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HYMS Block 13 > Airways Obstruction > Flashcards

Airways Obstruction Flashcards

1
Q

What questions are important to ask when making a diagnosis of occupational asthma

A
  • are symptoms worse at work?

- are symptoms better when you are away from work at the weekends or on holiday?

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2
Q
  1. Which resin used in soldering is a highly potent cause of occupational asthma
  2. name 4 other causes of occupational asthma
A
  1. colphony
  2. flour
    animal products
    wood dust
    paint spraying
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3
Q
  1. What is pneumoconiosis
  2. What is coalworker’s pneumocosis caused by?
  3. What is the CXR finding of simple coalworker’s pneumocosis?
  4. What is the CXR finding of complicated coalworker’s pneumocosis?
  5. What is silicosis caused by?
  6. What are the CXR findings?
  7. What does this predispose a person to?
  8. What is asbestosis?
  9. What condition is caused by trivial asbestos exposure?
  10. What is siderosis caused by?
  11. Is this a fibrotic condition?
A
  1. restrictive lung disease caused by inhalation of dusts
  2. inhalation of coal dust
  3. subtly abnormal
  4. reveals conglomerated masses of lung fibrosis
  5. inhalation of sillica dust (associated with stone occupations)
  6. upper lobe nodules and lymph node calcification
  7. TB and lung cancer
  8. fibrosis caused by asbestos inhalation
  9. diffuse, benign pleural thickiening
  10. inhalation and deposition of iron
  11. no
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4
Q
  1. What is pneumonitis?
  2. What is acute pneumonitis caused by?
  3. What type of individuals does it affect?
  4. What type of syndrome is it?
  5. What is the prognosis?
  6. What is hypersensitivity pneumonitis?
  7. Name 2 examples
A
  1. inflammation of the lung tissue
  2. acute inhalation of a variety of agents, including chlorine, ammonia, organic chemicals and metallic compounds
  3. otherwise healthy individuals
  4. Acute Respiratory Distress Syndrome
  5. Severe condition - 60% die within first 6 months; requires ICU treatment; patients who survive make full recovery
  6. alveolar inflammation caused by hypersensitivity to inhaled organic dusts
  7. farmer’s lung
    avian hypersensitivity
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5
Q
  1. Where are respiratory pollutants mainly derived from?

2. What is a major cause of COPD and childhood respiratory infection in the developing world?

A
  1. combustion of fossil fuels

2. cooking in poorly ventilated rooms

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6
Q

Define the following:

  1. FVC

2. FEV1

A
  1. the amount of air that can be forcibly exhaled from the lungs after taking the deepest breath possible
  2. the maximal amount of air that can be forcibly exhaled in one second
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7
Q
  1. What is a normal FEV1/FVC ratio?
  2. What is the effect of FEV1, FVC, and the ratio in:
    a) obstructive diseases
    b) restricted diseases
A
  1. 75%
    2a) FVC normal. reduced FEV1 and FEV1/FVC ratio
    2b) FVC and FEV1 reduced. Ratio normal
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8
Q

Name the three general mechanisms of airflow obstruction

A
  1. excess mucous
  2. hypertrophy of bronchial smooth muscle
  3. alveolar destruction (normally, the alveolar walls attach to the bronchial walls, and traction keeps the bronchioles open)
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9
Q

Name the three characteristics of asthma

A
  1. reversible airflow obstruction
  2. airway inflammation
  3. increased airway responsiveness
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10
Q
  1. Name 4 clinical features of asthma
  2. When are symptoms often worse?
  3. Describe the common findings in lung function tests in asthma:
    a) spirometry
    b) Peak Flow
A
  1. Wheeze, chest tightness, SOB, cough.
  2. Often worse at night

2a) greater than 15% improvement in FEV1 following the inhalation of a bronchodilator
2b) FLUCTUATIONS. greater than 15% improvement in FEV1 following the inhalation of a bronchodilator

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11
Q
  1. Which T helper cells are implicated in asthma?
  2. What do these T helper cells promote?
  3. Describe the process of immune sensitisation in asthma
  4. Which cytokines produced by these T cells promote this response?
  5. What medical treatment can inhibit these cytokines?
A
  1. Th2 cells
  2. enhances mast cells, eosinophils, and IgE synthesis
  3. dendritic cells present allergen to T cell → Th2 cell signals to B cells to produce IgE → IgE binds to airway mast cells →antigen binding promotes degranulation of mast cells → cytokines released activate T and B cells, and attract eosinophils
  4. IL-4 and IL-5
  5. IL-5 specific antibodies
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12
Q

Describe the remodelling that occurs in the airways in asthma:

  1. acute (5)
  2. chronic (2)
A
    • smooth muscle contraction
    • mucus hypersecretion
    • plasma leakage
    • oedema
    • sensory nerve activation
  2. subepithelial fibrosis
    smooth muscle hypertrophy
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13
Q
  1. What is status asthmaticus?
  2. Name 4 presentations of status asthmaticus
  3. When can this be life threatening?
A
  1. acute exacerbation of asthma that does not respond well to standard treatment (bronchodilators and corticosteroids)
  2. Inability to complete sentences in one breath
    tachypnoea
    tachycardia
    PEFR <50% of predicted normal or best
  3. if presenting with silent chest, cyanosis, altered mental state , bradycardia and PEFR <30% predicted.
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14
Q
  1. What is COPD?

