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PATHOPHYSIOLOGY > Asthma > Flashcards

Asthma Flashcards

1
Q

What 3 things make up the respiratory system?

A
  • airway passages
  • lungs
  • blood vessels
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2
Q

What is the purpose of the respiratory system?

A
  • provide oxygen and CO2 exchange between air and blood
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3
Q

How many processes are in respiration and what are the sub categories?

A
  • ventilation
  • inspiration; diffusion and perfusion
  • expiration
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4
Q

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

A

ventilation

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5
Q

What elements of the body compose the upper air passages?

A
  • nose
  • nasal passages
  • mouth
  • pharynx
  • larynx
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6
Q

What elements of the body compose the lower air passages?

A
  • trachea
  • bronchi
  • bronchioles
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7
Q

Definition: process of taking in air

A

inspiration

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8
Q

Definition: movement of blood through lungs

A

perfusion

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9
Q

Definition: movement of gases between 1 million alveoli in lungs and the capillaries that supply alveoli

A

diffusion

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10
Q

What are the steps in diffusion?

A

●Gases move across alveoli-capillary membrane
●Moves from the air that is in alveoli → blood in pulmonary capillaries
●C2 moves from blood into alveoli

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11
Q

Definition: process of expelling CO2

A

expiration

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12
Q

Asthma is known as

A
  • chronic reactive airway disorder
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13
Q

T/F: asthma involves hyposensitivity to reaction to stimuli

A

false; hyper

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14
Q

T/F: asthma involves increase resistance to air flow due to airway obstruction

A

true

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15
Q

What does asthma cause a release of?

A

chemical mediators from mast cells

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16
Q

T/F: asthma can be classified as intrinsic or extrinsic based on trigger factors

A

true

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17
Q

Asthma involves:

A
  • inflammation
  • bronchospasms
  • increased mucus secretion
  • injury to mucosal lining of airways
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18
Q

What initiates extrinsic or atopic asthma?

A
  • T1 hypersensitivity to extrinsic antigen
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19
Q

What does the antigen initiated by t1 hypersensitivity bind to?

A

mast cells; begins mast cell degranulates

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20
Q

The release of mast cell degranulates results in?

A

inflammation and bronchospasm resulting in edema, epithelial injury and impaired mucosilarily function

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21
Q

Intrinsic or non atopic asthma is initiated by

A

diverse non immune mechanisms

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22
Q

Which type of asthma has many types of overlapping symptoms?

A

intrinsic

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23
Q

What triggers intrinsic asthma?

A
  • irritant receptors and vagal reflex
  • viral infections
  • inhaled irritants
  • NSAIDS
  • sulfites
  • emotional stress
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24
Q

In what stage does asthma normally begin?

A

childhood

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25
Q

Can adults only get asthma with a previous history?

A

no; can get it without

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26
Q

What two factors are an arise to asthma?

A

hereditary and environmental

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27
Q

What is the time period of acute phase asthma?

A
  • 10 to 20 min of trigger
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28
Q

Acute phase asthma breakdown

A

● Mast cells react to antigens and degranulate
● Airborne antigens = antigen binds to mast cells on mucosal surface of the airway
● Release of inflammatory mediators → infiltration of inflammatory cells
● Allows antigens to reach submucosal mast cells
● Direct stimulation of parasympathetic receptors:
○ Bronchoconstriction
○ Increased vascular permeability
■ Mucosal edema
■ Increased mucus secretion

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29
Q

What is the time period of late phase asthma?

A

develops 4-8 hours after exposure to asthmatic trigger

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30
Q

Late phase asthma breakdown

A 
●	Release inflammatory mediators induces migration and activation of other inflammatory cells:
○	Basophils
○	Eosinophils
○	Neutrophils
Involves:
●	Inflammation
●	Increased airway responsiveness
●	Renewed bronchospasm
●	This leads to further air limitation and heightened airway responsiveness
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31
Q

Late phase asthma includes a vicious cycle of exacerbations including

A
  • edema
  • epithelial injury
  • impaired mucocillary function
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32
Q

What are the two ways asthma patients treatment is approached?

