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Cardiorespiratory > Lecture 23: COPD > Flashcards

Lecture 23: COPD Flashcards

1
Q

define COPD

A

A lung disease caused by inflammation of the small airways. Includes chronic bronchitis (characterized by productive cough ≥ 3 months in 2 consecutive years) and emphysema (dilation of the air spaces distal to the terminal bronchioles). Most cases of COPD (~ 90%) are caused by smoking.
• Group of diseases with respiratory symptoms of dyspnoea, cough, sputum production
• Airflow limitation and chronic inflammation of lung

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2
Q

does airflow limitation of COPD is reversible?

A

Its pulmonary component is characterized by airflow limitation that is not fully reversible.

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3
Q

what is the cause of airflow limitation in COPD?

A

The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.

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4
Q

FEV1/FEV is >80 % in COPD.T/F

A

False
COPD is a lung disease characterized by airflow limitation (FEV1/FVC ratio of less than 70%) that is not fully reversible (FEV1 increase of 200 ml and 12% improvement above baseline FEV1 following administration of either inhaled corticosteroids or bronchodilators).

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5
Q

FEV1 increase of 200 ml and 12% improvement above baseline FEV1 following administration of either inhaled corticosteroids or bronchodilators are suggesting of COPD. T/F

A

False

It is suggestive of Asthma (reversible obstruction)

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6
Q

COPD comprises of 2 predominant conditions:…

A

Chronic bronchitis and Emphysema

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7
Q

define chronic bronchitis

A

Chronic Bronchitis is defined as a productive cough for 3 months in each of 2 successive years in a patient whom other causes of chronic sputum has been excluded.

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8
Q

define the emphysema

A

Emphysema is defined as the presence of enlargement of airspaces distal to the terminal bronchioles or acinus with destruction of their walIs without obvious fibrosis.

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9
Q

what is the epidemiology of COPD?

A

• COPD affects >10% of the population of the USA; 200 million people worldwide
• Objective evidence of persisting and irreversible airflow obstruction
• Affects 14% of male smokers versus 3% of non- smokers (i.e smoking is not the only cause of COPD!)
• COPD is the fourth leading cause of death in western world
• The only common cause of death increasing in incidence
–Sex: 3:2 male/female ratio
–The third most common cause of death worldwide
–Prevalence: 6%

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10
Q

at what FEV value symptoms start to occur?

A
  • Accelerated decline in forced expiratory volume in 1 second from the normal rate in adults over 30 years of approximately 30 – 60 ml per year.
  • Initially asymptomatic but lung function is deteriorating
  • Symptoms occur once FEV is < 50% predicted
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11
Q

what are the causes of COPD?

A

• 90% of cases occur in chronic smokers
• 25% of heavy smokers have chronic bronchitis
• Age: high risk
• Environment: urban > rural
– Air pollutants including sulfur dioxide, nitrogen dioxide
• Dusty occupations (coal, quartz, silica, welding)
• Passive smoking
• Low birth weight; chest infections in the first year of life (eg adenovirus)

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12
Q

besides smoking, air pollutants also cause COPD. T/F

A

True

  • -Air pollutants including sulfur dioxide, nitrogen dioxide
  • -Dusty occupations (coal, quartz, silica, welding)
  • -onorganic dust: such as industrial bronchitis in coal miners
  • -Organic dust: ↑ incidence of COPD in areas where biomass fuel (e.g., wood, animal dung) is regularly burned indoors
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13
Q

does passive smoking increase the risk of COPD?

A

Yes
If precautions against smoke exposure not taken, those who live in close proximity to smokers (e.g., children, relatives) have a significantly higher risk of COPD. The risk of asthma progressing to COPD also increases with exposure to smoke.

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14
Q

Low birth weight; chest infections in the first year of life (eg adenovirus) can result in COPD.T/F

A

True

The lower the birth weight, the higher the risk of developing COPD.

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15
Q

what is the main causative factor of COPD?

A

Smoking is the main cause of COPD, but only one in five smokers is affected, so it is likely that a genetic predisposition also plays a role in development of the disease.

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16
Q

what are the endogenous factors increasing the risk of COPD?

