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MSS - RESP Exam 2 > Asthma, Allergies, and Anaphylaxis > Flashcards

Asthma, Allergies, and Anaphylaxis Flashcards

(61 cards)

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1
Q

type I hypersensitivities?

A 
systemic anaphylaxis
acute uriticaria
seasonal rhinoconjuctivitis
asthma
food allergy
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2
Q

systemic anaphylaxis?

A

intravenous

drugs, serum, food (peanut)

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3
Q

acute uriticaria?

A

wheal and flare
-through skin

local increase in blood flow and vascular permeability

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4
Q

seasonal rhinoconjuctivitis?

A

hay fever
inhalation
pollens and dust mite feces

sneezing and nasal mucosa

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5
Q

asthma?

A

inhalation
dander
pollen
dust mite feces

bronchial constriction, airway inflammation, increased mucus production

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6
Q

food allergy?

A

oral
tree nut, shellfish, peanuts, milk, egg, fish, soy, wheat

vomiting, diarrhea, pruritis, urticaria

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7
Q

pruritis

A

itching

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8
Q

urticaria

A

hives

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9
Q

allergens?

A

absence of inflammation

protein (T cell response)
small and highly soluble
carried on dry particles

bind MHC class II - activate Th2 cells**

low MW - can diffuse into mucus

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10
Q

allergens promote?

A

Th2 cell priming and IgE response

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11
Q

IgE production?

A

??

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12
Q

Th2 cytokines?

A

IL-4, 5, 9, 13

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13
Q

priming

A

T and B cell activation and expansion induced by allergen

production of IgE

multiple exposures leads to sensitized or atopic individuals

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14
Q

mast cells

A

skin and mucosa

pro-inflammatory:
histamine
serotonin
heparin
serine proteases

lipid mediators:
prostaglandin D2
leukotrienes

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15
Q

eosinophils

A

FceRI expression inducible

chronic allergic inflammation = high Eos #

major contributor to tissue damage

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16
Q

leukotrienes

A

SRS-A (slow release)
-synthesized from arachadonic acid

overlapping activities with histamine

slower onset, more powerful, longer duration

increase in capillary permeability and mucus production

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17
Q

LTB4

A

pro-inflammatory

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18
Q

IL-4

A

isotype switching to IgE

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19
Q

IL-13

A

airway eosinophilia
mucous gland hyperplasia
airway fibrosis and remodeling

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20
Q

IL-5

A

regulator of Eosinophil production and survival

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21
Q

TNF

A
  • recruitment and activation of inflammatory cells

- altered function and growth of airway smooth muscles

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22
Q

T-reg cells

A

limit inflammatory response

-inhibit

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23
Q

Th2

A

IL-5, 4, and 13

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24
Q

IL-5

A

eosinophils

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25
IL4 and 13?
B cells | -to activation of mast cells
26
IgE allergic response?
IgE coated mast cell | -IgE must be cross-linked
27
immediate reaction?
vascular/smooth muscle response
28
late phase reaction?
inflammation | -later released cytokines
29
early phase acute allergic response
degranulation of mast cells sneezing, pruritis, rhinorrhea, congestion recruitment of cells from circulation
30
late phase chronic allergic response
4-12 hours influx and activation of eosinophils, neutrophils, basophils, Th2 cells 10x increase mast cells present in area fatigue, myalgias, asthma
31
eosinophils
proinflammatory mediators local tissue damage, sinus infection chronic hyperplastic eosinophilic sinusitis (CHES)
32
mast cells result?
``` vasodilation vascular leak bronchoconstriction intestinal hypermotility inflammation tissue damage ```
33
eosinophil result?
killing of parasites and host cells | tissue damage
34
cationic granule cells?
from eosinophils
35
hygiene hypothesis
people without exposure as a child more likely to be atopic
36
counter regulation hypothesis
all types of infection lead to inflammation | -promotes Th1
37
symptom depends on?
allergen AND route of entry**
38
allergic rhinitis
seasonal rhinoconjunctivitis -paroxysms of sneezing, rhinorrhea, nasal obstruction, itchy eyes, nose, and palate either seasonal or perennial (year round)
39
allergic salute
itch up nose
40
allergic shiners
infraorbital edema and darkening due to subQ venodilation
41
acute urticaria
mediated by cutaneous mast cells in superficial dermis acute less than 6 weeks
42
early phase
release of mast cell mediators | onset of rhinitis and other overt symptoms
43
late phase
influx of inflammatory cells (Ts, Eos, Baso) | -chronic symptoms
44
asthma
heterogeneitic disease - can be non-atopic - exercise, cold, idiopathic atopic is with allergen trigger
45
asthma treated?
will result in slow increase in peak flow treats hyper responsiveness
46
early phase asthma
bronchoconstriction -contract smooth muscle and reflex neural pathways release of mast cell mediators
47
late phase asthma
bronchoconstriction influx of inflammatory cells Ts, Eos, Baso contract smooth airway muscles
48
risk factors
genetic environmental infectious
49
corticosteroids
IL4 IL5 TNF biogenic amines
50
cromolyn
inhibits mast cell release leukotrienes
51
leukotriene antagonist
limit bronchial constriction
52
anaphylaxis
most severe allergic response -systemic mast cell activation antigen gets into blood** hypotension, tachycardia, urticaria, flushing, bronchoconstriction, laryngeal edema, diarrhea, sense of doom IgE mediated
53
anaphylactoid
non-immunologic release of mediators drugs and complement components
54
idiopathic anaphylaxis
genetic mast cell disorder
55
risk factors for anaphylaxis
atopy route asthma delayed epinephrine
56
anaphylaxis and priming?
requires priming second exposure is the dangerous one
57
treatment for Th2 activation?
induce regulatory T cells
58
treatment for B cell IgE production?
block co-stimulation of Th2 cytokines inhibit IL-4 or IL-13
59
treatment of mast cell activation?
inhibits effects of mediators on specific receptors inhibit synthesis of specific mediators block IgE receptor
60
treatment of mediator action?
inhibit effects of mediators on specific receptors inhibits synthesis of specific mediators antihistamine drugs lipooxygenase inhibitors
61
treatment of eosinophil dependent inflammation
block cytokine and chemokine receptors that mediate eosino IL-5

MSS - RESP Exam 2 (2 decks)

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