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IK6 - Exams > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is the treatment for COPD?

A

O SHIT

oxygen
salbutamol
hydrocortisone
ipatropium
thiotropium

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2
Q

Why are COPD patients are higher risk of pneumothoraces?

A

due to bullae formation

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3
Q

what are the respiratory causes of clubbing?

A

carcinoma of bronchus
mesothelioma
abscess
bronchiectasis
empyema
cystic fibrosis

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4
Q

What are the clinical features of extrinsic allergic alveolitis?

A

fever
rigors
dry cough
SOB
coarse end-expiratory crackles
CXR mottling

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5
Q

Bob has a suspected respiratory tract infection. Tests come back with cold agglutinins.

What is the likely pathogen

A

mycoplasm pneumoniae

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6
Q

What organism might cause pneumonia and hyponatraemia?

A

legionella

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7
Q

what are the clinical features of fibrosing alveolitis?

A

SOB, clubbing, fine end-inspiratory crackles

honeycombing and ground glass shadowing on imaging

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8
Q

What are some differentials for unilateral pleural effusions?

A

usually: infection or neoplasm

other important factors:
RA, autoimmune disease, benign asbestos effusion, pancreatitis, haemothorax

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9
Q

what are some causes of ARDS?

A

common = pneumonia, aspiration, severe trauma, sepsis [PASS]

any severe systemic or pulmonary disease may lead to ARDS

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10
Q

what are the respiratory diseases linked to asbestos exposure?

A

BENIGN - pleural plaques, pleural thickening or pleural effusions

INTERSTITIAL LUNG DISEASE -> asbestosis

MALIGNANT = mesothelioma, lung cancer

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11
Q

what respiratory diseases may be caused by aspergillus

A

aspergilloma
allergic bronchopulmonary aspergillosis
invasive aspergillosis

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12
Q

what group of patients are more commonly affected by allergic bronchopulmonary aspergillosus ?

A

asthmatics

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13
Q

what test can be done for ABPA?

A

skin antigen sensitivity test for aspergillus

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14
Q

a 30 year old asthmatic presents to GP with recurrent pneumonia with associated wheeze, cough, fever and malaise.

what might be the underlying pathogen and disease?

A

aspergillus infection of the airways

causing allergic bronchopulmonary aspergillosis

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15
Q

What might one see on CT of invasive aspergillosis?

A

nodules surrounded by ground glass appearance (halo sign)

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16
Q

what is the halo signs associated with?

A

CT finding of invasive aspergillosis

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17
Q

what kind of a hypersensitivity reaction is asthma?

A

type 1

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18
Q

what investigations might one order for diagnosis of asthma?

A

peak flow
pulmonary function tests (obstructive picture - reversible)
bloods - eosinophils, IgE levels, aspergillus antibody titre
skin prick tests to identify allergens

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19
Q

what is the gold standard for diagnosis of asthma?

A

clinical diagnosis on history if strongly suggestive

if not do peak flow or spirometry before and after bronchodilator to demonstrate reversibility of obstruction

FeNO is becoming more commonly used to support asthma diagnosis

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20
Q

what test measures airway inflammation?

A

FeNO
fraction expired nitric oxide

as during inflammatory processes epithelial cells are activated to produce NO

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21
Q

what are the aims of asthma management?

A

no daytime symptoms
no night time waking due to symptoms
no need for rescue medications
no attacks
no limitations on daily activities
normal lung function

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22
Q

describe the long term management of asthma?

A

personalised asthma action plan
avoid triggers and allergens
ensure proper inhaler technique and good preventer compliance

  1. short acting beta agonist
  2. regular ICS + short acting beta agonist (if patient presents with significant symptoms at diagnosis start on step 2)
  3. SABA + ICS + LABA
    if inadequate control with LABA add high dose ICS
    no response to LABA stop and use high dose ICS
  4. high dose ICS and consider adding 4th drug (leukotriene antagonist, slow release theophylline)
  5. low does oral steroids, high dose ICS + steps above, refer for specialist care
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23
Q

what is the management of acute asthma

A
  1. ABCDE approach and resuscitation
  2. monitor O2, ABG and PEFR
  3. high flow oxygen
  4. salbutamol nebulisers (5mg) continuous
  5. ipatropium bromide nebulisers (0.5mg)
  6. steroids 100-200mg IV or 40mg prednisolone. continue for 5-7 days
  7. no improvement = magnesium sulphate, IV aminophylline infusion or IV salbutamol. get senior help

continue to monitor ABGs for normalising CO2 as sign of fatigue
may require anaesthesia and intubation if fatigued

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24
Q

what electrolyte abnormality can asthma treatment cause?

A

hypokalaemia

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25
Q

how do you grade the severity of an acute asthma attack?

A

PEFR 50-75% = moderate
PEFR 33-50% = severe
PEFR < 33% = life threatening
near fatal = hypercapnic, needs mechanical ventilation with increasing inflation pressures

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26
Q

what are the organisms commonly involved in bronchiectasis?

