens also Ab based
T
38
when IgG and IgM react with soluble antigens and form immune complexes
type III
39
failure to remove immune complexes leads to...
Type III Hypersensitivity
40
immune complexes can be deposited in _________ ____________and ______
blood vessels and organs
41
T or F. Immune complexes activate complement and immune cells (neuts) resulting in tissue damage/destruction
T
42
in order for type III hypersensitivity this must occur
point of equivalence = equal Ags and Abs
43
type III hypersensitivity conditions
autoimmune = rhematoid arthritis SLE persisitent infections = leprosy bacterial endocrditis malaria hepatitis trypanosomiasis **immune response does not completely clear antigens = persistent antigens = lon-gterm stimulation of immune response = immune complexes** Farmer's lung = moldy hay birds fancier's disease = fecal antigens
44
type IV hypersens
delayed hypersens = 24hrs for rxn to occur or later
45
this hypersens is mediated by activated immune cells only
delayed = no antibodies
46
this hypersens is often intiated by CD4+ Th cells
delayed
47
similar to type III, this hypsersens also requires persistent antigen exposure
type IV
48
mechanism of T4 hypersens
- antigen exposed to Th cells = active - CD4+ Th cells secrete cytokines that activate and recruit other immune cells such as macrophages and neutrophils - products released from activated macrophages and neutrophils cause the majority of the tissue damage and symptoms of type IV hypersensitivity

MLSCI 475 (22 decks)

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