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02F > Respiratory > Flashcards

Respiratory Flashcards

1
Q

how can lung cancer be classified histologically? what % of total lung cancers are each of them?

A
  • non-small cell lung cancer, 80%

- small cell lung cancer (SCLC), 20%

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2
Q

2 types of non-small cell lung cancer?

A
  • squamous cell carcinoma

- adenocarcinoma (more likely in a non-smoker)

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3
Q

which type of lung cancer can give rise to paraneoplastic syndromes? how?

A
  • SCLC

- the cells have granules which secrete neuroendocrine hormones

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4
Q

presentation of lung cancer?

A
  • SOB
  • cough, haemoptysis
  • finger clubbing
  • recurrent pneumonia
  • weight loss
  • lymphadenopathy
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5
Q

which lymph nodes are enlarged first typically in lung cancer?

A

supraclavicular ones

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6
Q

first line investigation in lung cancer? what are the findings?

A
  • CXR
  • hilar enlargement
  • peripheral opacity
  • pleural effusion, usually unilateral
  • collapse
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7
Q

investigations in lung cancer?

A
  • CXR
  • CT chest, abdomen and pelvis to stage
  • PET-CT
  • bronchoscopy with endobrachial ultrasound (EBUS)
  • biopsy and histology
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8
Q

when is surgical management used in lung cancer? what types are there?

A
  • non-SCLC isolated in one area
  • lobectomy
  • segmentectomy (wedge resection)
  • often done with adjuvant chemotherapy
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9
Q

management of SCLC? prognosis?

A
  • chemotherapy
  • radiotherapy
  • typically worse prognosis than non-SCLC
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10
Q

palliative treatment options for lung cancer?

A
  • palliative chemotherapy
  • endobrachial stenting
  • endobrachial debulking
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11
Q

complications of lung cancer relating to compression and hormone secretion?

A

compression:
- recurrent laryngeal palsy
- phrenic nerve palsy
- SVCO
- horner’s syndrome

hormonal:

  • SIADH
  • cushing’s syndrome
  • hypercalcaemia
  • limbic encephalitis
  • lambert-eaton myasthenic syndrome
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12
Q

how can lung cancer cause nerve palsy? which nerves are commonly affected?

A
  • tumour compresses them
  • recurrent laryngeal nerve
  • phrenic nerve
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13
Q

presentation of SVC obstruction?

A
  • facial swelling
  • difficulty breathing
  • distended veins in neck and upper chest
  • pemberton’s sign
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14
Q

what is pemberton’s sign? is it significant?

A
  • raising the hands over the head causes facial congestion and cyanosis
  • medical emergency!
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15
Q

how can lung cancer cause horner’s syndrome?

A

pancoast tumour compressing the sympathetic ganglion

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16
Q

presentation of horner’s syndrome?

A

triad:

  • partial ptosis
  • anhidrosis
  • miosis
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17
Q

what is a pancoast’s tumour?

A

tumour in the apex of the lung

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18
Q

how can lung cancer cause SIADH? key finding on bloods?

A
  • SCLC tumour secreting ectopic ADH

- hyponatraemia

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19
Q

how can lung cancer cause cushing’s syndrome?

A

SCLC secreting ectopic ACTH

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20
Q

how can lung cancer cause hypercalcaemia?

A

squamous cell carcinoma (non-SCLC) secreting ectopic PTH

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21
Q

describe limbic encephalitis

A
  • paraneoplastic syndrome caused by SCLC
  • immune reaction to the limbic system
  • anti-Hu antibodies
  • causes: memory impairment, hallucinations, confusion, seizures
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22
Q

pathophysiology of lambert-eaton myasthenic syndrome?

A

antibodies created against SCLC cells but which also happen to attack voltage-gated Ca channels in motor neurones

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23
Q

presentation of lambert-eaton myasthenic syndrome?

A
  • proximal muscle weakness, worse with prolonged use
  • diplopia
  • ptosis
  • slurred speech
  • dysphagia
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24
Q

top differential for lambert-eaton myasthenic syndrome?

A
  • myasthenia gravis

- onset is more insidious and symptoms less pronounced in lambert-eaton

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25
Q

which cells are affected in mesothelioma?

A

mesothelial cells of the pleura

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26
Q

biggest risk factor for mesothelioma?

A
  • asbestos inhalation / exposure

- latent period as long as 45 years

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27
Q

management of mesothelioma? prognosis?

A
  • palliative chemotherapy

- very poor

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28
Q

finding on CXR in pneumonia?

A

consolidation

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29
Q

what is hospital acquired pneumonia (HAP)?

A

pneumonia which develops >48h after hospital admission

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30
Q

different types of pneumonia?

A
  • CAP
  • HAP
  • aspiration pneumonia
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31
Q

presentation of pneumonia?

A
  • SOB
  • productive cough
  • fever
  • haemoptysis
  • pleuritic chest pain
  • delirium
  • sepsis
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32
Q

findings in a set of obs in pnuemonia?

A
  • tachypnoea
  • tachycardia and hypotension (shock)
  • hypoxia
  • fever
  • confusion (GCS)
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33
Q

lung signs on examination in pneumonia?

A
  • bronchial breathing
  • increased tactile vocal fremitus
  • focal coarse crackles
  • dullness to percuss
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34
Q

describe bronchial breathing

A

harsh breathing, equally loud on inspiration and expiration

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35
Q

scoring system for severity and risk of mortality from pneumonia in hospital? in community?

