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Respiratory SCE > Miscellaneous > Flashcards

Miscellaneous Flashcards

1
Q

What are the diagnostic criteria for ARDS?

A

An acute lung injury - within one week of the insult
Bilateral infiltrates on a chest x-ray, not explained by other lung pathology
Respiratory failure not explained by fluid overload
A Decreased PaO2/FiO2 ratio

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2
Q

A patient with COPD has saturations of 95% OA and MRC score of 1. They want to know if they need further investigations before they fly

A

No. No HCT required . Not meeting criteria for in flight oxygen

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3
Q

A patient with COPD has saturations of 95% OA and MRC score of 3. They want to know if they need further investigations before they fly

A

Yes , given MRC 3 , guidelines recommend 6MWT or SWT and if sats <84% review if hx of hypercapnia. If yes then need HCT, if no then inflight O2 @ 2l/min.

If sats on 6MWT/ SWT are > 84% then no need for HCT/ in flight O2

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4
Q

A patient with COPD has saturations of 91% OA and not on LTOT. They want to know if they need further investigations before they fly

A

Yes. Is there a history of hypercapnia ? If Yes then need HCT, if no then in flight O2 @ 2l/min

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5
Q

A patient with COPD has saturations of 91% on 1L LTOT. They want to know if they need further investigations before they fly

A

If known T1RF - no , just increase LTOT by 2l/min

If known T2RF - yes , needs HCT

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6
Q

Who needs a hypoxic challenge test for flying ?

A
  • those with sats ≤ 95% , not usually on LTOT and at risk of hypercapnia OR sats < 84% on 6MWT or SWT with concerns re hypercapnia
  • severe asthma with persistent symptoms or frequent exacerbations despite optimal treatment regardless of SpO2 at sea level
  • ILD patients with sats <95% on exercise and resting sea level PaO2 ≤9.42 or TLCO ≤ 50%
  • Severe chest wall deformity / severe resp muscle weakness FVC <1L
  • Those with existing or previous hypercapnia and those at risk of T2RF already on LTOT
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7
Q

What HCT results indicate need for in flight O2 ?

A

PaO2 < 6.6 or Sats <85%

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8
Q

Patient with IPF wants to know if they need in flight O2 . There sats are 96% following 6MWT

A

No , HCT not req and in flight O2 not required

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9
Q

Patient with IPF wants to know if they need in flight O2 . There sats are 92% following 6MWT and they are not on LTOT

A

Need ABG:

  • if PaO2 < 9.42 on room air then need to review TLCO. If TLCO < 50% predicted then need in flight O2 at 2l/min
  • if PaO2 > 9.42 then still review TLCO . If <50% predicted then should have HCT. If more then doesn’t require HCT
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10
Q

Patient with IPF on LTOT wants to know if they need in flight O2 .

A

Yes , 2L greater than usual prescription

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11
Q

What are recommendations for CF patients when flying ?

A

Review spirometry if FEV1 <50% should have HCT . If sats <90% will need in flight O2

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12
Q

What is the advice following thoracic surgery and air travel?

A

Four weeks for non essential travel , 2 weeks for essential

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13
Q

What is the advice for air travel following TBB/TBNA/EBUS/Endobronchial valve insertion?

A

Those with no PTX on X ray should wait 1 week

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14
Q

What is the advice for flying with PTX?

A

Can’t fly with untreated PTX
Can fly 1 week after resolution of PTX
Be aware those high risk of recurrence

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15
Q

What is the advice for patients who develop sinus barotrauma after flying ?

A

Topical / oral decongestants and appropriate analgesia.

If allergic component intranasal steroids for 1 week prior to travel and /or oral corticosteroids

Symptoms and signs of barotrauma should have resolved prior to flying

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16
Q

What is the advice for air travel following otitis media ?

A

Advised not to fly for 2 weeks

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17
Q

What are the viral infections you are advised not to fly with?

A

Measles , chicken pox , mumps , SARs, MERS, COVID

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18
Q

When can patients with TB fly?

A

Smear positive patients must not fly until there are two consecutive smear negative samples on treatment

Those starting TB treatment when all info not available should not fly for at least 2 weeks

For those who are smear negative treatment should render them non infectious in 2 weeks

For MDR/XDR TB this is prohibited until 2 negative samples produced and clinical evidence of improvement

Extra pulmonary TB no restrictions

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19
Q

When can patients with Pneumonia fly?

A

Air travel should be postponed for 7 days in those with sats < 94%

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20
Q

What is the advice for those with OSA/OHS re air travel?

