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Pathophysiology Exam 2 > Alterations in Pulmonary Function > Flashcards

Alterations in Pulmonary Function Flashcards

1
Q

Increased resistance to expired airflow due to reduction in caliber of airways

A

Obstructive Lung Disease

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2
Q

Obstructive lung disease caused by airway lumen

A

asthma, chronic bronchitis

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3
Q

Obstructive Lung Disease caused by airway wall

A

Asthma, Chronic Bronchitis

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4
Q

Obstructive Lung Disease caused by supporting structures surrounding the airway being damaged

A

emphysema

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5
Q

a disease of airway inflammation and variable airflow obstruction characterized by intermittent symptoms of wheezing, chest tightness, dyspnea, cough and bronchial hyperresponsiveness

A

asthma

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6
Q

Release of mediators due to response to allergen can cause what 3 things?

A

Alter airway smooth muscle tone and responsiveness
Induce mucus hypersecretion
Damage airway epithelium

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7
Q

Strongest identifiable predisposing factor for development of asthma is

A

Atopy

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8
Q

Atopy is the production of___antibodies in response to allergen exposure

A

IgE

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9
Q

What is the Atopic Triad

A

Asthma
Atopic Dermatitis
Allergic rhinitis

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10
Q

Samter’s Triad

A

Asthma
Nasal Polyps (sinusitis)
Aspirin Sensitivity

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11
Q

Why are BB a risk factor for asthma?

A

Many BB are nonselective… they can bind to B2 and cause bronchoconstriction

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12
Q

CELLS function as antigen-presenting cells that phagocytize foreign invaders

A

Dendritic

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13
Q

Once the dendritic cell engulfs the antigen, what is expressed on cell membrane

A

Antigen and MHC2 for Helper Tcell to recognize

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14
Q

essential to adaptive immunity as they activate B cells to secrete antibodies.

A

Helper T cells

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15
Q

Helper T cell are CD4 positive cells responsible for activation of __ cells and _______ T cells

A

Bcells
Cytotoxic T cells

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16
Q

Y-shaped proteins produced by B cells to identify and neutralize antigens in the body in mediating allergic reactions

A

IgE antibodies

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17
Q

white blood cells found in the connective tissues all over the body containing granules rich in histamine and leukotrienes

A

Mast Cells

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18
Q

What act on mast cells to cause them to undergo degranulation

A

IgE antibodies

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19
Q

white blood cells that play a significant role in the immune response to allergens and parasitic infections.

A

Eosinophils

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20
Q

What do Eosinophils release?

A

leukotrienes, cytokines, proteases

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21
Q

the release of leukotrienes and cytokines result in what response

A

proinflammatory

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22
Q

Release of proteases can do what?

A

directly damage airway epithelial cells resulting in chronic airway remodeling and hyperresposiveness over time.

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23
Q

Stages of Immune System Response to Allergens

A
  1. Allergens invades host
  2. Dendritic cell phagocytizes allergens
  3. expresses allergen antigen and MHC 2 complex
  4. Recognized by Helper T cell (CD4+) producing IL-4 and IL-5
  5. IL-4 stimulates production of IgE antibodies
  6. IgE antibodies stimulate degranulation of mast cells
  7. production of leukotrienes and histamines
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24
Q

IL-5 activates Eosinophils which causes the release of what 3 things

A

leukotrienes, cytokines, proteases

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25
Q

which proinflammatory Contracts airway smooth muscle, increase mucus secretion, activate inflammatory cells in airways

A

Leukotrienes

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26
Q

which proinflammatory is Involved in development of atopic state and chronic inflammatory process of asthma

A

Cytokines

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27
Q

which pro inflammatory causes Epithelial damage to airway tissue

A

Proteases

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28
Q

What are the histophologic features of asthma that reflect the disease

A
  1. Airway mucosa thickened, edematous, infiltrated with inflammatory cells
  2. Hypertrophied and contracted airway smooth muscle
  3. Bronchial and bronchiolar epithelial cell damage
  4. secretory gland hyperplasia and mucus hypersecretion
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29
Q

In asthma, airway inflammation, mucus hypersecretion, and smooth muscle hyperresponsiveness leading to bronchoconstriction results in what change to airway resistance?

A

Increased airway resistance

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30
Q

In asthma, is airway obstruction diffuse or not diffuse throughout the lungs?