A
  • control factors contributing to asthma severity

- pharmacological treatment

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33
Q

Pharm treatment includes

A
  • corticosteroids
  • bronchodilators
  • mast cell stabilizers
  • beta agonists
  • anticholinergic drugs
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34
Q

What is the percentage of the canadian population aged 12 years or older that have asthma?

A

10%

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35
Q

What nationality has a higher incidence of asthma in people 12 or older?

A

indigenous; greater by 12%

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36
Q

Globally asthma occurs in lower or higher income countries?

A
  • lower and middle income

- due to undiagnosed and under-treatment

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37
Q

What two groups of people have a higher prevalence of asthma?

A
  • boys and adult women
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38
Q

Where is asthma more and less prevalent in Canada?

A

■ HIGHER in Atlantic provinces (Ontario, Nova Scotia)

■ LOWER in BC and Prairies (Northwest territories, Yukon and Nunavut)

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39
Q

Risk factors for child asthma:

A

Family history of allergy and allergic disorders:
● Hay fever
● Asthma
● Eczema
● Genetic is complicated and multifactorial
● More than 100 genes play a role in susceptibility and pathogenesis

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40
Q

What specific gene is associated with asthma and bronchial hyper responsiveness?

A

Gene ADAM 33

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41
Q

High exposure of susceptible children to air-bone allergens including

A

● Pets
● House dust mites
● Cockroaches
● Mould
○ ALL IN FIRST YEARS OF LIFE
Exposure to tobacco smoke in utero or early in life
● Children are significantly more likely to have asthma than those in non-smoking houses

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42
Q

T/F: no links of asthma with income, urban or rural regions; in contrast to the US where prevelance of asthma is significantly higher in urban areas

A

true

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43
Q

Risk factors for adult onset asthma

A
  • occupation exposure

- exposure to infectious agents, allergens or pollution

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44
Q

T/F: Atmospheric pollution is likely as a primary cause

A

false; unlikely

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45
Q

For women what are three factors that can lead to asthma

A

● Smoking
● Obesity
● Hormonal influences

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46
Q

When is asthma more prevalent in the hospital for children 2-15?

A

September; after summer vacation

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47
Q

When do young adults 16-49 experience a peak in asthma?

A

Fall and December ; Christmas epidemic

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48
Q

When do older adults 50+ experience it?

A

December; 6 days after christmas

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49
Q

T/F: asthma can be transient, intermittent, or persistant; mild, moderate or severe

A

true

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50
Q

t/f: lower airway obstruction is normally reversible

A

true; in contrast to other diseases

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51
Q

Triggers of extrinsic asthma include

A

● Known as atopic or allergy asthma
● Type 1 IgE Hypersensitivity
● Results from exposure to extrinsic antigen/allergen

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52
Q

triggers of intrinsic asthma

A 
●	Known as non-atopic asthma; not as well understood 
●	Different explanations
●	Respiratory tract infections
●	Exercise
●	Hyperventilation
●	Cold air = weather changes
●	Drugs and chemicals
●	Irritants
●	Hormonal changes and emotional upsets
●	Airborne pollutants
●	GERD
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53
Q

Which type of asthma is thought to be due to parasympathetic stimulation through vagal paths?

A

intrinsic

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54
Q

Early phase begins and lasts up to

A

occurs within 10-20 min of trigger and lasts up to 2 hours

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55
Q

Early phase breakdown

A 
●	Allergen binds to preformed IgE on sensitized mast cells in mucosal surface of airway
●	Mast cells are activated
●	Results in degranulation of:
○	Histamine
○	Chemokines
○	Interleukins
○	TNF-a
●	Mast cells begin synthesizing these for the late phase:
○	Leukotrienes
○	Prostaglandin D2
○	TNF-a
○	Platelet activating factor
●	Inflammatory mediators cause infiltration of inflammatory cells
●	Open mucosal intercellular junctions
●	Allow access to submucosal mast cells
●	Results in more inflammation
●	Increased mucus secretion
●	Increased vascular permeability
●	Increased bronchoconstriction
●	Dendritic cells may receive antigen that will be processed and presented in late response
○	Present to naive T lymphocytes in lymph nodes or memory TH2 cells
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56
Q