A

Daytime flights where posssible and take CPAP in hand luggage

Avoid EtOH/sedation

If night flight should use CPAP, if day avoid falling asleep

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21
Q

What is the advice for muscle wall weakness for air travel

A

FVC < 1L then HCT

If can’t tolerate spiro then consider 6MWT /SWT

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22
Q

What is the advice we provide to avoid VTE with air travel?

A

Ensure hydrated , avoid alcohol , keep mobile , compression stockings , for high risk patients LMWH ie 40mg Enox /DOAC for long haul (6-8 hr) flight

Low risk - all
Mod risk- over 60, preggo , minor surgery , extensive varicose veins
High risk- precious VTE (and not on anticoag) , thrombophilia , 6/52 major surgery , malignancy

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23
Q

How long should air travel be delayed after acute PE/DVT?

A

2 weeks

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24
Q

For pulmonary HTN what NYHA category are patients advised to have in flight O2 ?

A

NYHA III or IV

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25
Q

Should patients with lung cancer / mesothelioma fly if on chemo?

A

No, high risk of infection and side effects

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26
Q

What are the contraindications to air travel?

A

Untreated respiratory failure
PTX (unresolved)
Active infection (TB, COVID, MERS, SARS)
Bronchogenic cysts - cerebral air embolism following rupture risk

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27
Q

How do they perform a HCT?

A

Patient inspires gas mixture containing 15% oxygen

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28
Q

What type of drug is Tacrolimus?

A

Calcineurin Inhibitor

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29
Q

What type of drug is Ciclosporin?

A

Calcineurin Inhibitor

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30
Q

What type of drug is Azathioprine?

A

Purine synthase inhibitor

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31
Q

What type of drug is MMF?

A

Purine synthase inhibitor

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32
Q

What type of drug is Sirolimus inhibitor?

A

An mTOR inhibitor

(mTOR is the mammalian target of Rapamycin)

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33
Q

What type of drug is Everolimus inhibitor?

A

An mTOR inhibitor

(mTOR is the mammalian target of Rapamycin)

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34
Q

Who may be harmed by unecessary high O2?

A

CO2 retainers
MI (may increase infarct size)
Paraquat poisoning or Bleomycin lung injury

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35
Q

What FiO2 and flow rate is the blue Venturi ?

A

24% (2-3l/min)

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36
Q

What FiO2 and flow rate is the white Venturi ?

A

28% (4-6L/min)

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37
Q

What FiO2 and flow rate is the yellow Venturi ?

A

35% (8-12l/min)

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38
Q

What FiO2 and flow rate is the red Venturi ?

A

40% (10-15 l/min)

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39
Q

What FiO2 and flow rate is the green Venturi ?

A

60% (12-15l/min)

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40
Q

How often should O2 saturations be measured in hospital?

A

4 hourly

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41
Q

What do we do with target sats in COPD?

A

ABG, if normal then for normal targets UNLESS hx of previous hypercapnia

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42
Q

What can happen with sudden cessation of oxygen?

A

Rebound hypoxia with rapid fall in O2 sats

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43
Q

Above what BMI should we lower target saturations?

A

40

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44
Q

What are the equivalent sats of pO2 <7

A

<85%

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45
Q

Patient on immunosuppressant medications should avoid what vaccines ?

A

Need to avoid live vaccines :

Measles
Mumps
Rubella
BCG
Yellow Fever
Oral Polio
Oral Typhoid

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46
Q

Patients on immunosuppressive medication who have never had varicella zoster and are exposed should have ?

A

Immunoglobulin therapy

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47
Q

Patients on immunosuppressive medication who have never had measles and and are exposed should have ?

A

Immunoglobulin

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48
Q

What should be checked prior to starting and during AZT treatment ?

A

Prior to starting : FBC, LFT, TPMT

During treatment : FBC ever 2/52 for 3/12 and then monthly , monthly LFTs

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49
Q

At what parameters should AZT /MTX be held ?

A

WCC <3
PLT < 100
ALP / transaminases > x3

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50
Q

What % of patients have no TPMT activity and should therefore should avoid AZT ?

A

0.3%

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51
Q

What is Azathioprine ?

A

Pro-drug of 6-mecaptopurine

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52
Q

What are the side effects of AZT?

A

Sore mouth, mouth ulcers , nausea , vomiting , diarrhoea , skin rash , alopecia , incr risk of skin cancer

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53
Q

What should be checked prior to starting and during treatment with MTX?

A

FBC/ U&E/LFT
CXR
Folic Acid
Pregnancy

Avoid if significant hepatic or renal impairment or if ascites / pleural effusion as can accumulate

During :
Bloods every 2/52 for 3/52 and then monitoring

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54
Q

What are the side effects of MTX?

