Airways disease Flashcards

(65 cards)

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
What is a spacer used for?
to optimise lung delivery and to reduce particle size and velocity
26
What is the pathophysiology of COPD?
- excessive inflammatory response by macrophages - CD8 lymphocytes and neutrophils - this causes scarring and thickening of the respiratory epithelium
27
What happens as a result of increased proteinase levels in COPD?
- hyper secretion of mucus - small airways obstruction - alveolar destruction
28
Which bronchus is more vertical?
right is more vertical, left is more horizontal
29
What are the coal cord important in?
coughing
30
What is stridor?
inspiratory wheeze due to large airways obstruction
31
What are the causes of stridor in children?
- infections (croup or epiglottitis from H. influenza) - foreign body - anaphylaxis
32
What are the causes of stridor in adults?
- tumour of larynx/ trachea, major bronchi - trauma - goitre (enlarged thyroid)
33
What are the investigations of stridor?
- laryngoscopy (dangerous in epiglottitis) - bronchoscopy - flow volume loop - CXR
34
What is treatment of a laryngeal obstruction?
- removal of foreign body - high flow O2 - cricothyroidotomy (army) - tracheostomy
35
What is the treatment of malignant airway obstruction?
- tumour removal - compression - radiotherapy - chemotherapy
36
What is acute anaphylaxis?
type 1 hypersensitivity reaction with IgE
37
What does acute anaphylaxis lead to?
oedema, hypotension and respiratory failure
38
What are the causes of acute anaphylaxis?
foods, insect venom, drug to other
39
What is the treatment of anaphylaxis?
- IM epinephrine - IV anti-histamine - IV corticosteroid - high flow O2 - nebulised bronchodilators - further is allergen avoidance, desensitisation and self-administered epinephrine
40
What causes snoring?
relaxation of pharyngeal dilator muscles leading to upper airway narrowing, turbulent airflow and vibration of soft palate and tongue base
41
What is obstructive sleep apnoea?
intermittent upper airway collapse with recurrent apnoeas
42
How common is instructive sleep apnoea?
1-4% of adult population
43
What are the risk factors for sleep apnoea?
enlarged tonsils, obesity, retrognathia, neurological, drugs or post-op
44
What are the consequences of sleep apnoea?
- excessive daytime sleepiness - personality change - cognitive impairment - hypertension - raised CRP - impaired endothelial function - glucose tolerance
45
How do you diagnose sleep apnoea?
snoring, EDS, sleep study with oximetry and domiciliary recording
46
What is the treatment for sleep apnoea?
remove underlying cause and CPAP (continuous positive airway pressure) which is very effective, mandibular advancement device or surgery
47
What is the circulation in the lungs?
dual circulation with pulmonary and bronchial arteries, low pressure system and pulmonary artery is a filter
48
Why is there low incidence of atherosclerosis in lungs?
thin walled vessels as it is a low pressure system
49
Where does pulmonary oedema occur?
in the interstitial and the alveolar spaces
50
How does pulmonary oedema present?
like ILD and causes restrictive pattern of disease
51
What are the causes of pulmonary oedema?
- 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
What is ARDS?
DADS or shock lung
53
What are causes of ARDS?
sepsis, diffuse infection, severe trauma or oxygen
54
What is the pathogenesis of ARDS?
- infiltration of inflammatory cells, cytokines and oxygen free radicals - injury to cell membranes
55
What is the pathology of ARDS?
- heavy lungs - fibrinous exudate lining alveolar walls - cellular regeneration and inflammation
56
What is the outcome of ARDS?
- death - resolution - fibrosis so chronic restrictive lung disease
57
What is the cause of neonatal RDS?
surfactant deficiency (produced by type 2 alveolar cells)
58
What is the result of neonatal RDS?
increased effort in expanding the lungs leading to physical damage to cells
59
What can emboli be?
- thrombus - gas - fat - foreign bodies - tumour clumps
60
What is the pathology of pulmonary infarct?
ischaemic necrosis
61
How does pulmonary infarct occur?
embolus and compromise of the bronchial arteries
62
What are the types of pulmonary hypertension?
- primary which is rare and occurs in young women | - secondary
63
What are the mechanisms of pulmonary hypertension?
- hypoxia - increased flow through pulmonary circulation - blockage or loss of pulmonary vascular bed - back pressure from left sided heart failure
64
What is the morphology of pulmonary hypertension?
- medial hypertrophy of arteries - intimal thickening - atheroma - right ventricular hypertrophy (necrosis and fibrosis in extreme cases)
65
What is cor pulmonale?
heart disease due to lung disease, pulmonary hypertension so right ventricular hypertrophy, right ventricular dilation and rough heart failure