Immuno - Resp Flashcards

1
Q

What is a type I hypersensitivity?

A

immediate with IgE, mast cells and lipid mediators

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2
Q

What is a type IV hypersensitivity?

A

delayed, CD4 mediated

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3
Q

What is Atopy? or an atopic individual? 3 things are high?

A

high IgE
eosinophils
IL-4 secreting TH2 cells

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4
Q

Will you know you’re being sensitized to an allergen?

A

Not necessarily, you may not even realize until next exposure

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5
Q

example of a local response to Type I hypersensitivity?

A

rhinitis,

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6
Q

Example of a systemic response to Type I hypersensitivity?

A

anaphylaxis

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7
Q

Responses to Type I hypersensitivity?

A

Immediate and late phase

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8
Q

are inhaled allergens lipids? sacharrides? or proteins?

A

protein via small carrier particles

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9
Q

are allergens usually insoluble?

A

usually soluble

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10
Q

You need high dose of allergen to be sensitized?

A

Only very low dose, like 1micro-gram per year

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11
Q

allergens are often proteins? enzymes? lipids?

A

enzymes

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12
Q

What’s Der p 1?

A

dust mite faeces allergen

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13
Q

T/F? DCs produce IL-4

A

Nope. They produce IL-33

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14
Q

What its the role of Basophils in Type 1 hypersensitivity?

A

Act as an APC

secrete IL-4 either after IL-33 or allergen binding

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15
Q

What do you need for TH2 differentiation?

A
  1. CD40 antigen binding
  2. Co-stim
  3. IL-4 cytokine
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16
Q

Where are mast cells usually located?

A

mucosal/epithelial/near blood vessels

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17
Q

Mast cells bind IgE using what?

A

high affinity FcER

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18
Q

What’s so special about FcER on mast cells?

A

The only one that can bind the antibody WITHOUT it’s antigen…

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19
Q

3 steps for mast cell activation

A
  1. secretion of preformed mediators (histamines)
  2. synthesis and secretion of lipid mediators (protaglandins/leukotrienes)
  3. cytokine production (slow)
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20
Q

initial (0-5min) wheal and flare is soft or hard feeling?

A

soft feeling

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21
Q

late phase (8-12 hours) mast cell activation is soft or hard feeling?

A

hard feeling due to mediators

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22
Q

Allergic response is dependent on what?

A

Type of tissue

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23
Q

What’s urticaria?

A

rashes/hives

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24
Q

Where and when are eosinophils usually found?