A

Mouth Ulcers, Skin rashes, nausea , macrocytosis , myelosuppression , pneumonitis

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55
Q

What should be checked prior to starting and during cyclophosphamide treatment ?

A

FBC /U&E/LFT
Urine Dip
Semen store
Pregnancy check - avoid & if BF (and for 6/12 after for both M & F)

Should have bloods weekly for 1 month then every 2 months

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56
Q

How long does cyclophosphamide take to work?

A

12-14/7 hence why usually combined with high dose steroids

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57
Q

What are the side effects of cyclophosphamide ?

A

Haemorrhagic cystitis , bladder cancer , nausea and vomiting , hair thinning , alopecia , cervical cancer

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58
Q

What should be checked prior to starting and during Rituximab treatment ?

A

FBC/U&E/LFT
Hep B and C
ECG
CXR

First week check FBC/ U&E/LFT and then weekly

Alternative to cyclophosphamide

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59
Q

Side effects of Rituximab

A

Abdominal pain; acne; alopecia; anaemia; anxiety; appetite decreased; arthralgia; asthenia; asthma; conjunctivitis; constipation; cough; cytokine release syndrome; depression; diarrhoea; dysphagia; ear pain; epistaxis; fever; gastrooesophageal reflux disease; headache; increased risk of infection; influenza like illness; infusion related reaction; leucopenia; lymphadenopathy; malaise; muscle complaints; muscle weakness; myocardial infarction; neutropenia; pain; pancytopenia; peripheral oedema; sensation abnormal; skin papilloma; stomatitis; sweat changes; throat irritation; thrombocytopenia; tremor; vomiting; weight decreased

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60
Q

What is the empey index?

A

The ratio of FEV1 (in ml) to PEFR (in L)

Useful in predicting if someone has upper airway obstruction , normal result is <10 and if >10 should prompt further evaluation

The PEFR is clipped first by the presence of upper airflow obstruction relative to the FEV2

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61
Q

Where are perfusion and ventilation greatest in the lungs ?

A

At the bases

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62
Q

What causes an increased DLCO?

A

Pulmonary haemorrhage
Polycythemia
Obesity
High altitude
Hyperthyroidism
AV malformations

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63
Q

What causes a decreased DLCO?

A

ILD
Emphysema
Severe anaemia
PE
Increased carboxyhaemoglobin
Hypothyroidism
CCF
Pneumonectomy

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64
Q

What is DLCO ?

A

The diffusing capacity for carbon monoxide and is the same as transfer factor for carbon monoxide. It is a measure of gas transfer from inspired air to the red blood cells . diseases that decrease blood flow to the lung or damage alveoli cause less efficient gas exchange resulting in lower DLCO

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65
Q

If the PaCO2 is normal the PaO2 for different FiO2 can be estimated how ?

A

FiO2 (%) x 0.75

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66
Q

In CPET what are indicators of a maximal test ?

A
  • Respiratory Exchange Ratio (RER) > 1.1 (switch from aerobic to anaerobic)
  • Low HRR (ie close to maximal HR)
  • Rise in lactate
  • Anaerobic threshold reached (if given as graph it’s where VCO2 raises faster than VO2)
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67
Q

What are the lung function changes seen in pregnancy?

A

Expiratory reserve volume decreased , FRC decreased , minute ventilation increased , TLC no change , arterial pCO2 decreased

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68
Q

What are the contraindications to CPET?

A
  • Known history of exercise induced syncope or pre-syncope
  • MSK problem limiting exercise
  • ACS/MI within 7 days
  • Unstable angina
  • Poorly controlled HF
  • Aortic dissection / Aneurysm
  • Acute exacerbation of COPD/Asthma
  • Severe Pulmonary HTN
  • Resp failure pO2<8
  • Acute PE
  • Recent DVT
  • Frailty
  • Hx of seizures / syncope
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69
Q

Most common adverse event during CPET?

A

Vasovagal / dizzyness

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70
Q

What should VO2 max be in normal individuals in CPET?

A

> 80% predicted
If > 80% predicted very unlikely that the individual has any significant pathology of heart or lungs (slight caveat with athletes but for purposes of exam)

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71
Q

What should HR be in normal individuals in CPET?

A

≥ 80% predicted maximal HR

(NB Maximal HR is 220 - age)

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72
Q

What should VE (minute ventilation) be in normal individuals in CPET?

A

Should not reach 80% of predicted during exercise (as should have ventilatory reserve, NB can be super maximal in athletes)

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73
Q

What is an abnormal fall of O2 sats in CPET?

