17-11-22 - Obstructive & Restrictive Lung disease Flashcards

1
Q

Learning outcomes

A
  • compare & contrast obstructive & restrictive lung disease
  • compare & contrast asthma & COPD
  • Understand the pathophysiology of obstructive lung disease
  • Name the different lung volumes mearured by spirometry and the changes you would expect in disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are obstructive lung disease defined by?

How can this by measured in spirometry?

What does this value reflect?

What are characteristics of this measurement?

What else can this measurement be used for?

A
  • Obstructive lung diseases are defined by an ‘obstructive’ deficit on lung function (measured by spirometry)
  • This can be measured in spirometry as Forced Expiratory Volume (in 1st second) as a fraction of the Forced Vital Capacity of <0.7:
  • FEV1 / FVC < 0.7 (FEV1 is less than 70% of the FVC) for obstructive lung diseases
  • This measurement reflects airway disease (compromised airflow)
  • This measurement is quantitative, reproducible, objective
  • This measurement can also be tracked to monitor the course of disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is Poiseuille’s equation (in picture)?

What does Poiseuille’s equation work on?

How does viscosity/length affect air resistance?

How does radius affect air resistance?

A
  • Poiseuille’s equation
  • Worked on liquids, air dynamics
  • R = airway resistance (Raw)
  • ƞ = airway ‘viscosity’, L = length of tube/airway
  • r = radius of tube/airway
  • Doubling viscosity/length doubles airway resistance
  • Halving radius = 16x increase in airway resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are normal bronchial airways held open?

What are the 3 different mechanisms of airflow obstruction in chronic obstructive lung disease?

A
  • Normal bronchial airways have elastic fibres that provide traction and hold the airway open
  • 3 different mechanisms of airflow obstruction in chronic obstructive lung disease:

1) Inflammation and fibrosis of the bronchial wall

2) Hypertrophy of submucosal glands and hypersecretion of mucus

3) Destruction of the elastic fibres that hold the airway open.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Loss of elastin in both small airways and alveoli of patients with COPD

A
  • Loss of elastin in both small airways and alveoli of patients with COPD
  • Control – a, c, e, g
  • COPD – b, d, f, h
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What measurements does spirometry consider?

What will cause an obstructive deficit?

What is the difference between an obstructive and restrictive disease?

What are 4 conditions that cause obstructive lung disease?

What are 5 conditions that cause restrictive lung diseases?

What are normal FEV1, FVC, and FEV1/FVC ratios for:
* Abnormalities
* Obstructive disorder
* Restrictive disorder (in picture)

A
  • Spirometry considers volume measurements and flow measurements
  • Anything that compromised airflow will give an obstructive deficit (FEV1 / FVC = <0/7)
  • Obstructive and restrictive lung diseases:
  • People with obstructive lung disease have shortness of breath due to difficulty exhaling all the air from the lungs.
  • Because of damage to the lungs or narrowing of the airways inside the lungs, exhaled air comes out more slowly than normal.
  • At the end of a full exhalation, an abnormally high amount of air may still linger in the lungs (air trapping – leads to reduced Forced expiratory volume (FEV1) and Forced vital capacity (FVC)
  • 4 conditions that cause obstructive lung disease:

1) Chronic obstructive pulmonary disease (COPD), which includes emphysema and chronic bronchitis

2) Asthma

3) Bronchiectasis

4) Cystic fibrosis

  • Obstructive lung disease makes it harder to breathe, especially during increased activity or exertion. As the rate of breathing increases, there is less time to breathe all the air out before the next inhalation.
  • People with restrictive lung disease cannot fully fill their lungs with air.
  • Their lungs are restricted from fully expanding.
  • Restrictive lung disease most often results from a condition causing stiffness in the lungs themselves.
  • In other cases, stiffness of the chest wall, weak muscles, or damaged nerves may cause the restriction in lung expansion.
  • 5 conditions that cause restrictive lung diseases

1) Interstitial lung disease, such as idiopathic pulmonary fibrosis

2) Sarcoidosis, an autoimmune disease

3) Obesity, including obesity hypoventilation syndrome

4) Scoliosis

5) Neuromuscular disease, such as muscular dystrophy or amyotrophic lateral sclerosis (ALS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is residual volume?

What is air trapping?

What conditions is it observed in?

How does gas trapping in these conditions affect residual volume?

How will this affect vital capacity?

A
  • Residual volume is the amount of air that remains in a person’s lungs after fully exhaling
  • Air trapping, also called gas trapping, is an abnormal retention of air in the lungs where it is difficult to exhale completely.
  • It is observed in obstructive lung diseases such as asthma, bronchiolitis obliterans syndrome and chronic obstructive pulmonary diseases such as emphysema and chronic bronchitis.
  • Gas trapping in these conditions will manifest in the residual volume
  • This will lead to an increase in residual volume, which will decrease the vital capacity of the lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is TLCO? What is it used for?