A

diffuse

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31
Q

In asthma, is airway obstruction homogenous or not homogenous throughout the lungs?

A

not homogenous

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32
Q

what does airway obstruction to the lungs being diffuse but not homogenous result in?

A

nonuniformity of ventilation

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33
Q

In asthma, you can have abnormally low V/Q ratio or high V/Q ratio. Why is this?

A

A high V/Q is a result of a lot of ventilation (alveoli are getting big, compressing the vessels) but no perfusion (air trapping).

A low V/Q ratio is a result from low ventilation due to mucous covering the alveoli, but adequate perfusion where mucous is not. This results in HYPOXEMIA

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34
Q

What is an ominous sign during a severe asthma attack?

A

Hypercapnia

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35
Q

What are the Clinical manifestations of Asthma?

A

Dyspnea and chest tightness
Wheezing
Cough
Tachypnea and Tachycardia
Pulsus paradoxus
Hypoxemia
Hypercapnia and Respiratory Acidosis

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36
Q

Why does dyspnea and chest tightness happen asthma?

A

there is greater muscular effort to overcomve the increase airway resistance

hyperinflation from the airway obstruction leads to thoracic distension

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37
Q

Worsening obstruction leads to V/Q mismatching which leads to what?

A

Hypoxemia

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38
Q

What happens to lung compliance in patients with asthma?

A

it decreases due to thickening of the airway and increase work of breathing

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39
Q

What causes asthmatic patients to wheeze

A

the short: prolonged turbulent airflow

Smooth muscle contraction and mucus hypersecretion leads to reduced airway caliber

40
Q

Why do you see Cough in asthmatic patients?

A

Airway narrowing, mucus hypersecretion and neural hyperresponsiveness caused from airway inflammation

41
Q

When do you see Tachypnea and Tachycardia and why?

A

Always seen in acute exacerbations

Theyre not getting enough oxygen… the hypoxemia results in the heart trying to compensate by increasing blood flow to try and get oxygen around to the muscles as much as possible

42
Q

What is pulsus paradoxus a result from and why does it occur in asthmatics

A

Consequence of lung hyperinflation

Compromised left ventricular filling and decreased output during inspiration (lowering systolic pressure during inspiration)

43
Q

Why do we see hypoxemia in asthmatics

A

Airway narrowing reduces ventilation to affected lung units
V/Q mismatch with low V/Q ratio

44
Q

When and why would we see hypercapnia and respiratory acidosis

A

Worsening airway obstruction and respiratory muscle fatigue during severe asthma attack –> alveolar hypoventilation causing increased pCO2 and decreased blood pH

45
Q

What would you see on chest xray of asthma?

A

hyperinflation

46
Q

in an asthmatic exaccerbation, what happens to FEV1 and FEV1/FVC ration

A

reduction

47
Q

what do you give asthmatics to reverse exacerbation?

A

bronchodilators

48
Q

a 12% or greater increase in the FEV1 in response to an inhaled bronchodilator
or
a 20% or greater decrease in FEV1 in response to a provoking factor that, at the same concentration, causes less than a 5% change in a healthy individual
is defined as what?

A

bronchial hyperresponsiveness

49
Q

What is the major cause of global morbidity and mortality and the 3rd leading cause of death worldwide?

A

COPD

50
Q

is mortality in COPD higher in men or women and does it increase with age?

A

Men
Increases with age

51
Q

Where do we see highest prevalence of COPD in the U.S. and why do you think that is?

A

South because of the exposure to irritants (smoke, farms) and due to increase comorbidities and less access to healthcare

52
Q

What 2 diseases is COPD broken down into?

A

Emphysema and Bronchitis

53
Q

What are the risk factors of COPD and which one is the most common worldwide?

A

Cigarette smoking (most common)
Chronic Dust
Air Pollutants
Genetics (alpha-1 antitrypsin) especially for emphysema

54
Q

What is the definition of chronic bronchitis?

A

Defined by a clinical history of productive cough for at least 3 months of the year for 2 consecutive years

55
Q

In chronic bronchitis, dyspnea and airway obstruction are ___________ present

A

continuously

56
Q

Where does chronic bronchitis mainly impact?

A

the airways

57
Q

in chronic bronchitis, Inflammation of the larger airways  mucosal thickening  mucosal hypersecretion cause what?

A

productive cough
airflow obstruction

58
Q

Layers of the airway lining?