A
  • -α1-Antitrypsin deficiency
  • -Antibody deficiency syndrome (e.g., IgA deficiency)
  • -Primary ciliary dyskinesia (e.g., Kartagener syndrome)
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17
Q

The defining feature of chronic bronchitis is that mucus hypersecretion is primarily a reflection of alveolar involvement. T/F

A

False

bronchial involvement

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18
Q

what is the cause of airflow limitation in chronic bronchitis?

A

• Airflow obstruction component is due to peripheral involvement with:
– Inflammation, fibrosis and resultant narrowing of bronchioles (small airway disease)
– Co-existent emphysema

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19
Q

what is the pathogenesis of chronic bronchitis?

A

• Hypersecretion of mucus, beginning in the large airways
• Irritants induce hypersecretion of the bronchial mucus glands -> hypertrophy of mucus glands -> metaplastic formation of mucin secreting goblet cells in the surface epithelium
• Irritants also induce inflammation with CD8+ T lymphocytes, macrophages and neutrophils
• Gross appearance: Airways swollen and erythematous, covered by a layer of mucin / mucopurulent secretions
• Histologically:
–Hypertrophy of mucus-secreting glands
–Increase in number of goblet cells in the lining epithelium
–Loss of ciliated epithelial cells
–Inflammatory cell infiltrate
–May eventually lead to squamous metaplasia -> dysplasia -> squamous cell carcinoma

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20
Q

CD4 T lymphocytes mediate inflammation in chronic bronchitis. T/F

A

False
Increased number of neutrophils, macrophages, and CD8+ T lymphocytes → release of cytokines → amplification of inflammation and structural changes of lung parenchyma (e.g., growth factor release)

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21
Q

CD8 vs CD4 T cells in obstructive lung diseases?

A

CD8+ T lymphocytes mediate inflammation in individuals with COPD. CD4+ T lymphocytes and eosinophils mediate inflammation in individuals with bronchial asthma.

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22
Q

what is the cause of goblet cell proliferation seen in COPD?

A

Irritants induce hypersecretion of the bronchial mucus glands -> hypertrophy of mucus glands -> metaplastic formation of mucin secreting goblet cells in the surface epithelium

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23
Q

what is the Reid index?

A

The ratio of the width of the mucus-secreting glands to the combined width of the epithelium and cartilage in the bronchial tree. > 0.5 is characteristic of chronic bronchitis.

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24
Q

what is the consequence of chronic irritant exposure in COPD?

A
  • -Overproduction of growth factor → peribronchiolar fibrosis → narrowing of airway → obliteration → emphysema (airflow limitation)
  • -Smooth muscle hyperplasia of the small airways and pulmonary vasculature (mainly due to hypoxic vasoconstriction) → pulmonary hypertension → cor pulmonale
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25
Q

how bronchopulmonary tissue is destructed in COPD?

A
  • -Bronchopulmonary inflammation ↑ proteases, and nicotine use (or other noxious stimuli) inactivates protease inhibitors (especially α1-antitrypsin) → imbalance of protease and antiprotease → ↑ elastase activity → loss of elastic tissue and lung parenchyma (via destruction of the alveolar walls), which causes:
  • -Enlargement of airspaces → ↓ elastic recoil and ↑ compliance of the lung → ↓ tethering of small airways → expiratory airway collapse and obstruction → air trapping and hyperinflation → ↓ ventilation (due to air-trapping) and ↑ dead space → ↓ DLCO and ↑ ventilation-perfusion mismatch (Va/Q) → hypoxemia and hypercapnia
  • -↓ Blood volume in pulmonary capillaries → ↑ dead space → ↓ DLCO and ↑ Va/Q → hypoxemia and hypercapnia
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26
Q

what are the hallmarks of chronic bronchitis?

A
  • -Mucus gland hypertrophy
  • -Increase in goblet cells
  • -Loss of ciliated cells
  • -May get squamous metaplasia
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27
Q

what is the clinical course of chronic bronchitis?

A
  • Cough with production of sputum may persist without ventilatory dysfunction
  • May progress to significant COPD with airflow obstruction -> hypercapnia, hypoxaemia and cyanosis
  • Severe forms may develop pulmonary hypertension and cardiac failure
  • Recurrent infections and respiratory failure
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28
Q

what is the morphologic definition of emphysema?

