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NURS 1650 - Here We Go Again > Pathophysiology of Asthma and COPD > Flashcards

Pathophysiology of Asthma and COPD Flashcards

1
Q

Obstructive vs. Restrictive Lung Disease

A

Obstructive:
- Increased resistance to airflow
- Asthma, emphysema, bronchitis

Restrictive:
- Decreased expansion of the lungs due to alterations in the lung tissue, pleura, chest wall or neuromuscular function
- Pneumothorax, pneumonia, TB

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2
Q

What characteristics define asthma?

A

Chronic obstructive lung disease

  • Airway inflammation
  • Reversible airway obstruction
  • Airway hyperresponsiveness
  • Airway remodeling over time
  • Episodic with acute exacerbations and symptom-free periods
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3
Q

Describe the pathogenesis of asthma:

A

Initiation: combo of genetics and environment, with symptoms, often beginning in childhood

Damage to lower airways due to inhaled agents stimulates abnormal immune responses in susceptible individuals

Recurrent episodes and aberrant repair lead to the sustained presence of inflammatory cells and mediators, airway remodeling, and airway hyperresponsiveness

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4
Q

Describe how the gut microbiota can be a risk factor for asthma

A

Gut microbiota trains the immune system to recognize pathogen vs. “friendly” bacteria

Dysbiosis is implicated in the dev. of allergies and asthma (skewing helper T cells toward increased type 2 TH cells)

Allergy has been associated with decreased gut microbiota diversity

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5
Q

What is atopy?

A

Predisposition toward developing allergic hypersensitivity

Typically associated with heightened immune responses to common allergens

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6
Q

What are some possible triggers in non-allergic asthma?

A

Cold air

Viral or bacterial infection

Exercise

GERD

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7
Q

What are some common atopy asthma triggers?

A

Pollen

Mold

Dust mites

Cigarette smoke

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8
Q

What kind of antibodies mediates allergic reactions?

A

IgE antibodies

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9
Q

What key cellular components promote airway remodeling?

A

Goblet cell hyperplasia

Smooth muscle hypertrophy and hyperplasia

Subepithelial fibrosis/stiffening of airway

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10
Q

What role do eosinophils have in an asthma attack?

A

They play a prominent role in the late phase of an asthma attack

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11
Q

Describe the role of these mediators in the early phase of bronchoconstriction, edema, mucosal thickening, and secretions:

ACh, histamine, leukotrienes, lipoxins, adenosine

A

ACh: bronchoconstrictor

Histamine: bronchoconstriction, vascular permeability, leakiness (edema), and increases mucus viscosity

Leukotrienes: bronchoconstriction, increased vascular permeability, increased mucus secretion, eosinophil recruitment

Lipoxins: anti-inflammatory DECREASED in asthma

Adenosine: AMP can cause bronchoconstriction in asthma and COPD patients

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12
Q

Describe the role of these mediators in the late phase of an asthma attack:

Eosinophil chemotactic factor, eotaxins, eosinophil major basic protein, ROS, interleukins, eosinophils

A

Eosinophil chemotactic factor: attracts additional eosinophils to the region of inflammation

Eotaxins: attracts eosinophils, mast cells

Eosinophil major basic protein: cause additional tissue damage

ROS: cause tissue damage

Interleukins: promote eosinophil survival activity (ex. IL-5)

Eosinophils: release numerous inflammatory mediators

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13
Q

Describe the airway remodeling that occurs in asthma and what causes it:

A

Bronchial smooth muscle hypertrophy and hyperplasia

Goblet cell (mucus-producing) hyperplasia, hypersecretion (thicker)

Subendothelial mucous gland hypertrophy: mucus plugs; partial or total occlusion of lumen, mucus in the airway lumen

Deposition of collagen and fibrocytes in epithelial basement membrane –> thickening and stiffening

Loss of ciliated epithelial cells –> more exposure of the airway to allergens, toxins, microbes

Increased number & size of blood vessels in bronchial tissue, tend to be leaky –> edema of airways

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14
Q

What can decrease the airway radius in asthma?

