copd Flashcards

1
Q

what are the most common symptoms of copd?

A

dyspnea, cough (early morning), sputum production

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2
Q

outline the mechanism of copd

A

exposure to smoke and environmental particles + host factor amplifying mechanisms causes lung inflammtion
this leads to oxidative stress, which can be inhibited by antioxidants and antiproteases. repair mechanisms are impaired by oxidative stress.
alveolar wall is destroyed, mucus is hypersecreted and fibroblasts cause abnormal tissue repair

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3
Q

why do the airways narrow in bronchitis?

A

remodelling

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4
Q

which airways narrow first in bronchitis?

A

smaller airways in periphery - have no cartilage to keep them open

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5
Q

which enzyme causes alveoli to lose elastic tissue?

A

proteolytic enzymes destroy elsatin and collagen

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6
Q

which inflammatory cells and mediators are involved in copd?

A

neutrophils
macrophages
t cells (more cd8 than cd4)
leucotriene B4 - attracts neutrophils and t cells
IL-8 and growth related oncogene alpha - amplifies pro inflammatory responses
TNF alpha, IL - 1 beta, IL-6 - proinflammatory
TGF beta - causes fibrosis

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7
Q

what pathological changes occur in the airway bronchial submucosal glands?

A

hypertrophy and hyperplasia

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8
Q

do goblet cell numbers increase or decrease?

A

increase

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9
Q

destruction of what cell causes difficulty expectorating?

A

cilia cells

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10
Q

expiratory flow limitation is caused by…

A

decreased elastic recoil of lungs
decreased gas exchange
hyperinflation
sputum production

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11
Q

what causes the wheeze in copd?

A

stenosis of bronchial tree - decreased diameter

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12
Q

what are some other clinical findings of copd?

A
increased respiratory rate
accessory muscle use
wheeze
reduced chest expansion
barrel chest
reduced breath sounds
asterixis (liver hand flap)
cyanosis
cor pulmonale
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13
Q

what are some non respiratory related features of copd?

A
weight loss
muscle wasting
cardiovascular comorbidities
depression
osteoporosis
normocytic anaemia
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14
Q

why does gas trapping occur in expiration?

A

small airways collapse and trap air

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15
Q

______flow limitation occurs in tidal breathing

A

expiratory

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16
Q

what are some effects on lung capacity?

A

increased end expiratory lung volume (FRC)
decreased inspiratory capacity and inspiratory reserve volume
functional weakness of the diaphragm

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17
Q

reduced muscle pump capacity + increased respiratory load = _____neural respiratory drive

A

increased

18
Q

what causes cor pulmonale in copd?

A

chronic hypoxia causes pulmonary vasoconstriction which leads to pulmonary hypertension.

19
Q

which viruses can cause copd exacerbations?

A

influenza/parainfluenza
rsv
human metapneumovirus
coronavirus

20
Q

which bacteria commonly cause exacerbations?

A

h. influenzae
m. catarrhalis
s. pneumoniae
s. aureus

21
Q

which bacteria are common in severe exacerbations?

A

pseudomonas aeruginosa

22
Q

what are features of an exacerbation?

A
increased breathlessness
increased cough
increased sputum
change in colour of sputum
impaired daily activities
raised temp, resp rate,heart rate, bp
low o2 sats
sweaty, confused
polyphonic wheeze
ankle oedema
23
Q

how should a mild exacerbation be treated?

A

short acting bronchodilators only

24
Q

how should a moderate exacerbation be treated?

A

short acting bronchodilator
antibiotics
oral corticosteroids

25
Q

why do peripheral muscles fatigue in exercise?

A

lower limb muscle atrophy
reduced muscle metabolism
decreased type 1 fibres
decreased myosin heavy chain 1 and oxidative enzyme activity

26
Q

what is a typical history for someone in the chronic bronchitis group?

A

hypoxic, obese, coughing using accessory muscles
productive cough
intermittent dyspnoea later
frequent and recurrent pulmonary infections
progressive cardiac/respiratory failure
oedema
weight gain (due to inactivity)

27
Q

what is a typical history for someone in the emphysema group?

A
thin, barrel chest, dry cough, effort in breathing, wheezing, hyperresonant chest
long history of progressive dyspnoea
later onset of non productive cough
occasional mucopurulent relapses
cachexia and respiratory failure
28
Q

how does the histology of the airways change in chronic bronchitis?

A
more squamous metaplastic epithelial cells
less columnar and ciliiated cells
mucous gland hyperplasia
basal cell metaplasia
squamous metaplasia
more macrophages as cd8 t cells
NO smooth muscle increase (thats asthma)
29
Q

what are neutrophils in the sputum a sign of?

A

exaerbation due to local infection

30
Q

what enzyme destroys elastic and collagen fibres in emphysema

A

proteases

31
Q

which genetic deficiency has high rates of emphysema?

A

alpha 1 antitrypsin deficiency

32
Q

which form of emphysema affects the area of the acinar proximal to the terminal bronchile and is characteristic of smokers?

A

centrilobar emphysema

33
Q

describe panacinar emphysema

A

affects the whole acinar
characteristic in exposure to smoke or noxious gases and alpha 1 antitrypsin deficiency
bullous subpleural airspaces can form due to ruptures

34
Q

what will a chest x ray for copd show?

A

hyperinflation

clear lung fields (unless pneumonia)

35
Q

what does an increase in sputum purulence in an exacerbation indicate?

A

bacterial infection

36
Q

how can a severe exacerbation be treated?

A
o2 therapy
sabd
b2 agonist plus anticholinergic therapy
systemic glucocorticoids
antibiotics
37
Q

what are the target sats for copd:

A

88% - 92%

38
Q

when should non invasive ventilation be considered?

A

acute resp acidosis
signs of fatigue
increased work of breathing
persistent hypoxaemia

39
Q

what indicates need for intubation?

A
post cardiorespiratory arrest
reduced consciousness
arrhythmia
haemodynamic instabiility
hypoxaemia
aspiration/vomiting
40
Q

decribe management of stable copd

A
flu vaccine
stop smoking
education
strengthen skeletal muscles
bronchodilators - sabas, labas, antimuscarinics, 
inhaled corticosteroids
surgical lung volume reduction
lung transplant
oxygen
41
Q

what are some side effects of beta 2 agonists

A

increased hr, arrythmias, hypokalemia