Late phase begins and lasts up to

A

4-8 hours after trigger and may last for days or weeks

57
Q

Late phase breakdown

A

● Release of inflammatory mediators
● Cause recruitment and persistent activation of:
○ Neutrophils
○ Eosinophils
○ Basophils
○ T-lymphocytes and TH2
● Causes epithelial injury and edema
● Increased mucus
● Changes in mucociliary function
○ Accumulation of mucus
● Increased airway responsiveness and bronchospasm
● Direct toxic effects of cellular products (eosinophils)
○ Causes epithelial damage and impaired mucociliary function
● Injury causes nerve endings to be stimulated through autonomic paths
○ May cause further bronchoconstriction and mucus secretion
● Macrophages are activated in resp tract

58
Q

Mast Cells factors

A

● Found in large numbers in skin and lining of GI and resp tract

59
Q

What activates mast cells?

A

○ Physical injury
○ Chemical agents
○ Immunologic
○ Infectious

60
Q

What is classified as a degranulate

A

○ Histamine
○ Chemotactic factors
○ Cytokines

61
Q

t/f: degranulates cause immediate effect

A

true

62
Q

Activated mast cell results in

A 
-synthesize inflammatory mediators (derived from plasma membrane lipid)
○	Platelet activating factor
○	Prostaglandin D2
○	Leukotrienes
○	Cytokines
○	Growth factors
63
Q

Histamine characteristics

A 
●	Potent vasodilator
●	Retracts endothelial cells
○	Increases vascular permeability
●	Cause smooth muscle contraction
○	Bronchoconstriction
64
Q

Leukotrines characteristics

A

● Similar to histamine
● More potent
● Stimulate SLOWER and more prolonged effects
● Cysteinyl leukotrienes (LTC4, LTD4 and LTE4) cause slow and sustained bronchoconstriction

65
Q

Prostagladins D2 characteristics

A

● Vasodilator
● Increases vascular permeability
● Bronchoconstriction

66
Q

Chemokines characteristics

A

● Cytokines that attract immune and inflammatory cells

● Primarily function to attract leukocytes

67
Q

Cytokines characteristics

A

● Proteins that modulate the function of other cells
● TNF-a, IL-4, 5, 8 and 13
● TNF-a increases activation and migration of inflammatory cells to express adhesion molecules

68
Q

TNF alpha and IL-1

A
  • alter muscarinic receptor function
    ○ Increases levels of Ach
    ○ Causes bronchoconstriction
    ○ Cause mucus secretion
69
Q

1L-4, 5,8, 13 are

A

TH2 cytokines

70
Q

● IL-4

A

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

71
Q

● IL-5

A

activates and promotes eosinophils

72
Q

● IL-8

A

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

73
Q

● IL-13

A

impairs mucus clearance, cause bronchoconstriction and increases fibroblasts

74
Q

Platelet activating factor

A 
●	Induce platelet aggregation
●	Increases vascular permeability
●	Activates neutrophils
●	Potent eosinophil chemoattractant
●	Cause bronchospasm
●	Cause eosinophil infiltration and non-specific bronchial hyperreactivity
75
Q

Cysteinyl leukotrienes

A

● Initially called “slow reacting substance of anaphylaxis”
● Due to their effect on bronchial smooth muscle of slow and prolonged contraction
● Cause bronchoconstriction
● Mostly produced by mast cells, eosinophils, and basophils

76
Q

T-Lymphocytes → TH2

A

● Important in pathogenesis of extrinsic asthma
● TH2 act as growth factors for mast cells
● Recruit and activate eosinophils by stimulating differentiation of B-cells into IgE-producing plasma cells
● In asthma = T-cell differentiation is skewed towards TH2 phenotype cells

77
Q

Leukocytes → eosinophils, basophils, neutrophils, lymphocytes, and macrophages

A

● Known as white blood cells
● Neutrophils, eosinophils, and basophils are granulocytes
● Neutrophils are first on the scene
○ Predominant phagocytes in EARLY inflammatory phase
● Eosinophils control the release of specific mediators from mast cells
● Basophils bind to IgE which is secreted by plasma cells
○ Release histamine and mediators of inflammation
● Macrophages arrive after neutrophils
○ They arrive in late phase response

78
Q

Bronchospasm results from

A

● Histamine
● Leukotrienes (late phase)
● Platelet activating factor
● Prostaglandins

79
Q

Within a bronchospasm does parasympathetic control of airway function properly why or why not?