A

Bronchoconstriction

Mucus production

Inflamed thickened airway wall

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15
Q

What does increased airway resistance in asthma lead to?

A

Accumulation of air behind closed airways –> air trapping and lung hyperinflation

In severe cases, no gas exchange can occur –> hypoxia

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16
Q

Is inspiration or expiration more difficult for patients with asthma? Why?

A

Expiration

The closing tendency of the airways is greatly increased during expiration

Because the bronchioles of the asthmatic lungs are already narrowed, further narrowing during expiration creates more obstruction –> air trapping

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17
Q

Sympathetic B2 adrenergic receptor activation results in:

A

Bronchodilation

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18
Q

Parasympathetic M3 cholinergic receptor activation results in:

A

Bronchoconstriction

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19
Q

What causes the symptoms of an asthma attack?

A

Airway narrowing due to bronchospasm (sudden constriction)

Edema/swelling

Increased mucus production

Increased mucus thickening

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20
Q

What are the clinical manifestations of an asthma attack?

A

Cough, wheeze, SOB

Sensation of chest tightness

Anxiety, tachycardia, palpitations

Tachypnea, cyanosis, use of accessory muscles

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21
Q

What is status asthmaticus?

A

An acute exacerbation of asthma that remains unresponsive to initial treatment with bronchodilators

Wheezing may disappear as airways constrict more and more

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22
Q

Intermittent vs. Persistent Asthma

A

Intermittent
- Less than 2
- No interference with daily activities
- FEV1 > 80%
- 0-1 exacerbations per year

Persistent:
- More than 2
- Any interference with daily activities
- FEV1< 80%
- 2 or more per year

23
Q

What is well-controlled asthma?

A

Rule of 2s

All must be met for asthma to be considered well-controlled

24
Q

What is a peak flow meter? What is it used for?

A

Meter used by asthma patients to compare their peak flow to their personal best and keep track of their asthma

