Lecture 6: The pathology of COPD Flashcards

(46 cards)

1
Q

What is Chronic Obstructive Pulmonary Disease (COPD)?

A

A chronic slowly progressive disorder characterized by airflow obstruction

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2
Q

How is COPD diagnosed?

A

Reduced FEV1 and FEV1/VC ratio

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3
Q

What is the pathophysiology of COPD?

A

Implicates varying degrees of airway remodelling, inflammation, and tissue destruction.

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4
Q

How does COPD affect large airways (trachea, bronchi) ?

A

Glandular hypertrophy, reduced number of cilia so increased cough with or without sputum.

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5
Q

How does COPD affect small airways (bronchioles)?

A

Goblet cell metaplasia; smooth muscle hypertrophy; fibrosis and scar tissue this increases mucus production, increased expiratory flow resistance.

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6
Q

How does COPD affect alveoli?

A

Loss of alveolar fine structure - Loss of lung recoil – this is important to push air out of the lungs, reduced gas exchange because of reduced surface area

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7
Q

What are the structural changes of COPD?

A
  • Remodelling of the upper airways
  • Dysanapsis: disproportionate scaling of airway dimensions to lung volume or a mismatch of airway tree caliber to lung size.
  • Inflammation and mucus hypersecretion
  • Ventilation heterogeneity
  • Loss of alveolar attatchment
  • Alveoli with emphysema
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8
Q

What are the clinical symptoms of COPD?

A
  • Symptoms include cough, sputum, dyspnea (shortness of breath), and wheeze.
  • Patients who have chronic cough and sputum production with a history of exposure to risk factors should be tested for airflow limitation, even if they do not have dyspnea.
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9
Q

What are the diagnostic features of COPD?

A
  • History of heavy smoking for many years.
  • Cough and sputum production for many years.
  • Cough often present only on waking at first; later cough occurs throughout the day.
  • Sputum usually mucoid – becomes purulent with exacerbation of disease, but not excessive.
  • Cough and sputum often worse in winter due to infection.
  • Insidious onset of breathlessness on exertion with wheezing or tightness of chest
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10
Q

What are the diagnostic features of COPD?

A
  • History of heavy smoking for many years.
  • Cough and sputum production for many years.
  • Cough often present only on waking at first; later cough occurs throughout the day.
  • Sputum usually mucoid – becomes purulent with exacerbation of disease, but not excessive.
  • Cough and sputum often worse in winter due to infection.
  • Insidious onset of breathlessness on exertion with wheezing or tightness of chest
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11
Q

What are the two clinical phenotypes of COPD?

A
  • Emphysema
  • Chronic bronchitis
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12
Q

What is the clinical diagnosis of chronic bronchitis?

A

Daily productive cough for three months or more, in at least two consecutive years

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13
Q

What are the signs of chronic bronchitis?

A
  • overweight and cyanotic
  • Elevated hemoglobin
  • Peripheral edema
  • Rhonchi and wheezing
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14
Q

What is the pathologic diagnosis of emphysema?

A

Permanent enlargement and destruction of airspaces distal to the terminal bronchiole

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15
Q

What are the sings of emphysema?

A
  • Older and thin
  • severe dyspnea
  • Quiet chest
  • Xray, hyperinflation with flattened diaphragsm
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16
Q

What are the three types of chronic bronchitis?

A
  1. Simple mucoid bronchitis
  2. Mucopurulent (pus) bronchitis
  3. Chronic obstructive bronchitis
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17
Q

What are the clinical manifestations of chronic bronchitis?

A
  • Excessive mucus production
  • Leading to Bronchospasm, dyspnea and wheezing
  • Hypoxia and hypercapnia (Blue in color)-elevated CO2
  • Productive cough
  • Increase body weight
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18
Q

What are the complications of chronic bronchitis?

A

Cor-pulmonale

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19
Q

What is cor-pulmonale

A

Also known as right sided heart failure, is an enlargement of the right ventricle due to high blood pressure in the lungs usually caused by chronic lung disease

20
Q

What is the clinical definition of chronic bronchitis?

A

Clinically defined as persistent productive cough for at least three consecutive months in at least two consecutive years.