A

H. influenza
Strep. pneumoniae
staph. Aureus
Pseudomonas aeruginosa

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27
Q

whats the aetiology of bronchiectasis?

A

repeated infections with causative organisms

cystic fibrosis, primary ciliary dyskinesia
bronchial obstruction, ABPA, RA
idiopathic (50%)
pneumonia, TB, HIV

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28
Q

what is bronchiectasis?

A

fibrosis and permanent dilation of airways due to chronic/recurrent lung infections

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29
Q

what might one notice on examination of a patient with bronchiectasis?

A

clubbing
coarse inspiratory crackles

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30
Q

what sign is seen on CXR in bronchiectasis patients?

A

tram lines and ring shadows

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31
Q

what is the management of an exacerbation of bronchiectasis?

A

Antibiotics (if known pseudomonas give ciprofloxacin)
ICS
bronchodilators (salbutamol neds/inhaler)
may require chest physio

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32
Q

what are the most serious complications of bronchiectasis?

A 
massive haemoptysis 
cor pulmonale (RHF)
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33
Q

what are the acute features of extrinsic allergic alveolitis?

A

4-6 hrs post exposure
rigors, fevers, myalgia, dry cough, dyspnoea, crackles

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34
Q

what are the chronic features of extrinsic allergic alveolitis?

A

increasing SOB
weight loss
exertional dyspnoea
type I resp failure
cor pulmonale

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35
Q

what are the CXR findings in extrinsic allergic alveolitis?

A 
upper zone mottling/consolidation 
honeycomb lung (chronic)
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36
Q

what are the HRCT findings of extrinsic allergic alveolitis?

A

patchy ground glass shadowing and nodules

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37
Q

what are the OE of idiopathic pulmonary fibrosis?

A

bibasal fine late inspiratory crackles
rarely - clubbing
dry irritation cough
dyspnoea
weight loss, fatigue

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38
Q

what are the types of lung cancer?

A

small cell cancer

non-small cell cancer (squamous, adenocarcinoma, large cell, carcinoid tumours, bronchoalveolar)

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39
Q

what is a pancoast tumour?

A

a lung cancer situated in the lung apices which compresses the sympathetic ganglion chain when large enough. this leads to horners syndrome (miosis, ptosis, anhidrosis)

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40
Q

what are common sites for lung cancers to metastasis to?

A

adrenal gland, bone, brain, liver, other lung

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41
Q

what is pneumoconiosis?

A

fibrosing interstitial lung disease caused by chronic inhalation of mineral dusts

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42
Q

what are the types of pneumoconiosis?

A

simple - asymptomatic
complicated - causing reduced lung function (symptomatic)

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43
Q

what materials or occupations are risk factors for pneumoconiosis?

A

Coalworker
silicosis exposure
beryllium exposure (chronic)
asbestos (causes asbestosis)

occupations: coal mining, quarrying, metal foundries, stone cutting, sandblasting, insulation, construction, plumbers, ship yards

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44
Q

what specific symptom suggests coalworker’s pneumoconiosis?

A

black sputum

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45
Q

what signs may be noted during examination of a patient with pneumonia?

A

tachypnoea, tachycardia, pyrexia
reduced chest expansion
over affected area: dull to percussion, increased tactile/vocal fremitus, bronchial breathing, coarse crepitations

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46
Q

what are the components of the CURB-65 score?

A

confusion (AMTS < 8)
urea ( > 7)
respiratory rate (>30)
blood pressure (low, SBP < 90 or DBP < 60)
age ( >65)

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47
Q

what findings would be detected in a patient with a pneumothorax?

A

may have deviated trachea if tension

resp distress, tachypnoea, cyanosis
increased resonance on percussion, reduced chest expansion, reduced breath sounds, reduced tactile/vocal fremitus

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48
Q

what is the first step of managing a tension pneumothorax?

A

high flow O2
insert a large bore needle/cannula in the 2nd ICS mid-clavicular line on affected side

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49
Q

where is a chest drain inserted?

A

triangle of safety = 4th or 5th ICS mid-axillary line above the rib

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50
Q

what are the risk factors for a PE?

A

previous PE/DVT
clotting disorders
long distance travel
recent immobility
recent surgery
OCP
smoking
malignancy

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51
Q

how does the Well’s score help determine management?

A

considers likelihood of patient having a PE

if < 4 then suggests unlikely and do D-dimer
if > 4 suggests high likelihood of PE so start LMWH therapy and order a CTPA to confirm

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52
Q

what are the skin manifestations of sarcoidosis?

A

lupus pernio, erythema nodosum

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53
Q

what are the drugs used to treat TB?

A

rifampicin, isoniazid, pyrazinamide, ethambutol

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54
Q

what are some of the SE of rifampicin?

A

orange urine
purple tears
hepatitis
induces liver enzymes

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55
Q

what are some of the SE of isoniazid?

A

hepatitis
peripheral neuropathy

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56
Q

what are some of the SE of pyrazinamide?

A

hepatitis
photo sensitivity
gout

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57
Q

what are some of the SE of ethambutol?

