6 Flashcards

(48 cards)

1
Q

What is spirometry?

A
  • measurement of the movement of air during breathing
  • records the volume of air that is breathed in and out
  • generates tracings of air flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the tracings from a spirometry used to calculate?

A
  • vital capacity, tidal volume

- flow rate of air movement

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

What are the reasons for pulmonary function tests?

A

Diagnosis

  • tests are rarely diagnostic on their own
  • results taken together with history and examination

Patient assessment

  • most usual reason for tests
  • serial changes
  • response to therapy
  • assessment for compensation
  • pre-surgical assessment

Research purposes

  • epidemiology
  • study of growth and development
  • investigation of disease processes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why is vital capacity useful in spirometry?

A

-measured value can be compared to the predicted vital capacity of an individual of the same age, height and sex to determine the status of patient

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

Why might vital capacity be reduced?

A
  • filled normally in inspiration
  • emptied normally in expiration
  • or both
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is “restrictive” deficit?

A
  • maximal filling of lungs usually determined by the balance between maximum inspiratory effect and force of recoil of the lungs
  • so if lungs are unusually stiff, or inspiratory effort is compromised by muscle weakness, injury or deformity, then this deficits is produced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is an “obstructive” deficit?

A

When airways are narrowed so expiratory flow is compromised much earlier in expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do modern spirometers work?

A
  • use electronic method of measuring the volume of gas inhaled/exhaled through a mouthpiece
  • recorded on a vitalograph which shows the volume expired during a vital capacity breath
  • FVCstanding > FVCseated but high intrathoracic pressure can result in reduced cardiac output and cerebral blood flow so pt. May faint
  • preferable to put nose clip on pt. So that air isnt lost through nose
  • must observe the subject
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a Collins water seal spirometer?

A
  • old spirometer
  • if pen records an upward deflection and the silver sinks, that means pt. Is breathing IN air
  • if pen shows downward curve and the silver rises then pt. Is breathing air OUT
  • floating bell-jar is inversely proportional to breathing
  • expired gas passes into water seal
  • increased pressure causes jar to rise
  • movement transmitted to pen
  • pen movement proportional to volume breathed in/out
  • see lecture 6.1 slides 5-7
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain what the movements of the TRACE mean?

A
  • INSPIRATION as an upward deflection

- EXPIRATION as a downward deflection

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

What lung capacities are shown on a Spirograph?

A
  • Vt= tidal volume
  • FRC= functional reserve volume
  • VC= vital capacity
  • inspiratory capacity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do we calculate inspiratory capacity?

A

Vt + IRV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do we calculate functional residual capacity?

A

-ERV + RV

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

How can we distinguish between restrictive and obstructive deficits on paper?

A
  • through time-volume graph
  • convention shows expiration as a downward deflection on spirometry trace
  • graph of volume (L) expired against time
  • follow normal graph conventions
  • pt. Inspires to vital capacity
  • rapid forced expiration
  • see session 6.1 slides 16-17
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What do forced flow-volume measurements show us?

A
  • how much air can the subject blow out?
  • could be reduced in restrictive disorders
  • may be airway narrowing precipitating early airway closure (ex. Asthma or CF)
  • how fast is the air expelled? (Could be reduced with airway narrowing)
  • pattern of change in flow-volume curve (insp and exp) can indicate site of obstruction
  • response to treatment (ex. B2 agonist)
  • change with age or growth
  • progression of disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define FVC, FEV1 and PEF on a time-volume graph

A
  • FVC: maximal amount of air that the pt. Can forcibly exhale after taking a maximal inhalation
  • FEV1: volume exhaled in the first second
  • PEF (peak expiratory flow): maximal only speed of airflow as the patient exhales
  • FEV1 is the most reproducible flow parameter and is especially useful in diagnosing and monitoring patients with obstructive pulmonary disorders (ex. Asthma, COPD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How will a volume-time graph look in obstructive disease (asthma, COPD)

A
  • FVC is nearly normal if given sufficient time to completely breathe out
  • narrowed airways reduces the speed at which air can be breathed out
  • FEV1 is markedly reduced
  • fraction or air expelled during first second (FEV1/FVC) is markedly reduced; ratio <70%
  • see graph on session 6.1 slide 18
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How will a volume-time graph look in restrictive disease? (Lung fibrosis)

A
  • FVC is markedly reduced (lungs stiff, cant be expanded adequately)
  • lungs not as stretchy anymore
  • however the speed at which air can be breathed out is normal (because no narrowing of airways)
  • FEV1 is reduced proportionately
  • fraction of air expelled during first second is normal or even greater than normal
  • FEV1/FVC ratio is greater or equal to 70%
  • see graph on session 6.1 slide 19
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is a flow volume curve/loop?