A
  • CURB-65 in hospital

- urea not checked out of hospital (CRB-65)

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36
Q

different parts of CURB-65?

A
  • Confusion, new onset
  • Urea >7
  • RR >30
  • BP <90 systolic, <60 diastolic
  • 65 or above years old
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37
Q

which CURB-65 score determines which treatment?

A
  • 0-1 = home treatment
  • 2 = hospital admission
  • 3 or more = ICU care
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38
Q

commonest bacterial causes of pneumonia?

A
  • strep pneumoniae (50%)

- H. influenzae (20%)

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39
Q

which organism causes pneumonia in immunocompromised / COPD patients?

A

moraxella catarrhalis

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40
Q

which organisms cause pneumonia in CF patients?

A
  • pseudomonas aeruginosa

- staph aureus

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41
Q

who is at higher risk of pneumonia from pseudomonas aeruginosa?

A
  • CF patients

- bronchiectasis patients

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42
Q

define atypical pneumonia

A

pneumonia caused by an organism which cannot be cultured in the normal way or detected by gram stain

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43
Q

which ABx should be used on atypical pneumonia?

A

macrolides

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44
Q

organisms which cause atypical pneumonia?

A
  • legionella pneumophila
  • mycoplasma pneumoniae
  • chlamydophila pneumoniae
  • coxiella burnetii
  • chlamydia psittaci
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45
Q

how is legionella pneumophila contracted? how does it present?

A
  • infected water supply, dodgy air con
  • pneumonia
  • hyponatraemia (it causes SIADH)
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46
Q

how does mycoplasma pneumoniae infection present?

A
  • mild pneumonia
  • erythema multiforme (“target” lesions)
  • warm-type AIHA
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47
Q

which demographic typically gets chlamydia pneumoniae infection? how does it present?

A
  • school aged children
  • chronic cough and wheeze
  • (be careful because this is a common presentation!)
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48
Q

another name for coxiella burnetii infection? how does it spread?

A
  • Q fever
  • animal bodily fluids
  • e.g. “farmer with a flu”
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49
Q

Legions of psittaci MCQs: 5 causes of atypical pneumonia?

A
  • legionella
  • psittaci (chlamydia)
  • Mycoplasma pneumoniae
  • Chlamydophila pneumoniae
  • Q fever (coxiella burnetti)
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50
Q

which organism could cause a fungal pneumonia?

A

pneumocystis jiroveci

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51
Q

which patients are at risk of pnuemocystis jiroveci pneumonia?

A
  • immunocompromised

- e.g. HIV+ with low CD4 count

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52
Q

presentation of fungal pneumonia?

A
  • dry cough
  • SOBOE
  • night sweats
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53
Q

management of fungal pneumonia?

A
  • co-trimoxazole (trimethoprim + sulfamethoxazole)
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54
Q

how can fungal pneumonia be prevented?

A

all HIV+ pts with CD4 count <200 are given prophylactic co-trimoxazole alongside their regular ART

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55
Q

investigations for pneumonia? findings?

A
  • CXR (consolidation)
  • FBC (raised WCC)
  • UEs (urea for CURB-65)
  • CRP (raised)
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56
Q

extra investigations done in severe pneumonia?

A
  • sputum cultures
  • blood cultures
  • legionella and pneumococcal urinary antigens
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57
Q

when might CRP be low in pneumonia? why?

A
  • immunocompromised patients

- they can’t mount an immune response

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58
Q

management of severe pneumonia?

A
  • hospital admission
  • IV ABx (check local guidelines to choose)
  • switch to oral once improving
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59
Q

management of mild CAP?

A

5 day oral course of either:

  • amoxicillin
  • macrolide
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60
Q

management of mod-sev CAP?

A

7-10 day course of BOTH amoxicillin AND a macrolide

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61
Q

SPELD: complications of pneumonia?

A
  • sepsis
  • pleural effusion
  • lung abscess
  • death
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62
Q

3 outcome measures of lung function tests?

A
  • spirometry
  • FEV1
  • FVC
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63
Q

in spirometry, what is reversible testing?

A

giving a bronchodilator (salbutamol) before doing the breathing exercises

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64
Q

what is FEV1? when is it reduced?

A
  • forced expiratory volume in 1 second
  • volume of air a person can forcefully exhale in 1 second
  • reduced in lung obstruction
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65
Q

what is FVC? when is it reduced?

A
  • forced vital capacity
  • total volume of air a person can exhale after inspiration
  • reduced in lung restriction (because capacity of lung is being restricted)
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66
Q

how is obstructive lung disease diagnosed?

A

FEV1/ FVC <0.75

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67
Q

examples of obstructive lung disease?

A
  • asthma (bronchoconstriction)
  • COPD (chronic damage leading to obstruction)
  • bronchiectasis
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68
Q

FEV1/FVC in restrictive lung disease? explain this

A
  • FEV1/FVC >0.75 (normal or raised)

- they’re both equally reduced, so the ratio doesn’t change

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69
Q

describe restrictive lung disease

A

restriction in lung’s ability to expand

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70
Q

examples / causes of restrictive lung diseases?

A
  • pulmonary fibrosis (or other ILD)
  • asbestosis
  • sarcoidosis
  • obesity
  • MND / other neuro disorders
  • scoliosis (e.g. in ank spond)
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71
Q

when is peak flow (PEFR) useful?