A

mucosal linings, found late in allergic response

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25
What increases Eosinophil production in bone marrow?
IL-5 by TH2 and mast cells
26
What are eotaxins?
mediators that attract eosinophils to inflammatory site
27
increased sensitivity happens how on mast cells?
more FcEr on surface and IgE binding
28
4 treatments for allergy?
1. adrenaline (anaphylaxis) 2. B2 adrenergic receptor agonists (asthma) 3. antihistamines 4. corticosteroids
29
What does T-cell desensitization/immunotherapy tolerance mean? 4 things
Anergy deviation of cytokines apoptosis Treg cells
30
What's anergy?
decreased allergen-induced proliferation
31
What kind of hypersensitivity involved T-cells/macrophages and CD8 cells?
Type IV
32
Why do you get Type IV hypersensitivity?
persistent antigenic stimulation
33
What is DTH?
Delayed type hypersensitivity
34
What happens in Delayed type hypersensitivity sensitization phase?
proliferation of TH1, helper T-cells, CD8 in lymph node, they go back to tissue and persist just waiting for next exposure
35
What does contact sensitivity TB celiac disease have in common?
All are Type IV Delayed type hypersensitivity
36
Mycobacterium TB is a what kind of pathogen?
facultative intracellular pathogen
37
What's the good news with DTH and TB?
restrict 90% of growth
38
What's the bad news with DTH and TB?
small % of ppl interrupts respiratory function
39
What's a telltale sign of TB infection in lung tissue on microscope?
Granuloma: multinucleate giant cells epithelioid cells, lymphocytes
40
>90% of celiac disease ppl are what positive?
HLA-DQ2 positive
41
What does the Delayed type hypersensitivity do to the small intestine?
damages villi
42
What's the incidence of celiac disease?
1 in 70
43
Normally, does gliadin peptides bind to HLA DQ2?
poorly
44
How does glutamine --> glutamate?
via tissue transglutaminase 2 (tTg2)
45
what's an autacoid?
local mediator
46
4 things autacoids can do?
smooth muscle tone glandular fluid leak/oedema sensory(pain/itch)
47
What is Cysteinyl
a Leukotriene in allergies
48
What's red man syndrome?
allergic reaction to morphine or vancomycin
49
What is a possible reason behind exercise induced bronchospasm?
increased air flow through bronchi created hypo-osmotic surface enough to trigger mast cells
50
ITAMS have no what?
intrgral kinase activity
51
Diacylglycerol protein kinase C + inositol triphosphate Ca2+ mobilisation = ??????
degranulation of mast cells
52
Once IgE is bound, it activates MAPK which does what?
arachidonic acid | cytokine gene transcription
53
Once IgE is bound, it activates phospholipase C which does what?
degranulation
54
How long does it take to cause mast cell degranulation?
30-45 seconds
55
When does mast cell activity peak?
10-30 minutes
56
4 immediate mast cell communication methods?
histamine heparin tryptase TNF-a
57
2 rapid mast cell communication methods?
cys-LTs | PGD2
58
3 slow mast cell communication methods?
IL-4 IL-5 GM-CSF
59
Why are antihistamines not used in asthma?
older antihistamines were H1 receptor blockers however H1 activation will cause bronchospasm/constriction
60
What does histamine do to H2 receptors? 2 things
1. positive inotropic and chronotropic | 2. Gastric acid secretion
61
H1 receptor activated by histamines does 6 things:
``` pain/itch bronchospasm mucus secretion vasodilation fluid leak CNS - wakefulness ```
62
Should you block prostaglandins or cysteinyl leukotrienes? Why?
Leukotrienes cause it will only affect inflammation unlike prostaglandins which have lots of other effects
63
What's 5-lipoxygenase? how activated?
the inflammation bitch. It's all it does. | Activated by increased intracellular calcium
64
Where does the leukotriene receptor antagonists block LTs?
At CysLT1 receptor
65
What leukotriene attracts leukocytes?
Leukotriene B4
66
Where does Aspirin, NSAIDS Coxibs act on?
Cyclooxygenase
67
What does phospholipase A2 do?
turns acyl lipid into Arachidonic acid
68
Cytokines are slow, what are they doing? 3 things
inducing gene expression changes structural changes inflammatory cell infiltration
69
Which cytokines are highly regulated by glucocorticoids?
IL-1, TNF-a
70
Which cytokines are not regulated by glucocorticoids?
IL-4
71
3 things in the body that can inhibit mast cells?
PGE2 (Prostaglandins) adrenaline cortisol
72
What do the older mast cell inhibitors like disodium cromoglycate and nedocromil sodium cause release of?
Annexin-1 which resolves inflammation
73
What's the cons of disodium cromoglycate and nedocromil sodium
modest working only prophylactic topical and local effects only
74
What is omalizumab?
expensive biologic: monoclonal antibody (Anti-human IgE antibody) that binds and prevents IgE to alpha chain of FcER1
75
Can you use omalizumab in asthma?
jury's still out on that one
76
What's RIT?
rushed immunotherapy
77
I have asthma, I might take some NSAIDS/COX-2 inhibitors, cool?
NO. NO. NO. doesn't do shit in asthma or hay fever, it might provoke symptoms.
78
Crap Doc, I took aspirin for my asthma and it's getting worse! what do I do?!
I'll give you LTRA (leukotriene receptor antagonists)
79
What do glucocorticoids do?
inhibit mediator (cytokine) production in airways
80
When would you use an H1 receptor antagonist for allergies? 6 things
``` urticaria atopic dermatitis hayfever anaphylaxis bites/stings motion sickness ```
81
When would you NOT use H1 receptor antagonist?
Asthma or colds
82
3 classes of H1 receptor antagonists
1. sedative (chlorpheniramine, promethazine) 2. non sedative but risk of ventricular arrhythmia 3. newer nonsedative (cetirizine, loratidine)
83
When are cysteinyl leukotriene receptor antagonists indicated? 2 things
1. Aspirin/exercise induced asthma | 2. combined with GCS/B2 agonist