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Year 3 > COPD > Flashcards

COPD Flashcards

1
Q

What is COPD?

A

A progressive lung disorder characterised by airflow obstruction:
1. Chronic bronchitis: chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years
2. Emphysema: pathological diagnosis of permanent obstructive enlargement of air spaces distal to the terminal bronchioles.

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2
Q

What is the prevalence/most commonly affected profile?

A

Very common (8%) of population, presents in middle age or late, more common in males

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3
Q

Describe aetiology

A

Chronic inflammation with neutrophilic infiltration and CD8+ T lymphocytes + macrophages

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4
Q

What is chronic bronchitis/emphysema characterised by?

A

CB:
1. Narrowing of the airways results in bronchiole inflammation (bronchiolitis)
2. Bronchial mucosal oedema
3. Mucous hypersecretion
4. Squamous metaplasia

Emphysema:
1. Destruction and enlargement of alveoli
2. Leads to loss of elasticity that keeps small airway open during expiration
3. Progressively larger air spaces develop known as bullae (>1cm diameter)

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5
Q

What are other causes of lung damage?

A
  1. Environmental toxins - predominantly affects upper lobes as they are better ventilated (smoking, air pollution, cadmium, coal etc)
  2. a1 antitrypsin deficiency - predominantly affects lower lobes (consider in young, never smoked patients with COPD like symptoms of cirrhosis and cholestasis)
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6
Q

What are symptoms of COPD?

A

Cough, often productive
Dyspnoea
Wheeze
RHF resulting in peripheral oedema

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7
Q

What would be revealed on chest inspection in a COPD patient?

A

Resp distress
Accessory muscle use
Barrel shaped over inflated chest
Decreased cricosternal distance
Cyanosis
Pursed lip breathing
Tar staining

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8
Q

What can be noticed on chest palpation and percussion?

A

Palpation:
- Decreased chest expansion
- Parasternal heave due to RV cardiomegaly secondary to cor pulmonale)

Percussion:
Hyper-resonance
Loss of liver/cardiac dullness

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9
Q

What can be noticed on chest auscultation?

A
  1. Quiet breath sounds
  2. Prolonged expiration
  3. Wheeze
  4. Rhonchi - rattling sounds caused by secretions in larger airways and obstructions
  5. Early inspiratory coarse crackles - infective exacerbation
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10
Q

What are signs of CO2 retention?

A
  1. Bounding pulse
  2. Warm peripheries
  3. Asterixis
  4. Signs of right heart failure (cor pulmonale) - right ventricular heave, raised jvp, ankle oedema
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11
Q

What are the 4 stages of COPD?

A

See table

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12
Q

What investigations are done for COPD?

A
  1. Spirometry
  2. ABG: Resp failure (hypoxaemia with or without hypercapnia)
  3. CXR
  4. FBC
  5. ECG
  6. Serum A1AT
  7. TLCO
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13
Q

What does a COPD CXR show?

A
  1. Flattened hemidiaphragms
  2. Horizontalisation of ribs
  3. More than 10 posterior ribs above diaphragm at MCL

Higher prominence of pulmonary vessels if pulmonary hypertension present.

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14
Q

How is COPD treated?

A

Start with SABA/SAMA
If features of steroid responsiveness present:
1. Graduate to LABA + ICS
2. LABA + LAMA + ICS

If features of steroid responsiveness not present:
1. LABA + LAMA
2. 3 month trial of LABA + LAMA + ICS

Oral theophylline may be used if symptoms not controlled.

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15
Q

What features suggest steroid responsiveness?

A

Asthmatic features
1. Previous diagnosis of asthma/atopy
2. Raised blood eosinophil
3. Substantial variation in FEV1 over time - 400ml
4. Substantial diurnal variation in PEF - over 20%

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16
Q

What are lifestyle aspects of managing COPD?

A
  1. Smoking cessation
  2. Encourage exercise + pulmonary rehab
  3. Vaccines - annual flu + one pneumococcal
  4. Depression screening
  5. Mucolytics like carbocysteine if chronic sputum production
  6. Long term oxygen therapy
17
Q

What are smoking cessation medicines?