A

optic neuritis

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58
Q

what are the skin manifestations of TB?

A

erythema nodosum
lupus vulgaris -> jelly like nodules on face and neck

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59
Q

what are the findings on CXR indicative of TB?

A

abscess/cavitating lesion in the lung apices

miliary TB - fine diffuse shadowing across both lungs

hila lymphadenopathy

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60
Q

what is the test for TB?

A

acid fast bacilli on a ziehl-neelson stain (+ve)

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61
Q

Risk factors for PE

A

clots in legs (DVT), previous PE, recent fracture, malignancy, recent surgery, recent immobility, oral contraceptive pill

long haul flight (immobility)

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62
Q

differentials of pleuritic chest pain

A

5 Ps
Pericarditis
PE
Pneumonia
Pneumothorax
Pleural pathology

sub-diaphragmatic pathology may cause it too e.g. hepatic abscess

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63
Q

differentials for breathlessness

A

seconds: pneumothorax, PE, foreign body

mins/hours: airway inflammation/obstruction, chest infection, acute heart failure

days/weeks: interstitial lung disease, malignancy, large pleural effusion, neuromuscular, anaemia, thyrotoxicosis, any of the above as chronic process

64
Q

what is the management of a PE?

A

give LMWH
start warfarin

continue LMWH until INR within therapeutic levels.

now use DOAC

65
Q

If the FEV1/FVC ratio is > 70% what sort of lung disease might a patient have?

A

restrictive

66
Q

If the FEV1/FVC ratio is < 70% what sort of lung disease might a patient have?

A

obstructive

67
Q

what might cause interstitial/alveolar shadowing on a CXR ?

A

fluid - pulmonary oedema
pus - pneumonia
blood - pulmonary haemorrhage

68
Q

what can cause reticulo-nodular shadowing on a CXR?

A

lung fibrosis

69
Q

what can cause a homogenous shadow on a CXR?

A

pleural effusion
lung or lobar collapse

70
Q

What are organisms that cause an atypical pneumonia?

A

mycoplasma pneumoniae
chlamydia pnuemoniae
legionella pneumoniae

71
Q

What might cause a cavitating lung lesion?

A

infection = Tb, staph, klebsiella

RA, PE, squamous cell carcinoma

72
Q

upper lobe fibrosis causes

A

A TEA SHOP

  • A - allergic bronchopulmonary aspergillosis
  • T - TB
  • E - extrinsic allergic alveolitis
  • A - ankylosing spondylitis
  • S - sarcoidosis
  • H - histiocytes
  • O - occupation (silicosis, berylliosis)
  • P - pneumoconiosis (coal worker’s)
73
Q

causes of lower lobe fibrosis

A

IPAS - BM

  • IP - infection, interstitial pneumonia
  • A - aspiration, alpha-1 anti-trypsin deficiency, asbestosis
  • S - systemic sclerosis, CTD e.g. RA
  • B - bronchiectasis
  • M - medications - busulfan, bleomycin lung toxicity, nitrofurantoin, hydralazine, methotrexate, amiodarone
74
Q

determine pleural effusion type

A

Determining exudative vs transudative

  • Generally consider effusions with protein > 35 g/L as exudative and < 35g/L as transudative
  • But if 25-35 should assess with Light’s criteria to be certain

Fluid considered exudative if Light criteria:

  • Pleural fluid-to-serum protein ratio > 0.5 or
  • Pleural fluid-to-serum LDH ratio > 0.6 or
  • Pleural fluid LDH concentration > 2/3 upper limit of normal for serum LDH
75
Q

causes of exudative effusion

A
  • Infection e.g. pneumonia, TB
  • Malignancy e.g. bronchial carcinoma, mesothelioma, lung metastases
  • Inflammation e.g. RA, SLE, acute pancreatitis
  • Pulmonary infarct e.g. secondary to PE and trauma
76
Q

causes of transudative effusion

A
  • ↑ capillary hydrostatic pressure
    • Heart failure
  • ↓ capillary oncotic pressure
    • Cirrhosis
    • Nephrotic syndrome
    • CKD
    • GI malabsorption or malnutrition e.g. Crohn’s
77
Q

medication causes of fibrosis

A

busulfan, bleomycin lung toxicity, nitrofurantoin, hydralazine, methotrexate, amiodarone

78
Q

management of severe PE in high risk/bleeding patient?

A

IV unfractionated heparin

can be stopped easily and rapidly reversed in event of bleeding while alteplase can’t.

79
Q

bronchitis definition + causes

A

Refers to a condition characterised by inflammation of medium sized airways (bronchials)

  • Predominantly affects smokers
  • Productive cough most days for 3/12, for 2 or more consecutive years

causes

  • viral - most common
  • bacterial
80
Q

management of bronchitis

A

Conservative - mainstay

  • Self-care strategies
    • Anti-pyretic e.g. paracetamol as required
    • Honey
    • OTC with guaifenesin (expectorant), cough suppressants (e.g. dextromethorphan)
  • Smoking cessation
  • Safety net + advise most self-resolve in 3-4 weeks

Medical

  • Antibiotic
    • Indicated: systemically unwell, high risk of complications (immediate or back up)
    • 1st line - oral doxycycline, 200mg on 1st day then 100mg for 4 days PO
      • Alternatives: amoxicillin (if pregnant or < 18)
81
Q

what is the berlin definition of ARDS?

