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Peds Patho > Asthma > Flashcards

Asthma Flashcards

1
Q

episodic asthma is characterized by:

A
  • -reversible airway constriction

- -increased airway responsiveness

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2
Q

chronic asthma is characterized by:

A
  • -chronic airway inflammation
  • -at least partially reversible airway obstruction
  • -increased airway responsiveness
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3
Q

pulmonary biochem: diff. layers

A

1) mucosal layer: potential for secretions

2) sub-mucosal layer: potential for mucosal edema, potential for bronchospasm

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4
Q

most common causes of narrowed airways

3 things

A

1) secretions
2) mucosal edema
3) bronchospasm

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5
Q

risk factors for asthma

A
  • -race/gender! Afr Amer. males most at risk!
  • -genetic predisposition
  • -airway hyperresponsiveness
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6
Q

what causes many symptoms of asthma?

A

airflow obstruction/narrowing of airway

risk factors –> INFLAMMATION –> airflow obstruction

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7
Q

inflammation with asthma causes:

A
  • -airflow obstruction

- -bronchial hyperresponsiveness

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8
Q

1 trigger of asthma hospitalizations

A

Viral respiratory infections

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9
Q

major trigger of acute asthma reaction

A

Upper Respiratory Infections (URI’s)

influenza vaccine recommended for ppl w/asthma!

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10
Q

triggers of acute asthma reaction

A

URIs, allergens, irritants, sudden or extreme changes in weather, exercise, intense emotions

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11
Q

major problem in poor areas: –>major environmental risk factor for development of asthma

A

roach excrement

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12
Q

other environmental risk factors for asthma development

A

indoor/outdoor allergens, occupational sensitizers, TOBACCO SMOKE, air pollution, resp. infections, parasitic infections, socioeconomic factors, FAMILY SIZE (larger fam –> more illness coming in), diet & drugs, obesity, hygiene hypothesis

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13
Q

hygiene hypothesis

A

idea that increased exposure to bacteria, viruses, & pathogens gives you a lesser risk of developing asthma

(ex: lower rates of asthma in rural areas, in kids who are around animals)
- -childhood exposure to germs and certain infections helps the immune system develop

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14
Q

Definition of Asthma (3 things)

A

1) Chronic inflammatory d/o of the airways
2) Excessive reaction to “minor” irritants results in a host of damaging airway changes
3) Patchy, mostly reversible regions of airway narrowing (cause asthma symptoms)

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15
Q

what causes chronic inflammatory d/o of the airway?

A
  • -mast cells, eosinophils, & lymphocytes infiltrate into the airway lining
  • -airway hyperresponsiveness develops
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16
Q

what harmful airway changes result from excessive reaction to “minor” irritants with asthma?
(3 things)

A
  • -bronchial wall edema
  • -smooth muscle contraction
  • -excess mucus production
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17
Q

w/asthma, it is not uncommon to see what on an x-ray?

A

atelectasis

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18
Q

what happens w/bronchial inflammation?

in terms of what happens to airway, acutely

A

excess mucus + muscle layer contracts = reduced airway

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19
Q

what happens w/bronchial constriction?

A

muscles tighten & alveoli are filled w/trapped air

“air trapping”

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20
Q

how does bronchial constriction appear on x-ray?

A

as flattening of the diaphragm

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21
Q

asthma physiology: 6 components

A

1) airway inflammation
2) bronchial hyperresponsiveness
3) bronchoconstriction
4) bronchial wall edema
5) excess mucous secretions
6) airway remodeling

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22
Q

how does bronchoconstriction occur?

physiologically, in terms of muscle

A

parasympathetic nerves contract smooth muscle–> causes bronchoconstriction

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23
Q

2 results of inflammation (long-term)

A

1) Reversibility

2) Remodeling

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24
Q

reversibility

A
  • -occurs in most asthma episodes
  • -airway returns to normal caliber
  • -flow of air through airways returns to normal “speed”
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25
Q

remodeling (4 things happen)

A
  • *permanent alterations in the airway structure**
  • -airway lining builds up persistent fibrotic changes
  • -airway caliber remains abnormal
  • -air flow is decreased
  • -permanent changes appear to begin in childhood, but become recognizable in adults
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26
Q

when do you see fibrotic changes?