A
  • when expiratory flow rate is plotted against lung volume

- obstructive deficient may be more revealed through this loop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Explain how to read a flow-volume loop

A
  • look at it like a clock, goes in clockwise direction
  • at the start of expiration, line goes up to produce peak expiratory flow
  • as expiration continues, there is a fall in expiratory flow rate since airways are narrowing
  • then residual volume is empty
  • inspiration begins, so producing a vital capacity
  • inspiration continues until total lung capacity produced
  • then cycle starts again
21
Q

What cheap device can patients use at home to produce a peak expiratory flow rate?

A

-Peak Flow Meter

22
Q

What is scolloping?

A
  • when the flow-volume loop produces a concave shape
  • means the small airways are narrower than expected; they are contracting abnormally
  • see session 6.1 slide 22
23
Q

Why do COPD and asthma produce the same flow-volume loop but COPD is worse than asthma?

A

-asthma loop can be fixed after taking bronchodilators but COPD loop cannot be fixed

24
Q

How would a flow-volume loop look like in obstructive airways disease?

A
  • mild obstruction of the small airways produces scalloping of the flow volume curve
  • more severe obstruction also reduces PEFR
25
How would a flow volume loop look in restrictive disease?
- characterized by a reduction in FVC - results in narrow flow volume loop - but PEFR is not significantly reduced as there is no airways obstruction - results in a narrow and tall flow volume loop
26
How can we measure residual volume?
- volumes of air remaining in the lungs after expiration | - may be measured by the helium dilution test
27
How can we measure dead space?
-measured by the nitrogen washout method
28
How can we measure diffusion capacity?
- “diffusion conductance”: resistance to diffusion across the alveolar membrane - estimated by the carbon monoxide transfer factor (TLCO)
29
What is bronchiectasis?
- chronic irreversible dilation of one or more bronchi - bronchi exhibit poor mucus clearance - predisposition to recurrent or chronic bacterial infection - results in abnormally enlarged bronchi - pathological condition that can be caused by many diseases or is idiopathic
30
What is the aetiology (causes) of bronchiectasis?
- common underlying mechanism of chronic inflammation - inflammation causes destruction of the elastic and muscular components of the bronchial wall and peribronchial fibrosis - post-infective: whooping cough, TB - immune deficiency: hypogammaglobulinaemia - genetic/mucociliary clearance defects: CF, primary ciliary dyskinesia, Young’s syndrome (triad of bronchiectasis, sinusitis and reduced fertility), Kartagener syndrome (triad of bronchiectasis, sinusitis and situs inversus) - obstruction: foreign body, tumour, extrinsic lymph node
31
What diagnostic tests will be done for bronchiectasis? What will you see?
- CXR: usually abnormal but inadequate in the diagnosis or quantification of bronchiectasis/bronchial dilation - Gold standard is a high resolution CT: willl see bronchial dilation bigger than the adjacent pulmonary arteriole and bronchial wall thickening
32
What is the signet ring sign?
- seen in CT-dilated bronchus and accompanying pulmonary artery branch are seen in cross-section - in healthy lung the bronchus is slightly smaller than the artery
33
What are the clinical symptoms of bronchiectasis?
Very common - chronic cough - daily sputum production: can vary in quantity, colour and consistency Common - breathlessness on exertion - intermittent Haemoptysis - nasal symptoms - chest pain - fatigue Less Common -wheeze
34
What are the clinical signs of bronchiectasis?
- pulse oximetry (measures o2 sat of blood) may reveal hypoxaemia in advanced cases of bronchiectasis - fever relatively common: more than half of bronchiectasis patients will have recurrent fever episodes - haemoptysis: present in about 50% of patients but usually mild - fine crackles (rales) due to the collapsed airways popping - high-pitched inspiratory squeaks - rhonchi: sounds that are lower in pitch, sounds like rumbling - sometimes can hear both crackles and wheezing - systemic signs: history of weight loss (common) and clubbing of digits (less common)
35
What are some common organisms that cause bronchiectasis?
