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RESPIRATORY > COPD > Flashcards

COPD Flashcards

1
Q

What characterises COPD?

A

Progressive disease
airway obstruction little or no reversibility
FEV1/FVC ratio <0.7. inc. chronic bronchitis and emphysema

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2
Q

What is chronic bronchitis?

A

clinically as cough, sputum production on most days for 3 months of two successive years.

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3
Q

What is emphysema?

A

defined histologically as enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls. It is classified according to the site of damage:
• centri-acinar - commonest; distension and damage is around resp bronchioles whilst distal alveolar ducts are preserved
• pan-acinar - less common; destruction involves whole acinus
• irregular - patchy scarring and damage; no regard for acinar damage

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4
Q

What are pink puffers?

  • SOB/ cyanosed
  • ventilation
  • PaO2 and PaCO2
  • Failure type?
  • Could develop?
A

breathless but not cyanosed
increased alveolar ventilation, are only slightly hypoxic and have a normal or low PaCO2
may progress to type 1 respiratory failure.

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5
Q

What are blue bloaters?

  • SOB/ cyanosed
  • ventilation
  • PaO2 and PaCO2
  • Failure type?
  • Could develop?
A

cyanosed but not breathless
decreased alveolar ventilation with low PaO2 and high PaCO2
may progress to type 2 respiratory failure. rely on their hypoxic drive to keep breathing
could develop cor pulmonale.

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6
Q

What age does it mainly affect?

A

> 40’s

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7
Q

How common cause of death?

A

Predicted to become 3rd most common cause of death and 5th most common disability worldwide by 2020
90% of COPD patients are smokers

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8
Q

What are 3 mechanisms have been suggested for this limitation of airflow in small airways?

A
  1. Loss of elasticity and alveolar attachments of airways due to emphysema. This reduces the elastic recoil and the airways collapse during expiration.
    o emphysema leads to expiratory airflow limitation and air trapping. The loss of lung elastic recoil = ↑ TLC and premature closure of airways limits expiratory flow, and loss of alveoli = decreased surface area for gas exchange
    • Chronic bronchitis – cough, sputum production on most days for 3 months of 2 successive years
    • Emphysema – enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls
  2. Inflammation and scarring cause the small airways to narrow.
    o Microscopically: infiltration with acute and chronic inflammatory cells.
    o Epithelial layer may become ulcerated, with squamous cells replacing the columnar cells on healing of the ulcer
    o Inflammation leads to scarring and thickening of the walls => narrowing of the small airways
    o Small airways especially affected in early disease (w/o any breathlessness); accounts for improvement in lung function if smoking is stopped early enough. Inflammation continues in later stages so smoking cessation not as effective.
  3. Mucus secretion which blocks the airways.
    o Increased number of mucus-secreting goblet cells in bronchial mucosa; bronchi may become inflamed and covered in pus.
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9
Q

Explain the FEV1 and FVC ratio?

A

In obstructive respiratory disease the FEV1 is decreased due to airway obstruction, the FVC remains normal as the lung capacity is unaffected. Therefore the FEV1:FVC ratio is decreased (<0.7). Normaly 75-80% of the FVC comes out in the first second hence the cut-off limit of 0.7 for the ratio. Common progressive disorder characterized by airflow obstruction (FEV1 <80% predicted; FEV1:FVC ratio <0.7) with little or no reversibility

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10
Q

What are the risk factors?

A
  1. Smoking
  2. Age
  3. a-1-antitrypsin deficiency
  4. Air polluaiton
  5. Infections often lead to exacerbations
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11
Q

Why is a-1-antitrypsin deficiency a problem?

A

accounts for 2% emphysema cases; major anti-protease. Alpha 1 antitrypsin is a protease I that inhibits enzymes able to destroy alveolar wall .
Smoking = inhibits a-1-antitrypsin

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12
Q

What are the symptoms?

A
  • Chronic cough
  • Sputum – white/clear; purulent during infective exacerbation
  • SOB
  • Wheeze
  • Recurrent chest infections
  • Dyspnea
  • Weight loss
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13
Q

When is SOB worse?

A

Worse in cold weather/pollution. Minimal diurnal variation

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14
Q

What signs should you look out for?