A

ARDS - acute, diffuse inflammatory lung injury

Berlin definition

  1. Acute, onset < 1 week
  2. Bilateral opacities on CXR or CT consistent with pulmonary oedema
  3. PF ratio < 300mg with a minimum of 5cmH2O PEEP or CPAP
    • PaO2/FiO2(ratio of arterial oxygen to fractional inspired O2) severity scaling:
      • 200-300/ <39.9 kPA = mild, 100-200/ <26.6 kPa = moderate, < 100/ <13.3 kPa = severe
  4. Cannot be fully explained by cardiac failure or fluid overload
82
Q

management of ARDS

A
  • Acute
    • A-E approach - airway protection, high flow O2, sepsis 6 + IV Abx, aim MABP > 60mmHg
  • Treat underlying cause + supportive
    • Admission to ICU
  • Managing inflammation
    • Corticosteroids - improvement in ventilator free days, no improvement in mortality
    • IV antibiotics if infective cause is identified, broad spectrum
  • Managing hypoxia
    • CPAP - mild cases, usually not sufficient
    • Mechanical ventilation
    • Prone positioning
    • Inhaled iNO (optimise V/Q mismatch), inhaled prostacyclin (optimise V/Q mismatch)
    • Surfactant replacement therapy
  • Follow-up
    • O/P respiratory clinic for f/up lung function tests
    • Psychological assessment (ICU, ventilation PTSD)
83
Q

what are the asbestos related lung diseases

A
  • Benign: pleural plaques, pleural thickening, benign pleural effusions
  • Interstitial lung disease: asbestosis
  • Malignancy: mesothelioma and lung cancer in particular
84
Q

management of pleural plaques

A
  • 20-60% asbestos exposed → pleural plaques
  • Asx or CP, normal lung function tests
  • reassure once malignancy is excluded
85
Q

asbestosis - definition, pathophysiology, key features

A
  • Diffuse interstitial lung fibrosis manifesting in patients with pleural plaque disease > 10 years after asbestos exposure
  • Latency period: 20-30 years
  • Phys:
    • inhaled fibres → alveolar macrophage alveolitis → active macrophages release cytokines e.g. TNF alpha which initiates fibrosis pathway.
    • Initially lower lobes → extensive fibrosis and honeycombing.
  • PC: SOB, reduced ET, non-productive cough + wheeze, fine bilateral inspiratory crackles, finger clubbing, cor pulmonale
86
Q

management of asbestosis

A
  • Conservative - smoking cessation, pulmonary rehabilitation, optimise any concurrent conditions e.g. COPD
  • Medical
    • Pneumococcal and influenza vaccines
    • O2 therapy to be considered if SpO2 < 89%
      • Long-term O2 therapy indicated on 2 ABG minimum 3 weeks apart while stable - if paO2 < 7.3kPA or paO2 kPa 7.3-8 + one of: secondary polycythaemia, peripheral oedema, nocturnal hypoxaemia, pulmonary hypertension
  • Surgical - lung transplant
  • if death due to → refer to coroner’s, family may get compensation
87
Q

indications for long term oxygen therapy

A

Long-term O2 therapy indicated on 2 ABG minimum 3 weeks apart while stable

  • if paO2 < 7.3kPA
  • paO2 kPa 7.3-8 + one of:
    • secondary polycythaemia, peripheral oedema, nocturnal hypoxaemia, pulmonary hypertension

used for COPD, interstitial lung disease/fibrosis

88
Q

definition of malignant mesothelioma + key features

A
  • Aggressive epithelial neoplasm arising from lining of lung, abdomen or pericardium.
  • Latency: 20-40 years (usually present in 60-90s age)
  • PC: SOB, chest pain (dull, diffuse, progressive), cough (usually dry), constitutional symptoms (FLAWS)
  • Signs: reduced breath sounds, dull to percuss
    • Finger clubbing - secondary to underlying asbestosis usually
    • Pericardial effusion
    • Palpable chest wall mass
    • Metastases - lymphadenopathy, hepatomegaly, bone pain
89
Q

investigations of mesothelioma

A
  • CXR: unilateral pleural effusion, pleural thickening, reduced lung volume, signs of asbestosis
  • CT chest: pleural thickening, enlarged hilar lymph nodes, invasion or spread of cancer
  • Thoracoscopy under LA
    • Pleural fluid sample - straw-coloured or blood stained
    • Pleural biopsy: specimen for pathological diagnosis
  • PET scan: asses primary tumour and look for any metastases
90
Q

management of mesothelioma

A
  • Surgery + chemotherapy (platinum based) + radiotherapy
    • Surgical - extrapulmonary pneumonectomy or lung-sparing debulking procedures, pleurectomy for palliation
91
Q