A

to demonstrate obstruction in asthma

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72
Q

how is peak flow measured?

A
  • stand tall and take a deep breath in
  • make a good seal with the device
  • blow hard and fast ;)
  • 3 attempts, take the best one
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73
Q

how is the peak flow result interpreted?

A
  • predicted peak flow obtained from chart

- record it as % of actual over predicted

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74
Q

factors taken into account in predicted peak flow?

A
  • sex
  • height
  • age
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75
Q

what is asthma?

A

chronic inflammatory condition where there is bronchoconstriction in exacerbations

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76
Q

how does asthma cause obstruction? is this reversible?

A
  • smooth muscles of bronchi contract
  • airway gets narrowed
  • obstructs airflow
  • reversible
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77
Q

how is obstruction in asthma reversed?

A

bronchodilator (salbutamol)

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78
Q

triggers of bronchoconstriction in asthma?

A
  • infection
  • time of day (night or early morn)
  • exercise
  • animals
  • cold / damp / dust
  • strong emotions
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79
Q

presentation of asthma?

A
  • episodic symptoms in Hx
  • diurnal variation
  • dry cough
  • wheeze
  • SOB
  • Hx of atopy (eczema, hayfever, food allergy)
  • FHx
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80
Q

what is heard on auscultation in asthma?

A

bilateral widespread polyphonic wheeze

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81
Q

what are the first line investigations in asthma diagnosis according to NICE?

A
  • fractional exhaled nitric oxide (FeNO)

- spirometry with bronchodilator reversibility

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82
Q

second line investigations in asthma diagnosis?

A
  • peak flow variability

- direct bronchial challenge with histamine / methacholine

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83
Q

full form of SABA? how long does the effect of a SABA last? what is the inhaler commonly called? example?

A
  • short acting beta 2 agonist
  • only lasts 1-2 hours
  • “reliever”, “rescue”
  • salbutamol
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84
Q

example of an ICS? how do they work? what is the inhaler commonly called?

A
  • beclometasone, budesonide, fluticasone
  • reduces inflammation in airway
  • “maintenance”, “preventer”
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85
Q

full form of LABA? example? what is the difference between LABA and SABA?

A
  • long acting beta 2 agonist
  • salmeterol
  • same MOA but LABA lasts much longer
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86
Q

full form of LAMA? example? how does it work?

A
  • long acting muscarinic antagonist
  • tiotropium
  • blocks ACh receptors, causing bronchodilation
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87
Q

full form of LTRA? example? how does it work?

A
  • leukotriene receptor antagonist
  • montelukast
  • blocks leukotriene action
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88
Q

what are the effects of leukotrienes?

A
  • inflammation
  • bronchoconstriction
  • mucus secretion
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89
Q

how does theophylline work?

A
  • relaxes bronchial smooth muscle

- reduces inflammation

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90
Q

why does theophylline need to be monitored? how is it monitored?

A
  • narrow therapeutic window, can cause toxicity
  • check blood theophylline levels 5 days after starting treatment
  • check 3 days after each dose change
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91
Q

what does MART stand for in asthma treatment? why is it useful?

A
  • maintenance and reliever therapy
  • one inhaler with a low dose ICS and LABA in it
  • replaces all other inhalers
  • convenient
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92
Q

step 1 in NICE asthma treatment ladder?

A

SABA (salbutamol), PRN

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93
Q

step 2 in NICE asthma treatment ladder?

A

add low dose ICS (beclometasone)

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94
Q

step 3 in NICE asthma treatment ladder? how does SIGN/BTS differ here?

A
  • NICE: add LABA (salmeterol)

- SIGN/BTS: add LTRA (montelukast)

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95
Q

step 4 in NICE asthma treatment ladder?

A

consider adding one of these:

  • LTRA (montelukast)
  • theophylline
  • PO SABA (salbutamol)
  • LAMA (tiotropium)
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96
Q

step 5 in NICE asthma treatment ladder?

A

increase ICS from low dose to high dose

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97
Q

step 6 in NICE asthma treatment ladder?

A

add oral steroids

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98
Q

other than regular medication, what else is part of asthma management?

A
  • yearly flu jab
  • yearly asthma review
  • advice on exercise and smoking
  • all patients should have a personalised plan
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99
Q

presentation of acute asthma exacerbation?

A
  • progressively worsening SOB
  • use of accessory muscles
  • tachypnoea
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100
Q

signs on auscultation in acute asthma exacerbation?

A
  • symmetrical expiratory wheeze

- “tight” chest sounds (reduced air entry)

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101
Q

how are acute asthma exacerbations graded?

A
  • moderate
  • severe
  • life-threatening
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102
Q

features of a moderate acute asthma exacerbation?

A
  • peak flow 50-75% of predicted
  • normal speech
  • RR <25/min
  • pulse <110/min
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103
Q

features of a severe acute asthma exacerbation?

A
  • peak flow is 33-50% of predicted
  • RR >25
  • HR >110
  • unable to complete a sentence
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104
Q

features of a life-threatening acute asthma exacerbation?

A
  • peak flow isn <33% of predicted
  • O2 sats <92%
  • becoming tired
  • silent chest (no wheeze)
  • haemodynamic instability (shock)
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105
Q

management of a moderate acute asthma exacerbation?

A
  • nebulised salbutamol 5mg, repeat as much as needed
  • nebulised ipratropium bromide
  • PO pred or IV hydrocortisone for 5 days
  • ABx if bacterial cause suspected
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106
Q

management of a severe acute asthma exacerbation?

A
  • O2 to maintain sats of 94-98%
  • aminophylline infusion
  • consider IV salbutamol
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107
Q

management of a life-threatening acute asthma exacerbation?

A
  • IV magnesium sulphate infusion
  • HDU / ICU admission
  • intubation if extreme severity
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108
Q

ABG findings in an acute asthma exacerbation? why?

A
  • respiratory alkalosis (drop in CO2 from tachypnoea)

- normal pCO2 means they are tiring and retaining more CO2

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109
Q

why is respiratory acidosis a worrying finding on ABG in asthma?

A

it means they have high CO2 because they’re not blowing any of it off

110
Q

how is treatment response monitored in acute asthma exacerbations?

A
  • RR
  • resp effort
  • peak flow
  • O2 sats
  • chest auscultation
111
Q

which electrolyte needs to be monitored in patients on salbutamol? why?

A
  • serum K+

- salbutamol causes K+ to move from blood into cells

112
Q

define COPD

A

non-reversible, long term obstruction in air flow through the lungs caused by damage to lung tissue

113
Q

presentation of COPD?

A
  • chronic SOB
  • cough with sputum
  • wheeze
  • recurrent resp infections
114
Q

main risk factor for COPD?

A

smoking

115
Q

how can breathlessness be assessed?

A

MRC dyspnoea scale

116
Q

describe the 5 grades of the MRC dyspnoea scale

A
  • 1 = breathless on strenuous exercise
  • 2 = breathless on walking uphill
  • 3 = breathessness that slows walking on the flat
  • 4 = stops to catch breath after walking 100m on the flat
  • 5 = unable to leave the house due to breathlessness
117
Q

how is COPD diagnosed?

A

both of:

  • clinical picture
  • spirometry showing: FEV1/FVC <0.7
118
Q

results of spirometry reversibility testing in COPD?

A

no dramatic reversal with salbutamol

119
Q

how can the severity of obstruction in COPD be assessed?

A

look at the FEV1 compared to the predicted value

120
Q

investigations (other than spirometry) and findings in COPD?

A
  • CXR (hyperinflated, exclude: cancer)
  • FBC (polycythaemia due to chronic hypoxia)
  • BMI (weight loss if COPD is severe, gain from steroids)
  • sputum culture (chronic infection)
  • ECG (cor pulmonale findings), echocardiogram
  • CT thorax (exclude: fibrosis, cancer, bronchiectasis)
  • serum A1AT (may be deficient)
  • TLCO (low)
121
Q

what is TLCO?

A

transfer factor for carbon monoxide

122
Q

non-drug management of COPD?

A
  • smoking cessation
  • pulmonary rehab
  • pneumococcal vaccine
  • annual flu jab
123
Q

step 1 in drug management of COPD?

A

SABA (salbutamol) or SAMA (ipratropium)

124
Q

step 2 in COPD management with NO features of asthma / response to steroids?

A
  • combined inhaler

- includes LABA and a LAMA

125
Q

which add-on meds can be used in COPD management?

A
  • PO theophylline
  • PO mucolytics (carbocisteine)
  • long term prophylactic ABx (azithromycin)
  • O2 therapy at home
126
Q

what determines step 2 of COPD medical management?

A
  • whether they have features of asthma

- whether it is steroid-responsive

127
Q

step 2 in COPD management with features of asthma / response to steroids? if this fails?

A
  • combined inhaler
  • LABA + ICS
  • if this fails: LABA + ICS + LAMA inhaler
128
Q

indications for long-term O2 therapy use in COPD?

A
  • chronic hypoxia
  • polycythaemia
  • cyanosis
  • cor pulmonale
129
Q

significant contraindication for O2 therapy?

A

smoking! fire hazard

130
Q

presentation of COPD exacerbation?

A

acute worsening of:

  • cough
  • SOB
  • sputum production
  • wheeze
131
Q

what causes a COPD exacerbation?

A

viral / bacterial infection

132
Q

ABG findings in someone acutely retaining CO2? why? what is this called?

A
  • low pH
  • the breakdown product of CO2 is acidotic
  • respiratory acidosis
133
Q

ABG findings in someone chronically retaining CO2? why?

A
  • raised bicarbonate

- kidneys compensate for the acid by producing something alkaline

134
Q

ABG findings in type 1 resp failure?

A
  • low pO2

- normal pCO2

135
Q

ABG findings in type 2 resp failure?

A
  • low pO2

- high pCO2

136
Q

investigations in COPD exacerbation?

A
  • ABG
  • CXR
  • ECG
  • UEs
  • sputum culture
  • blood cultures if septic
137
Q

why does O2 therapy need careful monitoring if someone is retaining CO2? how is it done?

A
  • too much O2 can depress their resp drive
  • repeat ABGs
  • use venturi masks to tightly control O2 flow
138
Q

target O2 sats in CO2 retainers?

A

88-92% titrated by venturi mask

139
Q

target O2 sats in COPD patient NOT retaining CO2?

A

> 94%

140
Q

treatment of COPD exacerbation at home?

A
  • pred 30mg for 7-14 days
  • regular inhalers / nebulisers
  • ABx if signs of infection
141
Q

treatment of COPD exacerbation in hospital?

A
  • nebulised salbutamol + ipratropium (bronchodilators)
  • steroids (either hydrocortisone or pred)
  • O2 via venturi mask
  • ABx if signs of infection
  • physio to clear sputum
142
Q

management of COPD exacerbation not responding to first line treatment?

A
  • IV aminophylline
  • NIV
  • intubation and ventilation
  • doxapram (resp stimulant)
143
Q

what are the types of non-invasive ventilation (NIV)?

A
  • BiPAP

- CPAP

144
Q

what does BiPAP stand for? when is it indicated?

A
  • bilevel positive airway pressure
  • type 2 resp failure
  • patient must have resp acidosis despite medication
145
Q

contraindications for BiPAP?

A
  • untreated pneumothorax

- any other serious pathology affecting face / airway / GI tract

146
Q

imaging done before BiPAP? why?

A
  • CXR

- to rule out pneumothorax

147
Q

what does CPAP stand for?

A

continuous positive airway pressure

148
Q

indications for CPAP?

A
  • obstructive sleep apnoea
  • congestive cardiac failure
  • acute pulmonary oedema
149
Q

describe interstitial lung disease (ILD)

A
  • an umbrella term
  • conditions which affect lung parenchyma to cause inflammation
  • results in fibrosis
150
Q

diagnostic investigation for ILD? findings?

A
  • high-res CT (HRCT)

- ground glass appearance

151
Q

prognosis in ILD?

A
  • poor

- the fibrosis is irreversible

152
Q

management of ILD? hint: supportive

A
  • remove / treat underlying cause
  • O2 at home if hypoxic at rest
  • stop smoking
  • physio, pulmonary rehab
  • pneumococcal and flu jab
  • advanced care planning / palliative where needed
  • lung transplant (rare)
153
Q

what is idiopathic pulmonary fibrosis?

A
  • pulmonary fibrosis without a clear cause

- type of interstitial lung disease

154
Q

typical demographic for idiopathic pulmonary fibrosis?

A

those aged >50 years old

155
Q

presentation of idiopathic pulmonary fibrosis?

A
  • insidious onset over >3 months
  • SOB
  • dry cough
156
Q

signs O/E in idiopathic pulmonary fibrosis?

A
  • bibasal fine inspiratory crackles

- finger clubbing

157
Q

prognosis in idiopathic pulmonary fibrosis?

A
  • poor

- life expectancy of 2-5 years

158
Q

2 medications which can slow progression of idiopathic pulmonary fibrosis?

A
  • pirfenidone

- nintedanib

159
Q

drugs which can cause pulmonary fibrosis?

A
  • amiodarone
  • cyclophosphamide
  • methotrexate
  • nitrofurantoin
160
Q

which conditions can pulmonary fibrosis be secondary to?

A
  • A1AT
  • RA
  • SLE
  • systemic sclerosis
  • sarcoidosis
161
Q

what is the other name for extrinsic allergic alveolitis (EAA)?

A

hypersensitivity pneumonitis

162
Q

describe EAA?

A
  • type III (delayed) hypersensitivity reaction to environmental antigen
  • causes inflammation in parenchyma
163
Q

investigation in EAA? findings

A
  • bronchoalveolar lavage
  • raised eosinophils
  • raised mast cells
164
Q

what does bronchoalveolar lavage involve? when is it used?

A
  • washing out the airways during bronchoscopy and collecting the fluid to test
  • used in EAA diagnosis
165
Q

4 specific causes of EAA? what is each one called?

A
  • bird droppings (bird-fanciers lung)
  • mould spores in hay (farmers lung)
  • mushroom antigens (mushroom workers lung)
  • mould spores in barley (malt workers lung)
166
Q

what is asbestosis?

A

lung fibrosis caused by inhaling asbestos

167
Q

conditions caused by asbestos inhalation?

A
  • lung fibrosis
  • pleural thickening and plaques
  • adenocarcinoma
  • mesothelioma
168
Q

what is a pleural effusion?

A

collection of fluid in the pleural space

169
Q

what is an exudative pleural effusion?

A

there is >3g/L (high) protein in the fluid

170
Q

causes of exudative pleural effusion? (hint: inflammation)

A

think inflammation:

  • lung cancer
  • pneumonia
  • RA
  • TB
171
Q

what is a transudative pleural effusion?

A

there is <3g/L (low) protein in the fluid

172
Q

causes of transudative pleural effusion? (hint: fluid shift)

A

think of things causing fluid to move:

  • CCF
  • hypoalbuminaemia (nephrotic syndrome)
  • hypothyroidism
  • Meig’s syndrome
173
Q

what is Meig’s syndrome?

A

R-sided pleural effusion with ovarian malignancy

174
Q

presentation (including O/E) of pleural effusion?

A
  • SOB
  • dull to percuss over the area
  • reduced breath sounds
  • tracheal deviation away from effusion if massive
175
Q

findings on CXR in pleural effusion?

A
  • blunting of costophrenic angle
  • fluid in lung fissures
  • meniscus in larger effusions
  • tracheal + mediastinal deviation if massive
176
Q

what can be tested for in a sample of pleural effusion fluid?

A
  • protein count
  • cell count
  • pH
  • glucose
  • LDH
  • microbiology testing
177
Q

management of pleural effusion?

A
  • conservative if small
  • pleural aspiration
  • chest drain
178
Q

what is empyema? when should you suspect it?

A
  • an infected pleural effusion

- when someone comes in with pneumonia-like signs but they are not responding to ABx

179
Q

findings on aspiration of empyema?