A
  • Inc. resp rate/tachypnoea
  • Accessory muscles of respiration
  • Pursed lips
  • Peripheral/central cyanosis – when more severe
  • CO2 flap – due to hypercapnia due to CO2 retention; usually when more severe and in respiratory failure
  • Decreased expansion
  • Resonant/hyper resonant to percussion – due to hyperinflation
  • Wheeze
  • Decreased vesicular breath sounds – over bullae
  • Peripheral oedema – when severe
  • Hyperinflation
  • Decreased cricosternal distance <3cm
  • Cyanosis
  • Cor pulmonale
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15
Q

What investigations would you request?

A 
CXR
Spirometry
FBC
ABG
ECG
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16
Q

What are looking for on a CXR?

A 
o	Hyperinflated lungs (>6 ant ribs seen above diaphragm in clavicular line)
o	Flat hemi-diaphragms
o	Large central pulmonary arteries
o	Decreased peripheral vascular markings
o	Bullae
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17
Q

What are you looking for in spirometry results?

A

o Patient sat down, breathes in fully, then breathes out as fast and hard as possible and keeps going until nothing left
o FEV1 <80% of predicted – predicted normal for a person of same sex, age and height
o FEV1:FVC <0.7
o Flow volume loop: decreased peak expiratory flow, decline in airflow to complete exhalation creating concave curve

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18
Q

What is the GOLD/NICE staging on COPD?

A

> = 80 Stage 1 (mild)*
50-79 Stage 2 (moderate)
30-49 Stage 3 (severe)
<30 Stage 4 (very severe)**

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19
Q

What are you looking for in blood results?

A

o Secondary polycythaemia

o Incr. PCV

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20
Q

What are you looking or in ABG results?

A

o To check for respiratory failure if sats drop
o To monitor oxygen
o Decreased PaO2
o +/- Hypercapnia

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21
Q

What are you looking for in ECG results?

A

o Cor pulmonale in advanced disease

o Right atrial and ventricular hypertrophy

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22
Q

What management would you suggest?

A
  1. Smoking cessation
  2. Pulmonary rehab
    3 .Diet advice and supplementation
  3. Vaccination and antiviral therapy
  4. Drug therapy (mucolytics)
  5. Oxygen therapy
  6. Surgery
  7. Palliative care
23
Q

What is pulmonary rehab?

A

Programme of physical training, disease education, nutritional assessment and advice, and psychological, social, and behavioural intervention.

24
Q

What vaccination do you offer?

A

Pneumococcal and annual flu vaccination

Antivirals recommended for influenza infections (zanamivir and oseltamivir)

25
Q

What are the surgical options?

A

o Bullectomy if single large bulla present on CT scan

o Lung transplant if remain breathless despite maximal medical therapy

26
Q

What palliative care do you consider?

A

o For people with end-stage COPD unresponsive to other medical therapy
o Opioids should be used as pain relief
o Use benzodiazepines, tricyclic antidepressants, major tranquillisers and oxygen to treat breathlessness

27
Q

When do you use short-acting b-agonist?

A

e.g. salbutamol, turbutaline – as needed, mild COPD

28
Q

Example and when do you use Short-acting muscarinic antagonist?

A

e.g. ipratropium – as needed

29
Q

Example and when do you use Long-acting beta agonist?

A

e.g. salmeterol, formoterol – more severe COPD, maintenance therapy

30
Q

Example and when do you use Long-acting muscarinic antagonist?

A

e.g. tiotropium – equally as effective as LABA

31
Q

When do you use Inhaled corticosteroids?

A

– if LABA/LAMA insufficient in severe COPD

32
Q

When do you give antibiotics?

A

acute exacerbations and sometimes long-term

33
Q

When do you give oral corticosteroids?

A

to decrease acute exacerbations in moderate to severe COPD

34
Q

When do we use theophylline?

A

use not encouraged; used only when corticosteroids and other medication have not helped

35
Q

When do you use mucolytics? How are they administered?

A

e.g. carbocisteine – chronic productive cough

Oral

36
Q

Acute Oxygen Therapy

A

o SaO2 aim 88-92%
o ABGs required to monitor changes to PaO2 and O2
o If PaO2 rises and PaCO2 drops then continue to give
o If pH drops and PaCO2 rises then consider non-invasive ventilation (NIV) instead – in hypercapnia patients lose their respiratory drive from low CO2 and so require hypoxia to keep them breathing

37
Q

Describe LTOT

A

o At least 15 hours a day
o Given at night if arterial hypoxaemia worsens overnight
o Considered for patients with FEV1 <30% predicted, cyanosis, polycythaemia, peripheral oedema, raised JVP, sats <92% on air
o Ambulatory oxygen can also be given to those already o LTOT who want to use it outside the house
o Hypercapnic patients should be considered for long-term NIV

38
Q

When do we consider short-burst oxygen therapy?