types of respiratory disease caused by aspergillus fumigates

A
  1. Aspergilloma
  2. Allergic bronchopulmonary aspergillosis (ABPA)
  3. Invasive aspergillosis
92
Q

features of aspergilloma + investigations

A
  • Growth of A. fumigates mycetoma ball in a pre-existing lung cavity occurs (e.g. post TB, infarct, abscess)
  • PC: asymptomatic or haemoptysis (erosion into vessel)
  • Signs:
    • tracheal deviation - indicator of very large aspergilloma
    • dullness in affected lung, reduced breath sounds
  • Investigations
    • CXR: round mass with crescent of air around it (monad sigh), usually in upper lobes
    • CT or MRI: if CXR was unclear
    • Sputum cultures: may be negative if no communication between aspergilloma and bronchial tree
93
Q

management of aspergilloma

A
  • Management
    • Life-threatening haemoptysis → A-E approach, resuscitation with IV fluids + blood, surgical resection of aspergilloma
    • Asymptomatic - observe
    • Symptomatic
      • surgical resection if acceptable pulmonary reserve
      • long term oral itraconazole
94
Q

features of allergic bronchopulmonary aspergillosis (ABPA)

A
  • Hypersensitivity reaction to colonisation of airways/sinuses/lungs with Aspergillus species.
  • Commonly occurs in asthmatics, CF patients, bronchiectasis patients
  • Pathophysiology:
    • Airway colonised → IgE and IgG mediated immune response → release of proteolytic enzymes, mycotoxins and antibodies → airway damage and central bronchiectasis
  • PC:
    • recurrent episodes of pneumonia w/ wheeze + cough + fever + malaise
      • May have large mucus plugs and haemoptysis
  • Signs:
    • wheeze, dullness in affected lung, reduced breath sounds
    • Poor asthma control
    • Associated chronic sinusitis with purulent discharge
95
Q

investigations for ABPA

A
  • Skin test: check for reactivity to aspergillus antigens
  • Bloods: FBC (↑eosinophils), raised serum IgE and IgG
    • ↑ A. fumigates specific IgE and IgG (serology)
  • CXR:
    • transient patchy shadows
    • collapse, distended mucous filled bronchi
    • complication signs = fibrosis in upper lobes or central bronchiectasis
  • CT: lung infiltrates, central bronchiectasis
  • Lung function tests: reversible airflow limitation, reduced lung volume/gas transfer
96
Q

management of ABPA

A
  • 1st line - Oral glucocorticoids, long term, high dose
  • 2nd line - itraconazole
97
Q

features of invasive aspergillosis + Ix

A
  • Disseminated Aspergillus infection affected organ systems outside of respiratory tract
  • immunocompromised
  • can affect any organ, haematogenous spread, causes coagulative necrosis
  • PC
    • SOB, rapid deterioration, septic
    • cyanosis, dull lung, reduced BS
  • Investigations:
    • Serum aspergillus spp IgG - +ve
    • Serum B-glucan - +ve, component of fungal cell wall
    • PCR for aspergillus species - serum, blood
    • Cultures (bronchial lavage fluid, sputum): positive for aspergillus
    • Chest CT: nodules surrounded by ground-glass appearance (halo sign).
      • Due to haemorrhage into surrounding tissue because of fungal infection
98
Q

management of invasive aspergillosis

A
  • Suspected - 1st line: liposomal amphotericin B or echinocandin
  • Confirmed
    • 1st line - anti-fungal agents: variconazole or posaconazole
    • 2nd line - Amphotericin B
    • Reversal or treatment of underlying immunodeficiency
    • Surgical resection of infection foci
  • Prevention - considered in patients with ongoing immunosuppression + previous invasive aspergillosis
    • Prophylactic posaconazole or voriconazole
    • Post-organ transplant - inhaled amphotericin may be used to manage aspergillus colonisation
99
Q

what is a moderate acute asthma attack?

A
  • Increasing symptoms
  • PEF 50-70% best or predicted
  • No features of severe acute asthma attack
100
Q

criteria for severe acute asthma attack?

A

Any one of:

  • PEF 33-50% best or predicted
  • RR > 25 /min
  • HR > 110/min
  • Inability to complete sentences in one breath
101
Q

criteria for life-threatening acute asthma attack

A

Any one of the following:

  • PEF < 33% best or predicted
  • SpO < 92%
  • PaO2 < 8 kPa
  • “normal” PaCO2 (4.6 - 6 kPa)
  • Altered conscious level
  • Exhaustion
  • Arrhythmia
  • Hypotension
  • Cyanosis
  • Silent chest
  • Poor respiratory effort
102
Q

spirometry diagnostic criteria for asthma

A
  • Lung function tests - spirometry with bronchodilator trial
    • Should demonstrate a reversible airway obstruction
    • FEV1/FVC < 70% predicted, FEV1 < 70%
    • Improvement in FEV1 > 12% and ↑ volume 200ml +
103
Q

what is a positive FeNO concentration

A

> 40 parts per billion

104
Q

what are the criteria for near fatal asthma attack?

