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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
NICE guidelines management of acute COPD exacerbation (if 1st line Rx do not work)
* 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
Treatments for acute severe asthma attack
* ***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
28
Stepwise management of asthma in adults
29
1st line (after lifestyle advice) of management of a stable COPD
_Bronchodilator therapy_ * a short-acting **beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA)**
30
What should be determined for COPD patients who remain breathless after use of SABA/SAMA (1st line)?
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
What are the criteria to determine if a patient has asthmatic features/steroid responsiveness?
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
What is the 2nd step in the management (after SABA/SAMA) for a COPD patient with no asthmatic features?
No asthmatic features/features suggesting steroid responsiveness * add a **long-acting beta2-agonist (LABA)** + **long-acting muscarinic antagonist (LAMA)**
33
What to add to the management\* of COPD patient with asthmatic features (suggesting steroid responsiveness)? \*after 1st line SABA/SAMA were tried
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
When an oral theophylline Rx should be prescribed in COPD patient?
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
When to consider use of mucolytics in COPD?
Mucolytics should be 'considered' in patients with a chronic productive cough and continued if symptoms improve
36
Features of cor pulmonare
***Cor pulmonale*** * fperipheral oedema * raised jugular venous pressure * systolic parasternal heave * loud P2
37
Drug management of cor pulmonare
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
Risk factors for ***pulmonary fibrosis***
* 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
Pathophysiology of ***Pulmonary Fibrosis***
40
Important differentiation in condition causing lung fibrosis
* conditions causing predominately **upper** or **lower** zone fibrosis \* more common causes (idiopathic pulmonary fibrosis, drugs) tend to affect the lower zones
41
Causes of u**pper zone fibrosis**
42
Causes of **lower zone fibrosis**
* 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
What's that?
CT scan showing advanced pulmonary fibrosis including 'honeycombing
44
What happens in ***Intestinal Pneumonitis***? (pathology)
* excessive extracellular matrix deposition * fibroblast and myofibroblast accumulation –between vascular and alveolar endothelium –disrupt normal lung structure –“***honeycomb***” appearance
45
Symptoms of pulmonary fibrosis
- dry cough - SOB - weight loss (sometimes)
46
Signs of ***pulmonary fibrosis***
* Finger clubbing * Reduced chest expansion * Fine end-inspiratory crackles –usually bilateral –sound like “velcro” •Signs of an associated condition –e.g. Rheumatoid arthritis
47
Ix in ***Pulmonary Fibrosis***
•**Oxygen saturations** –reduced •**Spirometry** –restrictive –reduced FEV1 and FVC –normal FEV1/FVC ratio •**Pulmonary function tests** –reduced lung volumes –reduced transfer factor
48
Restrictive flow volume loop
49
Features of ***pulmonary fibrosis*** on *CXR* (2)
* increased interstitial markings * reduced lung volumes
50
Features of ***Primary Fibrosis*** on CT
* *honeycomb* appearance * traction bronchial dilatation (“traction bronchiectasis”) * thickened interlobular septae * reduced lung volumes
51
General management steps in ***Pulmonary Fibrosis***
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
What two drugs to use for ***Idiopathic Pulmonary Fibrosis***?
– ***N-acetylcysteine*** (but evidence limited) – ***Pirfenidone & Nintedanib*** (nice criteria for use)
53
What's ***Idiopathic Pulmonary Fibrosis?***
***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
Clinical features of ***Idiopathic Pulmonary Fibrosis***
* progressive exertional dyspnoea * bibasal crackles on auscultation * dry cough * clubbing
55
Ix and results in ***Idiopathic Pulmonary Fibrosis***
* **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
Management of ***Idiopathic Pulmonary FIbrosis***
* 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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