Respiratory Flashcards

1
Q

What are the main classes of drugs used to treat respiratory disease?

A

inhaled corticosteroids
bronchodilators

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2
Q

What kind of drugs end in “…mab”?

A

monoclonal antibodies

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3
Q

What kind of drugs end in “…sone”?

A

corticosteroids

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4
Q

What kind of drugs end in “…lone”?

A

corticosteroids

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5
Q

What kind of drugs end in “…terol”?

A

bronchodilators

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6
Q

What kind of drugs end in “…nib”?

A

kinase inhibitors

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7
Q

What are the advantaged for inhaled medicines?

A

lungs are robust
large surface area for absorption
rapid absorption
fewer drug metabolising enzymes
fewer systemic side effects

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8
Q

What lung diseases are associated with bronchoconstriction?

A

Asthma
COPD

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9
Q

How does bronchoconstriction differ between asthma and COPD?

A

it is mostly irreversible in asthma and much less reversible in COPD

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10
Q

What are the categories of bronchodilator drugs?

A

adrenergic (sympathetic)
causes bronchodilation

anti-cholinergic (parasympathetic)
blocks bronchoconstriction

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11
Q

What is another name for adrenergic bronchodilators?

A

beta 2 adrenergic agonists

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12
Q

What diseases are associated with respiratory inflammation?

A

pneumonia
asthma
COPD
IPF (idiopathic pulmonary fibrosis)

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13
Q

How do you decide what drugs to use to treat respiratory inflammation?

A

determine whether it’s chronic or acute exacerbate inflammation and treat based on that

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14
Q

What class of drugs are used to treat respiratory inflammation?

A

glucocorticoids (inhaled corticosteroids: ICS)

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15
Q

What is a limitation of treated respiratory inflammation with glucocorticoids?

A

only really effective for asthma, relatively ineffective in COPD, CF, IPF

people with severe asthma can become resistant

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16
Q

What are the side effects of ICS?

A

loss of bone density
adrenal suppression
cataracts, glaucoma

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17
Q

What is the pleura?

A

lining of the lung

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18
Q

Describe the basic anatomy of the pleura.

A

2 layers:
visceral pleura- forms outer covering of lung
parietal pleura- forms inner lining of chest wall

between the 2 layers in the pleural space which contains about 5-10mls of fluid

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19
Q

What is the purpose of the pleura?

A

allows optimal expansion and contraction of lungs

pleural fluid and visceral and parietal pleurae to glide over with friction during respiration

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20
Q

What is a pneumothorax?

A

‘collapsed lung’

presence off air in the pleural space

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21
Q

What causes a pneumothorax?

A

air enters the lungs due to:
- hole in lung/ pleura
- chest wall injury

intra pleural pressure is negative, which leads to air being sucked into cavity

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22
Q

What are the classifications of pneumothorax?

A
  • primary spontaneous
  • secondary spontaneous
  • traumatic
  • iatrogenic
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23
Q

What is a primary spontaneous pneumothorax?

A

collapsed lung with no underlying lung disease

rupture of apical pleural bleb

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24
Q

What are the risk factors for a primary spontaneous pneumothorax?

A

male
smoker
tall
age 20-40 y/o

25
Q

What is secondary spontaneous pneumothorax?

A

collapsed lung in presence of known lung disease

26
Q

What type of lung disease causes secondary spontaneous pneumothorax?

A

60% COPD
asthma/ ILD/ CF/ lung cancer
cystic lung disease

also…

Infection:
- PCP/ TB
- lung abscess

Genetic predisposition:
- Marfan’s syndrome, Birt-Hogg Dube
- LAM (lymphangioleiomyomatosis)

Catamenial pneumothorax

27
Q

What is a traumatic pneumothorax?

A

penetrating chest wall injury

may be a puncture from a rib

may also rupture bronchus/ oesophagus

28
Q

What is iatrogenic pneumothorax?

A

‘doctor induced’ collapsed lung

risks include:
- pacemakers
- CT lung biopsies
- central line insertion
- mechanic ventilation
- pleural aspiration

29
Q

How does pneumothorax present?

A

asymptomatic
acute/ sudden
breathlessness
pleuritic chest pain
cough

30
Q

What is the worst possible complication of pneumothorax?

