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My Respiratory > Airways disease > Flashcards

Airways disease Flashcards

1
Q

What are the two pathophysiological features of the airway in asthma?

A
  • reversible airflow obstruction

- airway inflammation

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2
Q

What is airway hyper- responsiveness?

A

this is where the airway goes twitchy and into spasm

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3
Q

What are the histological signs of asthma?

A
  • thickening of the basement membrane
  • collagen deposition in the submucosa
  • hypertrophy in the smooth muscle
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4
Q

What are the extra histological signs in severe asthma?

A
  • epithelial shedding

- mucus plugging

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5
Q

What are the presenting symptoms and signs in asthma?

A
  • diurnal variability
  • a non-productive cough
  • associated atopy so increased IgE levels
  • responsiveness to steroids or beta-agonists
  • family history
  • wheezing due to turbulent airflow
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6
Q

How is the diagnosis of asthma achieved and what tests are carried out?

A
  • history taking
  • examination
  • diurnal variation of peak flow rate
  • reversibility to inhaled salbutamol
  • reduced FEV1/FVC ratio (below 75%)
  • provocation testing to bronchospasm with exercise and histamine
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7
Q

What are the histological signs of COPD?

A
  • tissue damage
  • mucociliary dysfunction
  • inflammation
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8
Q

What are the histological signs of chronic bronchitis?

A
  • neutrophilic inflammation
  • mucus hyper secretion
  • mucociliary dysfunction
  • altered lung microbiome
  • smooth muscle spasm
  • hypertrophy
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9
Q

What are the effects of emphysema?

A
  • alveolar destruction
  • impaired gas exchange
  • loss of bronchial support
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10
Q

Are emphysema and chronic bronchitis reversible or irreversible?

A

chronic bronchitis is partially reversible

emphysema is irreversible

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11
Q

What is the chemical factor that determines the severity of COPD and what is it affected by?

A
  • protease levels
  • antiprotenase levels are genetic
  • protease comes from alveolar destruction and emphysema from smoking
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12
Q

What are the signs and symptoms of COPD?

A
  • chronic symptoms
  • non-atopic
  • productive cough
  • breathlessness
  • exacerbations
  • wheezing from chronic bronchitis
  • reduced breath sounds from emphysema
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13
Q

What are the features of the chronic cascade in COPD?

A
  • fixed airflow obstruction
  • impaired alveolar gas exchange
  • respiratory failure
  • pulmonary hypertension
  • death
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14
Q

What happens to the FVC and TLCO in asthma?

A

it is preserved

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15
Q

What happens to FVC and TLCO in COPD?

A

it is reduced

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16
Q

What do ILDs usually present with?

A
  • progressive breathlessness
  • restrictive lung function
  • reduced transfer factor
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17
Q

How do you diagnose ILDs?

A

CT scan and sometimes a lung biopsy

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18
Q

What is the pathophysiology of DPLD?

A
  • impaired alveolar gas exchange (alveolar barrier to O2)
  • CO2 exchange is unimpaired because alveolar ventilation is normal
  • therefore, low PaO2 and normal PaCO2
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19
Q

What are the common causes of DPLD?

A

consolidation of the alveolar ai spaces from infective pneumonia or infarction

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20
Q

What is the treatment for DPLD?

A

remove trigger factor
- 1st line is systemic steroids
- 2nd line is oral azathioprine and O2 if hypoxaemic
treat secondary so pulmonary hypertension or lung transplant

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21
Q

What is pulmonary challenge testing?

A

methacholine is inhaled

the challenge will cause a >20% decrease in FEV1 in patients with asthma

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22
Q

What are examples of the causes of the extrinsic or intrinsic inflammatory cascades in asthma?

A
  • extrinsic causes are pollen, dust mite faeces, animal dander or mould
  • intrinsic causes are unknown
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23
Q

What is the pathophysiology of the asthma cascade?

A
  • Th2 CD4 cell-mediated immunity for allergenic or Th17 CD4 for non-allergenic
  • eosinophilic or neutrophilic airways inflammation
  • eosinophil and mast cell activation
  • nerve activation
  • smooth muscle cholinergic response
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24
Q

What is the result of the inflammatory cascade from asthma on the airways?

A
  • bronchoconstriction
  • mucus hyper secretion
  • vasodilation and oedema
  • airway remodelling
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25
Q

What is a spacer used for?

A

to optimise lung delivery and to reduce particle size and velocity

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26
Q

What is the pathophysiology of COPD?

A
  • excessive inflammatory response by macrophages
  • CD8 lymphocytes and neutrophils
  • this causes scarring and thickening of the respiratory epithelium
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27
Q

What happens as a result of increased proteinase levels in COPD?

A
  • hyper secretion of mucus
  • small airways obstruction
  • alveolar destruction
28
Q

Which bronchus is more vertical?

A

right is more vertical, left is more horizontal

29
Q

What are the coal cord important in?

A

coughing

30
Q

What is stridor?