A
  • does not function properly
    ● Due to heightened responsiveness to cholinergic mediators
    ● TNF-a and IL-1 cause an alteration of muscarinic receptor function
    ● Leads to increase in ACh
    ● This causes bronchoconstriction and mucus secretion
80
Q

What is mucus secretion triggered by?

A

inflammatory response

81
Q

Leukotrines in response to mucus stimulate or withhold mucus secretion?

A

stimulate

82
Q

The function of IL-9 AND IL-12 in mucus secretion are

A

to upregulate

83
Q

Mucus hypersecretion

A

● Submucosal glands and goblet cells produce mucus in the airways
● Both sources are effected in asthma
● Results in goblet cell hyperplasia and submucosal gland hypertrophy

84
Q

What is the most damaging effect of mucus hyper-secretion

A

is airway obstruction by mucus plugs

85
Q

How is airway obstruction by mucus plugs caused?

A

● This is caused by mucus hypersecretion and increased plasma exudation
● May also cause increased airway hyperresponsiveness
● Impaired mucociliary function worsens the situation
○ Not as able to clear the mucus as well

86
Q

What is one of the major contributors in the patho of asthma

A

airway remodelling

87
Q

When does airway remodelling begin?

A

early on in the disease process

88
Q

Airway remodelling

A

● Declining lung function in children with asthma = attributed to airway remodelling
● Changes to airway due to inflammation may include:
○ Submucosal infiltration w/ activated lymphocytes and eosinophils
○ Mast cell activation
○ Epithelial changes
○ Basement membrane thickening
● Structural changes in airway occur in parallel with inflammation
○ More inflammation = more airway remodelling

89
Q

More inflammation leads to more or less airway remodelling

A

more

90
Q

Severe asthma makes things common to have

A

○ Goblet cell hyperplasia
○ Smooth muscle hypertrophy
○ Mucus plugging

91
Q

Patho of asthma; understand its a big concept

A

● Allergen or irritant trigger mast cell degranulation
● Release of vasoactive mediators and chemokines
● Mast cell release histamine immediately
● Synthesize other vasoactive mediators for later release
○ Leukotrienes
○ Prostaglandin D2
○ PAF
● This results in:
○ Vasodilation
○ Increased capillary permeability
○ Bronchoconstriction
● Trigger causes immune activation
● TH2 cells release IL-4 which stimulates:
○ B cell activation
○ Proliferation
○ Production of antigen specific IgE
● IgE causes mast cell degranulation
● Mast cells release chemokines
● Chemokines cause cellular infiltration of other inflammatory cells
○ Neutrophils
○ Eosinophils
○ Lymphocytes
○ Cytokines
● Autonomic dysregulation results from alteration to muscarinic receptor function by TNF-a and IL-1
● This causes bronchoconstriction and mucus secretion

92
Q

Direct toxic effects of cellular products cause epithelial damage and impaired mucociliary function

A

○ Injury causes local nerve ending stimulation
○ This may cause more bronchoconstriction
○ May cause more mucus secretion

93
Q

Airway remodelling occurs b/c persistent inflammation and toxic effects of:

A

○ Eosinophils
○ Leukotrienes
○ TNF-a

94
Q

Vasoactive mediators and inflammatory cell infiltration causes:

A 
○	Bronchospasm
○	Vascular congestion
○	Mucus secretion
○	Impaired mucociliary function
○	Thickened airway walls
○	Increased contractile response of bronchial
○	Hyperresponsiveness and obstruction
95
Q

Patho of Early phase response

A

● Triggered by activation of presensitized IgE coated mast cells
● Mast cell degranulation occurs
● Inflammatory mediators cause:
○ Increase mucus production
○ Open mucosal inter cell junctions with exposure of submucosal mast cells to the antigen
○ Bronchospasm