21
Q

What is emphysema?

A

An abnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by destruction of their walls.

22
Q

What does emphysema cause?

A
  • loss of intricate alveolar architecture
  • progressive simplification of small and highly effective gas-exchanging units into large, inefficient cyst-like spaces.
  • loss of alveolar gas-exchanging units and the capillary bed so blood oxygen levels eventually fall and pressures within the pulmonary circulation rise
23
Q

What is the effect of emphysema?

A
  • Alveolar enlargement leads to progressively larger lungs that are fixed within an anatomically constrained chest cavity, limiting ventilation.
  • Severe difficulty breathing
  • Chronic respiratory failure, evidenced by low blood oxygen levels (hypoxemia), elevated levels of carbon dioxide (hypercapnia, hypercarbia, chronic respiratory acidosis)
  • Eventually death
24
Q

Describe the airways of obstructive chronic bronchitis

A
  • Thick, sticky mucous blocks up the airways rather than clears
  • Inflammation and swelling further narrows airways
25
What are the effects of emphysema?
- Dyspnea - Increased CO2 retention - Pink complexion (hyperventilation) - Minima cyanosis - Pursed lips breathing - Barrel chest - Thin (due to loss of appetite, muscle wasting)
26
What are the effects of chronic bronchitis?
- Recurrent productive cough - Hypoxic/hypercapnia - Cyanotic (blue!) - Increased respiratory rate - Ronchi (rattling) and wheezing - Cardiac enlargement
27
How is COPD diagnosed?
Spirometry
28
What is the expiratory airflow limitation?
Defined by a ratio of the forced expiratory volume in 1 s (FEV1) to the forced vital capacity (FVC) of less than 0.7
29
What is gold 1?
- Mild COPD - FEV1 >80%
30
What is gold 2?
- Moderate CODP - 50< FEV1
31
What is gold 3?
- Severe COPD - 30%< FEV1
32
What is gold 4?
- Very severe COPD - FEV1 <30%
33
What is BODE index?
Multidimensional index of disease severity in COPD that incorporates four independent predictors: BMI, degree of airflow obstrcution, dyspnea scale, exercise capacity assessed by the 6-min walking distance (6MWD) test.
34
How is the degree of airflow obstruction assessed?
Assessed by the Forced Expiratory Volume in one second (FEV1),
35
Why is COPD diagnosed at a stage when pathological changes are irreverible?
- lack of predictive biomarkers, - under-recognised clinical symptoms, - long latency period with no or minimal symptoms - reliance on spirometry, an insensitive diagnostic tool.
36
Why is COPD diagnosed at a stage when pathological changes are irreverible?
- lack of predictive biomarkers, - under-recognised clinical symptoms, - long latency period with no or minimal symptoms - reliance on spirometry, an insensitive diagnostic tool.
37
What are the risk factors for COPD?
- Genetics (alpha 1 atiitrypsin deficiency) - Occupational dust and chemicals - Indoor smoke from wood, coal, cow dungs, crop residues used for cooking - Frequent lung infections as a child - Smoking, passive smoking and smoke from crckers
38
What would greatly reduce the burden of COPD?
- prohibiting all kinds of smoking - eliminating exposure to any form of air pollution
39
Describe COPD histopathology
1. Cellular bronchiolitis - a narrowed and contracted airway is infiltrated by numerous inflammatory cells without a specific patterm 2. Loss of alveolar structure 3. Subepithelial fibrosis causes the airway lumen to narrow 4. Excessive mucus plug - the airway lumen is obstructed by mucus exudates
40
What is Alpha-1 anti-trypsin (α1-AT) ?
A protease inhibitor
41
What does Alpha-1 anti-trypsin (α1-AT) do?
Balances the activity of Elastin and other destructive enzyme proteases produced during an infection/immune challenge
42
What is crucial to alveolar homeostasis?
Protease:antiprotease balance
43
What does pathogenic mutation cause?
Cause α1-AT to self-associate into polymer chains
44
What abolishes antiprotease activity?
Polymerisation of α1-AT
45
What gives higher possibility of emphysema?
Deletion
46
What is alveolar and interstitial tissue destruction is driven by?
Excessive proteolysis.