Asthma, Allergies, and Anaphylaxis Flashcards

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
Q

IL4 and 13?

A

B cells

-to activation of mast cells

26
Q

IgE allergic response?

A

IgE coated mast cell

-IgE must be cross-linked

27
Q

immediate reaction?

A

vascular/smooth muscle response

28
Q

late phase reaction?

A

inflammation

-later released cytokines

29
Q

early phase acute allergic response

A

degranulation of mast cells

sneezing, pruritis, rhinorrhea, congestion
recruitment of cells from circulation

30
Q

late phase chronic allergic response

A

4-12 hours

influx and activation of eosinophils, neutrophils, basophils, Th2 cells

10x increase mast cells present in area

fatigue, myalgias, asthma

31
Q

eosinophils

A

proinflammatory mediators
local tissue damage, sinus infection
chronic hyperplastic eosinophilic sinusitis (CHES)

32
Q

mast cells result?

A
vasodilation
vascular leak
bronchoconstriction
intestinal hypermotility
inflammation
tissue damage
33
Q

eosinophil result?

A

killing of parasites and host cells

tissue damage

34
Q

cationic granule cells?

A

from eosinophils

35
Q

hygiene hypothesis

A

people without exposure as a child more likely to be atopic

36
Q

counter regulation hypothesis

A

all types of infection lead to inflammation

-promotes Th1

37
Q

symptom depends on?

A

allergen AND route of entry**

38
Q

allergic rhinitis

A

seasonal rhinoconjunctivitis
-paroxysms of sneezing, rhinorrhea, nasal obstruction, itchy eyes, nose, and palate

either seasonal or perennial (year round)

39
Q

allergic salute

A

itch up nose

40
Q

allergic shiners

A

infraorbital edema and darkening due to subQ venodilation

41
Q

acute urticaria

A

mediated by cutaneous mast cells in superficial dermis

acute less than 6 weeks

42
Q

early phase

A

release of mast cell mediators

onset of rhinitis and other overt symptoms

43
Q

late phase

A

influx of inflammatory cells (Ts, Eos, Baso)

-chronic symptoms

44
Q

asthma

A

heterogeneitic disease

  • can be non-atopic
  • exercise, cold, idiopathic

atopic is with allergen trigger

45
Q

asthma treated?

A

will result in slow increase in peak flow

treats hyper responsiveness

46
Q

early phase asthma

A

bronchoconstriction
-contract smooth muscle and reflex neural pathways

release of mast cell mediators

47
Q

late phase asthma

A

bronchoconstriction
influx of inflammatory cells
Ts, Eos, Baso

contract smooth airway muscles

48
Q

risk factors

A

genetic
environmental
infectious

49
Q

corticosteroids

A

IL4 IL5 TNF biogenic amines

50
Q

cromolyn

A

inhibits mast cell release leukotrienes

51
Q

leukotriene antagonist

A

limit bronchial constriction

52
Q

anaphylaxis

A

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
Q

anaphylactoid

A

non-immunologic release of mediators

drugs and complement components

54
Q

idiopathic anaphylaxis

A

genetic mast cell disorder

55
Q

risk factors for anaphylaxis

A

atopy
route
asthma
delayed epinephrine

56
Q

anaphylaxis and priming?

A

requires priming

second exposure is the dangerous one

57
Q

treatment for Th2 activation?

A

induce regulatory T cells

58
Q

treatment for B cell IgE production?

A

block co-stimulation of Th2 cytokines

inhibit IL-4 or IL-13

59
Q

treatment of mast cell activation?

A

inhibits effects of mediators on specific receptors

inhibit synthesis of specific mediators

block IgE receptor

60
Q

treatment of mediator action?

A

inhibit effects of mediators on specific receptors

inhibits synthesis of specific mediators

antihistamine drugs
lipooxygenase inhibitors

61
Q

treatment of eosinophil dependent inflammation

A

block cytokine and chemokine receptors that mediate eosino

IL-5