A

Permanent enlargement of air spaces distal to the terminal bronchioles accompanied by destruction of their walls

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29
Q

what is the epidemiology of emphysema?

A
  • Males >females
  • Heavy smokers
  • Develops over many years becoming clinically significant in later life
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30
Q

the air conducting part is lost in emphysema. T/F

A

False
Anatomically, emphysema involves the acinus, a structure distal to the terminal bronchiole
• This air exchanging portion of lung is lost in emphysema

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31
Q

what is the respiratory acinus?

A

A part of the airway distal to a terminal bronchiole. Each acinus contains multiple respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli.

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32
Q

what is the pulmonary lobule?

A
  • Hexagonal area of lung parenchyma 1 - 2 cm across outlined by fibrous septa
  • Contains lung tissue supplied by 3 - 5 terminal bronchioles
  • Consists of 3 - 5 respiratory acini
  • Grossly visible
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33
Q

what are the types of emphysema?

A

• Defined according to the distribution in the lobule and acinus
1)Centriacinar
- Central or proximal part of acini affected; sparing of distal alveoli
- More common and severe in upper lobes
2)Panacinar
– Acini are uniformly enlarged from the level of the terminal bronchiole to the terminal blind alveoli
– More commonly affects lower zones
3)Distal acinar
– Predominantly affects the distal part of the acinus
– Most striking adjacent to he pleura
– Most often associated with pneumothorax

34
Q

what is the centrilobular emphysema?

A

A morphologic subtype of emphysema characterized by centrally-located inflammation within the acini of the lung. Associated with smoking and frequently found in the upper lobes.

  • -Most common type of emphysema
  • -Classically seen in smokers
  • -Characterized by the destruction of the respiratory bronchiole (central portion of the acinus)
  • -Usually affects the upper lobe
35
Q

what is the panlobular emphysema?

A

A morphologic subtype of emphysema characterized by destruction of the entire acinus of the lung. Associated with alpha-1-antitrypsin deficiency and frequently found in the lower lobes.

  • -Rare type of emphysema
  • -Associated with α1-antitrypsin deficiency
  • -Characterized by the destruction of the entire acinus
  • -Usually affects the lower lobe
36
Q

list other types of emphysema except for centracinar and panacinar.

A

1) Cicatricial emphysema
- -Mainly caused by exposure to quartz dust
- -Results in chronic inflammation and nodular scar formation
2) Giant bullous emphysema
- -Characterized by large bullae (congenital or acquired) that extrude into the surrounding tissue
- -Bullae may rupture, leading to pneumothorax.
- -Depending on the shape of the bullae, resection should be considered.
3) Senile emphysema
- -Loss of pulmonary elasticity with age may lead to an emphysematous lung.
- -not considered pathological but a normal consequence of aging

37
Q

what is the pathogenesis of emphysema?

A

• At terminal bronchiole level the airflow suddenly decreases, dropping particulates into adjacent alveoli.
• Neutrophil and macrophage elastases are turned on by particulate or other compounds of smoke.
• Septal destruction is secondary to elastase and protease activity
–Imbalance between Proteases and Antiproteases in lungs
• Elastase is one of many proteases present in macrophages and neutrophils
• Elastases are released during the inflammatory process
• Antiproteases such as Alpha 1 Antitrypsin (A1AT) counteract their effects
• Patients with hereditary deficiency of A1AT have a high incidence of emphysema

38
Q

what is the role of neutrophils in the lung?

A
  • They are normally sequestered in the lung
  • Any stimulus that increases their number or the release of their elastase-containing granules increases the elastolytic activity
  • Macrophages also a significant source
  • Both sources play a role in smoking-related emphysema
  • Elastin degradation and imperfect repair are central in the pathogenesis of emphysema
39
Q

what process is central in the pathogenesis of emphysema?

A

Elastin degradation and imperfect repair are central in the pathogenesis of emphysema

40
Q

what is the bullous emphysema?

A
  • -Form of emphysema with large subpleural spaces or bullae (> 1 cm)
  • -Most often subpleural near the apex
  • -Rupture → pneumothorax
41
Q

what is the A1AD?