A

A fall >4% from resting value is abnormal and implies lung issue, PVD or opening of R to L shunt

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74
Q

What is oxygen pulse ?

A

A non invasive CPET given idea of CO

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75
Q

What should oxygen pulse be in normal individuals in CPET?

A

> 10ml/beat at peak exercise

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76
Q

What should AT (anaerobic threshold) be in normal individuals in CPET?

A

> 40% of predicted VO max (NB predicted, not achieved)

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77
Q

If VO2 max is >80% predicted , how would you interpret the CPET?

A

Normal

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78
Q

If VO2 max is <80% predicted, max HR <80% predicted and VE max <80% predicted how would you interpret the CPET?

A

Submaximal effort

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79
Q

If VO2 max is <80% predicted, max HR <80% predicted and VE max >80% predicted how would you interpret the CPET

A

Lung disease

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80
Q

If VO2 max is <80% predicted, max HR >80% predicted and fall in O2 says >4% how would you interpret the CPET

A

Pulmonary vascular disease

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81
Q

If VO2 max is <80% predicted, max HR >80% predicted and fall in O2 says not less than 4% how would you interpret the CPET

A

Heart disease
Or
Deconditioning

82
Q

What is the expected time length of CPET?

A

9 mins

83
Q

What is chronotropic incompetence V

A

Inability of HR to increase the rate to commensurate with increased activity or demand,

84
Q

What do we see on CPET demonstrating dysfunctional breathing ?

A
  • Relatively well preserved /low/normal VO2 max
  • Normal AT
  • High erratic RER (Resp exchange Ratio> aerobic to anaerobic )
  • Occ high resting HR that assumes normal chronotropic profile
85
Q

What do we see on CPET demonstrating Deconditioning ?

A
  • Low VO2 max (maybe within LLN)
  • Low HRR
  • High VE reserve
  • Maximum O2 pulse at border of low/normal
  • AT at 40-50% of predicted VO2 max
  • Following should be normal: Sats, ECG , BP
86
Q

What do we see on CPET demonstrating heart disease ?

A
  • Low VO2 max
  • Rapid early rise in HR
  • Low HRR
  • Flat O2 pulse with peak value below LLN
  • Early <40% anabolic threshold at predicted VO2 max
  • Abnormal BP (blunted systolic or very high BP rise)
87
Q

What do we see on CPET in lung disease ?

A
  • Low VO2 max
  • High HRR (ventilation limitation has stopped exercise)
  • Low VE reserve
  • Desaturation
  • High VECO2
88
Q

What do we see on CPET demonstrating Pulmonary Vascular Disease ?

A
  • Low VO2 max
  • Low HRR and steep chronotropic profile
  • Flat O2 pulse with low maximum value
  • Low AT
  • Desaturation +/- shunt open signal
89
Q

What do we see on CPET demonstrating muscle disease ?

A
  • Low VO2 max
  • Early AT
  • Early blood lactate rise with submaximal fixed work protocol
  • steep chronotropic profile because of impaired peripheral O2 extraction
  • Often low O2 pulse
90
Q

What do we see on CPET demonstrating peripheral vascular disease?

A
  • Low VO2 max
  • High HRR
  • High VE reserve
  • Low AT
  • Often heightened /exaggerated BP response
91
Q

When should oxygen supplementation be used in bronchoscopy as per BTS guidelines ?

A

When desaturation > 4% or sats <90% and prolonged for >1 minute to reduce risk of hypoxaemic complications

92
Q

What are the risk factors for hypoxaemic complications in bronchoscopy ?

A

Baseline arterial sats
Lung Function
Co-Morbidity
Sedation
Procedural sampling

93
Q

What is the most common arrhythmia during bronchoscopy?

A

Sinus tachycardia and atrial / ventricular premature contraction

94
Q

What is the risk of bleeding complications in bronchoscopy ?

A

Minor 0.19%
Severe 0.26%

95
Q

How many days prior to bronch should Clipidogrel be held ?

A

7 days

96
Q

What is the platelet cut off for bronch

A

BAL safe above >20 ; if biopsies speak to haem as may need transfusion prior

97
Q

What is the risk of pneumothorax in bronch?

A

1 in 1000 (0.1%)

98
Q

How long should bronch be delayed post MI?

A

4 weeks

99
Q

What is the desired depth of sedation in bronchoscopy ?

A

Verbal contact possible at all times

100
Q

Why is Midazolam preferred sedation agent in bronch?

A

Rapid onset of action, Required sedation depth , Reversible

101
Q

How many mg of Midazolam drawn up for <70 and > 70?