A

Innermost: simple columnar to cuboidal epithelium

surrounded by submucosal layer with attachment to mucosal glands producing mucous to humidify airway and trap pathogens

59
Q

Where are goblet cells found and what is their function?

A

found throughout the epithelium of conducting tissues with apical surface protruding into airway lumen

Function to produce mucus for a rapid response to inhaled airway insults

60
Q

What does ciliated epithelium do and where is it found

A

Found lining respiratory tract down to respiratory bronchiole
Cilia are essential to propelling mucus up and out of the airway to keep airway clear

61
Q

Pathophysiology pathway of Chronic Bronchitis due to tobacco smoke

A
  1. Inhale an Irritant
  2. increased production from mucosal glands and goblet cells resulting in hypersecretion
  3. Hypertrophy and hyperplasia of mucosal glands and goblet cells
  4. mucus plugging and obstructed airway
62
Q

What happens pathophysiology wise once mucus plugging occurs and airway is obstructed

A
  1. narrowing of airways (especially with exhalation)
  2. inability to bring air in and inability to move air out
  3. air trapping and low V/Q ratios
  4. results in Hypoxemia and Hypercapnia
63
Q

Clinical Manifestations of Chronic Bronchitis

A

Cough with sputum production
wheezing
inspiratory and expiratory ronchi
tachycardia
possible pulmonary HTN due to chronic hypoxemia

64
Q

in chronic bronchitis, sputum is purulent and thick. Why is this? Is the cough productive or less productive?

A

lysed cells from inflammatory process and increased inflammation resulting in mucosal injury. This cause fluid to sit and thicken, making the cough less productive.

65
Q

In chronic bronchitis, why is wheezing present

A

Persistent airway narrowing and mucus obstruction produce localized or diffuse wheezing

66
Q

Can wheezing be reversed? if so how?

A

potentially if responsive to bronchodilators

67
Q

Why is there a presence of inspiratory and expiratory ronchi in chronic bronchitis?

A

Increased mucus production and ciliary dysfunction leaves excess secretions in the airways despite increase in coughing

Rhonchi heard prominently in larger airways during tidal breathing

68
Q

What causes tachycardia to be present with chronic bronchitis and when would you expect to see pulmonary HTN?

A

tachycardia is present usually in conjunction with hypoxemia.

with significant and chronic hypoxemia, pulmonary HTN can result

69
Q

What do you think you would hear on cardiac examination if Pulm HTN present?

A
  1. abnormalities with the right side of the heart b/c that is where the pulmonary valve is
  2. increased JVD in the neck due to pulm arteries being constricted
70
Q

What would you expect to see on Chest Plaine Film?

A
  1. increased lung volumes with depressed diaphragm (diaphragm angle is not strong)
  2. Hyperinflamation due to airtrapping
  3. Tram Track lines (parallel linear densities) due to thickened bronchial walls
  4. If pulmonary HTn due to chronic hypoxemia you can see a prominent pulmonary trunk
71
Q

What would you see with PFTs with chronic bronchitis

A

FEV1 reduced
FVC reduced
FEV1/FVC reduced
increased RV and FRC

72
Q

What would you see with ABGs with chronic bronchitis

A
  1. V/Q mismatch with low V/Q ratio due to profound hypoxemia
  2. Increased obstruction increases hypercapnea and can cause respiratory acidosis
73
Q

Polycythemia can result due to chronic hypoxemia in chronic bronchitis. Why is this?

A

Low 02 sat in blood, stimulates EPO to produce and go to bone marrow to increase RBC synthesis

74
Q

why is Pneumonia a common Complication associated with Chronic Bronchitis

A

Increased risk of pneumonia is present due to the stasis of mucus in the lungs.

this is a breeding ground for bacterial colonization especially those bacteria associated wit pneumonia (H.influenza and M. Catarrhalis)

75
Q

Emphysema is marked by _________ enlargement of the airspaces ______ to the terminal bronchioles (small resp. airways) accompanied by destruction of their walls

A

Irreversible enlargement
Distal to the terminal bronchioles

76
Q

What pathologic defect within the walls of the respiratory unit is noted with emphysema

A

Acinus

77
Q

Loss of elastic tissue results in a loss of the recoil tension needed to support distal airways during expiration is what?

A

Acinus

78
Q

Acinus causes ________ dyspnea and ____________ obstruction due to the structural damage _______ mucus hypersecretion or productive cough in emphysema

A

Progressive dyspnea
Nonreversible obstruction
without mucus or cough

79
Q

What is the pathophysiology pathway of Emphysema?

