COPD Flashcards

1
Q

What is the micro pathology of COPD?

A
  • Hypertrophy and hyperplasia of mucus-secreting goblet cells of bronchial tree
  • Fibrosis and thickening of bronchial walls
  • Lymphocytic infiltrate
  • Emphysema – Dilatation and destruction of lung tissue distal to terminal bronchiole leading to reduced elasticity and gas exchange surface
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2
Q

What are the main differentials of COPD?

A

Asthma
Bronchiectasis
Lung cancer

In acute exacerbations:
Pneumothorax
Pneumonia
Pulmonary oedema
Large pleural effusion
PE
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3
Q

How would you manage an acute exacerbation of COOD?

A

ABCDE approach

  • Monitoring, iv access, bloods (consider theophylline level)
  • Early CXR and ABG

Oxygen

  • Titrated to maintain sats within individualised target range
  • Usually 88-92% if unsure
  • ABG to ensure not retaining CO2
Bronchodilators
- Salbutamol 5mg
- Nebulised (or inhaled via spacer – equally effective)
- Can run back to back
Ipratropium 0.5mg
- No evidence this is more effective than salbutamol but given anyway
Prednisolone 30mg
 - 7-14 days

Antibiotics
- If febrile, sputum purulent or signs of consolidation
Treat as pneumonia if consolidation on CXR
Empirical treatment – aminopenicillin, macrolide or tetracycline – refer to local guidelines

IV Thephylline
-Only if no response to bronchodilator therapy

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4
Q

What would you do to manage COPSMD if these medical steps are failing?

A

Non-invasive ventilation (CPAP or BiPAP)

  • In patients who are still hypercapnic and hypoxic despite medical therapy
  • Has been shown to improve survival
  • Must clearly document plan for what should happen if further deterioration and ceiling of treatment

Contraindications

  • Confusion or agitation
  • Unless this is due to high CO2
  • Severe dementia
  • Facial burns or trauma
  • Vomiting
  • Undrained pneumothorax
  • Copious secretions
  • Haemodynamically unstable, moribund or low GCS - Unless in HDU
  • Upper GI surgery or obstruction

Can use doxapram if NIV not available or inappropriate
- Stimulant of chemoreceptors. CI in epilepsy.

Invasive ventilation

  • Careful consideration regarding whether appropriate
  • Close liaison with ITU team
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5
Q

What is the definition of COPD?

A

Airflow obstruction that is:

  1. Not fully reversible
  2. Progressive
  3. Does not change markedly over several months
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6
Q

What is the pathophysiology of COPD?

A

Combination of airway and parenchymal damage
This occurs as a result of chronic inflammation and encompasses chronic bronchitis and emphysema
An exacerbations of COPD is a rapid and sustained worsening of symptoms beyond normal day-to-day variations

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7
Q

What is the epidemiology of COPD?

A

Prevalence: an estimated 3 million people have COPD in the UK
Incidence: approximately 1% overall and 10% in over 75 year olds

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8
Q

What are the causes/risk factors for COPD?

A

Smoking
- In UK, 90% of COPD is caused by long-term smoking
smokers of >30/day have a 20x risk compared to non-smokers, although only 10-20% of heavy smokers get COPD

Air pollution

Biomass fuels

Alpha-1-antitrypsin deficiency

Serum protease inhibitor

Can present with lung disease (75%) or liver cirrhosis (25%) - Pan-acinar (lower lobes) as opposed to centri-lobular in smoking and environmental exposures

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9
Q

What are the causes of acute exacerbation of COPD?

A

Viral
- Rhinovirus, influenza, coronvirus, adenovirus, RSV

Bacteria

1. Common
Strep. Pneumonia
Haemophilus
Moraxella
- WCC may be normal with mild symptoms
2. Rare
Staph aureus (during flu season)
Pseudomonas
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10
Q

What is the presentation of COPD?

A
Exertional breathlessness
Chronic cough
Sputum production
Wheeze
Frequent winter bronchitis
Fatigue
Ankle Swelling
Weight loss
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11
Q

What are the main differentials of COPD?

A

Asthma
Bronchiectasis
Lung cancer

In acute exacerbations:
Pneumothorax
Pneumonia
Pulmonary oedema
Large pleural effusion
PE
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12
Q

What are the investigations of COPD?

A
Bedside
Pulse oximetry
Sputum MCS
ECG
- May show tall P-waves of cor pulmonare, RBBB and RVH (right axis deviation, prominent V1 R-wave and V6 S-wave)
Calculate BMI

Bloods
FBC: Hb and Hct can be raised in response to chronic hypoxia
Blood cultures if pyrexial
Alpha-1-antitrypsin levels
Theophylline level if on maintenance therapy

ABG
Normal in mild disease
Hypoxia and hypercapnia in advanced disease
Respiratory acidosis +/- partial or full metabolic compensation

Imaging
CXR
- Classically shows bullae, hyperinflation and flattened diaphragms but can be normal
CT (high resolution CT – HRCT)
- Can do in expiration phase if looking for air trapping

Echo
Assess cardiac function (?cor pulmonare)

Lung function tests
High RV and TLC
Low VC
FEV1/FVC reduced (i.e. obstructive)
- FEV1/FVC < 0.7, FVC < 0.8 predicted
Little reversibility with salbutamol: <15%
Low KCO
- Carbon Monoxide gas transfer coefficient reduced in proportion to severity
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13
Q

What is the mangement of acute and chronic copd?

A

See notes

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14
Q

What are the complications of COPD?

A
Progressive respiratory failure
Cor Pulmonale
Recurrent LRTIs
Pneumothoraces
Post-infective bronchiectasis
Acute renal failure (likely pre-renal)
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15
Q

What is the prognosis of COPD?

A

Mortality is 70 per 100,000 per year (down from 200 25 years ago)
5 year survival approx. 75%
With acute exacerbations
- 1/3 will be re-admitted within 3 months and 14% will die within 3 months

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