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Medicine Part 2 > CBL_3 Obstructive and restrictive lung diseases > Flashcards

CBL_3 Obstructive and restrictive lung diseases Flashcards

1
Q

Changes in the airways and alveoli of COPD/obstructive

A

Airways:

–disruption of the epithelial barrier

–poor mucociliary clearance

–infiltration of the airway walls by inflammatory cells

–deposition of connective tissue in the airway wall

–repair leads to remodelling - thickened airway walls, reduced airway diameter, and restricts the normal increase in diameter when inflating lungs

Alveoli:

–Emphysematous lung destruction is associated with an infiltration of inflammatory cells

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2
Q

Neutrophils in an asthmatic airway is associated with what risk factors? (3)

A
  • sudden-onset, fatal asthma exacerbations
  • occupational asthma
  • patients who smoke
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3
Q

What happens in the asthamtic airway?

A

Chronic inflammation ->infiltration of inflammatory cells (neutrophils, eosinophils, mast cells, lymphocytes) -> hyper-responsivness and airflow limitation

Persistent inflammation leads to changes in the airways (on different flashcard)

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4
Q

Changes in asthmatic airway

A

–changes in airway structure

–sub-basement fibrosis

–mucus hypersecretion

–injury to epithelial cells

–smooth muscle hypertrophy

–angiogenesis

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5
Q

Symptoms of asthma

A
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6
Q

SYmptoms of COPD

A
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7
Q

Signs of a patient with an airway disease

A

Hyper-expansion

–reduced cricosternal distance

–reduced chest expansion

Wheeze

–Polyphonic

–Bilateral

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8
Q

Investigations for asthma/COPD

A
  • Blood tests

FBC – eosinophil count

  • Peak Expiratory Flow

Predicted based on age, gender, height

  • Spirometry

Obstructive:

–Reduced FEV1

–Reduced FEV1/FVC ratio (<70%)

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9
Q

How does the obstructive pattern look on flow volume loop?

A
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10
Q

CXR of an asthmatic patient - features

A

–usually normal

–may be hyperinflated

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11
Q

CXR of a patient with COPD - features

A

–Hyperinflated

–May be evidence of bullae

–May be evidence of associated disease e.g. pulmonary hypertension

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12
Q

CT of asthma - features

A

–May be normal

–Gas trapping – mosaicism – in expiration

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13
Q

CT of COPD - features

A

–Emphysema

–Bullae

–May be changes of associated conditions e.g. pulmonary hypertension

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14
Q

What does this CT show?

A

Mosaicism in asthma

(air trapping on expiration)

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15
Q

What do these CT scans show?

A

Emphysema - COPD

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16
Q

What is it?

A

Emphysema

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17
Q

What is this?

A

Emphysema with bullae

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18
Q

Initial treatment in asthma

A
  • Smoking cessation
  • Short- acting beta-agonist
  • Inhaled corticosteroids
  • Education

–peak flow monitoring, inhaler technique, asthma management plan

•Influenza/pneumococcal vaccine

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19
Q

Initial treatment of COPD

A
  • Smoking cessation
  • Short acting beta-agonist
  • Long acting muscarinic antagonist

or

  • Long acting beta agonist
  • Pulmonary rehabilitation
  • Education
  • Influenza/pneumococcal vaccine
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20
Q

What organisms are most likely to cause infective exacerbations of asthma?

A
  • Most often Viral (Rhinovirus, Influenza, Respiratory Syncitial Virus
  • Bacterial

Consider atypical organisms: Chlamydophila pneumoniae and Mycoplasma pneumoniae

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21
Q

Initial management steps of infective exacerbations of asthma

A
  • Consider sputum culture before starting antibiotics
  • Refer to local microbiology guidance
  • clarithromycin & doxycycline cover atypicals
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22
Q

Organisms likely to cause infective exacerbation of COPD

A

A. Viral (approximately 30%)

•Rhinovirus, Influenza, Respiratory Syncitial Virus

B. Bacterial

•Haemophilus influenzae, Streptococcus pneumoniae, Mycoplasma pneumoniae

C. May be bacterial and viral co-infection

D. In more severe COPD consider also: Klebsiella pneumoniae, MRSA, Pseudomonas aeruginosa (PsA)

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23
Q

Initial treatment of acute exacerbation COPD

A

–Consider sputum culture before starting antibiotics

–Refer to local microbiology guidance

–Amoxicillin/Clarithromycin/Doxycycline

–Ciprofloxacin is only oral agent effective for PsA

24
Q

What’s the only effective oral agent against Pseudomonas Auerginosa?