A
  1. Smoke/pollutant particles reach small airways
  2. Alveolar macrophages are activated and phagocytize incoming particles
  3. This causes a release of inflammatory cytokines
  4. there is recruitment and activation of neutrophils
  5. causing the release of the protease ELASTASE
  6. elastase causes the degredation of elastin within the acinar walls
  7. resulting in the reduction of elastin recoil tension
  8. this causes air trapping, loss of alveolar surface tension, and alveolar collapse in expiration
  9. Eventually hypoxia develops overtime with severe disease
80
Q

What is the relationship between Alpha 1 Antitrypsin Deficiency and Emphysema

A

A1A is a protease that inhibits elastase.
So when you have a deficiency in A1A, elastase is able to degradate elastin longer resulting in more structural damage and worsening emphysema

81
Q

What are the 3 physiologic changes in Emphysema

A

Parenchymal damages result in 3 changes
1. destruction of terminal respiratory units
2. loss of alveolar–capillary bed
3. loss of the supporting structures of the lung, including elastin-containing connective tissue

82
Q

What would you see on respiratory examination with Emphysema?

A

Breath sounds diminished (Decreased airflow, prolonged expiration)
Wheezes can be present but of diminished intensity

83
Q

What would you see on cardiac examination with Emphysema?

A

Tachycardia, especially with exacerbations or hypoxemia
Pulmonary HTN  consequence of destruction of alveolar capillaries

84
Q

What would you see with imaging of emphysema

A
  1. Hyperinflation common with flattened hemidiaphragms
  2. Increased AP chest diameter (barrel chest)
  3. Cystic or bullous changes may be seen (destroyed alveolar surface and enlarging acinus)
85
Q

What would you see in ABGs with emphysema

A
  1. High V/Q mismatch ratio due to Alveolar wall and capillary destruction
  2. Increased minute ventilation due to patient compensation of V/Q mismatch
  3. This compensatory mechanism Can maintain nearly normal PO2 and PCO2 early on
  4. Further destruction over time results in Hypercapnia and partially compensated respiratory acidosis with SEVERE DISEASE
86
Q

Restrictive Lung Disease is an interstitiall lung disease aka what

A

diffuse parenchymal lung disease

87
Q

What is Restrictive Lung Disease characterized by?

A

thickened alveolar interstitium resulting in fibrosis and capillary remodeling.

88
Q

What is interstitial pulmonary fibrosis caused by that leads to destruction of normal lung tissue?

A

Progressive Fibrosis

89
Q

Progressive fibrosis in pulmonary fibrosis results in what?

A

Produces a restrictive defect with altered ventilation, vascular alterations and increased work of breathing

90
Q

Is clinical presentation Insidious onset? if so, what are the manifestations?

A

yes, they do not come on suddenly

  1. Dyspnea that has progressed over months to years
  2. Chronic, non-productive cough
91
Q

Is Pulmonary FIbrosis common or uncommon compared to COPD

A

Uncommon

92
Q

What is the pathophysiology pathway of pulmonary fibrosis?

A
  1. Defects in type 2 alveolar cells increase susceptibility to injury
  2. repetitive microinjury to alveolar epithelium followed by failed wound repair
  3. failed wound repair results in profibrogenic mediators secreted and fibroblasts activated
  4. resulting in fibrosis
  5. causing tissue stiffness, decreased lung compliance, reduction in lung volume, and V.Q mismatch
93
Q

Why is there decreased lung compliance in pulmonary fibrosis?

A

lungs are stiffer and more resistant to expansion resulting in the lung compliance curve being shifted down and to the right

work of breathing is increased
and static recoil pressure is increased at TLC

94
Q

Why is FEV1/FVC ratio nearly normal in pulmonary fibrosis

A

The decreased lung compliance causes proportionally decreased lung volumes

95
Q

What are the clinical manifestations of Pulmonary Fibrosis?

A

Intermittent, non-productive cough
Dyspnea and tachypnea
Digital clubbing (no proven link to physiologic change)

96
Q

What would you see on PFTs with pulmonary fibrosis

A

Restrictive ventilatory pattern
Reduction in TLC, FEV1 (not as significant as with obstructive), and FVC
Preserved to Increased FEV1/FVC ratio

Pathophysiology Exam 2 (5 decks)

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