A

An autosomal codominant deficiency of α1-antitrypsin, a protease inhibitor that suppresses enzymes that break down proteins (e.g., elastase, trypsin). Presents with panacinar emphysema and cirrhosis.
• A1AT deficiency common in European population
• Autosomal recessive normal alleles PiMM
• Abnormal allele PiZZ
• Patients develop early onset COPD with lower lobe emphysema, bronchiectasis worsened by smoking

42
Q

what is the Alfa-1-antitrypsin?

A
  • A1AT is a serine protease inhibitor
  • It inhibits neutrophil elastase
  • A1AT is present in serum , tissue fluids and macrophages
  • > 80% of PiZZ phenotypes develop early onset emphysema especially severe if they smoke
43
Q

pink puffer vs blue bloater?

A

1) emphysema:
- - Noncyanotic
- -Cachectic
- -Pursed-lip breathing
- -Mild cough
- -PaO2 slightly reduced and normal PaCO2
2) Chronic bronchitis
- -Productive cough
- -Overweight
- -Peripheral edema
- -PaO2 markedly reduced and elevated PaCO2

44
Q

emphysema vs chronic bronchitis?

A 
1)chronic bronchitis:
•	40-45 onset
•	Mild late dyspnoea
•	Sputum abundant
•	Infections common
•	Cor pulmonale
•	Normal elastic recoil
•	CXR: cardiomegaly
•	Blue bloater
2)emphysema
•	50-75 onset
•	Severe early dyspnoea
•	Scant sputum
•	Infections uncommon
•	Cor pulmonale rare
•	Low elastic recoil
•	Hyperinflation, small heart
•	Pink puffer
45
Q

dyspnea is more characteristic of chronic bronchitis or emphysema?

A

emphysema

46
Q

cor pulmonale more commonly occurs with chronic bronchitis or emphysema?

A

chronic bronchitis

47
Q

abundant sputum is characteristic of emphysema. T/F

A

False

to chronic bronchitis

48
Q

PaCO2 in emphysema vs chronic bronchitis

A

normal vs markedly elevated

49
Q

The severity of Emphysema is more important than the type. T/F

A

True

  • -As it becomes more severe it becomes difficult to classify
  • -Pink Puffer and Blue Bloater represent opposite ends of the spectrum of Emphysema and Chronic Bronchitis
50
Q

what is the clinical presentation of emphysema?

A
  • -SOB, wheeze
  • -Productive cough
  • -Recurrent chest infections
  • -Pleuritic chest pain
  • -Features of right heart failure
  • -Narrowed airways lead to hyperinflation of lungs which are unable to empty
  • -This leads to exertional dyspnoea and progresses to dyspnoea at rest
51
Q

what is the disease course of emphysema?

A

• Asymptomatic early on until FEV1<50%
• Hyperinflation at rest and worsens with exercise
• Muscles of respiration have increased work due to increase functional residual capacity
• On examination:
- Use of accessory muscles of respiration
- Pursed lip breathing
- Hyperinflation
- Decreased breath sounds on auscultation; wheeze, rhonchi
- Features of right heart failure
• Diffusing capacity decreases

52
Q

what is the cause of pursed-lip breathing in emphysema?

A

To increase positive pressure and prevent airway collapse.

53
Q

what is the cause of weight loss and cachexia in emphysema?

A

The main causes are negative energy balance (increased work of breathing and systemic inflammation raise basal metabolism), muscle atrophy (glucocorticoid therapy), and increased oxidative stress (chronic hypoxemia). However, some patients experience weight gain because their overall activity level is reduced.

54
Q

what is the gold standard of COPD diagnosis?

A

Spirometry is the gold standard for diagnosis and assessment of COPD

55
Q

what is the reason for barrel chest in COPD?

A

This deformity is most commonly seen in patients with emphysema. It is caused by long-term use of the accessory respiratory muscles along with the flattening of the diaphragm in normal and quiet inspiration; this flattening is due to hyperinflation of the lungs.

56
Q

what is the cause of peripheral edema in COPD?