A

inspiratory wheeze due to large airways obstruction

31
Q

What are the causes of stridor in children?

A
  • infections (croup or epiglottitis from H. influenza)
  • foreign body
  • anaphylaxis
32
Q

What are the causes of stridor in adults?

A
  • tumour of larynx/ trachea, major bronchi
  • trauma
  • goitre (enlarged thyroid)
33
Q

What are the investigations of stridor?

A
  • laryngoscopy (dangerous in epiglottitis)
  • bronchoscopy
  • flow volume loop
  • CXR
34
Q

What is treatment of a laryngeal obstruction?

A
  • removal of foreign body
  • high flow O2
  • cricothyroidotomy (army)
  • tracheostomy
35
Q

What is the treatment of malignant airway obstruction?

A
  • tumour removal
  • compression
  • radiotherapy
  • chemotherapy
36
Q

What is acute anaphylaxis?

A

type 1 hypersensitivity reaction with IgE

37
Q

What does acute anaphylaxis lead to?

A

oedema, hypotension and respiratory failure

38
Q

What are the causes of acute anaphylaxis?

A

foods, insect venom, drug to other

39
Q

What is the treatment of anaphylaxis?

A
  • IM epinephrine
  • IV anti-histamine
  • IV corticosteroid
  • high flow O2
  • nebulised bronchodilators
  • further is allergen avoidance, desensitisation and self-administered epinephrine
40
Q

What causes snoring?

A

relaxation of pharyngeal dilator muscles leading to upper airway narrowing, turbulent airflow and vibration of soft palate and tongue base

41
Q

What is obstructive sleep apnoea?

A

intermittent upper airway collapse with recurrent apnoeas

42
Q

How common is instructive sleep apnoea?

A

1-4% of adult population

43
Q

What are the risk factors for sleep apnoea?

A

enlarged tonsils, obesity, retrognathia, neurological, drugs or post-op

44
Q

What are the consequences of sleep apnoea?

A
  • excessive daytime sleepiness
  • personality change
  • cognitive impairment
  • hypertension
  • raised CRP
  • impaired endothelial function
  • glucose tolerance
45
Q

How do you diagnose sleep apnoea?

A

snoring, EDS, sleep study with oximetry and domiciliary recording

46
Q

What is the treatment for sleep apnoea?

A

remove underlying cause and CPAP (continuous positive airway pressure) which is very effective, mandibular advancement device or surgery

47
Q

What is the circulation in the lungs?

A

dual circulation with pulmonary and bronchial arteries, low pressure system and pulmonary artery is a filter

48
Q

Why is there low incidence of atherosclerosis in lungs?

A

thin walled vessels as it is a low pressure system

49
Q

Where does pulmonary oedema occur?

A

in the interstitial and the alveolar spaces

50
Q

How does pulmonary oedema present?

A

like ILD and causes restrictive pattern of disease

51
Q

What are the causes of pulmonary oedema?

A
  • haemodynamic due to increased hydrostatic pressure

- due to cellular injury to the alveolar lining cells or endothelium, localised is pneumonia and generalised is ARDS

52
Q

What is ARDS?

A

DADS or shock lung

53
Q

What are causes of ARDS?

A

sepsis, diffuse infection, severe trauma or oxygen

54
Q

What is the pathogenesis of ARDS?

A
  • infiltration of inflammatory cells, cytokines and oxygen free radicals
  • injury to cell membranes
55
Q

What is the pathology of ARDS?

A
  • heavy lungs
  • fibrinous exudate lining alveolar walls
  • cellular regeneration and inflammation
56
Q

What is the outcome of ARDS?

A
  • death
  • resolution
  • fibrosis so chronic restrictive lung disease
57
Q

What is the cause of neonatal RDS?

A

surfactant deficiency (produced by type 2 alveolar cells)

58
Q

What is the result of neonatal RDS?

A

increased effort in expanding the lungs leading to physical damage to cells

59
Q

What can emboli be?

A
  • thrombus
  • gas
  • fat
  • foreign bodies
  • tumour clumps
60
Q

What is the pathology of pulmonary infarct?

A

ischaemic necrosis

61
Q

How does pulmonary infarct occur?

A

embolus and compromise of the bronchial arteries

62
Q

What are the types of pulmonary hypertension?

A
  • primary which is rare and occurs in young women

- secondary

63
Q

What are the mechanisms of pulmonary hypertension?

A
  • hypoxia
  • increased flow through pulmonary circulation
  • blockage or loss of pulmonary vascular bed
  • back pressure from left sided heart failure
64
Q

What is the morphology of pulmonary hypertension?

A
  • medial hypertrophy of arteries
  • intimal thickening
  • atheroma
  • right ventricular hypertrophy (necrosis and fibrosis in extreme cases)
65
Q

What is cor pulmonale?

A

heart disease due to lung disease, pulmonary hypertension so right ventricular hypertrophy, right ventricular dilation and rough heart failure

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