What are 11 differences between asthma and COPD (in picture)?

A
  • DLCO – The diffusing capacity for carbon monoxide (DLCO) is also known as the transfer factor for carbon monoxide or TLCO.
  • It is a measure of the conductance of gas transfer from inspired gas to the red blood cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is asthma?

What is it usually characterized by?

What are symptoms?

How does asthma affect expiratory airflow?

What does this mean for monitoring?

What is another way asthma can be defined?

What are 3 components in the pathophysiology of asthma?

What are 3 important mediators in asthma?

A
  • Asthma is a heterogeneous disease, usually characterized by chronic inflammation
  • Asthma has symptoms of wheeze, SOB, tightness, cough that vary over time and in intensity
  • Those with asthma can have variable expiratory airflow limitation
  • This means we will need to use tests other than static lung tests to monitor asthma
  • Asthma can also be defined as reversible airway inflammation of many types and many causes
  • 3 components in the pathophysiology of asthma:

1) Airway narrowing / obstruction (reversible)
* Mucous build up with inflammatory cell infiltrate

2) Airway hyper-responsiveness

3) Airway inflammation
* Eosinophils - Th2 response
* Non-eosinophilic - Th1 response

  • 3 important mediators in asthma

1) Interleukins IL-4, IL-5, IL-13

2) Leukotriene B4 and cysteinyl-leukotrienes (C4 and D4)

3) Tissue damaging eosinophil protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In what 5 things symptoms of asthma can worse in the presence of?

A
  • 5 things symptoms of asthma can worse in the presence of:

1) Viruses

2) Allergens - animal dander, dust mites, pollens, fungi

3) Foods/nutrition – vitamin D, A, E levels?

4) Chemicals – smoke

5) Exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are 3 non-pharmacological treatments of asthma?

A
  • 3 non-pharmacological treatments of asthma:

1) Achieve & maintain a normal BMI if overweight

2) Breathing exercise programmes

3) Stop smoking (patient +/- household members)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 4 steps in the treatment of asthma?

What can be added in addition to these therapies?

When do we move up and down steps?

A
  • 4 steps in the treatment of asthma:

1) Regular preventer
* Low-dose ICS (inhale corticosteroids)

2) Initial add on therapy
* Add inhaled LABA (long-acting bronchodilator inhalers) to low dose ICS

3) Additional controller therapies
* Consider increasing ICS to medium dose or add LTRA (leukotriene receptors agonist
* If there is no response to LABA, consider stopping LABA

4) Specialist therapies
* Refer patient for specialist care

  • During this whole period, add short acting B2 agonists (salbutamol) when required, and consider moving up a step if we are using three doses a week or more
  • We move up and down the steps to control as needed
  • We can move down to find and maintain the lowest controlling therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Biologics for severe asthma diagram

A

Biologics for severe asthma diagram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What 3 things indicate moderate acute asthma?

What 4 things can indicate acute severe asthma?

What 11 things can indicate life-threatening asthma in someone with severe asthma?

What indicates near fatal asthma?

A
  • 3 things indicate moderate acute asthma:
    1) Increasing symptoms
    2) PEF (peak flow) >50–75% best or predicted
    3) No features of acute severe asthma
  • What 4 things can indicate acute severe asthma (any one of the following):
    1) PEF 33–50% best or predicted
    2) Respiratory rate ≥25/min
    3) Heart rate ≥110/min
    4) Inability to complete sentences in one breath
  • 11 things can indicate life-threatening asthma in someone with severe asthma (any one of the following):
    1) Altered consciousness
    2) Exhaustion
    3) Arrythmia
    4) Hypertension
    5) Cyanosis
    6) Silent chest
    7) Poor respiratory effort
    8) PEF < 33% best/predicted
    9) SpO2 < 92%
    10) PaO2 < 8 kPa
    11) “Normal” PaCO2 (4.6-6.0kPa)
  • Near-fatal asthma is indicated by Raised PaCO2 &/Or requires ventilation/NIV (non-invasive ventilation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are 5 parts of the immediate treatment (adults) of acute severe asthma?

What 2 treatments should we consider if the patient is not improving?

What 3 other things do we need to consider?

A
  • 5 parts of the immediate treatment (adults) of acute severe asthma:
    1) Oxygen (maintain SpO2 94-98%)
    2) SABA (salbutamol or terbutaline) via nebuliser
    3) Steroids (hydrocortisone (IV) or prednisolone (PO))
    4) +/– antibiotics
    5) +/– muscarinic antagonist nebulised
  • 2 treatments should we consider if the patient is not improving:
    1) IV MgSO4 (bronchodilator, anti-inflammatory)
    2) IV salbutamol or IV methylxanthine (aminophylline)
  • 3 other things do we need to consider:
    1) Blood gases
    2) Patient exhaustion
    3) ICU
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Asthma treatment extension from previous slide

A

Asthma treatment extension from previous slide

17
Q

How common is COPD?

