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MD3001 > Obstructive and Restrictive Lung disease > Flashcards

Obstructive and Restrictive Lung disease Flashcards

1
Q

What are the main kinds of obstructive lung disease ?

A

Asthma
COPD
Bronchiesctasis (possibly due to CF)

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2
Q

What are the main kinds of restrictive lung disease ?

A

Idiopathic pulmonary fibrosis (IPF)

Sarcoidosis

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3
Q

How are obstructive and restrictive lung diseases distinguished from one another in diagnosis ?

A

Through spirometry measurements (repeatable measurement of lung function), which include FEV1.0 and FVC

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4
Q

State Poiseuille’s law, explaining its relevance to obstructive and/or restrictive lung disease.

A

R = 8ηL/πr^4
R being the resistance to flow when flow is laminar. This shows that resistance to flow is inversely proportional to radius, so small decrease in radius will have significant impact in resistance of flow and work of breathing, which is a major problem in some lung diseases.

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5
Q

What are the pathological changes in the airway causing reduced airflow in obstructive lung disease ? Compare these with the normal physiology of the airways.

A

Changes in airways, especially middle-sized bronchioles.

1) inflammation and fibrosis of the bronchial wall
2) hypersecretion of mucus (normally no mucus)
3) destruction of the elastic fibers that hold the airway open (normally present)

These results in reduced airflow in airways. These apply to COPD as well as asthma except for 3) which only applies to COPD.

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6
Q

Distinguish between spirometry results in normal conditions, in obstructive lung disease, and in restrictive lung disease (explaining the changes occurring). Graph the results of both obstructive and restrictive lung disease compared to a normal lung, in a spirometry test.

A

Spirometry indicates an abnormality if any of the following is present:

  • FEV1 < 80% predicted normal
  • FVC < 80% predicted normal
  • FEV1:FVC ratio reduced (< 0.7)

1) OBSTRUCTIVE LUNG DISEASE
-FEV1 reduced (< 80% predicted normal)
-FVC usually reduced but to a lower extent than FEV1
-FEV1:FVC ratio reduced (< 0.7)
Because air is trapped in the lungs rather than lost, so it mainly just takes more time to get it out (although FVC does decrease a little bit).

2) RESTRICTIVE LUNG DISEASE
-FEV1 reduced (< 80% predicted normal)
-FVC reduced (< 80% predicted normal)
-FEV1:FVC ratio maintained (> 0.7)
Because smaller size of lungs means lungs cannot expand more, so FVC must also decrease considerably.

Refer to slide 7 of lecture on “Obstructive Lung Disease”

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7
Q

Briefly explain the procedure of spirometry.

A
  • Clip on nose
  • Maximum breath in and blow out as hard and fast as possible and keep blowing
  • Normal, majority of air comes out in first second
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8
Q

Explain the change of air during spirometry in terms of lung volumes and capacities.

A

From total lung capacity to residual V

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9
Q

What volume/capacity is left in the lungs after a slow, maximal expiration ? (e.g. in spirometry) What volumes/capacities make this V/capacity ?

A 
Forced Vital Capacity
= 
inspiratory reserve volume 
\+ tidal volume
\+expiratory reserve volume

I.E.
total lung capacity
-residual volume

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10
Q

Define FEV1.0 and FVC.
What is FEV1.0 /FVC ratio a measure of ? What’s a normal FEV1.0 /FVC ratio ?
Graph spirometry of a normal lung, showing FEV1.0.

A 
FEV1.0 = forced expiratory volume in 1 sec.
FVC = forced vital capacity, the maximal volume of gas that can be exhaled from full inhalation by exhaling as forcefully and rapidly as possible.

FEV1.0 /FVC ratio is a measure of airflow obstruction

FEV1.0 /FVC > 0.7 is normal

Refer to slide 9 in lecture on “Obstructive Lung Disease”

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11
Q

Identify the changes in lung volumes and capacities in obstructive, and restrictive lung diseases.