A

< 70 years : 5 mg
> 70 years : 2 mg

To prevent inadvertent over sedation

102
Q

Which opioids are preferred in bronchoscopy ?

A

Fentanyl or alfentanyl

103
Q

When used in combination, should BDz or opioid be used first for bronchoscopy ?

A

Opioid should be given first

104
Q

What is the maximum dose of local anaesthetic for bronchoscopy ?

A

15.4mg/kg ; but often sx ≥ 9.6mg/kg

105
Q

What should be the diagnostic accuracy when comes to sampling visible endobronchial tumours ?

A

85%

106
Q

How many biopsy samples should be taken from each site ?

A

5 ; plus brush and wash to increase yield

107
Q

Investigations for invasive aspergillosis in bronch?

A

BAL Galactomannan
Microscopy for hyphae and fungal culture

Try to avoid TBLB and EBB

108
Q

What are the issues with BAL in tubed ICU patients ?

A

Post BAL worse O2 sats with change in lung compliance, mPAP and increased pCO2

Ideally take blind catheter aspirations first and if not getting answer from that then bronch

109
Q

What is used to disinfect bronchs?

A

Automated Endoscopic Reprocessor

110
Q

What are the rules for bronch re NBM?

A

No food 4 hours before; clear fluid upto 2 hours before

111
Q

What are the rules post procedure for bronch/EBUS with sedation?

A

Not to drive
Not to operate heavy machinery
Not to sign any legally binding documents

For 24 hours

112
Q

What diseases causes random nodules in the lungs ?

A

Mets
Miliary TB
LCH

113
Q

What diseases causes perilyhphatic nodules in the lungs ?

A

Sarcoid
Lymphangitic Carcinomatosis
Pneumoconiosis
Asbestosis
Silicosis

114
Q

What diseases cause centrilobular nodules in the lungs ?

A

HSP
Bronchoalveolar Carcinoma
RB-ILD

115
Q

What are the constrictions to spirometry?

A

Haemoptysis
Pneumothorax
CDV disease (recent MI, PE, Aneurysm , Unstable CDV status)
Nausea or vomiting
Recent chest / abdo / eye surgery

116
Q

What are the common side effects of spirometry?

A

Usually well tolerated but can cause transient headache or pain in the chest
Dizzyness, cough, occ syncope
Major complication is bronchospasm during

117
Q

Can we perform spirometry in acute respiratory infection?

A

In principle yes but the acute infection will affect the results and therefore rarely useful

118
Q

What is the standard way to perform spirometry?

A

Seated (normal values based on seated position and high intrathoracic pressures may cause patients to pass out, so sitting is safer)

Best of 3 blows , required to demonstrate maximal blow has been consistently achieved seeing two identical tracings where 2 best blows have FEV1 and FVC within 150mls of each other

119
Q

With LLN calculations for spirometry what parameters are included in calculation?

A

Age, Gender , Ethnicity and Height

120
Q

What is the z score in spirometry ?

A

Another way of describing LLN is the Z score or the standard score

Z score is the number of standard deviations a certain value is above the mean value of a data set

Spirometric value is considered too low if more than -1.64 standard deviations from the predicted value

121
Q

What is the LLN on spirometry?

A

The lower 5th percentile of the Gaussian bell curve: 95% of healthy people can blow better than the LLN

122
Q

What causes variable extra thoracic obstruction?

A

Vocal cord palsy
Extra thoracic goitre
Laryngeal tumour

123
Q

Why do we get the characteristic flattening of inspiratory limb with variable extrathoracic obstruction?

A

• Typically the expiratory part of the Flow Volume loop is normal: the obstruction is forced outwards by the force of the expiration
• During inspiration the obstruction is sucked into the trachea with partial obstruction and flattening of the inspiratory limb of the flow volume loop

124
Q

What causes variable intrathoracic compression?

A

Tumour located near the bottom thoracic part of the trachea as it is sucked outwards during inspiration

125
Q

What causes the characteristic flattening of the expiratory limb in variable intrathoracic obstruction?

A

• A tumour located near the intrathoracic part of the trachea is sucked outwards during inspiration with a normal morphology of the inspiratory limb of the Flow Volume loop
• During expiration the tumour is pushed into the trachea with partial obstruction and flattening of the inspiratory limb

126
Q

What causes fixed large airway obstruction?

A

Tracheal stenosis caused by intubation or circular tracheal tumour

127
Q

Why might patients not be able to produce reproducible flow volume loops ?