- haemophilus influenzae - pseudomonas aeruginosa - moraxella catarrhalis - strenotrophomonas maltophilia - fungi: aspergillus, candida - non-tuberculous mycobacteria (NTM) - staph aureus (less common)
36
Why is it important to consider whether a patient may have bronchiectasis?
- early diagnosis and treatment may impede disease progression - see if they have history of asthma or COPD - see if they have history of chest infections - see if sputum culture is positive for common organisms such as haemophilus, pseudomonas or atypical mycobacterium - check if they have IBD or rheumatoid arthritis
37
How would you manage bronchiectasis?
- treat underlying cause - physio/airways clearance: daily airway clearance is essential for treatment success - sputum sampling: routine culture and NTM - exclude immunodeficiency - consider long-term therapies at future visits - supportive: flu and routine vaccine - management plan for infective exacerbations
38
How can we define an exacerbation in bronchiectasis?
Has deterioration in 3 or more key symptoms for at least 48 hours: - cough - sputum volume and/or consistency - sputum purulence - breathlessness and/or exercise tolerance - fatigue - haemoptysis
39
What is the most common identifiable cause of bronchiectasis?
Cystic fibrosis
40
Define cystic fibrosis
- autosomal recessive disorder leading to mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) - can lead to multisystem disease (i.e. respiratory and GI) which is characterized by thickened secretions
41
How is cystic fibrosis diagnosed?
- one or more of the characteristic phenotypic features - or a history of CF in a sibling - or a positive newborn screening test result AND - increased sweat chloride concentration (>60mmol/L) SWEAT TEST - Or identification of 2 CF mutations (genotyping) - or demonstration of abnormal nasal epithelial ion transport (nasal potential difference)
42
What are the classic CF clinical presentations?
Meconium ileus - 15-20% newborn CF infants have bowel blocked by sticky secretions - signs of intestinal obstruction soon after birth with bilious vomiting, abd distension and delay in passing meconium Intestinal malabsorption - over 90% of CF individuals have intestinal malabsorption - most is evident in infancy - main cause is sever deficiency of pancreatic enzymes, potentially leading to type 3 diabetes Recurrent chest infections Newborn screening
43
What are some complications of CF?
Lungs - bronchiectasis - pneumothorax - haemoptysis - resp failure Nasal/upper resp tract - chronic sinusitis - nasal polyposis Pancrease - pancreatic insufficiency - diabetes mellitus Gut - distal intestinal obstruction syndrome (DIOS) - oesophageal reflux/oesophagitis Liver - chronic liver disease - portal hypertension Biliary tree -gallstones Heart -cardiac failure to right side of heart because pumping into a diseased lung Joints and bones - arthritis - osteoporosis Reproductive tract - male infertility - congenital bilateral absence of vas deferens (CBAVD)
44
What lifestyle advice should CF patients follow?
- no smoking - avoid other CF patients - avoid friends/relatives with colds/infections - avoid jacuzzies (pseudomonas) - clean and dry nebulisers thoroughly - avoid stables, compost or rotting vegetation (risk of aspergillus fumigatus inhalation) - annual influenza immunization - NaCl tablets in hot weather/vigorous exercise
45
What are the categories of defects due to CFTR mutation?
- no protein production - protein made but never gets to cell membrane - protein gets to membrane but DOESNT work at all - protein made but only partially active - protein expressed at gene level but substantial reduction in mRNA or protein, or both, synthesis - protein gets to membrane but partially unstable
46
What drug has been made to treat CF?
Orkambi (trade name for two drugs) Lumacaftor - CFTR chaperone during protein folding which increases the number of CFTR proteins that are trafficked to the cell surface - helps in people with Phe508del (most common mutation) Ivacaftor - CFTR potenitator which improves the transport of chloride through the ion channel by binding to the channels directly and increasing the probability that the channel is open - helps people with G551D mutation (in 4-5% cases of CF)
47
What is V/Q?
Ventilation/perfusion ratio
48
What will happen to v/Q if there is reduced ventilation of parts of the lung?
- occurs in pneumonia, asthma, COPD, and respiratory distress syndrome in newborns - V/Q < 1 since ventilation is low relative to perfusion