A
  • pus
  • acidic pH (<7.2)
  • low glucose
  • high LDH
180
Q

management of empyema?

A
  • chest drain

- ABx

181
Q

describe pneumothorax

A

air in the pleural space separating the lung from the chest wall

182
Q

causes of pneumothorax?

A
  • spontaneous
  • trauma
  • iatrogenic
  • lung pathology
183
Q

what are the iatrogenic causes of pneumothorax?

A
  • lung biopsy
  • mechanical ventilation
  • central line insertion
184
Q

which lung pathologies could cause a pneumothorax?

A
  • infection
  • asthma
  • COPD
185
Q

investigations in pneumothorax?

A
  • erect CXR

- CT thorax ( for smaller ones not seen on CXR)

186
Q

management of pneumothorax where there is no SOB and there is a <2cm rim of air on CXR?

A
  • nothing
  • will resolve spontaneously
  • follow up in a month
187
Q

management of pneumothorax where there is SOB +/- rim of air is >2cm on CXR?

A
  • needle aspiration and reassess
  • if aspiration fails twice, chest drain
  • talc pleurodesis if recurrent
188
Q

what is a tension pneumothorax? what causes it?

A
  • one-way valve forms in chest wall, which lets air in but not out
  • emergency
  • caused by trauma
189
Q

signs (including O/E) of tension pneumothorax?

A
  • tracheal deviation away from side of pneumothorax
  • reduced air entry on affected side
  • increased resonance on percussion of affected side
  • tachycardia
  • hypotension
190
Q

main complication of tension pneumothorax?

A

cardiorespiratory arrest

191
Q

management of tension pneumothorax?

A
  • insert a large bore cannula into the 2nd IC space in the midclavicular line
  • once some pressure is relieved, insert chest drain
  • do NOT wait for investigations
192
Q

describe the borders of the “triangle of safety”. why is this space important?

A
  • 5th IC space
  • mid-axillary line
  • anterior axillary line
  • this is where chest drains are inserted
193
Q

what is a pulmonary embolism (PE)?

A
  • a blood clot in the pulmonary arteries

- usually secondary to a DVT which has travelled

194
Q

risk factors for developing VTE?

A
  • recent surgery
  • long haul flights
  • pregnancy
  • oestrogen therapy
  • malignancy (hypercoagulable state!)
  • polycythaemia
  • SLE
  • thrombophilia
195
Q

what prophylaxis is offered to patients at risk of VTE?

A
  • LMWH (enoxaparin)

- compression stockings

196
Q

main contraindication for compression stockings?

A

peripheral arterial disease

197
Q

contraindications for LMWH?

A
  • active bleeding

- anyone on warfarin / NOAC (anticoag)

198
Q

presentation of PE?

A
  • cough +/- blood
  • pleuritic chest pain
  • hypoxia
  • tachycardia
  • tachypnoea
  • low grade fever
  • haemodynamic instability
  • hypotension
199
Q

what can be calculated if you suspect a PE?

A

wells score

200
Q

which factors are taken into account for wells score?

A
  • HR >100
  • immobilisation
  • prev DVT / PE
  • haemoptysis
  • malignancy
201
Q

how is the wells score outcome interpreted in suspected PE?

A
  • PE likely: CT pulmonary angiogram (CTPA)

- PE unlikely: D-dimer

202
Q

what is the next investigation in suspected PE if D-dimer is positive? hint: different for renal impairment

A
  • CTPA

- if renal impairment: VQ scan

203
Q

diagnostic investigations for PE?

A
  • CTPA

- VQ scan (ventilation-perfusion)

204
Q

what does the ABG pH show in PE? why?

A
  • resp alkalosis (high pH)
  • tachypnoea means they blow off their CO2
  • low CO2 makes blood alkalotic
205
Q

2 main causes of resp alkalosis?

A
  • PE

- hyperventilation syndrome

206
Q

supportive management in PE?

A
  • hosp admission
  • O2 as required
  • analgesia as required
  • monitor for deterioration
207
Q

medical management of PE?

A
  • IV fluids / oxygen if needed
  • start off with rivaroxaban + LMWH (dalteparin)
  • then long-term anticoag (warfarin or NOAC) for 3 months
  • carry on for longer if unsure of cause / malignancy present
208
Q

is D-dimer sensitive / specific to VTE?

A
  • sensitive but not specific

- if low, unlikely to be VTE but if raised can be something else

209
Q

causes of a raised D-dimer?

A
  • VTE
  • pneumonia
  • malignancy
  • HF
  • surgery
  • pregnancy
210
Q

management of a massive PE with haemodynamic instability? which agents can be used for this?

A
  • IV or catheter-directed thrombolysis
  • streptokinase
  • alteplase
  • tenecteplase
211
Q

causes of pulmonary hypertension?

A
  • primary (caused by nothing else)
  • connective tissue disease (SLE)
  • LSHF
  • chronic lung disease (COPD)
  • lung vascular disease (PE)
  • sarcoidosis
  • glycogen storage disorders
  • haematological causes
212
Q

presentation of pulmonary HTN?

A
  • SOB (main one)
  • syncope
  • tachycardia
  • raised JVP
  • hepatomegaly
  • peripheral oedema
213
Q

investigations for pulmonary HTN?

A
  • ECG
  • CXR
  • NT-proBNR (cor pulmonale)
  • echo (to check pulmonary artery pressure)
214
Q

ECG changes in pulmonary HTN?