A
  • Poor understanding
  • Bad Co-ordination
  • Exercise Induced Asthma (forced manoeuvre of the FVC can cause asthma attach in active patients , therefore subsequent flow volume loops worse)
128
Q

What is the simplest test for respiratory muscle weakness in clinic ?

A

Lying and standing VC

If the diaphragm is paralysed then on lying down the abdominal contents will push the diaphragm up and limit inspiration, on standing the abdominal contents drop and aid inspiration

129
Q

What is an abnormal fall in VC?

A

> 20% fall in VC when lying down , suggests significant, usually bilateral diaphragm weakness

10-20% suspicious for diaphragm weakness

<10% fall is normal

130
Q

What is a normal SNIP (Sniff Nasal Inspiratory Pressure)?

A

> 70cmH20 Men; > 60cmH20 women

131
Q

What is the calculation for TCLO?

A

TLCO = VA x KCO

132
Q

What does TLCO measure ?

A

The amount of gas exchanging surface available

TLCO - Total amount of CO transferred
KCO- when divided by total lung voulme

133
Q

How is TLCO calculated ?

A

Gas mixture containing diffuser tracer (usually Carbon Monoxide) and a mixing tracer (for example helium) is inhaled using a single breath technique and following maximal inspiration subject holds breath for 10 secs then exhales
Amount of CO that has disappeared (by crossing the alveolar capillary membrane and being taken up by red cells) is calculated

134
Q

What happens to TLCO and KCO in emphysema and why?

A

Both reduced
Alveoli have been destroyed

135
Q

What happens to TLCO and KCO in ILD and why?

A

Both reduced
Alveolar capillary membrane is thick, reducing CO passage (NB in early disease KCO will likely be normal)

136
Q

What happens to TLCO and KCO in weak respiratory muscles and why?

A

TLCO - Normal
KCO- Raised

Lungs poorly expanded and so more “concentrated” and transfers CO better when quoted per unit volume

137
Q

What happens to TLCO and KCO in pulmonary haemorrhage and why?

A

Both raised (for a few days)

Free red cells lining the alveoli take up the CO directly and falsely elevate the figure . As Hb is broken down KCO returns to normal unless there is another bleed

138
Q

What happens to TLCO and KCO in pneumonectomy and why?

A

TLCO reduced
KCO increased

More “concentrated”

139
Q

How do we calculate RV?

A

FRC- ERV

140
Q

How do we calculate TLC?

A

RV + VC

141
Q

How does body pleythsmography work?

A

Subject makes inspiratory effort against closed mouthpiece this leads to decreased intrathoracic pressure and lung expands pushing chest wall out
In turn this compresses the gas in closed box and the pressure changes in the box and at the mouthpiece (which equate to changes in alveolar pressure can then be used to calculate the unknown volume of the lung or FRC

142
Q

How do you detect the PTX/ bullae volumes on lung volume assessment?

A

The difference between the pleythsmographic lung volume and helium dilution lung volume

143
Q

What is sensitivity ?

A

How often the test is positive if the patient has disease

A/ A + C

144
Q

What is specificity ?

A

How often test is negative if patient is healthy

D/ D+B

145
Q

What is Positive Predictive Value (PPV)?

A

Likelihood patient has disease if test is positive

A/ A+B

146
Q

What is Negative Predictive Value (NPV) ?

A

Likelihood patient doesn’t have disease if test is -ve
D / (D+C)

147
Q

What is likelihood ratio?

A

likelihood that a given test result would be expected in a patient with the target disorder compared to the likelihood that that same result would be expected in a patient without the target disorder

Sensitivity / (1- Specificity)

148
Q

What are the variables in Qualitative Data?

A

Binary /Nominal

Ordinal (ie mild / mod/severe)

149
Q

What are the variables in quantitative data?

A

Discrete (ie no of vaccines)

Continuous ( ie height , weight , lung function)

150
Q

What is the mode ?

A

Most frequently occurring value in a data set

151
Q

What is the median ?

A

The middle value when data put in ascending order

152
Q

What are quantiles ?

A

Divides dataset into intervals with specified probabilities. Commonest quantile include the median (2nd quantile ) and Q1 and Q3

153
Q

What is the mean?

A

Sum of all the variables divided by number of observation

154
Q

What are measures of centrality ?

A

Mode, Median , Quantiles, Range

155
Q

If significant extremes in data set what is the most robust assessment of centrality ?

A

Median

156
Q

What measures of centrality can we use in Quantitative , Binary and Ordinal data sets?

A

Quantative : All
Binary: Mode
Ordinal: Mode and median

157
Q

What are measure of variability we can use ?

A

Range , IQR , SD

158
Q

What is the range?