96
Q

Patho of late response

A

● Involves release of other inflammatory mediators
● Recruit neutrophils, eosinophils, and basophils
● Increase vascular permeability
● Cause epithelial injury with decreased mucociliary function
● Increased airway responsiveness
● Bronchospasm

97
Q

Clinical manifestations: usually related to narrowed airways due to lower airway obstruction caused by:

A

○ Bronchospasm
○ Edema of bronchial mucosa
○ Mucus hypersecretion

98
Q

Clinical manifestations: air begins trapped or freed and there is impaired expiration

A

trapped

99
Q

Clincial manifestations

A

● Obstruction will worsen
○ Air flows to less resistant portions because ventilation is uneven
● Lungs become hyperinflated
○ Put resp muscles at disadvantage
● Alveolar hypoventilation occurs as gas exchange is impeded
○ Increase intrapleural pressure
○ Increase alveolar gas pressure
○ Cause ventilation perfusion mismatch
● Mucus inhibits alveolar ventilation
● Hyperventilation is triggered by lung receptors responding to increase lung volume + alveolar hypoxia

100
Q

Clinical manifestations: hypoxia causes

A

○ Decrease in serum CO2
○ Resp alkalosis
○ Accompanied by hypoxemia

101
Q

Clinical manifestations: work of breathing increases

A

○ Pt breathes close to functional residual capacity
○ Worsen SOB
○ Increase O2 demand
○ Fatigue results

102
Q

Clinical manifestations: cough becomes less effective

A

○ Due to air trapping and inspiration occurring at higher residual lung volume
○ Worsens hypoxemia
○ Retain CO2
○ Resp acidosis will result if obstruction persists

103
Q

Clinical manifestations: resp failure ensues

A

● During full remission asthmatic patients are asymptomatic in pulmonary function tests are usually normal

104
Q

Signs; objective and reported by HCP

A 
●	Physical assessment
●	Lab findings
●	Radiology
●	Pulmonary function tests
●	Peak flow monitoring
105
Q

Symptoms: subjective and reported by patient

A 
●	SOB
○	Inability to adequately ventilate
○	Abnormal ventilation-perfusion relationship
●	Chest tightness
○	Air trapping 
○	Result from hyperinflation of lungs
●	Cough
○	Pt tries to clear airway of mucus
●	Noisy breathing or wheezing
○	Passing of air through narrowed airways
106
Q

Physical Assessment Findings: Inspection

A 
●	Increased work of breathing
●	Use of accessory muscles
●	Prolonged expiration
●	Wheezing
●	Cough
●	Inability to maintain a conversation
107
Q

Physical assessment findings: Auscultation

A 
●	Wheezing
●	Distant or quiet breath sounds
○	Mean that air is not moving
●	Adventitious breath sounds
○	Crackles
○	May be related to infection
108
Q

Physical Assessment Findings: Vital Signs

A

● Tachypnea
● Tachycardia
● Decreased oxygen saturations
○ Hypoxemia

109
Q

Physical Assessment Findings: Tachycardia

A

● May be result of stress, anxiety, and use of ventolin

110
Q

Lab Values

A

***most important result in asthma is arterial blood gas
● Provides information about ventilation
● Givens the pCO2 and pO2 values

111
Q

Hyperventilation will cause

A

respiratory alkalosis

● May be accompanied with hypoxemia or low pO2 during an attack

112
Q

Persistent worsening of ventilation and ventilation-perfusion mismatch cause

A

respiratory acidosis

● This is result of hypercapnia or retention of CO2

113
Q

Acid Base Imbalances and Hypoxemia → address with O2 admin and pharm therapy

A

● Open airways and improve ventilation

● Mechanical ventilation and critical care management is required for severe acidosis and hypoxemia

114
Q

Normal Values

A

pH → 7.35-7.45
pCO2 → 35-45
HCO3 → 22-26
pO2 → 80-100

115
Q

Chest X-Ray

A

● Common to be done as a part of the work-up for patient in resp distress
● Hyperinflation flattening of hemidiaphragms are common radiological findings on chest x-ray
● May provide info on whether or not there is a resp infection
Bacterial infection suspected or confirmed = antibiotics used

116
Q

Viral infection suspected or confirmed

A

DO NOT use antibiotics

117
Q

Which is a more common trigger for asthma: bacteria or viral

A

• A viral respiratory infection is a more common trigger than a bacterial respiratory infection

118
Q

Pulmonary Function Tests

A 
●	Use spirometry
●	Used in initial diagnosis of asthma
●	Monitor the ongoing response to therapy
●	Assess airway function
●	Validate peak flow monitoring
119
Q

Spriometry offers??

