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3.24 > Lecture 6: The pathology of COPD > Flashcards

Lecture 6: The pathology of COPD Flashcards

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
Q

What are the effects of emphysema?

A
  • Dyspnea
  • Increased CO2 retention
  • Pink complexion (hyperventilation)
  • Minima cyanosis
  • Pursed lips breathing
  • Barrel chest
  • Thin (due to loss of appetite, muscle wasting)
26
Q

What are the effects of chronic bronchitis?

A
  • Recurrent productive cough
  • Hypoxic/hypercapnia
  • Cyanotic (blue!)
  • Increased respiratory rate
  • Ronchi (rattling) and wheezing
  • Cardiac enlargement
27
Q

How is COPD diagnosed?

A

Spirometry

28
Q

What is the expiratory airflow limitation?

A

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
Q

What is gold 1?

A
  • Mild COPD
  • FEV1 >80%
30
Q

What is gold 2?

A
  • Moderate CODP
  • 50< FEV1
31
Q

What is gold 3?

A
  • Severe COPD
  • 30%< FEV1
32
Q

What is gold 4?

A
  • Very severe COPD
  • FEV1 <30%
33
Q

What is BODE index?

A

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
Q

How is the degree of airflow obstruction assessed?

A

Assessed by the Forced Expiratory Volume in one second (FEV1),

35
Q

Why is COPD diagnosed at a stage when pathological changes are irreverible?

A
  • lack of predictive biomarkers,
  • under-recognised clinical symptoms,
  • long latency period with no or minimal symptoms
  • reliance on spirometry, an insensitive diagnostic tool.
36
Q

Why is COPD diagnosed at a stage when pathological changes are irreverible?

A
  • lack of predictive biomarkers,
  • under-recognised clinical symptoms,
  • long latency period with no or minimal symptoms
  • reliance on spirometry, an insensitive diagnostic tool.
37
Q

What are the risk factors for COPD?

A
  • 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
Q

What would greatly reduce the burden of COPD?

A
  • prohibiting all kinds of smoking
  • eliminating exposure to any form of air pollution
39
Q

Describe COPD histopathology

A
  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
Q

What is Alpha-1 anti-trypsin (α1-AT) ?

A

A protease inhibitor

41
Q

What does Alpha-1 anti-trypsin (α1-AT) do?

A

Balances the activity of Elastin and other destructive enzyme proteases produced during an infection/immune challenge

42
Q

What is crucial to alveolar homeostasis?

A

Protease:antiprotease balance

43
Q

What does pathogenic mutation cause?

A

Cause α1-AT to self-associate into polymer chains

44
Q

What abolishes antiprotease activity?

A

Polymerisation of α1-AT

45
Q

What gives higher possibility of emphysema?

A

Deletion

46
Q

What is alveolar and interstitial tissue destruction is driven by?

A

Excessive proteolysis.

3.24 (28 decks)

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