COPD Flashcards

1
Q

What is the pathophysiology of COPD?

A
  • Repeated injury to airways leads to structural and physiological changes and chronic inflammation
  • These changes include narrowing and remodeling of airways, increased number of goblet cells, enlarged mucus glands, alveolar loss and changes to vascular bed leading to pulmonary hypertension.
  • Elastin breakdown and loss of alveolar integrity leads to emphysema.
  • Increased goblet cell size and number causes excessive mucus secretion.
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2
Q

What is the physiological definition of COPD?

A

Increased airway resistance.
This is caused by reduced elastic recoil, fibrotic changes and luminal obstruction by secretions. The loss of elastic recoil leads to air trapping and therefore hyperinflation

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3
Q

What are the causes of COPD?

A
  • Smoking,
  • Alpha-1 antitrypsin deficiency
  • Others: Coal, cotton, cement, grain
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4
Q

What is alpha-1 antitrypsin deficency?

A

Autosomal recessive condition which causes a lack of alpha-1 antitrypsin, a protease inhibitor normally produced by the liver.
It’s role is to protect cells from enzymes such as neutrophil elastase

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5
Q

What are the features of alpha 1 antitrypsin deficiency?

A

Disease normally manifests in PiZZ genotype.
Lungs: Panacinar emphysema mostly in lower lobes.
Liver: Cirrhosis and hepatocellular carcinoma in adults, cholestasis in children.

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6
Q

What are the investigations for alpha-1 antitrypsin deficiency?

A

A1AT concentrations
Spirometry - obstructive picture

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7
Q

what are the symptoms and exam findings of COPD?

A

Symptoms - Productive cough, dyspnoea, wheeze, and in severe cases right sided heart failure which results in peripheral oedema.

Exam findings - Barrel chest, hyper-resonant percussion, wheezing, coarse crackles

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8
Q

What is the definition of chronic bronchitis?

A

Production of sputum on most days for at least 3 months in at least 2 years.
Affects large airways greater than 4mm in diameter. Inflammation leads to scarring and thickening of airways.

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9
Q

What is the definition of emphysema?

A

Abnormal, permanent enlargement of airspaces distal to the terminal bronchioles

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10
Q

What are the features of ‘blue bloaters’

A

Type 2 respiratory failure (high CO2 and low O2) due to COPD which presents with following symptoms:
- Cyanosis,
- Warm peripheries,
- Bounding pulse,
- Flapping tremor,
- Confusion/drowsiness,
- Right heart failure,
- Oedema
- Raised JVP

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11
Q

What are the features of ‘pink puffers’

A

Type 1 respiratory failure (low O2 and low CO2) due to COPD which presents with following:
- Desaturates on exercise,
- Pursed lip breathing,
- Use of accessory muscles,
- Wheeze,
- Indrawing of intercostals,
- Tachypnoea

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12
Q

What are the different types of emphysema?

A
  • Centri-acinar: damage occurs around bronchioles more in upper airways. Associated with smoking
  • Pan-acinar: Uniformly enlarged from level of** terminal bronchiole distally**. Large bullae and associated with alpha 1 anti-trypsin deficiency.
  • Paraseptal: Bullae are at risk of rupture and causing pneumothroax. Associated with fibrosis
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13
Q

What are the investigations for COPD?

A

Post-bronchodilator spirometry - FEV1/FVC ratio less than 70%.
Chest X ray - Hyperinflattion (>6 anterior ribs), flat hemidiaphragm, bullae
FBC - exculse secondary polycythaemia
Sputum culture
BMI

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14
Q

How do you classify severity of COPD

A

Based on % of predicted FEV1
Stage 1 = FEV1 >80%
Stage 2 = FEV1 of 50-79%
Stage 3 = FEV1 of 30-48
Stage 4 = FEV1 of < 30%

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15
Q

What is the management of stable COPD?

A

Step 1 - SABA or SAMA
Step 2 with NO asthmatic features - Add LABA and LAMA. If already taking a SAMA then discontinue and switch to SABA
Step 2 with asthmatic features - Add ICS and LABA. If already taking a SAMA then discontinue and switch to SABA
Step 3 - Trial triple therapy with LABA, LAMA and ICS
Additions: Mucolytics if severe congestions

Smoking cessation

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16
Q

When should oral theopylline be used in COPD?

A

People who cannot use inhaled therapy.
Dose should be reduced if macrolide or flouroquinolone is co-prescribed

17
Q

When are phosphodiesterase inhibitors recommended for COPD?

A

In severe asthma with FEV1 <50% predicted or 2+ exacerbations in last year despite triple therapy.

18
Q

What is the most common infective cause of COPD exacerbation?

A

Haemophilus influenza

19
Q

What are the features of an acute exacerbation of COPD?

A

Increase in dyspnoea, cough and wheeze.
Increase in sputum which may suggest infective cause
Hypoxia and confusion

20
Q

What is the primary care management of acute exacerbation of COPD

A

Increase frequency of bronchodialtor, consider nebs.
Give 30mg Prednisolone for 5 days
Antibiotics if sputum is purulent - Amoxicillin, doxycycline

21
Q

When should you admit a patient with IECOPD?

A

Severe breathlessness,
Acute confusion or low GCS,
Cyanosis,
O2 sats less than 90%
Social reasons
Significant comorbidity

22
Q

What is the management of IECOPD in secondary care?

A

Oxygen therapy - Aim sats 88-92%
Nebulised bronchodilator - Salbutamol or ipratropium
Steroids - Oral pred or IV hydrocortisone
IV theophylline if not responding to bronchodilators
If in type two resp failure with acidosis of <7.35 then use NIV.

23
Q

When should patient’s be offered long term oxygen therapy?

A

When pO2 < 7.3 kPa or pO2 of 7.8-8 kPa with one of following:
Secondary polycythaemia,
Peripheral oedema,
Pulmonary hypertension