A

Max - Min

159
Q

What is IQR?

A

Range between 1st and 3rd quartile , representing middle 50%

160
Q

What is confidence interval ?

A

The evaluation of a parameter of a population by computing an interval range within which parameter variable likely to lie

161
Q

What is the null hypothesis ?

A

The default assumption that there is no significant difference or effect

162
Q

What is the alternate hypothesis?

A

The hypothesis researchers aim to support

163
Q

What is the P value?

A

The probability of obtaining observed results (or more extreme) if the null hypothesis is true ; if P< significance level (0.05) we reject the null hypothesis

164
Q

What is a type 1 error ?

A

False positive (incorrectly rejecting the null hypothesis )

165
Q

What is Type II error?

A

False -ve (failing to reject a false null hypothesis )

166
Q

For normally distributed data sets what hypothesis tests can we use ?

A

Z test and T test : comparing means between 2 groups (ie BP pre and post treatment) ; if <30 sample size T test better

Chi Squared test: assess association between categorical variables ( and also compare properties) ie investigating relationship between smoking and development of specific health conditions

ANOVA (Analysis of Variance) - comparing means of 3 or more groups ie comparing effect of different drug dosages on pain relief

167
Q

What are the non parametric tests we can use if not normally distributed ?

A

Mann Whitney U test - comparing 2 groups

Wilcoxon Signed Rank test (compare 2 groups where same ie before and after tx)

Kruskal Wallis Test (if multiple groups)

Friedman test (repeated measures)

168
Q

What does correlation mean and how do we rank it ?

A

Strength of relationship between two variables

0-0.25 Little or no relationship
0.25-0.5 Fair
0.5-0.75 Moderate
0.75- 1 Strong
1 : Perfect correlation

169
Q

What can we use to assess correlation?

A

Pearson Correlation Coefficient - linear association between 2 continuous variables

Spearman’s rank - measures monotonic association between variables (not necessarily linear) suitable for ordinal or ranked data

170
Q

How do you calculate AA gradient ?

A

FiO2 - (pCO2x 1.25) - pO2

171
Q

What is normal AA gradient ?

A

<2 kPa

172
Q

Outline coal workers pneumoconiosis

A

Simple Pneumoconiosios - regional LN blackened

With cont exposure get :

PMF- aggregation of the fibrotic nodules to form larger 2-10cm, “black scar”

Clinically - cough productive of mucoid or blackened sputum and SOBOE. No crepitations

173
Q

What do you see on HRCT for pneumoconiosis ?

A

Simple- parenchymal nodule 1-10mm with upper zone predominance

PMF- nodules >1cm with irregular borders and associated parenchymal and distal emphysema

174
Q

How do you manage pneumoconiosis ?

A

Minimise exposure
Industrial Benefits
NB - no incr risk of lung cancer with simple pneumoconiosis or PMF

175
Q

What is Caplan’s Syndrome?

A

Seropositive RA (or RhF +ve) and pneumoconiosis - can occur with low exposure

176
Q

Outline the other pneumoconioses

A

Iron - Siderosis
Barium - Baritosis
Tin- Stannosis
Aluminum -like silicosis

177
Q

Outline silicosis

A

Caused by inhalation of silica particles - Quartz and Cristobalite forms

Very long lag time between exposure and clinical disease ; 10-30 years
Insidious and progressive onset

Acute /Sub-Acute/Chronic /Silicotuberculosis

Tx: All about prevention ; incr risk of cancer

178
Q

What are the image changes seen with Silicosis ?

A

Acute : CXR - patchy bilateral lower airspace consolidation ; HRCT- irregular fibrosis

Subacute: CXR upper and mid nodules 3-5mm , can progressive to PMF; eggshell calcification and BHL

Chronic- fewer upper and mid zones nodules with hilar lymphadenopathy

179
Q

Outline Berylliosis

A

Caused by Beryllium - fluorescent lights /aviation

Acute Beryllium Disease - acute alveolitis , widespread oedema / pulmonary oedema . Steroids may prevent progression.

Subacute and Chronic Berylliosis - delayed hypersensitivity reaction can be clinically indistinguishable from sarcoid

180
Q

What are the image changes in Berylliosis ?

A

CXR: Fine reticulonodular shadowing UL, Hilar lymphadenopathy

HRCT- subpleural micronodular change, thickened interlobular spare , traction bronchiectasis and honeycombing . May be ground glass shadowing

181
Q

What is the key ix for Berylliosis?

A

Beryllium Lymphocyte Proliferation test - Blood or BAL

NB on BAL will get non caseating granulomas

182
Q

What is the management for Berylliosis?

