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respiratory > COPD > Flashcards

COPD Flashcards

1
Q

caused by

A

smoking

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2
Q

who is more likely to get it

A

men working in unskilled manual occupations

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3
Q

complications

A
  • cor pulmonale
  • lower tract infections
  • depression
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4
Q

what is the overarching characteristic

A
  • airflow limitation

- destruction of lung parenchyma

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5
Q

associated with

A
  • ischaemic heart disease
  • hypertension
  • diabetes
  • heart failure
  • cancer
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6
Q

defined by

A

disease state characterised by airflow limitation that is not fully reversible

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7
Q

what is most common pathological finding

A

increase number of mucus-secreting goblet cels in bronchial mucosa

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8
Q

pathology in advanced stages

A

bronchi become overly inflamed and pus is seen in lumen

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9
Q

what is seen microscopically

A

infiltration of the walls of the bronchi and bronchioles

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10
Q

what is the predominant lymphocytic infiltrate

A

CD8

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11
Q

what can happen to epithelial layer

A

can become ulcerated

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12
Q

what metaplasia occurs over time

A

squamous epithelium replaces columnar cells

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13
Q

when are airways affected

A

early

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14
Q

what is emphysema

A

loss of elastic recoil of lung with collapse of small airways

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15
Q

what is pan-acinar emphysema associated with

A

alpha-1 antitrypsin deficiency

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16
Q

what does inflammation and scarring cause in small airways

A

narrowing

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17
Q

what does bronchoalveolar lavage and biopsies show

A

increased numbers of neutrophil granulocytes

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18
Q

what can granulocytes release

A

elastase and proteases

help produce emphysema

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19
Q

what imbalance is shown

A

in protease and antiprotease

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20
Q

what antiprotease is inactivated by smoking

A

alpha1- antitrypsin

21
Q

what causes mucous gland hypertrophy in larger airways

A

persistent irritation from inhalation of cigarette smoke

22
Q

where is alpha1-antitrypsin produced

A

in liver

23
Q

where is alpha1-antitrypsin secreted

A

into blood and diffuses into lung

24
Q

what dose alpha1-antitrypsin inhibit

A

neutrophil elastase

25
Q

what does neutrophil elastase destroy

A

alveolar wall connective tissue

26
Q

symptoms

A
  • productive cough
  • clear sputum
  • wheeze
  • breathlessness
  • frequent infective exacerbation
27
Q

when are symptoms worsened

A

cold or damp weather

28
Q

what are some systemic effects

A
  • depress
  • hypertension
  • osteoporosis
  • weight loss
  • reduce muscle mass
29
Q

what can patients develop

A

pulmonary hypertension (cor pulmonale)

30
Q

what is diagnosis

A

clinical

31
Q

what investigations can be done

A
  • Lung function test
  • CXR
  • CT
  • blood gases
  • sputum exam
  • ECG
  • echo
32
Q

what is the FEV1:FVC ratio

A

reduced

33
Q

what is seen on CXR

A
  • overinflation
  • flattened diaphragms
  • pruned blood vessels

can be normal so would do CT

34
Q

what causes exacerbation

A
  • step pneumonia

- H.influenza

35
Q

ECG shows

A

often normal

in pulmonary hypertension

  • tall p wave
  • right bundle branch block
  • right ventricular hypertrophy
36
Q

what is the single most useful thing for treatment

A

smoking cessation

37
Q

what drugs are used

A
  • beta-adrenoreceptor agonist
  • antimuscarinic drug
  • theophyllines
38
Q

example of beta agonist

A

salbutamol

39
Q

LAMA example

A

tiotropium

40
Q

SAMA example

A

ipatropium

41
Q

do theophyllines work for COPD

A

no

42
Q

PDE4 inhibitor

A

roflumilast

43
Q

how long should prednisolone be given for

A

2 weeks

44
Q

in an exacerbation what is oxygen given through

A

venturi mask

initially 24%

45
Q

what is there a loss of in emphysema

A

distal lung parenchyma

46
Q

causes of centrilobar emphysema

A
  • smoking

- coal dust

47
Q

where is centrilobar emphysema mostly

A

upper lobes

48
Q

where is pan lobar emphysema

A

lower lobes

49
Q

who gets pan lobar emphysema

A

alpha-1 antitrypsin

respiratory (20 decks)

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