A

with airway remodeling

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27
Q

fundamentally, asthma is:

A

a chronic inflammatory disease

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28
Q

with asthma, what cells are damaged?

A

see damage to epithelial cells

also: damaged cilia!

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29
Q

consequences of persistent asthma (2 things)

A

1) changes in subepithelial layer:
- -collagen deposition (collagen where it doesn’t belong)
- -not as effective
- -increasing mass
2) smooth muscle hyperplasia

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30
Q

effects of smooth muscle hyperplasia (d/t persistent asthma)

A

muscle mass increases can really change airway!
(by about 12%)
–narrowing large & small airways permanently

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31
Q

changes in subepithelial layer d/t persistent asthma:

A
  • -collagen deposition (collagen where it doesn’t belong)
  • -not as effective
  • -increasing mass
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32
Q

inflammatory cell infiltrate consists mainly of:

A

eosinophils & lymphocytes

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33
Q

“sudden death” asthma is assoc. w/?

A

a massive neutrophil infiltration

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34
Q

in asthma, what happens to the epithelium?

A

it wears away (denudation)

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35
Q

w/asthma, what happens to mucus glands?

A

hyperplasia & hypersecretion

36
Q

w/asthma, what happens vascularly?

A

vascular dilatation (& submucosal edema)

37
Q

what causes airway remodeling?

A

fibrin & collagen deposition

38
Q

how does inflammation lead to clinical sx w/asthma?

A

inflammation causes:

  • -airway hyperresponsiveness (AHR) & airway obstruction
    - -> which interact together and cause sx!
39
Q

Where can mucosal edema and bronchospasm occur?

A

Sub-mucosal layer

40
Q

What can occur at the mucosal layer?

A

There is the potential for secretions

41
Q

“mediator soup” is made up of these inflammatory mediators (cell types):

A
  • -mast cells
  • -macrophages
  • -T-lymphocytes
  • -Epithelial cells
  • -Platelets
  • -Neutrophils
  • -Myofibroblasts
  • -Basophils
42
Q

what are the effects of inflammatory mediators?

(4 things) – “Be Mine Max Always Hyper”

A

1) bronchoconstriction
2) microvascular leakage
3) mucus hypersecretion
4) airway hyperresponsiveness

43
Q

what does “airway responsiveness” mean?

A

“twitchiness” of the airways

44
Q

what does the term “inflammatory mediators” mean?

A

cell products that are secreted and exert functional effects

45
Q

“mediator soup” is made up of these inflammatory mediators: (in addition to cells)

A
  • -histamine
  • -lipid mediators (prostaglandins, leukotrienes)
  • -peptides (bradykinin, tachykinin)
  • -cytokines (TNF)
  • -growth factors
46
Q

2 examples of lipid mediators

A
  • -leukotrienes

- -prostaglandins

47
Q

example of a cytokine

A

Tumor Necrosis Factor (TNF)

also: IL-4, IL-5, IL-6

48
Q

2 examples of peptides

A
  • -bradykinin

- -tachykinin

49
Q

definition of atopy

A

the genetic predisposition of an individual to produce high quantities of IgE in response to allergens in the environment
**is the strongest identifiable predisposing factor for developing asthma

50
Q

what restricts or blocks airflow

A

bronchoconstriction of bronchiolar muscle bands

51
Q

w/asthma, you may hear:

A

decreased breath sounds at bases

52
Q

is wheezing always asthma?

A

NO!

“Not all that wheezes is asthma, and not all asthma wheezes.”

53
Q

acute sx of asthma usually arise from… ?

A

bronchospasm (–> respond to bronchodilator therapy)

54
Q

what does bronchial hyperresponsiveness do?