What is COPD characterised by?

What is it also associated with?

What contributes to the overall severity of COPD in individual patients?

What are 7 different types of COPD? What is a description/cause for each of them? (In picture)

A
  • COPD is common, preventable, and treatable
  • COPD is Characterized by persistent airflow limitation, which is usually progressive
  • It is also associated with an enhanced chronic inflammatory response in the airways to noxious particles or gases
  • Exacerbations and comorbidities contribute to the overall severity in individual patients
18
Q

How is cannabis smoking linked to COPD?

How can a cannabis smokers lungs appear on an x-ray?

What are bullae?

What is large bullae?

What are 3 things a contaminated joint can cause?

What are 3 increased risks of cannabis smoking?

A
  • Cannabis smokers can get COPD at a younger age (frequently smoked with tobacco – causing COPD – C)
  • If there are large bullae on an x-ray when the patient is young, we should think cannabis
  • A bulla is defined as an air space in the lung measuring more than one centimetre in diameter in the distended state.
  • The term giant bulla is used for bullae that occupy at least 30 percent of a hemithorax
  • 3 things a contaminated joint can cause

1) TB

2) Aspergillosis
* Aspergillosis is an infection caused by Aspergillus, a common mould (a type of fungus) that lives indoors and outdoors.
* Most people breathe in Aspergillus spores every day without getting sick

3) NTM
* Non-tuberculous mycobacteria, or NTM, are a group of bacteria that cause rare lung infections

  • 3 increased risks of cannabis smoking:

1) Emphysema

2) Pneumothorax

3) Lung cancer

19
Q

Describe the GOLD ABE assessment tool for classifying COPD

A

Describe the GOLD ABE assessment tool for classifying COPD

20
Q

What are the essential, recommended, and local guideline treatment of the different forms of COPD?

A

What are the essential, recommended, and local guideline treatment of the different forms of COPD?

21
Q

When should α1 anti-trypsin deficiency (AATD) be suspected (causes COPD-G)?

How does it present with?

What is α1 antitrypsin?

What is the phenotype that can lead to AATD?

What % of AAT levels does the ZZ phenotype account for?

A
  • α1 anti-trypsin (AAT) deficiency (AATD) should be suspected (causes COPD-G) if there is early onset of COPD (<45 years)
  • It presents with lower-dominant emphysema which can be seen on an x-ray
  • α1 antitrypsin is a liver enzyme that counteracts proteinases which cause tissue damage
  • AATD is caused by the presence of the ZZ phenotype in the e A1AT gene-peptide can lead to M = normal, S = reduced, Z = abnormal α1 antitrypsin, with reduced leading to worse outcomes
  • The ZZ phenotype accounts for about 10-20% if AAT levels
22
Q

Describe the flow chart of how smoking can cause emphysema

A

Describe the flow chart of how smoking can cause emphysema

23
Q

How are normal bronchial airways held open?

What are the 3 different mechanisms of airflow obstruction in chronic obstructive lung disease?

Which one is not present in asthma?

When should we consider diagnosis of COPD in smokers?

What % of those with COPD have never smoked?

A
  • Normal bronchial airways have elastic fibres that provide traction and hold the airway open
  • 3 different mechanisms of airflow obstruction in chronic obstructive lung disease:

1) Inflammation and fibrosis of the bronchial wall

2) Hypertrophy of submucosal glands and hypersecretion of mucus

3) Destruction of the elastic fibres that hold the airway open (emphysema) – not present in asthma

  • Consider the diagnosis of COPD in ever-smoker with breathlessness, chronic cough/sputum production & exposure to risk factors
  • 10-20% of those with COPD have never smoked
24
Q

What are 7 parts of the usual clinical presentation of COPD?

A
  • 7 parts of the usual clinical presentation of COPD:

1) Insidious onset
* An insidious disease is any disease that comes on slowly and does not have obvious symptoms at first.
* The person is not aware of it developing

2) Usually, 50s or 60s

3) Chronic cough

4) Sputum production (typically worse in the morning)

5) Steadily worsening shortness of breath

6) Diminishing exercise tolerance (remember to quantify e.g. stairs, walking distance, ‘activities of daily living’ or ADLs)

7) History of exposure to risk factors, not just cigarettes

25
Q

What are 5 key aspects of COPD care?

What are the 2 goals of COPD care?

A
  • 5 key aspects of COPD care:
    1) Smoking cessation
    2) Vaccination – flu, pneumonia, COVID etc.
    3) Pulmonary rehab (PR)
    4) Self-management plan
    5) Optimise co-morbidities
  • The 2 goals for COPD care are to:

1) Reduce symptoms
* Relieve symptoms
* Improve exercise tolerance
* Improve health status

2) Reduce risk
* Prevent disease progression
* Prevent and treat exacerbations
* Reduce mortality

26
Q

What is the initial pharmacological treatment for Groups A, B, and E of COPD (in picture)?

