Asthma - COPD Flashcards

(64 cards)

1
Q

what is COPD?

A

Chronic Obstructive Pulmonary Disease

Chronic - It is a long-term condition that doesn’t go away.
Obstructive - The airways are narrowed -> harder to breathe out quickly, causing air trapping in chest
Pulmonary - It affects the lungs
Disease - medical condition .

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2
Q

What causes COPD?

A

Long-term exposure to harmful gases/particles combined with individual factors such as childhood lung development + genetics.

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3
Q

What type of symptoms characterize COPD?

A

Persistent and progressive respiratory symptoms, including difficulty in breathing + hpersistent cough (sometimes with phlegm).

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4
Q

What environmental exposures are major contributors to COPD?

A

Tobacco smoke, indoor air pollution, and occupational dusts/fumes/chemicals.

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5
Q

Is COPD curable?

A

No — not curable, but early diagnosis and treatment required to slow progression of symptoms and reduce flare ups

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6
Q

What age group is COPD usually diagnosed in?

A

older patients - diagnosis unlikely before 40-50 years

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7
Q

COPD is a major cause of what?

A

morbidity and mortality
accounts for 12 % of hospital admissions

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8
Q

COPD usually involves a combination of which two conditions?

A

Chronic bronchitis and emphysema.

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9
Q

What structural change occurs in emphysema and what does It lead to?

A

Walls between alveoli are damaged or destroyed.
leads to reduced gas exchange

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10
Q

What structural changes occur in chronic bronchitis?

A

Inflamed airways, thickened lining, and overproduction of mucus/sputum/phlegm

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11
Q

what are the causes of/risk factors for COPD?

A

long term exposure to lung irritants e.g. - smoking, occupation, air pollution
Genetics - AAT deficiency in 1-2% cases
Age>40 years
Asthma (20% COPD patients)
Infections - HIV, TB e.g.
Poor growth in utero or prematurity
Frequent/ severe respiratory infections in childhood
socioeconomic factors

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12
Q

In COPD pathobiology, what do chronic irritants do to normal inflammation responses?

A

They modify normal inflammation ->
leading to more inflammatory cells-

and release of multiple inflammatory mediators that attract more inflammatory cells from circulation - amplifying inflammatory process

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13
Q

Which inflammatory cells are increased in COPD due to chronic irritants?

A

Increased macrophages, activated neutrophils, and lymphocytes.

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14
Q

What major structural changes occur in COPD pathobiology and what drives them?

A

Structural changes occur via excessive growth factor production, including peribronchiolar fibrosis and interstitial opacities.

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15
Q

What is oxidative stress in COPD associated with?

A

Increased biomarkers in exhaled breath, sputum, and systemic circulation (example: H₂O₂).

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16
Q

What is the protease–antiprotease imbalance in COPD and what does it cause?

A

It causes increased breakdown of connective tissue components, e.g. elastin.

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17
Q

what lung irritants can cause COPD?

A

smoking
indoor pollution - e.g. cooking fires, especially poorly ventilated or biomass fuelled
Outdoor pollution
Occupational irritants - dusts, chemical irritants

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18
Q

Passive smoking contributes to what?

A

COPD development

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19
Q

What percentage of smokers develop COPD?

A

About 20%.

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20
Q

What is “pack years” and how is it calculated?

A

A measure of tobacco exposure:
Risk can be modelled using pack years
Helpful for screening
Pack years = (cigarettes per day × years smoked) ÷ 20.
1 pack years equivalent to smoking 20 cigarettes per day for 1 year

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21
Q

what reduces likelihood of disability or death?

A

smoking cessation

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22
Q

What rare genetic condition predisposes to early-onset COPD?

A

Alpha-1 antitrypsin (AAT) deficiency.

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23
Q

What percentage of COPD patients have AAT deficiency?

A

1–2%
may develop COPD younger

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24
Q

what does the AAT protein normally do?

A

Protects tissues from damage during acute inflammation.