A

OBSTRUCTIVE
TLC normal or increased
Tidal Volume increased
FVC decreased (but to a lower extent than FEV1)
FEV1.0 decreased
FRC increased
RV increased (because air trapping so bronchioles close and alveoli cannot empty)

RESTRICTIVE
TLC decreased
FVC decreased
FEV1.0 decreased 
FRC decreased
Residual V decreased
Tidal Volume decreased
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12
Q

Give an example of physiological V/Q mismatching. What happens in lung disease wrt this ?

A

Top of lungs ventilated more than bottom.
Perfusion of lungs greater at bottom than at the top.
Mismatch.

In lung disease, increased mismatch so some alveoli ventilated but no blood supply so blood cannot pick up O2.
In both obstructive and restrictive lung disease, the cause of hypoxia is increase in V/Q mismatching

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13
Q

Define bronchiectasis.

A

Chronic pus in bronchioles.

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14
Q

Distinguish between asthma and COPD wrt:

  • Smoking patterns
  • Allergic ?
  • Age groups affected
  • Timeline
  • Rate of decline
  • Immune cells involved
  • Diurnal variations
  • Corticoid response
  • Bronchodilator response
  • Change in FVC and TLCO
  • Quality of gas exchange
A

COPD:

  • Smokers
  • Non-allergic
  • Over 50s
  • Chronic
  • Progressively decline (but through treatment can reduce slope of decline)
  • Neutrophils
  • No diurnal variations
  • Poor corticosteroid response
  • Poor bronchodilator response (measure spirometry both before inhaled bronchodilators, and after that)
  • Reduced FVC and TLCO
  • Impaired gas exchange

ASTHMA:

  • Non-smoking related (but can trigger asthma)
  • Allergic (patients tend to have history of allergic rhinitis, eczema)
  • Tends to be younger patients
  • Intermittent
  • Non-progressive (spirometry can be perfectly normal)
  • Eosinophil infiltration
  • Diurnal variation (nocturnal cough and wheeze)
  • Good corticosteroid response
  • Good bronchodilator response (measure spirometry both before inhaled bronchodilators, and after that )
  • Preserved FVC and TLCO (i.e. thicker walls)
  • Normal gas exchange
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15
Q

How is asthma diagnosed ?

A

♦ Clinical diagnosis, based on symptoms of:
• Wheeze
• Breathlessness
• Chest tightness
• Cough
♦ Especially if:
-Diurnal variations on symptoms and history of atopy
-Symptoms arise in response to allergen, exercise, cold air
-PEFR shows abnormalities

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16
Q

Define asthma.

A

Chronic inflammatory disorder of the airways…in susceptible individuals, inflammatory symptoms are usually associated with widespread but variable airflow obstruction and an increase in airway response to a variety of stimuli. Obstruction is often reversible, either spontaneously or with treatment.

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17
Q

Describe the pathophysiology of asthma.

A

Three components:
1) Airway narrowing / obstruction (reversible)
2) Airway hyper-responsiveness in response to trigger (e.g. allergen, infection) (and edema secondary to histamine release)
3) Airway inflammation
• Eosinophilic inflammation

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18
Q

Identify important mediators of asthma.

A
  • Leukotriene B4 and cysteinyl-leukotrienes
  • (C4 and D4) interleukins IL-4, IL-5, IL-1
  • Tissue damaging eosinophil proteins
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19
Q

Describe a hypothesis which has been presented to explain why there has been an increase in asthma diagnoses over the past few years.

A

Hygiene hypothesis: houses are becoming too clean, leading to under-exposure to allergens to trigger T-lymphocytes (moderators of asthma) which would mediate a response.

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20
Q

Identify possible exacerbators/triggers of asthma.

A
  • Virus
  • Allergens - animal dander, dust mites, pollens, fungi
  • Cold
  • Foods / nutrition – vitamin D, A , E levels? • Chemicals – smoke
  • Exercise
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21
Q

Describe non-pharmacological treatment of asthma.