A

Ciprofloxacin *

*Ciprofloxacin belongs to a fluoroquinolone class

25
Q

NICE guidelines management of acute COPD exacerbation (if 1st line Rx do not work)

A
  • increase frequency of bronchodilator use and consider giving via a nebuliser
  • give prednisolone 30 mg daily for 7-14 days
  • Oral antibiotics ‘if sputum is purulent or there are clinical signs of pneumonia’
  • oral antibiotics first-line: amoxicillin or tetracycline or clarithromycin
26
Q

Treatments for acute severe asthma attack

A
  • magnesium sulphate recommended as next step for patients who are not responding (e.g. 1.2 - 2g IV over 20 mins)
  • IV aminophylline
  • if no response consider IV salbutamol
27
Q
A
28
Q

Stepwise management of asthma in adults

A
29
Q

1st line (after lifestyle advice) of management of a stable COPD

A

Bronchodilator therapy

  • a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA)
30
Q

What should be determined for COPD patients who remain breathless after use of SABA/SAMA (1st line)?

A

for patients who remain breathless or have exacerbations despite using short-acting bronchodilators the next step is determined by whether the patient has ‘asthmatic features/features suggesting steroid responsiveness’

31
Q

What are the criteria to determine if a patient has asthmatic features/steroid responsiveness?

A

Criteria NICE suggest to determine whether a patient has asthmatic/steroid responsive features:

  • any previous, secure diagnosis of asthma or of atopy
  • a higher blood eosinophil count - note that NICE recommend a full blood count for all patients as part of the work-up
  • substantial variation in FEV1 over time (at least 400 ml)
  • substantial diurnal variation in peak expiratory flow (at least 20%)
32
Q

What is the 2nd step in the management (after SABA/SAMA) for a COPD patient with no asthmatic features?

A

No asthmatic features/features suggesting steroid responsiveness

  • add a long-acting beta2-agonist (LABA) + long-acting muscarinic antagonist (LAMA)
33
Q

What to add to the management* of COPD patient with asthmatic features (suggesting steroid responsiveness)?

*after 1st line SABA/SAMA were tried

A

COPD patient with asthmatic features/features suggesting steroid responsiveness

  • LABA + inhaled corticosteroid (ICS)
  • if patients remain breathless or have exacerbations offer triple therapy i.e. LAMA + LABA + ICS
  • NICE recommend the use of combined inhalers where possible
34
Q

When an oral theophylline Rx should be prescribed in COPD patient?

A

Oral theophylline

  • NICE only recommends theophylline after trials of short and long-acting bronchodilators or to people who cannot used inhaled therapy
  • the dose should be reduced if macrolide or fluoroquinolone antibiotics are co-prescribed
35
Q

When to consider use of mucolytics in COPD?

A

Mucolytics

should be ‘considered’ in patients with a chronic productive cough and continued if symptoms improve

36
Q

Features of cor pulmonare

A

Cor pulmonale

  • fperipheral oedema
  • raised jugular venous pressure
  • systolic parasternal heave
  • loud P2
37
Q

Drug management of cor pulmonare

A

Use a loop diuretic for oedema, consider long-term oxygen therapy

ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICE

38
Q

Risk factors for pulmonary fibrosis

A
  • Smoking
  • Family history
  • Increasing age
  • Men more than women
  • Expose to toxins (miner, farmers, construction, ship workers, asbestosis, cotton workers, birds and animal dropping exposure)
  • Connectives Tissue Disorder (sarcoidosis, SLE, systemic sclerosis, dermatomyositis and polymyositis)
  • Medication (methotrexate, amiodarone, chemotherapy, nitrofurantoin, azathioprine, rituximab)
  • Radiation and exposure to radiotherapy
39
Q