A
  • RV hypertrophy
  • R axis deviation
  • RBBB
215
Q

CXR changes seen in pulmonary HTN?

A
  • dilated pulmonary arteries

- RV hypertrophy

216
Q

prognosis in pulmonary HTN?

A
  • poor

- 30% life expectancy at 5 years post-diagnosis

217
Q

treatment for primary pulmonary HTN?

A
  • IV prostanoids (epoprostenol)
  • endothelial receptor antagonists (macitentan)
  • phosphodiesterase-5 inhibitors (sildenafil)
218
Q

complications of pulmonary HTN?

A
  • cor pulmonale
  • resp failure
  • arrhythmias
219
Q

management of secondary pulmonary HTN?

A

manage the underlying cause

220
Q

what is sacrdoidosis?

A
  • granulomatous inflammatory condition

- gives chest signs and extrapulmonary signs

221
Q

what do the granulomas in sarcoidosis contain?

A

macrophages

222
Q

demographics affected by sarcoidosis?

A
  • 2 spikes in incidence
  • young adulthood and 60s
  • F>M
  • Black people more affected
223
Q

organs affected by sarcoidosis? (hint: literally everything)

A
  • lungs
  • liver
  • eyes
  • skin
  • heart
  • kidneys
  • CNS and PNS
  • bones
224
Q

what can sarcoidosis cause in the lungs?

A
  • mediastinal lymphadenopathy
  • pulmonary fibrosis
  • pulmonary nodules
225
Q

what can sarcoidosis cause in the liver?

A
  • nodules
  • cirrhosis
  • cholestasis
226
Q

what can sarcoidosis cause in the eyes?

A
  • uveitis
  • conjunctivitis
  • optic neuritis
227
Q

what can sarcoidosis cause on the skin?

A
  • erythema nodosum
  • lupus pernio
  • granulomas
228
Q

systemic signs of sarcoidosis?

A
  • fever
  • fatigue
  • weight loss
229
Q

what can sarcoidosis cause in the heart?

A
  • bundle branch block
  • heart block
  • myocardial muscle involvement
230
Q

what can sarcoidosis cause in the kidneys?

A
  • stones (hypercalcaemia)
  • nephrocalcinosis
  • interstitial nephritis
231
Q

what can sarcoidosis cause in the nervous system? (hint: split into central and peripheral)

A

central:
- diabetes insipidus (pituitary)
- encephalopathy
peripheral:
- bell’s palsy
- mononeuritis multiplex

232
Q

what can sarcoidosis cause in the bones?

A
  • arthralgia
  • arthritis
  • myopathy
233
Q

what is lofgren’s syndrome?

A

a specific presentation of sarcoidosis

234
Q

presentation of lofgren’s syndrome? hint: triad

A
  • erythema nodosum
  • bilateral hilar lymphadenopathy
  • polyarthralgia (joint pain)
235
Q

differentials for sarcoidosis?

A
  • TB
  • lymphoma
  • EAA
  • HIV
  • toxoplasmosis
  • histoplasmosis
236
Q

investigations and findings for sarcoidosis?

A
  • blood tests (lots)
  • CXR (hilar lymphadenopathy)
  • HRCT thorax (HL and pulmonary nodules)
  • MRI (CNS changes)
  • PET scan (inflammation)
237
Q

findings of blood tests in sarcoidosis?

A
  • raised serum ACE (screening)
  • raised Ca
  • raised IL-2 receptor
  • raised CRP
  • raised Ig
238
Q

gold standard investigation to diagnose sarcoidosis?

A

biopsy and histology

239
Q

what is seen on histology in sarcoidosis?

A

non-caseating granulomas with epithelioid cells

240
Q

management of asymptomatic / mild sarcoidosis?

A
  • nothing

- resolves spontaneously

241
Q

1st line treatment of symptomatic sarcoidosis? 2nd line?

A
  • PO steroids for 6-24 months
  • give bisphosphonates concurrently (stops osteoporosis)
  • 2nd line: methotrexate or azathioprine
  • lung transplant if severe lung disease
242
Q

prognosis of sarcoidosis?

A
  • good
  • 60% resolve spontaneously in 6 months
  • in some patients goes on to cause pul fibrosis / HTN
243
Q

what causes obstructive sleep apnoea (OSA)?

A

collapse of the pharyngeal airway in sleep

244
Q

risk factors for OSA?

A
  • middle age
  • male
  • obesity
  • alcohol
  • smoking
245
Q

features of OSA?

A
  • apnoeic episode, noticed by partner
  • snoring
  • morning headache
  • waking up unrefreshed from sleep
  • daytime sleepiness
  • reduced concentration
  • reduced O2 sats in sleep
246
Q

describe an apnoeic episode

A
  • the person stops breathing for a few minutes

- typically unaware of this themselves

247
Q

complications of OSA?

A
  • HTN
  • HF
  • increased risk of MI and stroke
248
Q

investigations for OSA?

A
  • sleep studies

- done by ENT specialists or sleep clinics

249
Q

management of OSA?

A
  • stop drinking
  • stop smoking
  • lose weight
  • CPAP at night
  • surgery (UPPP)
250
Q

ECG changes seen in PE?