A
  • Achieve and maintain a normal BMI if overweight (since increased weight increases work of breathing)
  • Breathing exercise programmes
  • Stop smoking (patient +/- household members)
22
Q

Identify the clinical signs of acute severe asthma, life-threatening asthma, and near fatal asthma

A

ACUTE SEVERE ASTHMA

  • PEF 33-50% best or predicted
  • Respiratory rate (>25/min) (i.e. hyperventilation, so likely low PaCO2)
  • Heart rate (>110/min)
  • Inability to complete sentences in one breath

LIFE THREATENING ASTHMA

  • PEF < 33% best or predicted
  • Sp02 < 92%
  • PaO2 < 8 kPa
  • Hyperventilation
  • Normal PaCO2 (4.6 - 6.0 kPa) (normalised from acute severe asthma because respiration is a muscular work and after a while muscles tire so hyperventilation not so effective)
  • Silent chest
  • Cyanosis
  • Poor respiratory effort
  • Arrythmia
  • Exhaustion
  • Altered conscious level (due to hypoxia)
  • Hypotension

NEAR FATAL ASTHMA
-Raised PaCO2 (muscles get more tired so respiration rate falls and CO2 accumulates) and/or requiring ventilation with increased inflation pressures.

23
Q

What happens if life threatening asthma is not treated ?

A

Respiratory arrest, followed by cardiac arrest

24
Q

Is there any overlap between COPD and asthma ? Explain.

A

Yes.
Overlap is partly artificial because both are difficult to specifically define. Also, if you have lungs which tend to hypersecrete and go into bronchospasm (i.e. asthma), they are more vulnerable to cigarette smoke, so if you do smoke you are more likely to end up with COPD .

25
Q

State what COPD stands for and explain what each word making up COPD means.

A
  • Chronic: Symptoms for more than 3 months in 2 consecutive years
  • Obstructive: Predominant sign wheeze. Needs spirometry for assessment
  • Pulmonary: Affects both the airways & the lung
  • Disease
26
Q

How common, preventable, and treatable is COPD ?

A

COPD is a common, preventable and treatable disease.

27
Q

What are the main pathological characteristics of COPD ?

A

Characterized by persistent airflow limitation that is usually progressive and associated with chronic inflammatory response in the airways and the lungs to noxious particles or gases.

28
Q

What factor can contribute to the overall severity of COPD in individual patients ?

A

Exacerbations and comorbidities contribute to the overall severity in individual patients

29
Q

Identify risk factors for COPD.

A

MODIFIABLE

1) Tobacco/cannabis smoking (number of cigarettes/bidis smoked + individual susceptibility of the lungs)
2) Indoor / outdoor pollution from biomass fuels (esp. in less economically developed countries)

NON-MODIFIABLE (i.e. host factors)

1) Genetic abnormalities (e.g. α1 antitrypsin deficiency, especially if early onset COPD)
2) Abnormal lung development (e.g. premature neonate)
3) Age and gender (females at increase risk)

30
Q

How developed are the countries which COPD affects most ?

A

Upper and lower middle class-income countries (low income not so much, high income not so much)

31
Q

What is a characteristic sign of cannabis smoking in CXR ?

A

Large (black) bullae on CXR, showing lots of emphysema

32
Q

Why is cannabis relevant wrt COPD ? What illness can cannabis smoking result in besides COPD ?

A
  • Frequently smoked with tobacco and although it has a different pattern of inhalation, still contributes to COPD (cannabis smokers get COPD at a younger age). Hotboxing is an especially unhealthy practice (associated with TB).
  • Cannabis inhalation can lead to aspergillosis (contaminated joints).
33
Q

What kind of patient may have α1 antitrypsin deficiency ?

A

Patient with early onset COPD (< 45yrs)

34
Q

What does α1 antitrypsin normally do ?

A

Enzyme produced in the liver which counteracts proteinases

35
Q

Describe the inheritence pattern of α1 antitrypsin deficiency.

A

Autosomal codominant pattern

  • M allele, produces normal levels of alpha-1 antitrypsin
  • S allele produces moderately low levels of this protein
  • Z allele produces very little alpha-1 antitrypsin

ZZ-AT have α1 antitrypsin deficiency

36
Q

What is the treatment for α1 antitrypsin deficiency?