A

it enhances susceptibility to bronchospasm

55
Q

the dominant physiological event leading to clinical

symptoms

A

airway narrowing and a subsequent interference with airflow

caused by bronchoconstriction

56
Q

role of cytokines in asthma

A

direct and modify the inflammatory response in asthma and likely determine its severity

57
Q

IgE

A

–the antibody responsible for activation of allergic reactions –is important to the pathogenesis of allergic diseases & the development and persistence of inflammation

58
Q

Type I Hypersensitivity Reaction

A
  • -Immediate type hypersensitivity

- -involves IgE antibody on mast cell

59
Q

Type IV Hypersensitivity Reaction

A
  • -Delayed Type Hypersensitivity
  • -Involves T-cell mediated response
  • -other immune system cells activate
60
Q

Airway Inflammation: Early phase response

A
  • *IgE mediated**
  • -involves Type I Hypersensitivity
  • IgE antibody w/mast cells
61
Q

Airway Inflammation: Late Phase Response

A
    • T-cell mediated **
  • -involves Type IV Hypersensitivity
  • -T-cell mediated response activates:
    - -eosinophils, B cells, others
62
Q

airway hyperresponsiveness: definition

A

an exaggerated bronchoconstrictor response to a wide variety of stimuli
–contractile responses to challenges w/methacholine –> correlates w/the clinical severity of asthma

63
Q

what influences airway hyperresponsiveness (AHR)?

3 things

A

1) inflammation
2) dysfunctional neuro-regulation
3) structural changes

64
Q

how can we reduce AHR?

A

by giving tx aimed towards reducing inflammation

should also improve asthma control

65
Q

1 physio event occurring with asthma

A

INFLAMMATION

66
Q

2 physio event occurring w/asthma

A

bronchoconstriction

a dominant physio event, but 2nd to inflammation

67
Q

what causes allergen-induced acute bronchoconstriction?

A

IgE-dependent release of mediators from mast cells

68
Q

Non-IgE dependent bronchoconstriction can be caused by:

A

other stimuli: irritants, exercise, cold air, aspirin & other NSAIDs
–stress may also play a role!

69
Q

what causes swollen airways?

A

bronchial wall edema

& excess mucus secretion!

70
Q

what releases mucus in the lung?

A

Goblet Cells secrete mucus

71
Q

other changes w/asthma that limit airflow?

A
  • -edema
  • -inflammation
  • -mucus hypersecretion
  • -formation of inspissated mucus plugs
72
Q

definition of inspissated

A

thickened, congealed

73
Q

structural changes you can see w/asthma

A

hypertrophy & hyperplasia of the airway smooth muscle

74
Q

is airway remodeling reversible?

A

–can be reversible in some pts!

75
Q

structural changes of airway remodeling (8 things!)

A
  • -Vascular Dilation
  • -Edema
  • -Subbasement Membrane Thickening
  • -Smooth Muscle Hypertrophy & Hyperplasia
  • -Mucous Gland Hyperplasia & Hypersecretion
  • -Inflammatory Cell Infiltration
  • -Epithelial Damage
  • -Subepithelial Fibrosis
76
Q

is asthma an obstructive or restrictive process?

A

depends…bad asthma can be both!

77
Q

asthma: restrictive or obstructive?

A

mild asthma is primarily obstructive

–bad asthma can be both

78
Q

cystic fibrosis: restrictive or obstructive?

A

restrictive

79
Q

when should you perform spirometry?

A
  • -at initial assessment
  • -after tx is initiated & sx and PEFs have stabilized
  • -at least every 1-2 yrs to assess maintenance of airway function if well-controlled
  • -more often if poor asthma control
80
Q

when should Peak Flows be performed?

A
    • In all moderate & severe persistent asthmatics! **
  • -establish a personal best
  • -useful in exacerbations & maintenance/changes of therapy
  • -can be helpful w/ “poor perceivers”
81
Q

what is a “poor perceiver”?

A

someone who accepts their chronic asthma sx as the norm

82
Q

do you always have asthma w/reactive airway disease?

A

no! some kids have reactive airway disease and will never have asthma

83
Q

3 major sx of asthma

A

1) cough
2) wheezing (tightness, noisy breathing)
3) dyspnea (breathlessness)

84
Q

a cough may be particularly assoc. w/ asthma if it occurs:

5 things

A

1) after exertion
2) breathing cold air
3) at night
4) after colds
5) paroxysmal

85
Q

meaning of paroxysmal

A

from time to time

86
Q

dyspnea (breathlessness) be be especially assoc. w/asthma if it is:
(3 things)

A

1) intermittent or variable
2) after exertion
3) at night

87
Q

if you have 1 case of bronchiolitis, then:

A

at risk for asthma

Peds Patho (8 decks)

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