A

the single most objective measurement of lung function available

120
Q

Bronchial provocation tests use:

A 
●	Histamine
●	Methacholine
○	Cholinergic agonist
○	Acts on PNS
○	Causes bronchoconstriction
●	Or exposure to non-pharm agent (cold air)
121
Q

Airway obstruction is assessed following bronchial provocation using baseline and post B-agonist measurements of:

A

● Forced vital capacity → FVC
● Forced expiratory volume in 1 second → FEV 1
● Ratio of forced expiratory volume in 1 sec and forced vital capacity → FEV1/FVC
● Forced expiratory volume 25-75% → FEV 25-75%

122
Q

Reversible airway obstruction is confirmed when

A

post challenge data shows 12% or greater improvement

123
Q

PEF can be used to

A

to validate peak flow monitoring results if value is multiplied by 60

124
Q

Peak Flow Monitoring

A

● Measure the peak expiratory flow
● Measure how quickly a person can exhale
● Done at home using a handheld device comparing the result to the patient’s personal best
● Should be measure around the same time each day
● Best of three readings should be recorded

125
Q

PEF greater than 80% of personal best indicates that the person is in the

A

green zone

● Asthma is well controlled

126
Q

PEF btw 50-80% of personal best indicates the person is in the

A

yellow zone
● Caution should be taken
● Person should use their short acting bronchodilator
● Repeat PEF measurement
● Patient should contact their HCP if they do not return to green

127
Q

PEF less than 50% of personal best indicates

A

medical alert and red zone
● Person should take their short acting bronchodilator
○ Increase if needed
● Should seek medical attention

128
Q

Pharm Therapy

Long Term Control Medications or Controllers

A

● Address inflammation and airway obstruction

129
Q

Quick Relief Medications

A

● Reverse acute airflow obstruction

130
Q

T/F: all medications are given inhally

A

true; except for monoclonal antibody is given subq

131
Q

Quick relief meds: beta 2 agonists

A

● Result in bronchodilation
● Act on beta 2 pulmonary receptors increasing levels of cAMP
● Relax smooth muscle
● They can affect beta 1 receptors in heart causing tachycardia
● Preferred quick relief medications

132
Q

Quick Relief Medications;Anticholinergics

A

● Inhibit muscarinic cholinergic receptors
● Reduce vagal tone of airways
● Result in bronchodilation
● Add on therapy with others

133
Q

Quick Relief Medications: Systemic Corticosteroids

A

● Used in severe asthma exacerbations

134
Q

Long-term Control Medications: Long-term Control Medications

A

● Block COX and lipoxygenase paths in inflammation
● Decrease inflammation by suppression of polymorphonuclear leukocytes and fibroblasts
● Reduce capillary permeability
● LABA’s and SABA’s

135
Q

What are the medications of choice?

A

***SABA and LABA are the medication choice for all individuals with persistent asthma

136
Q

Long term control medications: leukotriene modifiers

A

● Interfere with leukotriene action

137
Q

Long-term Control Medications: Mast Cell Stabilizers

A

● Stabilize membrane of sensitized mast cell after antigen IgE interaction
● Prevent release of inflammatory mediators such as histamine

138
Q

Long-term Control Medications: Monoclonal antibody

A

● Subcut injection

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

139
Q

Patient teaching:

A

● Avoid triggers; Recognize signs of impending asthma attack
● Participate in development of written action plan for med titration and symptom management
● Use peak flow monitoring
● Take medication as prescribed; Use proper inhaler technique

PATHOPHYSIOLOGY (9 decks)

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