A

Steroids
Associated with delayed skin sensitivity to Tuberculin, granulomas don’t always resolve

183
Q

What are pneumoconioses?

A

Non neoplastic pulmonary diseases caused by the reaction of the lung to mainly mineral but also organic dusts

<5 microns reach the terminal airways of the alveoli and settle on epithelial layer of lung

184
Q

What drugs reduce theophylline levels

A

Carbamazepine

185
Q

What drugs increase theophylline levels ?

A

BB
Clarithromycin
Ciprofloxacin

186
Q

In health where are majority of eosinophils ?

A

90% GIT

187
Q

Outline Lofflers (Simple Pulmonary Eosinophilia)

A
  • Caused by ASCARIS LUMBRICOIDES but also strongyloides and hookworm
  • Occurs worldwide but particularly SE Asia , Africa , Central and South America
  • CXR shows transient bilateral shadowing - disappears 6-12/7 can take a month
  • Sputum contains Eos and Hyphae ; stool will reveal but only 2-3 months after , blood Eos not raised

Tx: Antihelminth agent : Albendazole or Mebendazole for 3 days ; may need steroids if pulmonary manifestation severe

*ACUTE, Perihilar on CT , Sinus and stool involvement

188
Q

Outline Tropical Pulmonary Eosinophilia

A
  • Hypersensitivity to migrating larvae of filiarial worms - WUCHERIA BANCROFTI
  • Occurs in India / Pacific
  • May get cavitation and pleural effusion
  • Sputum and BAL see Eos , blood Eos raised

Tx- Filaricide diethylcarbamazine for 3/52

** Indolent ; Cavities on CT

189
Q

Outline drug induced pulmonary eosinophilia

A

Shadowing within hours of starting drug and resolves within 1 week of stopping

Essentially an allergic reaction of the pulmonary vessel wall can be associated with a skin reaction, avoid the drug in future and give steroids if needed

Severity ranges from mild to severe

190
Q

What drugs cause drug induced pulmonary eosinophilia ?

A

Penicillin, Phenytoin
Carbamazepine , Cocaine
NSAIDs, Nitrofurantoin , Tetracycline , Methotrexate

191
Q

Outline Chronic Eosinophilic Pneumonia

A

Unknown cause ; 2:1 F:M

Insiduous onset ; dx usually clinical and radiological but may need BAL

Peripheral dense opacities on CT

Have sputum eosinophilia and BAL high Eos , may not have blood eosinophilia

Tx : Steroids - should improve quickly

192
Q

Outline acute eosinophilic pneumonia

A

Unknown cause ; any age /sex

Diagnostic Criteria:
- Acute febrile illness <7 days
- Hypoxic resp failure
- Interstitial or alveolar CXR infiltrates
- BAL Eos >25%
- No parasitic /fungal / other infection
- Prompt and complete response to steroids
- Failure to relapse after completing steroids

193
Q

Outline Hypereosinophilic Syndrome

A

Rare , common around 30-40 years

Fever , WL, cough , pruritius

Dx:
- Marked eosinophilia >1.5
- Signs /sx of eosinophilic tissue infiltration
- No evidence of another cause of eosinophilia

Get pulmonary involvement with interstitial infiltrates and effusions ; can get CDV involvement with myocarditis or cardiomyopathy ; skin - urticaria , GIT, alcohol intolerance ; Hepato/Splenomegaly

Can be fatal
IgE often high

Tx - High dose steroids

194
Q

When should NIV be started in MND when acutely unwell

A

If VC <1L and RR > 20

195
Q

What are the absolute contraindications to NIV?

A

Severe facial deformity
Facial Burns
Fixed upper airway obstruction

196
Q

What are the relative contraindications to NIV?

A

pH <7.15
GCS <8
Confusion/agitation
Cognitive impairment

197
Q

What is morbidity /mortality associated with bronch?

A

1.1% serious complications
0.02% mortality

198
Q

When should O2 supplementation be used in bronchoscopy?

A

When detect a desaturation of >4% for more than 1 minute

199
Q

What is significant pCO2 rise with LTOT?

A

> 1kPa of pCO2 or develop acidosis ; may have clinically unstable disease if so further medical optimisation needed and reassess 4 weeks. I’d have on 2 separate occasions when clinically stable should only have domicillary oxygen in conjunction with nocturnal ventilatory support

200
Q

What is the pO2 aim with LTOT?

A

Greater than or equal to 8

201
Q

What should non hypercapnic patients do during sleep?

A

Increase flow rate by 1L/min

Respiratory SCE (15 decks)

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