25
What is a spirometer/spirometry?
Measures how fast and how much air you breathe out
26
What is body plethysmography?
Used to measure residual volume (RV), total lung capacity (TLC) and any other lung volume that incorporates RV
27
PFT Healthy People vs. People with Asthma
Asthma: Decreased FVC, FEV1 Increased RV (air trapping), TLC (hyperinflation)
28
What is COPD?
Chronic Obstructive Pulmonary Disease a common preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases
29
What are the most common respiratory symptoms of COPD?
Dyspnea **Cardinal symptom*** Cough and/or sputum production
30
What are the different "types" of COPD? Describe them
Chronic Bronchitis: cough and sputum for at least 3 months in at least 2 consecutive years Emphysema: abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, accompanies by the destruction of their walls and without obvious fibrosis
31
Why do females have higher rates of COPD than males?
Smaller lungs --> higher concentrations of cigarette toxins Role of estrogen in metabolism and inhibition of excretion of toxins
32
Describe how alpha-1 antitrypsin (AAT) deficiency is a risk factor for COPD
Normal function: inhibit the proteolytic breakdown of alveolar tissue, especially by inhibiting neutrophil elastase produced by pulmonary neutrophils in the presence of inflammation Deficiency: neutrophil elastase and macrophage proteases function unchecked --> destruction of alveolar walls and dev. of emphysema
33
What can the most severe form of AAT deficiency lead to?
Liver disease
34
Describe mucus production in chronic bronchitis
Increased mucus production 2/2 hyperplasia of goblet cells and hypertrophy of bronchial mucous glands
35
How is the consistency of mucus different in bronchitis?
Mucus is thicker and more tenacious than normal Lead to mucus plugging of airway
36
How can chronic infection result from chronic bronchitis?
Bacteria become embedded in the airway secretions leading to chronic infection
37
How is cilia affected in chronic bronchitis?
Cilia function is impaired --> decreased mucociliary clearance Fewer cilia // remaining cilia is less able to function
38
How does the airway narrow in chronic bronchitis?
Edema and accumulation of inflammatory cells lead to bronchial wall inflammation and thickening --> narrowing of the airway lumen
39
Why does air become trapped in chronic bronchitis? What does this result in?
Airway wall enlargement, loss of elastic recoil in the alveoli trap air Limits outflow Obstructed airways are likely to close on expiration
40
What does air trapping result in?
Hypoventilation --> hypercapnia (more CO2 in blood // hypoventilation does not allow CO2 to be expired) Ventilation/perfusion mismatching Hypoxemia (decreased oxygen in blood)
41
What do elastase and other proteases do? (emphysema)
Released by neutrophils and macrophages --> cause alveolar wall destruction and breakdown of elastic tissue Alveoli become untethered from the bronchiole wall
42
What happens to the alveolar wall, airways, and gas exchange in emphysema?
Alveolar wall destruction due to elastase and proteases (and AAT deficiency or inactivation due to smoking) Narrowing and collapse of the small airways --> increased airway resistance --> more likely to close on expiration reduction of pulmonary capillary bed necessary for gas exchange alveolar enlargement and loss of elastic recoil combine to trap air and cause lung hyperinflation
43
What happens to the lungs and alveoli in patients with emphysema?
They become enlarged
44
Chronic bronchitis vs. Emphysema: Defining Features
Chronic Bronchitis: - Mucus build-up - Inflamed airway Emphysema: - Collapsed airways - Damaged air sacs - Damaged blood vessels
45
How does smoking lead to COPD?
Smoking inactivates AAT, even in the absence of the genetic deficiency AAT then cannot inhibit elastase/protease damage to the alveolar wall
46
What is needed to diagnose COPD?
Patient has dyspnea, chronic cough, or sputum production A history of exposure to risk factors for the disease Spirometry is REQUIRED: FEV1/FVC of < 0.70
47
Signs and Symptoms of COPD
- SOB, DOE - Fatigue, exercise intolerance - Wheezing - Cough - Cyanosis (late stage) - Decreased FEV, increased TLC
48
Chronic Bronchitis Clinical Presentation Picture Summary:
- Excess body fluids (edema plethora) - Chronic cough - SOB upon exertion - Increased sputum - Cyanosis (late sign)
49
Emphysema Clinical Presentation Picture Summary:
- Use of accessory muscles to breathe - Pursed-lip breathing - Minimal or absent cough - Leaning forward to breathe - Barrel chest - Digital clubbing - Dyspnea on exertion (late sign)
50
Why does barrel chest occur in patients with emphysema?
Hyperinflation of the lungs Loss of lung elasticity (bc elastase) --> chest wall recoils to a position closer to the total lung capacity position
51
Describe how pursed-lip breathing is used in emphysema
Helps maintain higher end-expiratory pressure in the airways Slows exhalation, reduces pressure drop in the airway walls, reduces airway collapse, allows more air to flow out
52
What is a COPD exacerbation? What causes them?
An acute worsening of respiratory symptoms that results in additional therapy Increased airway inflammation, increased mucus production, and marked gas trapping --> increased dyspnea The most common causes are viral upper respiratory tract infections (even the common cold!!)
53
Asthma vs. COPD: Onset, Symptoms, Causes, Airflow limitation, Exacerbations
Onset: Asthma- young age COPD - middle-to-older age Symptoms: Asthma - intermittent, may vary from day to day COPD- Progressive, not much day to day variation Causes: Asthma - Allergic and non-allergic COPD - Years of smoking Airflow limitation: Asthma - Reversible with bronchodilator COPD - Irreversible or partially reversible Exacerbations: Asthma - Yes, but not well-defined COPD - Yes, better-defined

NURS 1650 - Here We Go Again (20 decks)

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