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pathophysiology > Asthma > Flashcards

Asthma Flashcards

1
Q

movement of air from the atmosphere into and out of the lungs

A

ventilation

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2
Q

nose, nasal passages, mouth, pharynx and larynx.

A

upper airway passages

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3
Q

trachea, bronchi, and bronchioles

A

lower airway

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4
Q

the movement of blood through the lungs

A

perfusion

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5
Q

the movement of gases between the roughly 1 million alveoli or air filled sacs within the lungs and the capillaries that supply the alveoli

A

diffusion

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6
Q

_____ moves from the air that is in the alveoli to the blood flowing through the pulmonary capillaries

A

oxgyen

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7
Q

___ passes from the blood into the alveoli

A

carbon dioxide

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8
Q

completing the respiration process, carbon dioxide is expelled.

A

expiration

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9
Q

chronic reactive airway disorder characterized by increase resistance to air flow due to episodic airway obstruction.

A

asthma

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10
Q

is initiated by diverse, non-immune mechanisms

A

intrinsic (non-atopic)

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11
Q

triggered by irritant receptors and vagal reflex

A

intrinsic

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12
Q

initiated by type 1 hypersensitive response to an extrinsic antigen

A

extrinsic (atopic)

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13
Q

Mast cells, which in people which asthma are in a pre-sensitized state, react to antigens and release histamine, leukotrienes, interleukins and prostaglandins.

A

early phase

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14
Q

occurs 4-8 hours after exposure to an asthmatic trigger. Release of inflammatory mediators induces the migration and activation of other inflammatory cells: basophils, eosinophils, and neutrophils.

A

late phase

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15
Q

higher prevalence in

A

boys and women

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16
Q

highest prevalence in ____

A

women between 45 and 64

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17
Q

risk factors for childhood asthma

A

family history, high exposure to airborne allergens, exposure to tobacco smoke, low birth weight and RDS

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18
Q

risk factors for adult onset asthma

A

occupational exposures to low molecular weight sensitizers, exposure to infectious agents, allergens or pollution, women- smoking, obesity, hormonal influences

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19
Q

adults tend to experience more exacerbations in the ____ months

A

winter

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20
Q
  • exposure to allergen/antigen

- type I IgE mediated hypersensitivity reaction

A

extrinsic asthma (atopic/allergy asthma)

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21
Q

respiratory tract infection, exercise, hyperventilation, cold air, drugs/chemicals, irritants, hormonal changes, emotional upsets, airborne pollutants, GERD, etc.

A

intrinsic asthma (non-atopic asthma)

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22
Q
  • allergen binds to preformed IgE on sensitized mast cells on mucosal surface of airways
  • mast cell activation releasing inflammatory mediators
  • increase mucus secretion, increased vascular permeability and bronchoconstriction
A

early phase response

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23
Q
  • release of inflammatory mediators causes recruitment of neutrophils, eosinophils, basophils, T lymphocytes (TH2)
  • cause epithelial injury and edema, increased mucus, changes in mucociliary function
A

late phase response

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24
Q

are cellular bags of granules found in large numbers in the skin and linings of GI and respiratory tract. They are activated by several means including physical injury, chemical agents, immunologic and infectious means. They degranulate releasing histamine, chemotactic factors and cytokines which can an immediate effect.

A

mast cells

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25
Q
  • is a potent vasodilator that causes increased vascular permeability through retraction of endothelial cells
  • causes smooth muscle to contract causing bronchoconstriction when simulated in the bronchi
A

histamine

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26
Q
  • functions are similar and complementary to that of histamine.
  • more potent and stimulate slower and more prolonged effects compared to histamine.
  • cause slow and sustained constriction of the bronchioles
A

Leukotrienes

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27
Q

causes vasodilation, increased vascular permeability and bronchoconstriction

A

Prostaglandin D2

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28
Q

are cytokines that attract immune and inflammatory cells. They primarily function to attract leukocytes.

A

chemotactic chemokines

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29
Q

are proteins that modulate the function of other cells.

A

cytokines

30
Q
  • increases the activation and migration of inflammatory cells (specifically eosinophils and neutrophils) and contributes to airway remodeling.
  • causes endothelial cells to express adhesion molecules
A

TNF alpha

31
Q

alter muscarinic receptor function resulting in increased levels of acetylcholine which causes bronchial smooth muscle contraction and mucus secretion

A

TNF-alpha and IL-1

32
Q

stimulates activation, proliferation and production of antigen-specific. IgE by B cells

A

IL-4

33
Q

activates and promotes eosinophil activity

A

IL-5

34
Q

causes a more exaggerated inflammatory response through activation of basophils, neutrophils, and eosinophils.

