Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MLSCI 475 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Th2 produces these cytokines which stimulates B cells to produce IgE

A

IL4,5,13

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

this cytokine stimulates eosinophils for worm killing

A

IL-5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

synonym to allergy

A

hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

define hypersensitivity

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

hypersensitivity rxns requires this

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how are the types of hypersensitivities distinguised?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

immediate hypersiytivity responses

A

antibody-mediates
I-III
5 mins to 10 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

delayed hypersensitivity

A

T cell mediated
type IV
24-48 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

common sources of allergens

A

inhaled = pollen, mold

injected = insect venom, vaccines, etc.

ingested = food, etc.

contact = plant leaves ,etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

this is a requirement for type I hypersens

A

preference in IgE production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

intracellular Calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why is IgE produced?

A
  • nature of antigen
  • history of exposure
  • heredity
  • TH2 cells and IL-4 = IgE production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

IL-4

A

important for B cells to make memory and proliferate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

mast cell granule mediators

A

histamine = preformed and short-lived

lipid mediators = synthesized and longer lasting = leukotrienes, prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

A

IL 4,13

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
Q

asthma vs allergic rhinitis

A

asthma = lower airwys = danders, pollens, dust mite feces

allergic rhin = nasal passages = pollen (ragweed, oak, etc.), dust mite feces

26
Q

treatment of anaphylaxis

A

nullify effects of mast cells
- anti-histamines, epinephrine

27
Q

what does epinephrine do?

A

reduce perm of blood vessels
diminish tissue swelling
raise BP
relax constricted smooth muscles
stimulates heart

for more systemic/significant rxns

28
Q

the treatment of choice to save life of person experiencing severe systemic anaphylactic shock

A

epinephrine

29
Q

T or F. Type IV hypersensitivity is rooted in the normal anti-helminth immune response

A

F! type I

30
Q

Th1 vs Th2 in allergies

A

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
Q

Type II hypersens

A
  • 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
Q

T or F. In Type II Hypersens, Ab-Ag interact first then Fc receptors recognizes them

A

T!

33
Q

drug rxns hypersens

A

type II
- penicillin covalently bind to RBCs surface = proteins altered = targets for Abs

34
Q

rheumatic fever

A

type II
- antibodies formed against bacteria (GAS) but cross react with antigens found on heart valves

35
Q

HDN

A

type II hypersens

36
Q

blood transfusion rxns

A

type II hypersens

37
Q

T or F. Type III hypersens also Ab based

A

T

38
Q

when IgG and IgM react with soluble antigens and form immune complexes

A

type III

39
Q

failure to remove immune complexes leads to…

A

Type III Hypersensitivity

40
Q

immune complexes can be deposited in _________ ____________and ______

A

blood vessels and organs

41
Q

T or F. Immune complexes activate complement and immune cells (neuts) resulting in tissue damage/destruction

A

T

42
Q

in order for type III hypersensitivity this must occur

A

point of equivalence = equal Ags and Abs

43
Q

type III hypersensitivity conditions

A

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
Q

type IV hypersens

A

delayed hypersens
= 24hrs for rxn to occur or later

45
Q

this hypersens is mediated by activated immune cells only

A

delayed
= no antibodies

46
Q

this hypersens is often intiated by CD4+ Th cells

A

delayed

47
Q

similar to type III, this hypsersens also requires persistent antigen exposure

A

type IV

48
Q

mechanism of T4 hypersens

A
  • 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions