Respiratory - Pleural and Pulmonary Vascular Diseases Flashcards

1
Q

The structure of the pleura

A

The pleural space is bounded by the parietal and visceral membranes covered by a continuous layer of mesothelial cells

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2
Q

What can result in the accumulation of excess pleural fluid

A

Disturbances in either formation or absorption

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3
Q

When can we determine pleural fluid is an exudate - Light’s criteria

A

Pleural fluid proteins divided by serum proteins is >0.5
Pleural fluid LDH divided by serum LSD > 0.6
Pleural fluid LDH > 2/3 the upper limits of labs normal value for serum LDH

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4
Q

Determining transudates vs exudates

A

Hx
Examinations
Ix

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5
Q

Ix to help determine transudates vs exudates

A
Radiology 
Bloods - clotting screen, FBC, LFTs etc 
Light's criteria 
CT, PET 
Bx
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6
Q

Most important examples of condns causing transudates

A

Usually caused by failures

HF
Liver cirrhosis
Nephrotic syndorme
Hypoalbuminaemic status

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7
Q

Other condns causing transudates

A

Mitral stenosis
Meigs syndrome
Constrictive pericarditis

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8
Q

Features of transudates

A

Slower time scale

Usually bilateral but R side may be larger - may find fluid in other areas e.g. ascites, pitting oedema

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9
Q

Treatment of transudates

A

Treat the case- if pt fails to respond will need to reconsider dx

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10
Q

Causes of pleural exudates

A
Parapenumonic effusions and empyema 
Malignancy 
Pulmonary infarction 
TB 
Drugs 
RhA
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11
Q

Clinical assessment of pleural exudates

A

Risk factors (smoking, asbestos)
Red flag symptoms
A/c and subacute symtoms - timescale
Look for systemic signs (should be minimal) and effusion is often unilateral

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12
Q

Examination findings of pleural exudates

A

Reduced chest expansion
Percussion - stony dullness
Absent breath sounds

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13
Q

Use of ultrasound when determining between transudates and exudates

A

Fluid vs thickening - darker fluid. is usually transudate
Loculations
Guided thoracocentesis (Light’s criteria)

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14
Q

What do we send pleural aspiration for

A
Cytology 
Protein 
LDH 
pH/ glucose 
Gram stain 
Culture & sensitivity
Optional extras depending on likely cause
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15
Q

Thoracoscopy

A

Placing camera in pleural space under anaesthetic

Can also take fluid from parietal pleura during this procedure

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16
Q

Why should an ultrasound be done before a thoracospy

A

To guide needle placement

Should be above rib to avoid neurovasc bundle

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17
Q

Ddx for complete white-out on CXR w/ trachea deviation

A

Complete lung collapse
Massive pleural effusion
Pneumonectomy

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18
Q

Pleural plaques

A

Benign condn

Sign of asbestos exposure

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19
Q

When might a pt develop diffuse pleural thickening

A
Heavy exposure to asbestos **
Previous haemothorax 
TB 
Chest surgery 
Radiation 
Infection 
drugs
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20
Q

What can diffuse pleural thickening lead to

A

SOB, restricted lung function - requires follow up

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21
Q

What are the majority of pleural effusions. (90%) caused by

A

Infection - treat w/ abx, CXR in 6-8 weeks (exudate)
HF - treat cause, don’t drain (transudate)
Malignancy (exudate)
PE (exudate)

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22
Q

Clinical px of PTX pts

A

Hx - cigarette, cannabis smoking
PMH - lung disease
A/c onset symptoms - pleuritic chest pain, breathlessness

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23
Q

Examination findings in PTX pts

A
Trachea/ mediastinum - pushed 
Reduced/ absent expansion 
Percussion - hyper resonant 
Reduced/ absent breath sounds 
Hypoxamia esp if underlying lung disease
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24
Q

Hypoxaemia

A

Low levels of oxygen in blood nOT tissues

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25
Q

Causes of PTX

A

Primary spontaneous
Secondary spontaneous
Iatrogenic
Trauma

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26
Q

Which group of people do we tend to see primary sponatanoues PTX in

A

Taller pts
Alveoli at the lung apex in tall individuals are subject to significantly greater distending pressure than those at the base of the lung

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27
Q

What are apical pleural blebs associated with

A

High risk of PTX

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28
Q

What should you ask spontaneous PTX pts about

A

Smoker - 12% risk of developing PTX

Lung disease

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29
Q

Causes of secondary spontaneous PTX

A
COPD 
PJP
CF
TB
Others - incl Marfan
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30
Q

PJP

A

Pnemoctitis jiroveci pneumonia

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31
Q

Tension PTX

A

Air trapped in between parietal and visceral pleura resulting in lung collapse, displacement of mediastinal structure and compromised cardiopulmonary function

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32
Q

Medical emergency - Tension PTX

A

Low BP and low HR

Emergency needle decompression

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33
Q

Anterior border of safe triangle for chest drain

A

Lateral border of Pec Major

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34
Q

Superior border of safe triangle for chest drain

A

Base of axilla

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35
Q

Inferior border of safe triangle for chest drain

A

Line of 5th ICS

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36
Q

Lateral border of safe triangle for chest drain

A

Lateral edge of Lat Dor

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37
Q

Complications of Chest Drain

A
Infection/ pain 
Drain dislodgement 
Drain blockage 
Visceral injury 
Death
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38
Q

Methods of chest drain insertion

A

Seldinger technique

Surgical blunt dissection approach

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39
Q

Suction recommendations for chest drain

A

High volume low-pressure suction systems

Wall suction or digital suction system

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40
Q

Conservative mx of PTX

A

Shouldn’t dive until definitive prevention strategy
Avoid air travel until 7/7 post PTX resolution
Smoking cessation
Organise follow up CXR to ,omit resolution
Manage comorbidities

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41
Q

Definitive prevention strategy for ptx

A

Surgical pleurectomy

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42
Q

Why do PTX pts need to stop smoking

A

Reoccurrence risk for smokers is 32%

8% in non-smokers

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43
Q

When should a follow up CXR be organised for a PTX

A

2 - 4 weeks

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44
Q

Risk factors for recurrence of SSP

A

Age
Pulmonary fibrosis
Emphysema

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45
Q

Surgical intervention to prevent recurrence of PTX

A

Medical Chemical Pleurodesis (Talc)

Done for recurrent pneumothoraces and non-resolving PTX

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46
Q

When is melatonin secreted

A

As a result of darkness, from the pineal gland

Retinal hyper thalamic pathway

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47
Q

Stages of sleep

A

REM (dream sleep)

Non-REM - light sleep, slightly deeper, deep sleep

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48
Q

When do we experience non-REM sleep

A

First half of sleep

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49
Q

Which sleep refreshes cells

A

Deep sleep

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50
Q

Breathing in NREM sleep

A

Normal

Regular muscle tone

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51
Q

Breathing in REM sleep

A

Breathing is erratic

Muscles are atonic except diaphragm

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52
Q

Which stage of sleep generally exacerbates sleep apnoea

A

REM sleep

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53
Q

Sleep Disordered Breathing Classification

A

OSA
Central Sleep Apnoea
Mixed obstructive/ central apnoea
Obesity hypoventilation Syndrome

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54
Q

Most common pattern seen in Sleep disordered breathing

A

OSA

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55
Q

2nd most common pattern seen in sleep disordered breathing

A

Obesity Hypoventilation Syndrome

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56
Q

Hx and clinical px of OSA pts

A
Snoring 
Witnessed apnoea 
Excessive daytime sleepiness (EDS)
Nocturia 
Unrefreshed sleep 
Morning headaches
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57
Q

Witnessed apnoea in OSA

A

Bed partner will note pt stopped breathing and then took a v loud breath on inspiration

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58
Q

Nocturia

A

Urinating <4 a night

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59
Q

Things to ask about in hx of OSA pts

A
Occupation and riving 
Medications 
PMH 
Trisomy 21 
Past surgical hx
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60
Q

What medication can be a ppts factor in OSA

A

Opiod analgesics

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61
Q

What diseases should be screened for in PMH of OSA pts

A

Thyroid disease
DM
Systemic hTN
CDV and CBV disease

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62
Q

Why do we ask about trisomy 21 in OSA pts

A

High risk for OSA (reduced muscle tone)

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63
Q

What is relevant in the past surgical hx of OSA pts

A

Tonsillectomy

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64
Q

Measuring EDS

A

Epworth Sleepiness Scale

Scores of 11/24 = EDS

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65
Q

Epworth Sleepiness Scale

A

Looks at high likely a pt is to fall asleep during following situations e.g sitting, watching TV, talking to someone, in a car
Rated from 0 (would never dose) - 3 (high chance)

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66
Q

Limitations of ESS

A

Pt may be worried to accurately report lapse in judgement e.g. driving
Timescale - values may may change by the time the pt is seen

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67
Q

Possible sleep questionnaires

A

Pittsburgh sleep quality index index (PSQ1)
ESS
STOP BANG (pre-op screening)
4 variable screening tool used in Norfolk

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68
Q

Examination for OSA

A

Obesity - BMI >30kg/m2, measure waist circumference
Upper airways -
Look for signs of acromegaly, hypothyroidism, Cushing’s syndrome
Look for cranial abnormalities

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69
Q

What do you look for in upper airways when examining OSA pts

A

Enlarged tonsils esp in younger pts

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70
Q

Which craniofacial abnormalities should you look for in OSA pts

A

Micrognathia (small jawline)
Retrognathia (receding jawline)

These can cause smaller airways

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71
Q

Mallampati Score

A

Class I (Complete visualisation of soft palate) to Class IV (soft palate is covered)

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72
Q

Desaturation in apnoea

A

Cessation of breathing for 10s or more

Usually scored w/ >4% desaturation (SpO2)

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73
Q

Hypoapnoea

A

Reduction in the airflow (nasal flow) by 50% or more

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74
Q

Does hypoapnoea always cause O2 desaturations

A

No - may not cause O2 desaturation

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75
Q

Apnoea Hypoapnoea Index scores for OSA

A

2-15 - mild OSA
15 - 30 - moderate OSA
>30 severe OSA

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76
Q

Desaturation index criteria fro OSA

A

> 4%

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77
Q

OSAS

A

OSA syndrome

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78
Q

OSA vs OSAS

A

Abnormal Sleep study and EDS - OSAS

Abnormal Sleep Study and no EDS - OSA

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79
Q

Measurements in sleep disordered breathings

A
Nocturnal oximetry 
Resp Polygraphy (Home Sleep Test)
Polysomnography - Gold standard
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80
Q

Treatment of sleep disordered breathing

A

Lifestyle modifications - mild OSA/ OSAS
Wt reduction
Sleep Hygiene - excessive caffeine
Positional training

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81
Q

Mandibular advancement devices

A

Used in mild OSA(S)

Boil and bite devices - pushes lower jaw forward creating more room at back of throat

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82
Q

CPAP

A

Continuous Positive Airway Pressure

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83
Q

When is CPAP given for OSAS

A

Definitive treatment - moderate/ severe disease
Given after attempting lifestyle modification and mandibular advancement devices
Relieves symptoms majorly

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84
Q

Driving and sleep apnoea

A

Pts have to declare dx to DVLA
CPAP compliance > 4hrs/ night
HGV/ public transport drivers need to inform employers and occupational health - asked not to drive unless established in treatment

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85
Q

Obesity Hyperventilation Syndrome

A

Morbid obesity BMI > 35kg/m2
Mean SpO2 < 90% in sleep study
Need to measure time spent <90% SpO3 - shallow breathing, reduced TV

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86
Q

ABG of pts w/ obesity Hypoventilation Syndrome

A

Day time CO2 retention and/or elevated HCO3 (.27mmol/L)

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87
Q

Mx of Obesity Hypoventilation Syndrome

A

Wt loss

NIV (+ve pressure)

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88
Q

Co-existent lung disease in sleep disordered breathing

A

Asthma and OSA

COPD/ emphysema: overlap syndrome of OSA/COPD

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89
Q

Consequences of SDB (sleep disordered breathing)

A

Systemic HTN
AF
MI, CVA
Pulmonary arterial hypertension

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90
Q

Ventilation

A

Rate at which air enters or leaves the lungs

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91
Q

Minute ventilation

A

Volume of air moving in and out per unit time

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92
Q

Alveolar ventilation

A

Amount of air utilised for gas exchange (VT - dead space) x RR

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93
Q

Perfusion (Q)

A

Movement of blood in to lungs through pulmonary capillaries

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94
Q

V/Q ratio

A

Alveolar ventilation/ pulmonary blood flow

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95
Q

When do we see hypoxaemia

A
Reduction in altitude 
Hypoventilation 
Diffusion 
Shunts 
VQ mismatch
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96
Q

When are V and Q matched

A

When pulmonary blood flow is proportionally matched to the pulmonary ventilation
Results in greatest efficiency for gas exchange

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97
Q

VQ ratio for single alveolus

A

Alveolar ventilation/ capillary blood flow

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98
Q

How many zones are there for perfusion and ventilation in the lungs

A

3

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99
Q

Pressures in zone I (apex) for perfusion and ventilation

A

PA > Pa > Pv

A - systemic arteries
a - alveoli
v - pulmonary vein

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100
Q

Pressure in zone II for V & Q

A

Pa > PA > Pv

A - systemic arteries
a - alveoli
v - pulmonary vein

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101
Q

Pressures in zone III

A

Pa > Pv > PA

A - systemic arteries
a - alveoli
v - pulmonary vein

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102
Q

How does V/Q vary in diff zones of the lung

A

Highest in apex and lowest in base (but has higher O2 content)
Clinical rel - certain infections attack apex as less aerobic than base

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103
Q

Shunt

A

Physiological phenomena where deoxygenated blood mixes w/ oxygenated blood
Occurs when there’s an intracardiac defect - doesn’t participate in gas exchange

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104
Q

Pulmonary shunt

A

Mixing of blood without participating in the gas exchange at level of pulmonary capillaries

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105
Q

When do we see a pulmonary shunt

A

Occurs when alveoli are perfused like normal but ventilation fails to supply perfused region - pathological condn (VQ = 0)

106
Q

Examples of intrapulmonary shunting

A

Fluid in alveoli e.g. pulmonary oedema & pneumonia

107
Q

Shunt fraction

A

% of blood pumped by heart that is not ventilated (oxygenated)

108
Q

When is the shunt fraction increased

A

Greater in pulm contusion or haemorrhage even at breathing 100% oxygen

109
Q

What can minimise shunt fraction

A

Vasoconstriction - compensatory mechanisms of hypoxaemia

110
Q

What can cause a VQ mismatch

A
Dead space (physiological) - ventilation of poorly perfused alveoli (V > Q)
Shunts; perfusion of poorly ventilated alveoli (V < Q)
111
Q

Pathologies resulting in VQ mismatch - low VQ ratio

A
Pneumonia 
Pulmonary oedema 
ILD/ pulm fibrosis 
Asthma 
Mucous plugging 
Airway obstruction
112
Q

Pathologies resulting in AQ mismatch - high VQ

A

PE

Emphysema

113
Q

What does a VQ mismatch respond to

A

100% oxygen

114
Q

Normal VQ in healthy lung

A

0.8

115
Q

Aa gradient

A

Alveolar to capillary oxygen gradient

116
Q

Mechanisms of hypoxaemia

A
Shunt 
Diffusion impairment 
VQ mismatch 
Hypoventilation 
Low ambient oxygen
117
Q

Aetiology of primary pleural malignancy

A

Mesothelioma

118
Q

Aetiology of secondary pleural malignancies

A

Lung - 1st most common
Breast - 2nd most common
Lymphoma - 3rd most common

But almost any cancer can metastasise to the pleura

119
Q

What do pleural malignancies commonly cause

A

Malignant pleura effusions and/or pleural thickening

120
Q

Pathology of exudative effusion caused by pleural malignancy

A

Tumour dissemination
Angiogenesis - w/ vasc hyperpermeability
Tumour secreted vasoactive mediators (VEGF)

121
Q

Asbetsos-related resp disease

A
Asbestosis 
Malignant pleural mesothelioma 
Pleural plaques 
Benign pleural thickening 
Benign pleural effusion
122
Q

Why is asbestos considered an ILD

A

Asbestos in lung tissue –> fibrosis and scarring

123
Q

When can pts get compensation for benign pleural thickening after asbestosis exposure

A

If disabled by SOB

124
Q

Epidemiology of pleural malignancy

A

Common - incidence about 30,000/ yr
Breast cancer commonest in women and lung cancer commonest cause in men
Increasing incidence w/ age (max at 80-85)

125
Q

Ddx of pleural effusion

A
Transudative pleural effusion - cardiac, renal or hepatic failure 
Pleural infection 
PE 
CTD 
Benign asbestos pleural disease
126
Q

What should be asked in the hx of a pt w/ pleural malignancy

A
Symptoms spp to effusion 
Constitutional symptoms 
Symptoms of other malignancy 
PMH - previous malignancies 
SH
127
Q

Symptoms spp to effusion in pts w/ pleural malignancy

A

Breathlessness, cough, dull chest pain

Time course: months - weeks

128
Q

Constitutional symptoms seen in pts w/ pleural malignancy

A

Wt loss
Loss of appetite
Fatigue

129
Q

Symptoms of the malignancies that may be seen in pts w/ pleural malignancy

A

Dysphagia
Change in bowel habits
Lumps

130
Q

Relevant SH in pts w. pleural malignancy

A

Smoking
Asbestos exposure
Perfomance status

131
Q

ECOG performance status

A
Looks at effects of malignancy on pts lifestyle 
From 0 (fully active, able to carry on pre-disease performance) to 4 (completely disabled, cannot cary on self-care)
132
Q

Why is ECOG performance status important for pleural malignancy

A

Helps determining what ix the pt is fit for e.g <2 fit for thoracoscopy
Helps determine mx, 4 is usually disseminated and not fit for treatment

133
Q

Examination of pts w/ pleural malignancy

A

Increased RR
Cachexic
not usually hypoxic
Decreased air entry, decreased lung expansion, dull percussion note, decreased vocal resonance
Other signs of malignancy e.g. breast lumps, testiuclar lumps, lymphadenopathy

134
Q

Main ix for pleural malignancy

A

Bloods - U&Es, FBC, CRP, clotting, PSA

CXR

135
Q

Addn ix for pleural malignancy

A

Thoracic ultrasound
CT
Pleural aspiration
Thoracoscopy

136
Q

What might you see in a thoracic ultrasound in pleural malignancy

A

Pleural effusion
Pleural thickening
Pleural modularity

137
Q

Difference in CT scan for men and women for suspected pleural malignancy

A

CT scans in men of chest and upper abdomen

For women also do pelvis

138
Q

What do you send pleural aspiration for in suspected pleural malignancy

A

Biochem: total protein, LDH (malignant effusions typical transudative)
MC&S - excl infection
Cytology - +ve in 90% MPE, only 20% in mesothelioma

139
Q

MPE

A

Malignant Pleural effusion

140
Q

Main procedures done in thoracoscopy

A

Fluid drainage and pleural biopsy

After procedure can perform pleurodesis (using sterile talc), IPC insertion

141
Q

IPC

A

indwelling pleural catheter

142
Q

Complication of thoracosocpy

A

Re explosion pulmonary oedema

143
Q

Making a dx of pleural malignancy - role of MDT

A

Team reviews hx and ix
Make a dx - radiological or definitive
Mx plan

144
Q

Possible mx plans for pleural malignancy

A

Further biopsies
Cancer treatment
Watch and wait
Palliative care

145
Q

Treatment for pleural malignancy

A
Treat underlying malignancy - lymphoma, small cell lung cancer, breast cancer 
Therapeutic aspiration 
Chest drain and pleurodesis 
IPC insertion 
Pleurectomy
146
Q

Chest drain and pleurodesis for pleural malignancy

A

Inpt 2-5 days
Seldinger chest drain and underwater seal
~75% success rate

147
Q

Why is talc used in pleurodesis

A

4g talc creates infl causing pleura to fuse together

148
Q

What can pts be left w/ after chest drain and pleurodesis

A

Residual pleural thickening –> breathlessness

149
Q

IPC for pleural malignancy treatment

A

Day case
intermittent drainage at home using vacuum bags, 3x/ week initially
Definitive treatment
Can give talc to perform pleurodesis

150
Q

What IPC the treatment of choice for

A

Trapped lung

Failed pleurodesis

151
Q

Risk associated w/ IPC

A

Blockage

Infection

152
Q

Trapped lung

A

Thickened visceral pleura so unable to expand fully

153
Q

Pulmonary HTN

A

Pathophysiological disorder that may involve multiple clinical condns, where mPAP > 20 mmHg

154
Q

mPAP

A

Mean pulmonary artery pressure

155
Q

What can pulmonary HTN complicate

A

Majority of CDV and resp diseases

156
Q

What kind of symptoms are seen in pulm HTN

A

Non-spp

157
Q

What does pulmonary HTN dx and classification require

A

R heart catheterisation

158
Q

Calculating PVR

A

80(mPAP - PAWP)/ CO

159
Q

PAWP

A

Pulm artery wedge pressure

160
Q

Normal pulmonary artery pressure

A

14 mmHg +/- 3.3 mmHg at rest

161
Q

Criteria for Pulm HTN

A

Precapillary PH mPAP > 20mmHg, PVR > 3 WU and PAWP < 15mmHg

Combined pre and post capillary PH - mPAP > 20mmHg, PVR > 3 WU, PAWP > 15

162
Q

WU

A

Wood units

163
Q

Classification of pulm HTN

A
Pulm arterial HTN (PAH)
Left heart disease - PAWP > 15
Lung disease 
CTEPH 
Unclear/ multifactorial
164
Q

Epidemiology of pulmonary HTN

A

Global PH incidence data is poor
In the UK, prevalence of 97/1,000,000
F:M ratio of 1.8
L heart disease believed to be most common cause

165
Q

How is clinical presentation of Pulm HTN classed

A
By functional class 
From Class I (nob symptoms w/ exercise or rest) to Class IV (symptomatic at rest, syncope and fatigue)
166
Q

Determinants of prognosis in pulmonary HTN

A

Clinical signs of R heart failure
Progression of symptoms
Syncope
WHO functional class
Cardiopulmonary exercise testing
NT-proBNP plasma levels - higher is worse
Imaging - increased RA area, pericardial effusion

167
Q

General mx of pulmonary HTN

A
Avoid pregnancy 
Influenza and pneumococcal vaccinations 
Psychosocial support 
Pulm/ cardiac rehab 
Diuresis if evidence of volume overload 
LTOT if pO2 consistently less than 8kPa
Correct anaemia
168
Q

Spp mx for pulm HTN

A

Group I - depends on functional class, assess severity
Group 2 - targeted therapy not currently licensed
Group 3 - no targeted therapy
Group 5 - v difficult to mx

169
Q

CTEPH

A

C/c thromboembolic pulmonary HTN

170
Q

What is CTEPH

A

Fibrotic transformation of a pulmonary arterial thrombosis, causing fixed mechanical obstruction of pulmonary arteries
Microvascular remodelling causing a progressive increase in PVR

171
Q

What % of CTEPH pts lack a hx of a/c PE

A

~25%

172
Q

Treatment for CTEPH

A

PEA (pulmonary endarterectomy) surgery - removing central obstructing lesions
BPA (Balloon pulmonary angioplasty)

173
Q

CTEPH prognosis

A

In operable pts, treated w/ drugs, 3 yrs survival varies from 41-805
3-yr survival of 89% in operated PEA pts and 70% in non operated pts

174
Q

Drugs given for CTEPH

A

IV prostacyclin analogues or oral PAH targeted drugs

175
Q

What does BPA in non-operable CTEPH pts show significant improvement in

A
Functional status 
QoL
Pulm pressure 
Exercise capacity 
PVR
176
Q

Causes of cardiac chest pain

A

MI/ infarction
Pericarditis
Aortic dissection (pleurite chest pain)

177
Q

Resp causes of chest pain

A

PE
PTX
Pneumonia
Pleural infl (pain happens even at rest)

178
Q

GI causes of chest pain

A

Oesophageal spasm
Dysmotility/ reflux
Oesophageal rupture (Boerhavve’s)

179
Q

MSK causes of chest pain

A

Rib frature/ metastasis
Muscle spasm/ strain
Costochondritis (localised pain - can be elicited)

180
Q

Psychological states causing chest pain

A

Panic attack

Hyperventilation

181
Q

Ix for differentiating between causes of chest pain

A

Bloods - FBC, CRP/ESR, LFT, D-dimer etc
ECG - cardiac causes, arrhythmia
CXR +/- further imaging

182
Q

What is a PE

A

Occlusion of a segment of pulmonary arterial circulation through embolism from a distant source - lower limbs

183
Q

Embolic material that can cause a PE

A

Commonly blood clots
May be fat embolism - following major trauma
Air embolism following invasive procedures e.g. central line insertion

184
Q

Causes of a PE

A

Virchow’s triad

Hypercoagulable stae
Stasis (local/ systemic) - VV, immobilisation
Endothelial damage - c/c infl

185
Q

What can cause a hyper coagulable state –> PE

A

Factor V Leiden, Protein S/C deficiency
Malignancy
Loss of proteins incl clotting factors - myeloma

186
Q

Major risk factors for a PE

A
Recent immobility 
Major surgery incl obstetric 
Leg fracture 
Previous DVT/ PE 
Thrombotic disorder 
Metastatic cancer
187
Q

Minor risk factors for PE

A
Oestrogen 
Travel 
Known thrombophilia 
Obesity 
Minor surgery
188
Q

Presentation of a PE

A
SOB 
Pleuritic chest pain 
Cough 
Leg swelling/ pain 
Haemoptysis
189
Q

Well’s score for PE - criteria

A
Previous VTE 
Tachycardia 
Recent surgery/ immobilisation 
Clinical signs of DVT - 3 point 
Haemoptysis 
Cancer
190
Q

Bloods for a PE

A

ABG
D-dimer
FBC/ clotting profile

191
Q

ECG for PE

A

Sinus tachycardia
Fast AF
S1Q3T3

May also be normal

192
Q

Ix for PE

A
Bloods 
ECG 
CXR - doesn't excl/ confirm dx
CTPA
V/Q
193
Q

D-dimer for PE

A

Highly sensitive
High -ve predictive value
Used in combo w/ probability score

194
Q

What is D-dimer commonly elevated in

A

Pts w/ infl states, infection, ACS, malignancy recent surgery

195
Q

What might you see on a CXR for for PE

A

Pulmonary infarct

Pleural effusion

196
Q

CTPA

A

CT pulmonary angio
Gold standard for PE
Involves higher dose of ionising radiation and risk of nephrotoxicity w/ contrast
Embolus is dark grey - found in white area

197
Q

VQ scan for a PE

A

Compares radioactive material uptake in lungs via inhalation and iV injection
Reported as probability risk

198
Q

Pulmonary angio for PE

A

Invasive
Superseded in a/c setting by CTPA
Relevat in dx CTEPH

199
Q

Echo for PE

A

Looks for evidence of R heart dilatation/ strain
Relevant in a/c setting/ peri-arrest situation
To screen for 2’ pulmonary HTN

200
Q

Treatment of a/c PE

A

Heparin - LMWH, unfractionated heparin (IV)
Warfarin

Anticoagulants for 3/12

201
Q

Massive PE

A

PE w/ evidence of systemic compromise - central/ proximal/ multiple clots
Hypotension, R heart strain

202
Q

Thrombolysis of a massive PE

A

Dissolution of a clot
Improvement of physiological parameter
Reduce risk of death

203
Q

Follow up for PE

A

Echo
Consider VTE risk factors and their modification
Consider lifelong anticoagulants

204
Q

Who gets lifelong treatment after a PE

A

Idiopathic PE - cause unknown
First episode and ongoing risk factors
2 or more VTE events - IVC filter

205
Q

Canonball metastases on CXR

A

Discrete lesion, multiple opacities

206
Q

Mx of tension PTX

A

Urgent needle decompression

Chest drain and admission

207
Q

Ddx of whole lung field white out

A

Collapse
Large pleural effusion
Pneumonectomy
Consolidation

208
Q

Pneumonectomy

A

Surgical removal of lung or part of lung

209
Q

What direction does the trachea move in lung collapse

A

Pulls trachea towards it

210
Q

What direction does a large pleural effusion push the mediastinum

A

Away

211
Q

Why might you see a white out on a CXR following a pneumonectomy

A

Fluid fills up space where lung has been taken out

212
Q

What direction does a pneumonectomy move the mediastinum

A

Moves in or may be normal

213
Q

When do you see a meniscus sign on a CXR

A

Pleural effusion

214
Q

What do we see in hydro PTX on CXR

A

Fluid line

215
Q

What side do you normally see surgical emphysema in

A

The side of the chest drain

216
Q

Pancoasts tumour

A

Apical lung tumour

May cause denervation

217
Q

Signs in Horner’s syndrome

A

Anhydrosis
Ptosis
Miosis

218
Q

What does it mean if the cricothyroid distance is <3 fingers

A

Hyperinflation of the chest

219
Q

What types of crackles do we hear

A

Coarse (infection and bronchiectasis) and fine end inspiratory (pulm fibrosis)

220
Q

Features of vesicular breathing

A

Normal breathing
Longer inspiratory phase (2:1)
Gentle sound

221
Q

Features of bronchial breathing

A

Seen in infections
Longer espiratrxy phase (1:3)
Break in between inspiratory and expiratory phases
Louder sound

222
Q

Features of rhonci

A

Sounds similar to snoring
Can be cleared by coughing
Combination of wheeze and crackles - low pitched

223
Q

Cause of rhonci

A

Build up of secretions

224
Q

Features of a wheeze

A

Heard in expiratory
High pitched
Whistling/ musical tone

225
Q

When do we hear a pleural rub

A

Pleurisy

226
Q

Added breath sounds

A
Crackles 
Bronchial breathing 
Wheeze 
Stridor 
Rhonci 
Pleural rub
227
Q

Signs of anaphylaxis

A

V quick onset
Stridor (inspiratory wheeze)
Angiodema
Urticarial rash

Crash call should be put out

228
Q

Where do we aspirate PTXs from

A

2nd IC space, mid clavicular

229
Q

Where do we insert a chest drain for PTX

A

5th IC space mid axillary

230
Q

How do we measure a PTX

A

From edge of lung to hilum

231
Q

Mx of PSP

A

If >2cm and/or breathless - aspirate

If no success, insert chest drain and admit

232
Q

Mx of SSP

A

Insert chest drain if >2cm and/or breathless

Aspirate if 1-2cm

233
Q

Which hilum is higher

A

L

234
Q

What can a cavitating mass be caused by

A

Carcinoma of bronchus
SCC metastasis
Pulm infarct
Bacterial abscess

235
Q

Definition of apnoea

A

Cessation of breathing for 10 seconds, causing 4% destauration

236
Q

Ideal V/Q ratio

A

1 for maximally efficient pulmonary function

237
Q

Usual VQ ratio

A

0.84 overall

Diff ratios for diff areas due to where area lies in relation to heart

238
Q

How does VQ ratio change at the apex and base of lung

A

When standing up straight, ratio is 3.3 in apex and only 0.63 in base
V > Q in apex
V < Q in base

239
Q

Examples of diseases causing Class I PHTN

A

Idiopathic/ heritable PAH - pts usually px quite young

PAH 2’ to drugs of CTD

240
Q

Examples of diseases causing Class II PHTN

A

LV systolic/ diastolic dysfunction

Valvular disease e.g. MS, MR

241
Q

Examples of diseases causing Class III PHTN

A

COPD

ILD

242
Q

Examples of disease causing Class V PHTN

A

Sarcoidosis

Sickle cell anaemia

243
Q

What mutation causes familial PAH

A

BMPR2

244
Q

PAH

A

Pulm arterial HTN

245
Q

Symptoms of Pulm HTN

A
(Non-spp) 
Progressive exertion dyspnoea
Syncope
Fatigue 
Limb swelling 
Chest pain 
Haemoptysis
246
Q

Examination findings for pulm HTN

A

Looking for associations w/ CTD e.g. Raynaud’s, calcinosis, telangiectasia, sclerodactyly

247
Q

Main ix for pulm HTN

A

R heart catheterisation
Echo
ECG
Bloods - NTproBNP, FBC (anaemic pts have worse prognoses)
Cardiac MRI
6 in walking test (stamina and desaturations)

248
Q

Why do we measure glucose in pleural aspirate

A

To rule out Rh effusion when glucose is low

249
Q

What is the pleural effusion most likely to be if the pH of the aspirate is below 7.2

A

Acidotic fluid implies parapneumonic effusion or empyema

Chest drain must be inserted ASAP (5th IC space)

250
Q

What can be done for a PTX pt if a chest drain has not worked

A

Insert large bore cannula
Surgery
Talc pleurodesis

251
Q

Key mechanism of hypoxaemia in pE

A

Physiological dead space - no gas supply to alveoli

252
Q

Key mechanism of hypoxaemia in pleural effusion

A

Physiological shunting

253
Q

What must HGV and public transport drivers do after a dx of OSA is made

A

Declare to DVLA and stop driving ASAP

Once established on treatment for 2-3/52, and assessed, they can resume

254
Q

Indications for CPAP

A

ESS 11/24 and moderat/severe apnoea

Mild apnoea but CDV risk factors

255
Q

Which CTD is most likely to cause heart failure

A

SScl

Specifically R heart

256
Q

h

A
257
Q

Example of a drug that may cause PAH

A

Fenfluramine - anti-epileptic

258
Q

Drug therapy for PAH

A

Sildenafil
Bosentan
Both venodilators

259
Q

Absolute contraindications for thrombolysis in PE

A
Haemorrhage stroke 
Ischaemic stroke within 3/12
Recent head injury 
Recent surgery 
Current active bleeding 
Bleeding disorder
260
Q

Mechanism of tension PTX

A

The opening in the pleura creates a flap that acts as a one-way valve
This allows air to enter the cavity during inspiration but stops it from leaving during expiration

261
Q

Mechanism of a spontaneous PTX

A

Small bleb/ weakness ruptures - more common in tall pts
Air in pleural space can results in pain - variable in intensity
Feeling breathless - dependent on air leak
Air in pleural space may result in the lung collapsing

262
Q

Key landmark for insertion of a needle in a tension PTX

A

2nd IC space in the mid-clavicular line (urgent needle decompression)