A

Edema occurs in COPD as a result of water retention (secondary aldosteronism due to sympathetic activation) and pulmonary vasoconstriction (due to chronic hypoxemia). Heart failure is not always the cause. Diuretic treatment is often unnecessary, as edema improves with increased pulmonary function.

57
Q

nail clubbing is typical to COPD.T/F

A

False
Nail clubbing is not a finding specific to COPD; its presence usually suggests comorbidities such as bronchiectasis, pulmonary fibrosis, or lung cancer.

58
Q

what is the gold classification of COPD?

A

1)GOLD 1 (Class I)
–Mild
–FEV1≥ 80%
2)GOLD 2 (Class II)
–Moderate
50% ≤ FEV1 < 80%
3)GOLD 3 (Class III)
–Severe
30% ≤ FEV1 < 50%
4)GOLD 4 (Class IV)
–Very severe
–FEV1< 30%

59
Q

low and high-risk CAT score of COPD?

A
  • -Low risk = FEV1/FVC ratio ≤ 0.7, FEV1≥ 50% predicted, and 0–1 exacerbation in the last year
  • -High risk = FEV1/FVC ratio ≤ 0.7, FEV1 ≤ 50% predicted, and ≥ 2 exacerbations in the last year
60
Q

what is the prevalence of COPD stages?

A
  • Stage 1 prevalence 2.5%
  • Stage 2 -3 prevalence 1.1%
  • Normal total air exchange area is the size of a squash court size
  • A minority of smokers develop COPD (approx 15% of whites, 5% of Asians)
  • Genetic factors may determine in which smokers airflow obstruction will develop
  • Familial clustering of COPD
  • Different prevalence in different racial groups
  • TNF
  • Microsomal epoxide hydrolase
  • Glutathione-S-transferase
  • MMP12
  • IL4RA
61
Q

what is COPD mortality?

A
  • PROBABLY UNDERESTIMATED
  • Identifying precise cause of death in elderly patients is difficult
  • Patients may have cardiac arrhythmias, ischaemic heart disease, pulmonary emboli etc
62
Q

Death in COPD is due to:

A
  1. Respiratory acidosis and coma
  2. Cor pulmonale = Right-sided heart failure due to chronic pulmonary hypertension
  3. Massive collapse of lungs secondary to pneumothorax
63
Q

how much is the number of alveoli in advanced COPD?

A
  • -Normal number of alveoli is 300 million

- -In advanced emphysema may be decreased to 40 million

64
Q

at what age COPD is usually diagnosed?

A
  • -COPD diagnosed in 5th and 6th decades

- -Probably starts much earlier

65
Q

what are the general measures of COPD treatment?

A

1) Cessation of tobacco use (single most effective step to slow the decline in lung function)
2) Vaccinations
- -Pneumococcal: reduces the incidence of community-acquired pneumonia and invasive pneumococcal diseases
* Age 19-64 years: Administer PPSV23.
* Age ≥ 65 years
a) Vaccinated: Administer PPSV23 (should be at least 5 years after the previous PPSV23 dose and at least 1 year after PCV13).
b) Not vaccinated or unknown vaccination history: Administer PCV13 followed by PPSV23
* *Immunocompetent patients: Administer PPSV23 after 1 year.
* *Individuals with immunocompromising conditions, cerebrospinal leaks, or cochlear implants: Administer PPSV23 after 8 weeks.
- -Influenza (annual): reduces serious illness and death in COPD patients

66
Q

what is the single most effective step to slow the decline in lung function

A

smoking cessation

67
Q

Pulmonary rehabilitation includes…

A
  • -Pursed lip breathing: A breathing technique in which the patient breathes in through the nose and breathes out slowly through pursed lips. This technique increases airway pressure and prevents bronchial collapse during the last phase of expiration.
  • -Physical activity helps maintain endurance and alleviate dyspnea.
68
Q

why vit D is administered in CPD?

A

Vitamin D3 also reduces the risk of acute exacerbations.

69
Q

what bronchodilators are used n COPD?

A
  • -either parasympatholytics or β2-agonists
  • -Long-acting parasympatholytics (long-acting muscarinic antagonists, LAMAs): tiotropium bromide
  • -Long-acting β2-agonists (LABAs): salmeterol, formoterol
  • -Short-acting parasympatholytics (short-acting muscarinic agonists, SAMAs): ipratropium bromide
  • -Short-acting β2-agonists (SABAs): salbutamol, fenoterol
70
Q

LAMA vs SAMA?