A

What is the initial pharmacological treatment for Groups A, B, and E of COPD (in picture)?

27
Q

What are the 5 stages in the management of COPD (in picture)?

A

What are the 5 stages in the management of COPD (in picture)?

28
Q

What are the surgical and interventional therapies in advanced COPD (In picture)?

A

What are the surgical and interventional therapies in advanced COPD (In picture)?

29
Q

Prescription of supplementary oxygen to COPD patients

A

Prescription of supplementary oxygen to COPD patients

30
Q

How is lung inflation affected in restrictive lung disease?

What is restrictive lung disease often a result of?

What can be the cause in other cases?

What are normal FEV1, FVC, and FEV1/FVC ratios for restrictive disorders (in picture)?

A
  • People with restrictive lung disease cannot fully fill their lungs with air.
  • Their lungs are restricted from fully expanding.
  • Restrictive lung disease most often results from a condition causing stiffness in the lungs themselves.
  • In other cases, stiffness of the chest wall, weak muscles, or damaged nerves may cause the restriction in lung expansion
31
Q

What type of disease is restrictive lung disease/deficits usually caused by?

What is interstitial lung disease (ILD)?

What does scarring from interstitial lung disease cause?

What are 4 examples of ILDs that cause restrictive lung disease?

What are 4 examples of ILDs?

What different types of causes do we have to consider?

What are 5 extrathoracic causes of restrictive lung disease?

A
  • Restrictive lung disease/deficits are usually caused by interstitial lung diseases (ILD)
  • Interstitial lung disease describes a large group of disorders, most of which cause progressive scarring of lung tissue.
  • The scarring associated with interstitial lung disease eventually affects your ability to breathe and get enough oxygen into your bloodstream
  • 4 examples of ILD that cause restrictive lung disease:

1) Idiopathic pulmonary fibrosis (IPF)

2) Hypersensitivity pneumonitis (HP)
* Hypersensitivity pneumonitis (HP) happens if your lungs develop an immune response – hypersensitivity - to something you breathe in which results in inflammation of the lung tissue - pneumonitis

3) Sarcoidosis

4) Connective tissue disease (CTD)

  • We have to consider intrinsic vs extrinsic (extra-thoracic) causes of restrictive lung disease
  • Above diseases are intrinsic causes, as they affect the lung parenchyma
  • Extrathoracic causes can be pleural, neuromuscular, rib cage/bony abnormality
  • Also, the acronym ‘PAINT’: pleural, alveolar, interstitial, neuromuscular, thoracic cage
32
Q

What are 4 effects of restrictive lung diseases on lung function?

A
  • 4 effects of restrictive lung diseases on lung function:

1) Overall lungs are smaller (restricted)

2) Decreased VC (decreased FEV but not as much as VC – vital capacity)

3) Decreased other volumes – classically TLC (total lung capacity)

4) Decreased gas transfer – if disproportionate to decreased lung volumes, consider co-existent emphysema or pulmonary hypertension

33
Q

How many causes of restrictive lung diseases are there?

What are 4 prognostic indicators of restrictive lung diseases?

What are 3 treatments for restrictive lung disease?

A
  • There are 200 different pathologies that can cause restrictive lung diseases, with probably <10 being clinically relevant
  • 4 prognostic indicators of restrictive lung diseases:
    1) 6 min walk test
    2) Change in FVC over 6 months
    3) Composite physiological scores (CPI)
    4) ‘GAP’ score (in IPF)
  • 3 treatments for restrictive lung disease:
    1) Steroids
    2) Anti-fibrotics
    3) ‘Best supportive care’ (BSC)
34
Q

What are 2 symptoms of ILD?

What 2 types of exposures should we consider for ILD?

What is a common sign on examination for ILD?

A
  • 2 symptoms of ILD:
    1) Steady worsening of breathlessness
    2) Ongoing usually dry cough
  • 2 types of exposures should we consider for ILD:
    1) Consider work exposures – dusts (stone), chemicals, asbestos
    2) Consider home exposures/interests – birds, farms, mould
  • On examination, fine velcro-like crackles are the most discriminating sign of ILD (compare reduced air entry and wheeze in airway disease)
35
Q

What is IPF (idiopathic pulmonary fibrosis) in relation to ILD?

How is it diagnosed?

How is it treated? How is it cured?

A
  • Idiopathic pulmonary fibrosis (IPF) is the most common ILD type
  • It is the most progressive/feared ILD
  • IPF is diagnosed on CT scan (>90%)
  • It is treated with anti-fibrotic therapy
  • IPF is incurable, with the median survival being 3.5 years