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Zero to Finals: Medicine A.S. > 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

3 main types of non-small cell lung cancer?

A
  • adenocarcinoma (40%)
  • squamous cell carcinoma (more likely in a non-smoker) (20%)
  • large cell carcinoma
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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? (6)

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 (4)?

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 endobronchial ultrasound (EBUS)
  • biopsy and histology
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8
Q

when is surgical management used in lung cancer? Types of surgery available?

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
  • endobronchial stenting
  • endobronchial debulking
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11
Q

complications of lung cancer relating to compression (4) and hormone secretion (3) and immune (2)?

A

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

hormonal:

  • SIADH
  • cushing’s syndrome
  • hypercalcaemia

Immune

  • 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 (as the thoracic inlet becomes obstructed)
  • 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

(caused by? / pathophys?/ features?)

A

= paraneoplastic syndrome caused by SCLC

  • immune reaction to the limbic system
  • anti-Hu antibodies
  • causes: memory impairment, confusion, hallucinations, seizures
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22
Q

pathophysiology of lambert-eaton myasthenic syndrome?

A

antibodies created against SCLC cells ➡️ BUT also 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
  • EYE - 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

CHEST:

  • SOB
  • productive cough +/- haemoptysis
  • pleuritic chest pain

SYSTEMIC

  • fever
  • Sepsis

OTHER:
- delirium

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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 TO REMEMBER ➡️”69 😉”
  • 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

**REMEMBER - “legions of psittaci MCQs”

  • 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
  • additional features = COLD-type AIHA
  • erythema multiforme (“target” lesions) (= a COMPLICATION)
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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? (3)

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? 6

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? (5 symps; 2 Hx)

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 LTRA (montelukast)
  • BTS: add LABA (salmeterol)
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95
Q

step 4 in NICE asthma treatment ladder? (VS BTS)

A

NICE

Add LABA inhaler (e.g. salmeterol). Continue the LABA only if the patient has a good response.

BTS
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? (VS BTS)

A

Consider changing to a maintenance and reliever therapy (MART) regime.

BTS…
Titrate inhaled corticosteroid up to “high dose”. Combine additional treatments from step 4. Refer to specialist.

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97
Q

step 6 in NICE asthma treatment ladder? (Vs BTS)

A

Increase the inhaled corticosteroid to a “moderate dose”.

BTS
add oral steroids

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98
Q

other than regular medication, what else is part of asthma management? (1 medical? 1 follow up? 2 conservative)

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? 5

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
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? (5)

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? (9)

A
  • CXR (hyperinflated, exclude: cancer)
  • CT thorax (exclude: fibrosis, cancer, bronchiectasis)
  • echocardiogram - cor pulm
  • ECG (cor pulmonale findings),
  • BMI (weight loss if COPD is severe, gain from steroids)
  • FBC (polycythaemia due to chronic hypoxia)
  • sputum culture (chronic infection)
  • 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 (2)? (+prevention (2))

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? (6)

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? (5)

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? (4)

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 (7): supportive

A

remove / treat underlying cause

SUPPORTIVE

  • O2 at home if hypoxic at rest
  • Stop smoking
  • physio, pulmonary rehab
  • advanced care planning / palliative where needed

VAX = pneumococcal and flu jab

SURGERY 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 (antifibrotic + anti-inflammatory)
  • nintedanib (nintedanib - mAb targeting tyrosine kinase)
159
Q

drugs which can cause pulmonary fibrosis? 4

A
  • amiodarone
  • cyclophosphamide
  • methotrexate
  • nitrofurantoin
160
Q

which conditions can pulmonary fibrosis be secondary to? (5)

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? (*1st line investigation + findings)

A
    • bronchoalveolar lavage
      • raised lymphocytes
      • ^ 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? 4

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? (4)

(key symp, resp exam, trachea position)

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? (4)

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? (6)

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? (4)

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? 3

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? (5)

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? (8)

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? (8)

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? (5)

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

Zero to Finals: Medicine A.S. (11 decks)

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