A

Varenicline + Bupropion

18
Q

What is long term oxygen therapy and evidence for it?

A

PaO2 of above 8 maintained for 15 hours a day - 3 year survival increased by 50%

19
Q

Who is long term oxygen therapy considered for?

A
  1. Non smoker on maximal treatment with consistent PO2 below 7.3
  2. Consistent PO2 between 7.3-8.0 with:
    - Secondary polycythaemia
    - Cor pulmonale
    - Peripheral oedema
    - Nocturnal hypoxia
20
Q

What is hypoxic drive?

A

In someone with healthy lungs, stimulation to breathe comes from detection of high CO2 in the blood. However, in chronically hypercapnic people, body starts to use the hypoxic drive which kicks in when saturations are very low - therefore, usually have sats of around 92%.

21
Q

What are surgical management options for COPD?

A
  1. Lung volume reduction: removes emphysematous tissue and helps the diaphragm contract more effectively to improve ventilation.
  2. Lung transplant - patients such as those with A1AD
  3. Bullae removal
22
Q

What are bullae?

A

Focal areas of emphysema with smaller ones called blebs. Can encroach on lung tissue and worsen symptoms. May burst and cause pneumothoraces. Can also be caused by connective tissue disease.

23
Q

What is alpha 1 antitrypsin and why is smoking particularly injurious?

A

Alpha 1 antitrypsin is made in the liver and breaks down elastase. Elastase damages connective tissue in the lungs (COPD) and liver (cirrhosis). Cigarette smoke inactivates A1AT so people with A1AD even more susceptible to damage from smoking.

Think of this in COPD symptoms, under 40, never smoked

24
Q

How is alpha 1 antitrypsin deficiency diagnosed?

A
  1. Low serum A1AT
  2. Liver biopsy showing cirrhosis and acid-Schiff-positive staining globules
  3. Genetic testing for the A1AT gene
  4. High resolution CT thorax diagnoses bronchiectasis and emphysema
25
Q

What organisms are the most common causes of a IECOPD?

A
  1. Haemophilus influenzae
  2. Streptococcus pneumoniea
  3. Moraxella catarrhalis
  4. Rhinovirus
  5. Pseudomonas aeruginosa
26
Q

How is a COPD exacerbation treated?

A
  1. Salbutamol and ipratropium via nebuliser
  2. Oxygen - if retainer, aim for lower sats via venturi mask (do an ABG within an hour when starting/changing oxygen)
  3. Steroids - IV hydrocortisone/prednisolone (continued for 1-2 weeks)
  4. Antibiotics - amoxicillin, doxycycline, clarithromycin
  5. If nebulisers and steroids don’t help, add IV aminophylline
27
Q

When should ICU and non-invasive positive pressure ventilation be considered?

A

ICU + NIPPV if
RR >30
pH <7.35
PaCO2 continuing to rise

If NIPPV not effective and pH drops below 7.26 + PaCO2 still rising, then consider intubation + ventilation and then ICU
Where NIV/intubation is not appropriate, doxapram can be used as a respiratory stimulant.

28
Q

When is NIPPV used and what are the forms?

A

Used when patients still hypoxaemic despite medical management.
BiPAP - in inhalation phase, pressure higher than exhalation phase. Helps to recruit alveoli that are normally under ventilated/collapsed.
CPAP - high pressure maintained in inspiration and expiration to keep the airway open.
Airway is scored using the Mallampati score.

29
Q

When is BiPAP and CPAP used?

A

BiPAP: Used in Type 2 resp failure (COPD exacerbation) when there is respiratory acidosis
CPAP: OSA, CCF, acute pulmonary oedema

30
Q

What are complications of COPD?

A

Acute respiratory failure
Infections (haemophilus influenzae)
Pulmonary hypertension - chronic hypoxia leading to vasoconstriction of pulmonary vessels
Right sided heart failure
Pneumothorax secondary to bullae rupture
Secondary polycythaemia due to hypoxic state
Increased risk of lung cancer

Year 3 (18 decks)

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