A

o Should be considered for patients not eligible for LTOT but who remain breathless after minimal exertion

39
Q

How do we treat mild COPD?

A

Antimuscuarinic eg ipratropium or B2 agonist inhaled PRN

40
Q

How do we treat moderate COPD?

A

Regular anticholinergic eg ipratropium or tiotropium or long acting B 2 agonist eg salmetrol + inhaled corticosteroid eg beclomethasone esp if FEV1 <50% and >2 exacerbations/yr eg seretide. May consider oral theophylline

41
Q

How do we treat severe COPD?

A

Long acting B2 agonist + inhaled steroid + anticholinergic
Refer to specialist
Consider steroid trial or home nebs

42
Q

How do we deal with pulmonary hypertension?

A

Assess need for long term O2 therapy
UK DoH guidelines suggest LTOT for:
1.) Clinically stable non smokers with PaO2 <7.3kPa despite max Rx
2.) If PaO2 7.3-8.0 AND pul HTN (eg RHV; loud S2) + cor pulmonale
3.) Terminally ill patients
Treat oedema with diuretics

43
Q

What are the indications for surgery?

A

Recurrent pneumothoraces
Isolated bullous disease
Lung vol reducing surgery (selected pts)

44
Q

How do we deal with an acute exacerbation of COPD?

A

Increasing cough, breathlessness, wheeze. Decr exercise capacity
Look for cause eg infection, pneumothorax
Controlled O2 therapy (start 24-48%; vary according to ABG. Aim for PaO2 >8.0kPa with prise in PaCO2 <1.5kPa
Nebulised bronchodilators – salbutamol 5mg/4hr and ipratropium 500mcg/6hr
Steroids – IV hydrocortisone (200mg) and oral prednisolone 30-40mg for 7-14d
Antibiotics – if evidence of infection – amoxicillin 500mg/8hr PO or clarithromycin or doxycycline
Physio to aid sputum expectoration
If no response – repeat nebs and consider IV aminophylline
If still no response, consider NIPPV if RR >30 or pH <7.35
Consider intubation and ventilation if pH <7.26 and PaCO2 is rising
Consider a resp stimulant drug eg doxapram 1.5-4mg/min IV. SE: agitation, confusion, tachycardia, nausea. In pt who not suitable for mechanical ventilation. Short term measure and rarely sued now NIPPV available.

45
Q

Are symptoms common in <35yrs?

A

Uncommon

46
Q

Is a chronic productive cough common or uncommon?

A

Common

White/clear/grey sputum

47
Q

Is night time waking with SOB common or uncommon?

A

Uncommon

48
Q

Is significant diurnal/day-to-day variation common or uncommon?

A

Uncommon

49
Q

How do you differentiate between COPD and Asthma?

A

Asthma – does not usually coincide with COPD; no sputum; presents earlier; reversible airway obstruction

50
Q

How do you differentiate between COPD and Bronchictasis?

A

Bronchiectasis – purulent sputum; presents earlier; absence of smoking Hx

51
Q

How do you differentiate between COPD and congestive heart failure?

A

Congestive heart failure – no cough;

52
Q

How do you differentiate between COPD and Pneumonia?

A

Pneumonia - acute; consolidation on CXR

53
Q

What is the prognosis?

A

Five-year survival from diagnosis is 78% in men and 72% in women with clinically mild disease (defined as not requiring continuous drug therapy), but falls to 30% in men and 24% in women with severe disease defined as requiring oxygen or nebulised therapy.

54
Q

What are the complications?

A
  • Acute exacerbations/infections
  • Respiratory failure
  • Secondary polycythaemia – hypoxia stimulates erythropoietin increasing number of red blood cells
  • Cor pulmonale – hypoxia leads to vasoconstriction of lulmonary vessels in order to improve ventilation-perfusion; leads to right-heart strain resulting in right-sided hypertrophy
  • Pneumothorax – bullae; thin, brittle alveolar walls; prone to rupture

RESPIRATORY (8 decks)

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