A

life threatening respiratory failure/ cardiac arrest

31
Q

What are the symptoms of lung cancer?

A

LOCAL:
- increasing shortness of breath
- continuous cough for more than 3 weeks
- haemoptysis
- recurrent chest infections

GENERALISED/ SYSTEMIC:
- general malaise
- weight loss
- paraneoplastic syndrome

32
Q

What type of cancer are most lung tumours?

A

90% are carcinomas

others include:
- benign tumours
- salivary gland tumours
- soft tissue tumours (sarcomas)
- lymphoma

33
Q

What is the classification of lung carcinomas?

A

non-small cell lung carcinoma (NSCLC)
small cell lung carcinoma (SCLC)

34
Q

How is non-small cell lung cancer treated?

A

resection +/- chemotherapy

35
Q

What % of lung carcinomas are non-small cell?

A

85%

36
Q

What are the 3 main types of non-small cell lung carcinoma?

A

adenocarcinoma
squamous cell carcinoma
large cell carcinoma

37
Q

How do you differentiate between types of non-small cell carcinomas?

A

can only really differentiate from the histology

38
Q

What risk factor is most associated with small cell carcinoma?

A

cigarette smoking

39
Q

What is ILD?

A

interstitial lung disease

40
Q

What is an example of restrictive lung disease?

A

emphysema
interstitial lung disease

41
Q

How can interstitial lung diseases be physiologically measured?

A
  • restriction of lung volumes (measured by FVC)
  • reduction in lung gas transfer efficiency (DLCO/ TLCO)
  • hypoxia, particularly on exertion
  • reduction in exercise capacity
42
Q

Why is not possible to lump all ILDs together?

A

because treatment varies massively depending on the type of ILD

43
Q

Describe the pathophysiology of idiopathic pulmonary fibrosis.

A
  • fibroblasts repair damaged tissue
  • fibroblasts migrate to the lungs and become myofibroblasts
  • myofibroblasts deposit collagen in the extracellular matrix
  • In IPF, these fibroblasts are resistant to apoptosis (cell death)
  • my-fibroblasts proliferate and form fibroblastic foci
  • the thickened tissue leads to lower gas exchange efficiency in the lungs
44
Q

What are the key features of idiopathic pulmonary fibrosis?

A
  • collections of fibroblasts
  • thickening of alveolar interstitium
  • destruction (honeycombing) of alveoli
  • affects periphery and base of lungs
  • spatial heterogeneity (normal lung tissue next to abnormal tissue)
45
Q

How is IPF treated?

A

pirfenidone and nintedanib

46
Q

What are the main side effects of pirfenidone?

A

photosensitivity (skin rash)
gastrointestinal upset

47
Q

How does pirfenidone affect the progression of IPF?

A

does not improve the condition, patients will still worsen but the decline won’t be as steep

48
Q

What is the main side effect of nintedanib?

A

diarrhoea

49
Q

What is the mechanism of action of nintedanib?

A

inhibitor or multiple tyrosine kinase receptors

interferes with processes such as fibroblast proliferation, migration and differentiation and secretion of extracellular matrix (collagen)

50
Q

Can nintedanib improve IPF?

A

no- same as pirfenidone in that sense, won’t reverse any damage but will slow down deterioration

51
Q

What is hypersensitivity pneumonitis?

A

also called extrinsic allergic alveolitis

inflammation of the lungs as part of an allergic reaction

52
Q

What type of reaction is hypersensitivity pneumonitis?

A

type III hypersensitivity reaction

53
Q

What is the typical presentation of TB?

A

lung infection, productive cough, blood in the sputum

54
Q

What vaccine protects against TB?

A

BCG vaccine

55
Q

What is the leading killer of people with HIV?

A

TB

56
Q

What does “smear positive” mean in TB?

A

if there is enough bacteria in the sputum to see the bacterium under the microscope

57
Q

How do acquire TB if not from other people?

A

drinking unpasteurised cows milk- cows can be infected with m.bovis which can give humans TB of the gut

58
Q

What is the historical name for TB?

A

consumption

59
Q

What is the classic x-ray sign of TB?

A

cavity in apex of lung (white ring at top of lung)