Obstructive lung disease Flashcards

1
Q

What is asthma

A

hypersensitivity (type 1) response to allergens (dust mite, fungi, pollen)., leading to reversible obstruction.

mast cell, histamine, cytokines

Atopic (genetic) and environmental.

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2
Q

pathophysiology of asthma

A

Primarily mast cell degranulation and histamine
release as a result of allergen exposure in the
acute phase, causing mucus plugging and airway
bronchoconstriction

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3
Q

Examples of obstructive lung disease

A

asthma, chronic bronchitis, emphysema, bronchiectasis

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4
Q

Asthma treatment BTS

A
  1. Inhaled SABA, salbutamol
  2. Inhaled corticosteroid (ICS) 200-800mcg/day. beclometasone, ciclesonide, budesonide
  3. Inhaled LABA, salmeterol
    >if good response, continue LAA
    >if benefit from LABA but not controlled, continue LABA and increase ICS to 800 mcg/day
    >if no response to LABA, stop LABA. increase ICS to 800 mcg/day, and consider using leukotriene receptor antagonist. montelukast, zafirlukast, and pranlukast
    4.increase ICS to 2000 mcg/day, or add leukotriene receptor antagonist
  4. offer daily steroid tablet and ICS 2000 mcg /day, prednisone (mainly gluco)
    >refer to speailist
    >omalizumab (Subcut), monoclonal antibody against IgE, stops mast cell degranulation
    >bronchial thermoplasty
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5
Q

COPD definition

A

Airway limitation secondary to inflammation caused by stimuli, not reversible. Emphysema and chronic bronchitis.

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6
Q

COPD in the young should make you suspect which genetic cause of COPD?

A

alpha 1 antitrypsin deficiency.

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7
Q

what in alpha 1 antitrypsin deficiency?

A

a lack of A1AT, so there is not stopping the breakdown of elastin by neutrophil elastine.

This leads to alveolar destruction.
a. Congestion of the liver with the enzyme alpha-1 antitrypsin (which is produced there in an attempt to compensate)
eventually causes destruction of hepatocytes,
leading to liver disease.

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8
Q

what is centrilobular emphysema?

A

Smokers tend to develop centrilobular emphysema
which typically affects proximal acini
and the upper lung

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9
Q

what is panlobular emphysema?

A

patients
with alpha-1 antitrypsin deficiency tend
to develop panlobular emphysema,
broadly affecting the lower lung

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10
Q

Which organism is the most common cause of COPD exacerbation?

A

Haemophilus

influenzae

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11
Q

Clinical features of COPD?

A
exertional breathlessness
wheeze
sputum production
haemoptysis
bronchitis in the winter
weight loss
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12
Q

MRC dyspnoea scale

A
  1. not troubled by SOB unless on exertion
  2. SOB when hurrying up a hill
  3. walks slower than contemporaries, or has to stop for breath at own pace
  4. stops after 100 yards for breath, or a few minutes
  5. too breathless to leave the house or upon dressing
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13
Q

what is the difference between emphysema and chronic bronchitis

A

e: alveolar wall destruction due to inflammatory changes

CB: goblet cell hyperplasia and increased mucus secretion leading to chronic cough.

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14
Q

Investigation of COPD

A
  1. Spirometry
  2. MRC dyspnoea
  3. CXR (hyperinflation)
  4. sputum culture
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15
Q

management of COPD

A
  1. inhaled SABA (salbutamol) or SAMA (muscarinic antagonists, ipratropium)
    2.Use FEV1 ad a guide
    FEV1> 50%: LABA (salmeterol) or LAMA (tiotropoum) and discontinue SAMA
    FEV1<50%, LABA +ICS. Or LAMA
  2. Theophylline oral modified release(a xanthines, a muscle relaxer) and mucolytics (Carbocisteine and acetylcysteine, oral)
  3. Long term oxygen therapy, when PaO2< 7.3 or PaO2 <7.3–8kPa with secondary polycythaemia,
    nocturnal hypoxaemia, or pulmonary
    hypertension
  4. Surgical, bullectomy, or lung transplant
    Bullectomy is considered in patients who have a single large bulla on CT scan and an FEV1 <50% predicted
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