Obstructive & Restrictive Lung disease Flashcards

1
Q

how are obstructive respiratory diseases categorised and why is this method effective

A
  • the pattern of spirometry
  • this is useful as it is quantitative, objective and is an accurate measurement of the lung function
  • it is also repeatable and can be used to monitor the course of the disease
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2
Q

what are the two main measurements in spirometry

A

FEV1.0 and FVC

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3
Q

Poiseuilles Law

A

especially states that if the radius narrows then the resistance to air flow increases and the work load of breathing increases and therefore the lungs have to work harder causing shortness of breath

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4
Q

what is the physiology of asthma

A

essentially what happens in asthma is that, there is inflammation and swelling and fibrosis and increases in mucus secretion.

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5
Q

what is the physiology of COPD

A

essentially what happens in COPD is that, there is inflammation and swelling and fibrosis and increases in mucus secretion. There is also destruction of the elastic fibres that hold open the airway, this can lead to narrowing and potentially collapse

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6
Q

at what level in spirometry is an abnormality identified

A
  • FEV1 <80% of predicted normal
  • FVC<80% of predicted normal
  • the FEV1//FVC ratio is < 0.7
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7
Q

spirometry findings in an obstructive disorder

A
  • FEV1 is reduced
  • FVC is usually reduced but to a lesser extent than FEV1
  • the ratio is reduced <0.7
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8
Q

spirometry in restrictive disorder

A
  • FEV1 reduced
  • FVC reduced
  • ratio is normal >0.7
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9
Q

what is FVC

A

forced vital capacity

F = this means the patient exhales as hard and as long as possible
V = total volume in the lungs minus the residual volume 
C = sum of more than one volume
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10
Q

what is the fev1//FVC ration a measure of

A

the airflow obstruction, which is why in restrictive lung disease it is normal

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11
Q

what happens to the lungs in a restrictive lung disease

A

the lungs become stiff and fibrosed so all measurements tend to be reduced, as the lungs are less expansive

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12
Q

what happens to lungs in obstructive lung disease

A

this causes the trapping of air.
The working proportion of the lungs shifts upwards, the air is trapped in the alveoli and they are not ventilated but they are still perfused. this increased ventilation perfusion mismatching leads to the patient becoming hypoxic

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13
Q

ventilation rate (V)

A

refers to the volume of gas inhaled and exhaled from the lungs in a given time period

multiplying the tidal volume (volume of air inhaled and exhaled in a single breath) by the respiratory rate. In an average man, the ventilation rate is roughly 6L/min.

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14
Q

perfusion

A

refers to the total volume of blood reaching the pulmonary capillaries in a given time period.

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15
Q

what leads to this mismatching and how is it made worse

A

ventilation increases from the top to the bottom of the lungs (this means there is more at the bottom) this is the same with perfusion.
There is a mismatch however which causes:
top of the lung = under-perfused and preferentially ventilated
bottom of the lung = preferentially perfused and under-ventilated

this mismatch is made worse by obstructive and restrictive lung diseases

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16
Q

what are the most common obstructive lung diseases

A

asthma and COPD

also bronchiectasis and cystic fibrosis

17
Q

what is important about the eosinophil and neutrophil count in asthma and COPD

A

in regards to eosinophils and neutrophils. If there is a high level of eosinophils and normal neutrophils then it is likely to just be asthma, however if there is normal eosinophils and high neutrophils then it is likely to be COPD. If both are high, COPD is not usually treated with steroids but if there is a high eosinophil count then this suggests an element of asthma which you should then treat with steroids

18
Q

what are symptoms od asthma

A

cheese
breathlessness
chest tightness
cough

however could be asymptomatic between attacks

look for diurnal variation in symptoms and history of atopy (PEFR is useful)

OR symptoms could be in response to allergies or exercise or cold air

19
Q

what is the pathophysiology of asthma

A
  • airway narrowing/obstruction which can be reversible
  • airway hyper-responsiveness
  • airway inflammation (look for eosinophils)
20
Q

what are the important mediators in asthma

A

leukotriene B4 and cysteinyl-leukotrines C4 and D4
interleukins IL-4, IL-5, IL-13
tissue damaging eosinophil proteins
(drugs tend to target these mediators)

21
Q

genetic predisposition and potential triggers

A

symptoms can become worse in the presence of:

  • viral
  • allergens (e.g animal dander, dust mites, pollens and fungi)
  • cold
  • foods/nutrition (vitamin D, A, E levels?
  • chemicals (smoke)
  • exercise
22
Q

non-pharmacological treatment

A
  • achieve and maintain a normal BMI if overweight
  • breathing exercise programmes
  • stop smoking (patient and household members)
23
Q

what is the criteria for COPD

A

symptoms have to be for more than 3 month in two consecutive years
predominant sign of a wheeze (spirometry assessment)
it effects both the airways and the lungs

24
Q

how is COPD characterised

A

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

25
Q

epidemiology of COPD

A
  • smoking
  • indoor/outdoor pollution from biomass fuels
  • genetic abnormalities (alpha 1 antitrypsin def. if early onset COPD)
  • abnormal lung development
  • age and sex (females at increased risk)
26
Q

cannabis diagnosis

A

large bullae on xray

beware of a contaminated joint (aspergillosis)

27
Q

alpha 1 antitrypsin def.

A
early onset COPD 
it is an enzyme produced in the liver that counteracts the proteinases (the enzyme that breaks down the lung tissue)
autosomal codominance
emphysema most marked in the lower lobe
gene therapy research phase
28
Q

pathophysiology of COPD

A
  • inflammation and fibrosis of the bronchial wall
  • hypertrophy of the submucosal glands and hyper secretion of mucous
  • loss of elastic, parenchymal lung fibres (emphysema)
29
Q

clinical presentation of COPD

A

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

30
Q

pink puffer

A
increasing SOB but little cough 
pursed lips as alveoli tend to collapse 
barrel chest due to air trapping 
use of accessory muscles 
decreased breath sounds
31
Q

blue bloater

A

blue = cyanosed
bloater = signs of right heart failure
expectorant cough
crackles and wheezes

could be weight loss 
skeletal dysfunction 
CVS disease 
depression 
osteoporosis
32
Q

what are the five fundamentals of COPD care

A
  1. support the stopping of smoking
  2. pneumococcal and flu vaccine
  3. pulmonary rehab
  4. co-develop a personalised self-management plan
  5. optimise co morbidities
33
Q

Domiciliary oxygen therapy

A

patients with a Pao2 < 7.3 - 8 kPa
must have stopped smoking
must be breathed for >15 hours/day to improve mortality

NON INVASIVE POSITIVE PRESSURE VENTILATION

34
Q

Examples of restrictive lung diseases

A
  1. idiopathic pulmonary fibrosis
  2. hypersensitivity
  3. sarcoidosis
  4. connective tissue disease related to lung disease

dyspnoea, dry cough and malaise
bilateral fine crackles ad finger clubbing

35
Q

characterises of restrictive lung diseases

A

overall lungs are smaller
decreased VC and decreased fev1.0 but ratio maintained
6 minute walk test
often palliative pathway