2. Name the 5 pathological findings in COPD

A
  1. chronic airflow obstruction that does not change markedly over several months
    Pathological evidence of chronic bronchitis and emphysema
2. mucus gland hypertrophy
goblet cell hyperplasia
excess mucus
smooth muscle hypertrophy
inflammatory cell infiltrate - CD8 cells and neutrophils
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15
Q
  1. What is emphysema?
  2. Which lobes of the lungs are commonly affected in smokers?
  3. Why?
  4. What is a bullous?
  5. What are pathological complications of bullae?
  6. How does emphysema cause airway obstruction?
A
  1. abnormal enlargement of the airpsace distal to the terminal bronchiole, accompanied by destruction of their walls, without any fibrosis
  2. upper lobes
  3. ventilation is better here
  4. large distension of the alveoli
  5. no gas exchange takes place; can rupture, leading to pneumothorax
  6. loss of radial traction - elastic recoil is lost therefore alveolar airways collapse prematurely
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16
Q

what genetic defects are associated with increased risk of COPD?

A

alpha1-antitrypsin deficiency

17
Q
  1. Why does airflow obstruction cause hypoxia?
  2. What is cor pulmonale?
  3. How can COPD cause cor pulmonale?
A
  1. V/Q mismatch - many alveoli will be poorly ventilated because of bronchial narrowing
  2. right sided heart failure as a consequence pf pulmonary hypertension
  3. pulmonary arteries construct to account for the V/Q mismatch
18
Q
  1. What is minute ventilation?

2. What is alveolar ventilation?

A
  1. tidal volume x respiratory rate

2. (tidal volume - dead space) x respiratory rate

19
Q

what are the components of the capillary diffusion membrane? (3)

A
  1. type 1 pneumocytes of the alveolar walls
  2. fused basement membranes
  3. endothelial cells of the capillaries
20
Q
  1. How much faster does CO2 diffuse across the membrane than O2
  2. Why does a pathology affecting gas exchange lead to hypoxia?
A
  1. 20x
  2. blood will not spend enough time in the vessels for gas exchange to take place. Under normal conditions, O2 equilibration just occurs in the time available (unless membrane is thickened)
21
Q
  1. Where does maximal perfusion occur?
  2. Which areas of the lungs are best ventilated?
  3. What happens when there is reduced ventilation/normal perfusion?
  4. what happens when there is normal ventilation/reduced perfusion
A
  1. lung bases when upright
  2. apices
  3. shunt of deoxygenated blood to systemic circulation
  4. increased alveolar dead space - wasted ventilation
22
Q
  1. What are flow volume loops used for?
  2. What does TLCD/DLCO measure?
  3. Describe the test
A
  1. provide graphical analysis of inspiratory and expiratory FLOW. Can be used to gather peak flow rates
  2. Used to measure gas exchange
  3. Inhale air with low concentration of CO
    Concentration change during a 10 second breath hold reflects absorption (and is proportional to thickness of alveolar membrane)
23
Q

What is the PO2 and PCO2 in:

  1. Type 1 respiratory failure
  2. Type 2 respiratory failure
  3. What is type 2 respiratory failure associated with?
A
  1. low PaO2; low/normal PCO2
  2. low PaO2; high PCO2
  3. hypoventilation
24
Q

Name 4 causes of respiratory lung disease

A
  1. pulmonary fibrosis
  2. obesity
  3. chest wall deformity
  4. neuromuscualr dysfunction
25
Q

What is the shape of the flow volume loop in obstructive lung disease?

A

Concave expiration, due to collapse of small airways

26
Q

What are the effects of pulmonary fibrosis on:

  1. diffusion
  2. perfusion
  3. what is the shape of the flow volume loop in restrictive lung disease?
A
  1. impaired - increased thickness of interstitium
  2. normal
  3. displaced to the left (due to reduced volumes)
27
Q
  1. What type of respiratory failure is seen in pulmonary fibrosis
  2. Name 3 types of restrictive lung diseases that cause type 2 respiratory failure
A
  1. type 1 (CO2 diffusion is faster)
  2. chest wall deformities
    neuromuscular disorders
    obesity
28
Q
  1. Name 2 antifibrotic drugs used to treat idiopathic pulmonary fibrosis
  2. Name 5 supportive therapies for idiopathic pulmonary fibrosis
A
  1. pirfenidone, nintendanib

2. oxygen, pulmonary rehabilitation, breathlessness management techniques, opiates, transplantation (in selected cases)

29
Q
  1. What does SABA stand for?
  2. What does LABA stand for
  3. Name an example of a SABA
  4. Name two examples of LABAs
A
  1. Short Acting Beta 2 agonist
  2. Long Acting Beta 2 agonist
  3. salbutamol
  4. salmeterol; formaterol
30
Q
  1. What are used to treat the underlying inflammation in asthma?
  2. Why do these not cause systemic effects?
A
  1. inhaled corticosteroids

2. majority is swallowed. Metabolised and inactivated at first pass

31
Q
  1. How do Lekotriene receptor antagonists treat asthma?
  2. Name an example
  3. What is the MOA of theophyline?
  4. How does it treat asthma?
A
  1. antagonises the effects of leukotrienes, which are potent bronchoconstrictors and nerve sensitisers
  2. Montelukast
  3. phosphodiesterase inhibitor
  4. increases cAMP, which promotes bronchodilation and prevents the synthesis of leukotrienes
32
Q
  1. Name 2 short acting bronchodilators used in the treatment of COPD and their MOA
  2. Name a long acting bronchodilator used in the treatment of COPD, and its MOA
  3. Why should inhaled steroids not be used to treat COPD?
  4. Why can oxygen therapy cause deterioration in COPD?
A
  1. Salbutamol - beta2 agonist
    Ipratropium - antimuscarinic
  2. Tiotropium - antimuscarinic
  3. Systemic effects with little benefit on COPD
  4. change in hypoxic drive

HYMS Block 13 (4 decks)

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