Pathophysiology of Pulmonary Fibrosis

A
40
Q

Important differentiation in condition causing lung fibrosis

A
  • conditions causing predominately upper or lower zone fibrosis

* more common causes (idiopathic pulmonary fibrosis, drugs) tend to affect the lower zones

41
Q

Causes of upper zone fibrosis

A
42
Q

Causes of lower zone fibrosis

A
  • idiopathic pulmonary fibrosis
  • most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
  • drug-induced: amiodarone, bleomycin*, methotrexate
  • asbestosis

*bleomycin - anti tumor antibiotic/ cytotoxic

43
Q

What’s that?

A

CT scan showing advanced pulmonary fibrosis including ‘honeycombing

44
Q

What happens in Intestinal Pneumonitis? (pathology)

A
  • excessive extracellular matrix deposition
  • fibroblast and myofibroblast accumulation

–between vascular and alveolar

endothelium

–disrupt normal lung structure

–“honeycomb” appearance

45
Q

Symptoms of pulmonary fibrosis

A
  • dry cough
  • SOB
  • weight loss (sometimes)
46
Q

Signs of pulmonary fibrosis

A
  • Finger clubbing
  • Reduced chest expansion
  • Fine end-inspiratory crackles

–usually bilateral

–sound like “velcro”

•Signs of an associated condition

–e.g. Rheumatoid arthritis

47
Q

Ix in Pulmonary Fibrosis

A

•Oxygen saturations

–reduced

•Spirometry

–restrictive

–reduced FEV1 and FVC

–normal FEV1/FVC ratio

•Pulmonary function tests

–reduced lung volumes

–reduced transfer factor

48
Q

Restrictive flow volume loop

A
49
Q

Features of pulmonary fibrosis on CXR (2)

A
  • increased interstitial markings
  • reduced lung volumes
50
Q

Features of Primary Fibrosis on CT

A
  • honeycomb appearance
  • traction bronchial dilatation (“traction bronchiectasis”)
  • thickened interlobular septae
  • reduced lung volumes
51
Q

General management steps in Pulmonary Fibrosis

A

In general:

–assess for a cause or associated condition

–assess for oxygen

–assess for pulmonary rehabilitation

–consider symptomatic treatments e.g. morphine for breathlessness/cough

52
Q

What two drugs to use for Idiopathic Pulmonary Fibrosis?

A

– N-acetylcysteine (but evidence limited)

– Pirfenidone & Nintedanib (nice criteria for use)

53
Q

What’s Idiopathic Pulmonary Fibrosis?

A

idiopathic pulmonary fibrosis (IPF, previously termed cryptogenic fibrosing alveolitis)

  • progressive fibrosis of the interstitium of the lungs
  • idiopathic cause (e.g. not due to asbestos etc)
  • IPF is typically seen in patients aged 50-70 years and is twice as common in men
  • poor prognosis - usually life expectancy is 3-4 years
54
Q

Clinical features of Idiopathic Pulmonary Fibrosis

A
  • progressive exertional dyspnoea
  • bibasal crackles on auscultation
  • dry cough
  • clubbing
55
Q

Ix and results in Idiopathic Pulmonary Fibrosis

A
  • spirometry: classically a restrictive picture (FEV1 normal/decreased, FVC decreased, FEV1/FVC increased)
  • impaired gas exchange: reduced transfer factor (TLCO)
  • imaging: bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’) may be seen on a chest x-ray but high-resolution CT scanning is the investigation of choice and required to make a diagnosis of IPF
  • ANA positive in 30%, rheumatoid factor positive in 10% but this does not necessarily mean that the fibrosis is secondary to a connective tissue disease
56
Q

Management of Idiopathic Pulmonary FIbrosis

A
  • pulmonary rehabilitation
  • very few medications have been shown to give any benefit in IPF. There is some evidence that pirfenidone (an antifibrotic agent) may be useful in selected patients
  • many patients will require supplementary oxygen and eventually a lung transplant

Medicine Part 2 (12 decks)

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