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Jason's Respiratory Block > Immuno - Resp > Flashcards

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
Q

What increases Eosinophil production in bone marrow?

A

IL-5 by TH2 and mast cells

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26
Q

What are eotaxins?

A

mediators that attract eosinophils to inflammatory site

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27
Q

increased sensitivity happens how on mast cells?

A

more FcEr on surface and IgE binding

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28
Q

4 treatments for allergy?

A
  1. adrenaline (anaphylaxis)
  2. B2 adrenergic receptor agonists (asthma)
  3. antihistamines
  4. corticosteroids
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29
Q

What does T-cell desensitization/immunotherapy tolerance mean? 4 things

A

Anergy
deviation of cytokines
apoptosis
Treg cells

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30
Q

What’s anergy?

A

decreased allergen-induced proliferation

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31
Q

What kind of hypersensitivity involved T-cells/macrophages and CD8 cells?

A

Type IV

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32
Q

Why do you get Type IV hypersensitivity?

A

persistent antigenic stimulation

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33
Q

What is DTH?

A

Delayed type hypersensitivity

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34
Q

What happens in Delayed type hypersensitivity sensitization phase?

A

proliferation of TH1, helper T-cells, CD8 in lymph node, they go back to tissue and persist just waiting for next exposure

35
Q

What does
contact sensitivity
TB
celiac disease have in common?

A

All are Type IV Delayed type hypersensitivity

36
Q

Mycobacterium TB is a what kind of pathogen?

A

facultative intracellular pathogen

37
Q

What’s the good news with DTH and TB?

A

restrict 90% of growth

38
Q

What’s the bad news with DTH and TB?

A

small % of ppl interrupts respiratory function

39
Q

What’s a telltale sign of TB infection in lung tissue on microscope?

A

Granuloma: multinucleate giant cells epithelioid cells, lymphocytes

40
Q

> 90% of celiac disease ppl are what positive?

A

HLA-DQ2 positive

41
Q

What does the Delayed type hypersensitivity do to the small intestine?

A

damages villi

42
Q

What’s the incidence of celiac disease?

A

1 in 70

43
Q

Normally, does gliadin peptides bind to HLA DQ2?

A

poorly

44
Q

How does glutamine –> glutamate?

A

via tissue transglutaminase 2 (tTg2)

45
Q

what’s an autacoid?

A

local mediator

46
Q

4 things autacoids can do?

A

smooth muscle tone
glandular
fluid leak/oedema
sensory(pain/itch)

47
Q

What is Cysteinyl

A

a Leukotriene in allergies

48
Q

What’s red man syndrome?

A

allergic reaction to morphine or vancomycin

49
Q

What is a possible reason behind exercise induced bronchospasm?

A

increased air flow through bronchi created hypo-osmotic surface enough to trigger mast cells

50
Q

ITAMS have no what?

A

intrgral kinase activity

51
Q

Diacylglycerol protein kinase C + inositol triphosphate Ca2+ mobilisation = ??????

A

degranulation of mast cells

52
Q

Once IgE is bound, it activates MAPK which does what?

A

arachidonic acid

cytokine gene transcription

53
Q

Once IgE is bound, it activates phospholipase C which does what?

A

degranulation

54
Q

How long does it take to cause mast cell degranulation?

A

30-45 seconds

55
Q

When does mast cell activity peak?

A

10-30 minutes

56
Q

4 immediate mast cell communication methods?

A

histamine
heparin
tryptase
TNF-a

57
Q

2 rapid mast cell communication methods?

A

cys-LTs

PGD2

58
Q

3 slow mast cell communication methods?

A

IL-4
IL-5
GM-CSF

59
Q

Why are antihistamines not used in asthma?

A

older antihistamines were H1 receptor blockers however H1 activation will cause bronchospasm/constriction

60
Q

What does histamine do to H2 receptors? 2 things

A
  1. positive inotropic and chronotropic

2. Gastric acid secretion

61
Q

H1 receptor activated by histamines does 6 things:

A 
pain/itch
bronchospasm
mucus secretion
vasodilation
fluid leak
CNS - wakefulness
62
Q

Should you block prostaglandins or cysteinyl leukotrienes? Why?

A

Leukotrienes cause it will only affect inflammation unlike prostaglandins which have lots of other effects

63
Q

What’s 5-lipoxygenase? how activated?

A

the inflammation bitch. It’s all it does.

Activated by increased intracellular calcium

64
Q

Where does the leukotriene receptor antagonists block LTs?

A

At CysLT1 receptor

65
Q

What leukotriene attracts leukocytes?

A

Leukotriene B4

66
Q

Where does Aspirin, NSAIDS Coxibs act on?

A

Cyclooxygenase

67
Q

What does phospholipase A2 do?

A

turns acyl lipid into Arachidonic acid

68
Q

Cytokines are slow, what are they doing? 3 things

A

inducing gene expression changes
structural changes
inflammatory cell infiltration

69
Q

Which cytokines are highly regulated by glucocorticoids?

A

IL-1, TNF-a

70
Q

Which cytokines are not regulated by glucocorticoids?

A

IL-4

71
Q

3 things in the body that can inhibit mast cells?

A

PGE2 (Prostaglandins)
adrenaline
cortisol

72
Q

What do the older mast cell inhibitors like disodium cromoglycate and nedocromil sodium cause release of?

A

Annexin-1 which resolves inflammation

73
Q

What’s the cons of disodium cromoglycate and nedocromil sodium

A

modest working
only prophylactic
topical and local effects only

74
Q

What is omalizumab?

A

expensive biologic: monoclonal antibody (Anti-human IgE antibody) that binds and prevents IgE to alpha chain of FcER1

75
Q

Can you use omalizumab in asthma?

A

jury’s still out on that one

76
Q

What’s RIT?

A

rushed immunotherapy

77
Q

I have asthma, I might take some NSAIDS/COX-2 inhibitors, cool?

A

NO. NO. NO. doesn’t do shit in asthma or hay fever, it might provoke symptoms.

78
Q

Crap Doc, I took aspirin for my asthma and it’s getting worse! what do I do?!

A

I’ll give you LTRA (leukotriene receptor antagonists)

79
Q

What do glucocorticoids do?

A

inhibit mediator (cytokine) production in airways

80
Q

When would you use an H1 receptor antagonist for allergies? 6 things

A 
urticaria
atopic dermatitis
hayfever
anaphylaxis
bites/stings
motion sickness
81
Q

When would you NOT use H1 receptor antagonist?

A

Asthma or colds

82
Q

3 classes of H1 receptor antagonists

A
  1. sedative (chlorpheniramine, promethazine)
  2. non sedative but risk of ventricular arrhythmia
  3. newer nonsedative (cetirizine, loratidine)
83
Q

When are cysteinyl leukotriene receptor antagonists indicated? 2 things

A
  1. Aspirin/exercise induced asthma

2. combined with GCS/B2 agonist

Jason's Respiratory Block (20 decks)

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