A

IL-8

35
Q

impairs the clearance of mucus, contributes to bronchoconstriction and increases fibroblast secretion.

A

IL-13

36
Q

induces platelet aggregation, increases vascular permeability through endothelial cell retraction, activates neutrophils and is a potent eosinophil chemoattractant

A

PAF

37
Q

are mostly produced by mast cells, eosinophils and basophils are the leukotrienes that play a major role in the pathophysiology of asthma. They were initially called “slow reacting substance of anaphylaxis” due to their effect on bronchial smooth muscle of slow and prolonged contraction and hence, bronchoconstriction.

A

Cysteinyl leukotrienes

38
Q
  • play an important role in the pathogenesis of extrinsic asthma.
  • act as growth factors for mast cells as well as recruiting and activating eosinophils by stimulating the differentiation of B cells into IgE producing plasma cells.
A

T lymphocytes (TH2)

39
Q

neutrophils, eosinophils, and basophils

A

granulocytes

40
Q

are first on scene and the predominant phagocytes in the early inflammatory phase.

A

neutrophils

41
Q

controlling the release of specific mediators from mast cells

A

eosinophils

42
Q

bind to IgE which is secreted by plasma cells and release histamine and mediators of inflammation such as IL-4.

A

basophils

43
Q

What is mucus secretion triggered by?

A

the inflammatory response

44
Q

What stimulates increased mucus production?

A

Leukotrienes

45
Q

What produces mucus in the airways?

A

submucosal glands and goblet cells

46
Q

what is the most damaging effect of mucus hypersecretion?

A

airway obstruction by mucus plugs which is caused by mucus hypersecretion and increased plasma exudation.

47
Q
  • begins early in the disease process

- declining lung function

A

airway remodeling

48
Q

the result of an inability to adequately ventilate and an abnormal ventilation-perfusion relationship where parts of the lung that are well perfused are not adequately ventilated.

A

dyspnea

49
Q

results from air trapping and resultant hyper inflation of the lungs.

A

chesr tightness

50
Q

results as the asthmatic patient tries to clear his or her airway of mucus

A

coughing

51
Q

is the result of the passing of air through narrowed airway

A

wheezing

52
Q

triggered by lung receptors responding to increasing lung volume and alveolar hypoxia.

A

hyperventilation

53
Q

causes vasoconstriction which in turn decreases vascular perfusion contributing to ventilation-perfusion mismatch.

A

hypoxia

54
Q

causes a decrease in serum carbon dioxide resulting in respiratory alkalosis usually accompanied with hypoxemia

A

hyperventilation

55
Q

the most helpful result is an ____

A

arterial blood gas

56
Q

provides information about ventilation through the pCO2 and PO2 values

A

arterial blood gas

57
Q

will initially cause respiratory alkalosis which may be accompanied with hypoxemia or a low PO2 during an asthma attack.

A

hyperventilation

58
Q

pH=7.50, pCO2=29, HCO3=22, PO2=70

A

respiratory alkalosis and hypoxemia

59
Q

pH=7.32, pCO2=49, HCO3=27, PO2=70

A

respiratory acidosis and hypoxemia

60
Q

____ infections are more common.

A

viral

61
Q

___ offers the single most objective measurement of lung function available

A

spirometry

62
Q

bronchial provocation tests cause _____

A

bronchoconstriction

63
Q

____ is confirmed when post challenge data shows a 12% or greater improvement

A

reversible airway obstruction

64
Q

assesses peak expiratory flow (PEF) by comparing to patient’s personal best

A

peak flow monitoring

65
Q

PEF >80% of personal best

A

green zone

66
Q

PEF 50-80% of personal best

A

yellow zone

67
Q

PEF <50% of personal best

A

red zone

68
Q

address inflammation and airway obstruction

A

long-term control medications

69
Q

reverse acute airflow obstruction

A

long-term control medications

70
Q

block the COX and lipoxygenase pathways in the inflammatory process.

A

corticosteroid medications

71
Q

stabilize the membrane of a sensitized mast cell after an antigen-IgE interaction preventing the release of inflammatory mediators such as histamine.

A

mast cell stabilizers

72
Q

is anti-IgE antibody that prevents binding of IgE to basophils and mast cells.

A

Monoclonal antibody SC injections

pathophysiology (5 decks)

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