A

Gene therapy, in research phase

37
Q

What are the main features of α1 antitrypsin deficiency on a CXR ?

A

Emphysema most marked in lower lobe (black, whereas normally whiter towards bottom than top).

38
Q

Describe the mechanism of α1 antitrypsin deficiency.

A

Smoking leads to the attraction of inflammatory cells, which in turns results in release of elastase. However, the action of this enzyme (destruction of elastic fibers in the lung) is inhibited by α1 antitrypsin. In decreased α1 antitrypsin activity (due to smoking) and inherited α1 antitrypsin deficiency, this means elastase does result in destruction of elastic fibers in the lung, and thus emphysema.

39
Q

Describe the pathophysiology of COPD.

A

• Inflammation and fibrosis of the bronchial wall
• Hypertrophy of the submucosal glands and
hypersecretion of mucous
• Loss of elastic, parenchymal lung fibres (emphysema) which holds the bronchioles open by radial traction

40
Q

Which symptoms are we looking for in the diagnosis of COPD (i.e. presenting complaint) ?

A

Consider the diagnosis of COPD in patients with breathlessness, chronic cough/sputum production and exposure to risk factors.

41
Q

Describe the clinical presentation of COPD.

A

Usually 50s or 60s, chronic cough, sputum production (typically worse in the morning), increasing (over time) shortness of breath, diminishing exercise tolerance, history of exposure to risk factors.

42
Q

What is the onset of COPD ?

A

The onset of COPD is usually insiduous (i.e. patients do not present early because they adapt their activity. For instance if cannot walk to shops, they’ll get the bus. By time they present, little to be done )

43
Q

What are the main categories of patients in COPD ? Identify the main characteristics of each group.

A

Pink puffer

  • Pink
  • Increased SOB but little cough
  • Increased work to breathe so tripod position (fixed shoulder girdles to help) + use of accessory muscles + pursed lips (to prevent alveolar collapse and thus reduce work to breath)
  • Barrel chest due to air trapping
  • Decreased breath sounds

Blue bloaters

  • Blue (cyanosed so pulmonary hypertension, raised JVP, edema, cor pulmonale)
  • Bloater = sign of RH failure
  • Expectorant cough (brings out mucus)
  • Crackles and wheezes
44
Q

Identify systemic effects of COPD.

A 
• Weight loss (problem: high BMI or low BMI do worse in prognosis)
• Skeletal muscle dysfunction
• CVS disease (hypertension, arrhythmia,
peripheral vascular disease)
• Depression
• osteoporosis
45
Q

Identify a non-pharmacological treatment of COPD.

A

Stop smoking (slows downward progression)

46
Q

When is domiciliary oxygen therapy given ?

A
  • Patients with a PaO2 <7.3 -8 kPa
  • Must have stopped smoking
  • Willing to breath it for > 15 hours / day to improve mortality
47
Q

Identify the main restrictive lung diseases. How many are there ?

A
  1. Idiopathic pulmonary fibrosis (i.e. lost elasticity in the lungs)
  2. Hypersensitivity pneumonitis (i.e. due to allergens)
  3. Sarcoidosis
  4. Connective tissue disease related lung disease (e.g. rheumatoid can give you a fibrotic restrictive lung disease)

Total about 200 separate restrictive lung diseases.

48
Q

Which symptoms are we looking for in the diagnosis of restrictive lung disease (i.e. presenting complaint)

A

Dyspnoea, dry cough, malaise

49
Q

What findings upon examination would fit with restrictive lung disease ?

A

Bilateral fine crackles + finger clubbing

50
Q

Identify a good prognostic indicator for restrictive lung diseases.

A

6 minute walk test (i.e. measurement of distance walked over a span of 6 minutes)

51
Q

What is the treatment for restrictive lung diseases ?

A

Often palliative pathway, unless relatively young and otherwise fit and thus candidate for heart and lung transplant

MD3001 (75 decks)

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