A

Raise PaCO2 and/or requiring mechanical ventilation with ↑ inflation pressures

105
Q

acute management of asthma

A

ABCDE approach

  1. Monitor oxygen saturations, RR, HR. regular ABG and PEFR
  2. High flow oxygen, aim for 94-98%
  3. Salbutamol nebulisers
    • 5mg, continuous with oxygen.
    • Once improved give 2-4 hourly and slowly increase gap
    • Monitor potassium level can cause ↓ K+ serum
  4. Ipratropium bromide nebuliser (0.5mg 4-6 hourly)
  5. Steroid treatment
    • 40-50mg prednisolone PO - continue until recovery, minimum 5 days
    • 100-200mg IV hydrocortisone (2nd line)
  6. If no improvement urgent senior review/ICU. Treatment can consider:
    • IV Magnesium sulphate (1st line IV treatment, 1.2-2g IV infusion over 20 minutes)
    • IV aminophylline infusion
    • IV salbutamol
  7. Intubation and mechanical ventilation
    • Indicated in exhaustion
    • Signs may be required include ↓ GCS, normal or rising PCO2
  • Admission - severe, life-threatening or near-fatal attack. Consider in moderate depending on clinical circumstance
106
Q

what are the discharge criteria following asthma attack (adult)

A
  • PEFR > 75%
  • Diurnal variation < 25%
  • Correct inhaler technique demonstrated
  • Stable on discharge medication for 24 hours
  • Patient must leave with bronchodilator + steroids + follow up appointment
107
Q

aims for asthma care

A
  • no daytime symptoms
  • no night-time waking due to asthma
  • no need for rescue medication
  • no attacks
  • no limitations on activity
  • normal lung function (FEV1 and/or PEF > 80% predicted or best)
  • Minimal side effects from medications
108
Q

medical management of asthma (NICE)

A
  1. Short-acting beta-agonist (SABA) reliever inhaler
    • Salbutamol (2-10 puffs, repeat every 10-20 minutes)
  2. Add low dose inhaled corticosteroid (ICS) BD
    • SABA + ICS
    • Low does < 400 micrograms budesonide or equivalent
  3. Add leukotriene receptor antagonist (LTRA)
    • SABA + ICS + LTRA
    • e.g. Montelukast, PO
  4. Add Long-acting beta-agonist (LABA)
    • Continue LTRA depending on response
    • SABA + ICS + LABA + LTRA
    • e.g. salmeterol (inhaled)
  5. Switch LABA/ICS to maintenance and reliever therapy which has low-dose ICS
    • SABA + MART + LRTA
  6. Increase dose of ICS steroids to medium dose
    • Medium/moderate dose is 400-800 micrograms budesonide or equivalent
    • SABA + MART with medium dose ICS + LRTA
    • SABA + LABA + medium dose ICS + LTRA
  7. Referral to specialist
    • May consider high dose ICS as fixed dose (not part of MART)
      • > 800 micrograms of budesonide or equivalent
    • Trial additional drugs
    • Biologics - only under specialist prescription + monitoring
109
Q

what are the biologics used in asthma?

A
  • Omalizumab - for difficult and severe asthma, for confirmed allergic IgE asthma
  • Mepolizumab - severe refractory eosinophilic asthma
  • Benralizumab or reslizumab - add on for severe eosinophilic asthma
110
Q

what drugs are contraindicated/cautioned in asthmatics?

A
  • Beta-blockers
  • NSAIDs
  • ACEi
  • Adenosine
111
Q

what is the BTS medical management for adult asthma?

A
  1. SABA + low dose ICS
  2. SABA + low dose ICS + LABA (salmeterol)
    1. can consider mart
  3. SABA + LABA + medium dose ICS or LTRA
    1. consider stopping LABA is no response
  4. specialist
112
Q

definition and causes of bronchiectasis

A

Persistent or progressive chronic disease characterised by permanent dilatation of bronchi following irreversible damage to elastic and muscular components of bronchial wall

  • causes
    • Idiopathic (40%)
    • Post-infectious after severe LRTI → most common cause
      • Common pathogens: H. influenzae (20-40%), P. aeruginosa (10-30%), M. Catarrhalis, S. Pneumoniae, S. Aureus, Enterobacteriaceae
    • Aspiration or inhalation injury
    • COPD
    • Asthma
    • Disorders of mucociliary clearance - e.g. PCD
    • Endobronchial tumours
    • ABPA
    • Immunodeficiency - hypogammaglobulinemia
    • CTD + IBD - e.g. RA
113
Q

investigations for bronchiectasis

A
  • Bedside
    • Sputum MC&S - identify colonising pathogens
  • Bloods
    • FBC (infection), CRP (infection)
    • serology - aspergillus, asses immunodeficiency
    • HIV test
    • Alpha-1 antitrypsin deficiency (exclude as cause)
  • Imaging
    • CXR
      • cystic shadows, thickened bronchial walls (tramline and ring shadows). Dilated airways. May see atelectasis
    • HRCT - diagnostic, signet ring sign, dilated bronchi with thick walls
  • Specialist or scoring
    • Spirometry - obstructive picture
    • Bronchoscopy
    • CF testing - sweat test or genetic testing
      • All children, adults up to 40 years and those > 40 with features of CF
    • PCD testing - children where no other cause found, Hx of rhinitis (continuous), neonatal resp. distress, dextrocardia
114
Q

management of bronchiectasis acute

A
  1. Admit if: sig. comorbidities, severely unwell (e.g. cyanosis, confusion, marked SOB or respiratory distress, peripheral oedema, temp > 38)
  2. Antibiotics (adult)
    • 1st line
      • amoxicillin 500mg TDS 7-14/7
      • doxycycline 200mg 1st day then 100mg OD 7-14/7
      • Clarithromycin 500mg BD 7-14/7
    • If high risk for treatment failure consider co-amoxiclav
    • 1st line IV (severely unwell or unresponsive to oral Abx) - co-amoxiclav, piperacillin with tazobactam
  3. Bronchodilators as required
115
Q

long term management of bronchiectasis

A

Review/referral to secondary care - high risk of future exacerbations

  • > 3 exacerbations/year
  • Chronic Pseudomonas, MRSA or non-TB mycobacterial colonisation
  • Deteriorating with ↓ lung function, advanced, ? transplant
  • Long-term antibiotics therapy
  • Associated: RA, immunodeficiency, IBD, APBA, PCD

Long term management

  • Conservative
    • Smoking cessation
    • Respiratory physiotherapy → airway clearance
    • Patient education + support group
  • Medical
    • Annual influenza vaccination, up to date on pneumococcal
    • Antibiotic prophylaxis - > 3 exacerbations/year under specialist advice
      • 1st line: azithromycin 500mg 3x/week, azithromycin 250mg OD, erythromycin ethyl succinate 400mg BD
    • Mucolytic - ↓ viscosity of sputum e.g. Carbocysteine, nebulised saline
    • Bronchodilators e.g. salbutamol - if comorbid asthma, COPD or ABPA
    • ABPA - corticosteroids (prednisolone)
  • Surgical
    • Radiological embolization or surgical intervention for haemoptysis
    • Lung transplant
116
Q

conservative management of COPD

A
  • Stop smoking
  • Nutritional support
  • Flu and pneumococcal vaccination
  • Pulmonary rehabilitation
    • Offered if MRC grade 3 or above
  • Chest physiotherapy - beneficial for patients with significant mucus production
  • Minimum annual review
117
Q

mMRC (modified medical research council) scale of COPD

A
  • 0 only breathless with strenuous exercise
  • 1 SOB when hurrying or walking slightly uphill
  • 2 slower than average person (same age); need to stop for breaks
  • 3 stop for breath after walking 100m or after a few minutes
  • 4 too breathless to leave the house; breathless when dressing
118
Q

long term medical management of COPD

A
  1. SABA or SAMA - used for symptom relief, retained through all steps
    • Salbutamol (SABA), ipratropium bromide (SAMA)
  2. Assess for asthmatic features of still uncontrolled
    • Asthmatic features - previous diagnosis of asthma/atopy; ↑ blood eosinophil could; substantial FEV1 over time (>400ml) or diurnal variation in PEFR (at least 20%), evidence of steroid responsiveness
    • Asthmatic features → add LABA + ICS
      • e.g. symbicort (LABA + ICS)
    • No asthmatic features → add LABA and LAMA
      • LAMA - tiotropium, glycopyrronium, aclidinium
      • LABA - salmeterol, formoterol, vilanterol
  3. 3 month trial of LAMA + LABA + ICS
    • If no improvement return to previous regime
    • Indicated: ongoing daily symptoms or 1 severe exacerbation/year or 2 moderate exacerbations/year
  4. Specialist referral
    • Long-term oxygen therapy
119
Q

what are the asthmatic features in COPD?

A

Asthmatic features - previous diagnosis of asthma/atopy; ↑ blood eosinophil could; substantial FEV1 over time (>400ml) or diurnal variation in PEFR (at least 20%), evidence of steroid responsiveness

120
Q

what are the surgical management options for COPD?

A
  • Bullectomy
  • Lung volume reduction surgery
    • Consider if:
      • Upper lobe predominant emphysema
      • FEV1 < 20% predicted
      • PaCO2 < 7.3 kPa
      • TICO > 20% predicted
121
Q