A
  • sinus tachycardia
  • R-axis deviation
  • complete / partial RBBB
  • S waves in lead I
  • Q waves in lead III
  • T wave inversion in lead III
251
Q

what is ARDS? explain the pathophysiology of it

A
  • acute respiratory distress syndrome
  • a non-cardiac cause of pulmonary oedema (e.g. alveolar damage)
  • gives acute resp failure
252
Q

risk factors for ARDS? hint: most common first and there’s a LOT

A
  • sepsis
  • major trauma with shock
  • hypovolaemic shock
  • pneumonia
  • gastric aspiration
  • smoke inhalation
  • burns
  • DKA
  • pregnancy and eclampsia
253
Q

features of ARDS?

A
  • worsening dyspnoea
  • cyanosis
  • tachypnoea
  • tachycardia
  • peripheral vasodilation
254
Q

signs O/E of ARDS?

A
  • cyanosis

- bilateral fine inspiratory crackles

255
Q

management of ARDS?

A
  • ITU admission
  • CPAP in early disease
  • mechanical ventilation when more severe
  • monitor BP with arterial line
  • treat underlying cause (e.g. ABx for sepsis)
256
Q

differentials for a “white out” on CXR?

A
  • consolidation
  • pleural effusion
  • collapse
  • pneumonectomy
  • tumours
  • fluid (pulmonary oedema)
  • hernia
257
Q

differentials for a “white out” on CXR where the trachea is central?

A
  • consolidation
  • pulmonary oedema
  • mesothelioma
258
Q

differentials for a “white out” on CXR where the trachea is PULLED towards it?

A
  • pneumonectomy
  • complete lung collapse
  • pulmonary hypoplasia
259
Q

differentials for a “white out” on CXR where the trachea is PUSHED away from it?

A
  • pleural effusion
  • diaphragmatic hernia
  • large thoracic mass
260
Q

poor prognostic factor in CF?

A

chronic infection with either:

  • pseudomonas
  • burkholderia
261
Q

indications for corticosteroids in sarcoidosis?

A
  • parenchymal lung disease
  • uveitis
  • hypercalcaemia
  • neurological signs
  • cardiac signs
262
Q

what is bronchiectasis?

A

permanent dilation of bronchi / bronchioles from chronic infection

263
Q

main causative organisms of pts affected by bronchiectasis?

A
  • H. influenzae
  • pseudomonas aeruginosa
  • streptococcus pneumoniae
  • staph aureus
264
Q

causes of bronchiectasis?

A
  • post-infection (TB, HIV, measles, pertussis, pneumonia)
  • foreign body / tumour obstructing bronchioles
  • CF
  • idiopathic
265
Q

presentation of bronchiectasis?

A
  • cough with large amounts of purulent sputum
  • haemoptysis
  • finger clubbing
  • coarse inspiratory crackles
  • dyspnoea
  • wheeze
266
Q

findings on spirometry in bronchiectasis?

A

obstructive pattern

267
Q

findings on CXR in bronchiectasis?

A
  • tramlines

- ring shadows

268
Q

features of legionnaire’s disease?

A
  • muscle aches
  • headache
  • dry cough
  • high fever
269
Q 
What is bronchiectasis?
causes 
RF
Features
IX
Management
A

chronic obstructive lung disease characteristed by permanent dialation of the bronchi
Pneumonia, TB, whooping cough CF
Rheumatoid arthritis
Sjogren’s syndrome
Allergic bronchopulmonary aspergillosis (ABPA)
Inflammatory bowel disease

Age, smoking, female, genetics
SOB, copious sputum. production, haermoptysis, clubbing, auscultation
high res ct- bronchial dialation and bronchial wall thickening
CXR- tram tracks
Treat underlying cause, chest phyiotherpay annual influenza, abx, carbocystine
Bronchodilator: especially in patients with a degree of bronchoconstriction
Nebulised isotonic or hypertonic saline: these increase the hydration of the airway which make it easier to cough up sputum
Long-term antibiotics [5]:
Long term macrolide: e.g. azithromycin can be considered if patients have three or more exacerbations in a year
Nebulised anti-pseudomonal antibiotic: e.g. colistin can be considered if more than three exacerbations per year and grown Pseudomonas aeruginosa
Long term oxygen therapy: same eligibility criteria as COPD

270
Q 
what is cystic fibrosis?
RF
Features
IX 
management
A

Cystic fibrosis (CF) is an inherited, autosomal recessive, multi-system disease, which occurs due to mutations in the CF transmembrane conductance regulator (CFTR) on chromosome 7. Δ-F508

FHX
KNown parental carriers
caucasian

SEE DIAGRAM

airway clearence techniques
salbutamol
irst-line: rhDNase e.g. dornase alfa / recombinant human deoxyribonuclease
Second-line: hypertonic sodium chloride

271
Q 
what is ards
causes
features
IX
Management
A

Lung damage causes release of inflammatory mediators, leading to ^ capillary permeability, pulmonary oedema and
multi-organ failure

infection: sepsis, pneumonia
massive blood transfusion
trauma
smoke inhalation
acute pancreatitis
cardio-pulmonary bypass

dyspnoea
elevated respiratory rate
bilateral lung crackles
low oxygen saturations

A chest x-ray and arterial blood gases are the key investigations.

Management
due to the severity of the condition patients are generally managed in ITU
oxygenation/ventilation to treat the hypoxaemia
general organ support e.g. vasopressors as needed
treatment of the underlying cause e.g. antibiotics for sepsis
certain strategies such as prone positioning and muscle relaxation have been shown to improve outcome in ARDS

02F (18 decks)

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