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25
Why does mutated AAT cause lung damage?
It is produced in the liver but cannot be released in sufficient amounts if mutated
26
What is the hallmark symptom of COPD?
Chronic and progressive dyspnoea, especially on exertion. may feel like gasping or breathing takes more effort
27
What is the classic COPD cough called?
Chronic productive or “smoker’s” cough.
28
What typical respiratory findings occur in COPD?
Wheezing, whistling, squeaking when breathing Regular sputum production chest tightness or heaviness Susceptibility to colds or damage from smoke/air pollution (weakened lungs)
29
What systemic symptoms, signs and complications appear in severe COPD?
Fatigue, muscle loss, weight loss, anorexia due to severe COPD Ankle swelling, possibly due to Cor pulmonale Hyperinflation/gas trapping Polycythaemia Depression/anxiety
30
what are symptoms of acute exacerbations of COPD?
Tachycardia/Tachypneoa – Infection/Fever (may be the cause of the flare-up) – Sputum changes – Cyanosis/Respiratory failure
31
What vascular complication can develop from COPD?
Cor pulmonale is right-sided heart failure secondary to lung disease Enlargement of the right ventricle caused by pulmonary hypertension as a consequence of hypoxia
32
who should be suspected of cor pulmonale?
people with Peripheral oedema – Raised jugular venous pressure – Systolic parasternal heave – A loud pulmonary second heart sound (over the second left intercostal space) – Hepatomegaly
33
What initial lung abnormality triggers the development of cor pulmonale?
Alveolar hypoxia.
34
What vascular response occurs in the lungs in response to alveolar hypoxia?
Hypoxic pulmonary vasoconstriction.
35
What is the normal physiological purpose of hypoxic pulmonary vasoconstriction in healthy lungs?
This construction response to local hypoxia diverts blood away from poorly oxygenated alveoli to lung segments that are better oxygenated.
36
What happens when hypoxic pulmonary vasoconstriction becomes widespread and chronic?
It leads to increased pulmonary vascular resistance.
37
What additional factors increase pulmonary vascular resistance in COPD?
Acidosis Capillary destruction (emphysema)
38
How does emphysema contribute to pulmonary hypertension?
Capillary destruction reduces the pulmonary vascular bed, increasing resistance.
39
How does polycythaemia contribute to pulmonary hypertension in COPD?
Increased blood viscosity raises pulmonary vascular resistance.
40
What condition develops as a result of chronically increased pulmonary vascular resistance?
Pulmonary hypertension (disease)
41
What is the effect of pulmonary hypertension on the right ventricle
It causes increased right ventricular afterload.
42
How does the right ventricle initially respond to increased afterload?
By developing right ventricular hypertrophy.
43
What happens when the right ventricle can no longer compensate?
Right ventricular failure develops -> cor pulmonale
44
Which COPD complications directly contribute to cor pulmonale development?
Chronic hypoxia Emphysema (capillary loss) Polycythaemia Acidosis
45
Why does COPD commonly lead to cor pulmonale?
Chronic hypoxia causes pulmonary hypertension, increasing right ventricular workload over time.
46
What is the primary goal in managing cor pulmonale due to COPD?
Treat the underlying lung disease and chronic hypoxia, not the heart directly.
47
How does treating hypoxia slow progression of cor pulmonale?
By reducing pulmonary vasoconstriction, pulmonary hypertension, and right ventricular afterload.
48
what are the 3 symptoms that suggest COPD and what are the risk factors ?
Symptoms: shortness of breath chronic cough sputum Risk factors host factors tobacco occupation indoor/outdoor pollution
49
what test is required to establish diagnosis of COPD?
spirometry test
50
what other tests are used to diagnose COPD?
Chest sounds - checking for abnormal sounds Chest X-ray or CT scan - checking for complications Arterial blood gas test - checking for hypoxia or hypercapnia Full blood count - checking for anaemia or polycythaemia Calculate BMI - checking whether need nutritional assistance AAT deficiency - especially if early onset, minimal smoking, or family history
51
Describe the spirometry test
main lung function test for COPD can detect COPD before severe symptoms develop simple non-invasive
52
what is PEF?
peak expiratory flow -> maximal flow (speed) achieved during maximally forced expiration initiated at full inspiration
53
what is TLC?
total lung capacity (L) - maximum volume at full inspiration
54
what is RV?
residual volume (L) - volume left after maximum expiration
55
what is VC and FVC ?
Vital capacity (L) and forced vital capacity (L) difference in volume between inspiration and expiration measured when relaxed (VC) or when forced with maximal effort (FVC)
56
How are FVC and VC different in obstructive breathing disorders ?
FVC is smaller than VC due to gas trapping and airway collapse
57
What is FEV1?
Forced Expiratory Volume in 1 second (L) Volume that can be forcibly expelled in the first second of the test (following a full inspiration) abnormally low in obstructive diseases
58
what is FVC?
Total volume of air that a patient can forcibly exhale in one breath
59
What is a normal FEV1/FVC ratio?
for healthy lungs - FEV1/FVC is usually 70% or above
60
what is the FEV1/FVC?
The ratio of these values (expressed as a %) i.e. how much of the forced expiration volume was exhaled within the 1st second of testing
61
How is spirometry affected in obstructive breathing disorders?
restrictive - FVC low, FEV1/FVC NOT reduced Obstructive - FEV1/FVC significantly reduced Severe Obstructive - Both FVC and FEV1/FVC significantly reduced
62
when is COPD diagnosed?
when FEV1/FVC is <70%
63
Describe the 4 stages of COPD severity categorised by FEV1 as a %
Stage 1 Mild - FEV1 ≥ 80% May be winded on moderate exercise Stage 2 Moderate - 50 - 80% Frequent stops to catch breath, coughing/wheezing and breathlessness Stage 3 Severe - 30 - 50% Shortness of breath worsens; frequent flare-ups leading to hospitalisation Stage 4 Very severe - < 30% * Constant shortness of breath, flareups can be life- threatening
64
What are the goals of COPD treatment?
Relieving symptoms – Slowing the progress of the disease – Improving exercise tolerance or ability to stay active – Preventing and treating complications – Improving overall health * LIFESTYLE CHANGES