A

tiotropium vs pratropium

71
Q

LABA vs SABA?

A

salmeterol, formeterol vs salbutamol, fenoterol

72
Q

what other medications are also used in COPD?

A
  • -Inhaled corticosteroids (ICS): budesonide, fluticasone, beclomethasone
  • -PDE type 4 inhibitors: roflumilast (A selective phosphodiesterase type 4 inhibitor. Roflumilast is used to improve lung function and prevent exacerbations in patients with severe cases of chronic obstructive pulmonary disease (COPD).)
73
Q

treatment of a patient with COPD and FEV1/FEV<70 and FEV1>80% of predicted?

A

SAMA or SABA

74
Q

treatment of a patient with COPD and FEV1/FEV<70 and FEV1<80% but >50 of predicted?

A

LABA/LAMA, pulmonary rehabilitation

75
Q

treatment of a patient with COPD and FEV1/FEV<70 and FEV1<50% but >30 of predicted?

A

add inhaled glucocorticoids

76
Q

treatment of a patient with COPD and FEV1/FEV<70 and FEV1<30 of predicted?

A

add home oxygen therapy

77
Q

If exacerbations still occur, escalate to triple therapy:

A

1) If eosinophil count is ≥ 100/μl: LABA, LAMA, and ICS
2) If eosinophil count is < 100/μl: LABA, LAMA, and either:
- -PDE-4 inhibitor (roflumilast) or
- -If non-/ex-smoker: azithromycin

78
Q

If exacerbations still occur with LABA, LAMA, and ICS triple therapy:

A
  • -If FEV1 < 50 % and chronic bronchitis: add roflumilast
  • -If non-/ex-smoker: add a macrolide (e.g., azithromycin)
  • -Stop ICS (due to possible adverse effects such as pneumonia)
79
Q

what is the indication of theophylline?

A

1)Mechanism of action: adenosine receptor blockade and nonspecific PDE inhibition
2)Indication: usually only severe and refractory COPD
3)Metabolism by the liver cytochrome P450 oxidase system
4)Significant risk for drug interactions (e.g., ciprofloxacin, cimetidine) and variable serum concentrations
5)Side effects: Drug monitoring is necessary because theophylline has a very low therapeutic index and elimination time varies among individuals.
–Severe, refractory nausea and vomiting with abdominal pain
–Cardiotoxicity: tachycardia that may degenerate into arrhythmias and hypotension in severe cases
–Neurotoxicity: CNS involvement (e.g., tremor, agitation, insomnia, psychotic symptoms), seizures in severe cases
6)Contraindications: damaged cardiac muscle (Mechanism of action: adenosine receptor blockade and nonspecific PDE inhibition
Indication: usually only severe and refractory COPD
Metabolism by the liver cytochrome P450 oxidase system
Significant risk for drug interactions (e.g., ciprofloxacin, cimetidine) and variable serum concentrations
Side effects: Drug monitoring is necessary because theophylline has a very low therapeutic index and elimination time varies among individuals.
Severe, refractory nausea and vomiting with abdominal pain
Cardiotoxicity: tachycardia that may degenerate into arrhythmias and hypotension in severe cases
Neurotoxicity: CNS involvement (e.g., tremor, agitation, insomnia, psychotic symptoms), seizures in severe cases
Contraindications: damaged cardiac muscle )

80
Q

Long-term oxygen therapy (LTOT) indicated in the case of…

A

1) PaO2 ≤ 55 mm Hg or SaO2 ≤ 88 % at rest
- -Increases the chance of survival in patients with COPD
- -Supplemental O2 can worsen hypercapnia
- -The target oxygen saturations is 90–93%.
2) PaO2 between 55 and 60 mmHg or SaO2 of 88 mmHg if there is evidence of pulmonary hypertension, congestive cardiac failure, or polycythemia

81
Q

Surgery may be beneficial in severe cases…

A
  • -Lung resection for giant bullae in emphysema

- -Lung transplantation for nonrepairable damage

Cardiorespiratory (24 decks)

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