COPD lms Flashcards

1
Q

chronic bronchitis

A

chronic inflammation of airways with excess mucous production
leads to narrowing of airways

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2
Q

emphysema

A

dilatation of the airways distall to the terminal branchioles
destruction of alveili with bullae formation and lossof lung elaasticity leading to trapping of air and lung hyperinflation

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3
Q

alpha-1 antitrypsin deficiency

A

rare cause of emphysema
autosomal recessive
normal genotype is PiMM, heterozygotes are PiMz and homozygotes are PiZZ
homozygotes with pool antitrypsin in the liver because they cannot transport it out of the liver causing liver cirrhosis
deficiency of antitrypsin in the blood means they cannot protect the lungs from endogenous proteases

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4
Q

suspect alpha 1 antitrypsin deficiency in

A

emphysema with no or minimal smoking history
or severe emphysema in smoker aged under 40

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5
Q

typical histroy of COPD

A

generally over 50
a smoker or ex smoker with a smoking history of at least 20 pack years
presents with gradually worsening cough, often productive of sputum, shortness of breath, wheeze

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6
Q

signs on mild/moderate COPD

A

may hear wheeze or crackles if predominant bronhcitis
breath sounds in emphysema are quiet due to loss of lung tissue or may be normal

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7
Q

signs of severe COPD

A

hyperexpanded barrel chest
may be using accessory muscles of respiration
may exhibit pursed lip breathing (to keep the pressure of the small airways up so they dont collapse on expiration)
cyanosed
angle oedema
cechectic with muscle wasting

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8
Q

ssigns of respiratory failure

A

if in respiratory failure with carbon dioxide retention, may have a flapping treemor, papilloedema, confusion and peripheral vasodilatation

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9
Q

confirming the diagnosis of COPD

A

full smoking histroy
spirometry - FEV1 and FVC
CXR is not a diagnsotic test - often normal in mild/moderate cases

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10
Q

imporrtance of spirometry

A

better measure of small airway function
prognostic value
FEV1 60-80% : mild
FEV1. 40-60% : moderate
FEV1<40 : severe

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11
Q

CXR in severe COPD

A

flattened diaphragm due to hyperinflation
large volume lungss
hyerlucent areas due to the presence of bullae

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12
Q

differential diagnoses

A

asthma - wheeze and cough
bronchiectasis - cough and excessive sputum production
idiopathic. pulmonary fibrosis - gradually worsening breathlessness and cough
lung cancer - chronic cough, although history usually shorteer than in COPD

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13
Q

distinguishing featuress beetween COPD and asthma

A

COPD: not usually woken at night by symptoms, little variation in severity, never completely free of symptoms, may be some improvement on coritocsteroids but often none
asthma: symptoms often worse at night or cause waking, may be marked day to day variability, may be entirely well between attacks, marked therapeutic response to corticosteroids

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14
Q

complications of COPD

A

exacerbations
resppiratory failure (type 1 if normocapnia, or type 2 if hypercapnia)
pulmonary hypertension (causing right heart failure)
pneumothorax

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15
Q

management of COPD

A

smoking cessation
inhaled bronchodilators -
short: beta 2 agonsits (salbutamol and terbutaline) or antimuscarinics (iprotropium)
long: beta 2 agonists and antimuscarinics

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16
Q

why not use inhaled steroids

A

increasing body of evidence for risk of long term high dose inhaled. steroids including oneumonia and mycobacterial infection
reserve inhaled steroids for COPD exacerbations

17
Q
A