management of acute exacerbation of COPD

A
  1. Ensure patent airway
  2. Ensure oxygen saturations of 88-92%
    • Venturi masks to titration of O2 if known CO2 retainer, start on blue 24%
    • Repeat ABG 1 hour after altering oxygen level
    • Aim to raise PO2 > 8 kPa with < 1.5 kPa rise in CO2
  3. Nebulisers
    • salbutamol (5mg, back-to-back)
    • ipratropium bromide (0.5mg every 4 hours)
    • Should be air driven
  4. Steroids - oral prednisolone (30 mg, 5 days) or IV hydrocortisone (200mg) if severe
  5. Antibiotics - if evidence of infection e.g. fever, ↑ inflammatory markers
    • 1st line - 5 days of either: amoxicillin 500mg TDS for severe infection, doxycycline 200mg 1st day then 100mg OD or clarithromycin 500mg BD
    • IV or PO depending on severity
  6. Further support - ITU/HDU
    • IV aminophylline - under senior review/instruction
    • Non-invasive ventilation e.g. BiPAP (always required if hypercapnic)
      • Indications for NIV: respiratory alkalosis (7.25-7.35), T2RF, cardiogenic pulmonary oedema, weaning from tracheal intubation
    • Intubation - pH < 7.25, continuing to deteriorate
122
Q

definition of COPD

A

Chronic, progressive lung disorder characterised by irreversible airflow obstruction

Associated with:

  • Chronic bronchitis - chronic cough + sputum production on most days for at least 3/12 in a year over 2 consecutive years
    • Hypertrophy and hyperplasia of mucus glands in bronchi
  • Emphysema - pathological permanent destructive enlargement of air spaces distal to terminal bronchioles with destruction of alveolar walls
123
Q

pathophysiology of CF and most common mutation

A

AR condition caused by a number of gene mutations which result in impaired or complete loss of function of CFTR leading to impaired chloride transport with systemic effects.

  • delta F508 (class II defect)
124
Q

definition of extrinsic allergic alveolitis

A

Interstitial inflammatory disease of distal gas-exchanging parts of lung secondary to exposure to inhaled organic allergens

  • form of ILD
  • aka hypersensitivity pneumonitis
  • type III hypersensitivity reaction (Ag-Ab immune complex formation)
125
Q

types of hypersensitivity pneumonitis

A
  • Farmer’s lungs - one of the most common
    • Due to exposure to mouldy hay, major antigen is Saccharopolyspora Rectivirgula
  • Bird-fanciers - one of the most common
    • Avian proteins e.g. proteins in bird dropping
    • Pigeons, parakeets
  • Malt workers lung due to aspergillus clavatus in mouldy malt
126
Q

presentation of hypersensitivity pneumonitis

A
  • 4-6 hours post exposure → reversible episodes of:
    • fever, rigors
    • Myalgia
    • dry cough
    • Dyspnoea
    • crackles (no wheeze) → wheeze and productive cough may develop if repeat high-level exposure
    • Rarely - can develop life threatening respiratory failure with respiratory distress + cyanosis
  • Chronic:
    • increasing dyspnoea, exertional dyspnoea
    • fine inspiratory crepitations
    • Weight loss
    • type I respiratory failure, cor pulmonale
127
Q

investigations for hypersensitivity pneumonitis

A
  • Full occupational history as well as hobbies and pets
  • Bloods
    • FBC (↑ neutrophils)
    • ESR (↑)
    • ABG (low PO2 and normal CO2 - type 1 respiratory failure, severe)
    • Serology - IgG for fungal or avian antigens
  • Imaging
    • CXR
      • upper zone mottling/consolidation, hilar lymphadenopathy (rare), honeycomb (late, severe)
      • During acute may be normal
    • High resolution CT - patchy “ground glass” shadowing and nodules
  • Specialist or scoring
    • Pulmonary function test - restrictive, ↓ gas transfer, ↓ total lung capacity
    • Bronchoalveolar lavage - ↑ lymphocytes and mast cells
128
Q

management of hypersensitivity pneumonitis

A

Conservative - Avoid exposure

Medical

  • Steroids - acute or long term
  • Immunosuppressants or immunomodulators in advanced disease with fibrosis
129
Q

investigations for idiopathic pulmonary fibrosis?

A
  • Diagnosis should be made by specialist ILD respiratory consultant
  • Bedside
    • O2 sats and RR
  • Bloods
    • ABG (normal early, late PO2 ↓ & ↑PCO2 (type 2))
  • Imaging
    • CXR - areas of opacities
      • early shows ground glass shadowing
      • late shows reticulonodular shadowing, cor pulmonale signs, honeycombing
    • High resolution CT - diagnostic, increased reticulation, honeycombing, possible traction bronchiectasis
    • Echocardiogram - assess heart
  • Specialist or scoring
    • Pulmonary function tests (spirometry) - restrictive changes (↓FVC, ↓TLC)
    • Lung biopsy - gold standard, not always needed
    • BAL - exclude ?infection or ?malignancy
    • 6 minute walk test
130
Q

management of IPF?

A

best supportive care pathway within a specialist respiratory MDT.

  • Conservative
    • Chest physiotherapy
    • Pulmonary rehabilitation
    • Smoking cessation
  • Medical
    • Anti-fibrotic - Pirfenidone, ninatadinib
      • Slows FVC decline by around 100ml/year
      • NICE eligibility - must have FVC between 50-80%
        • Treatment must stop of FVC falls below 50 or if FVC falls > 10% in 12 months
    • Managing cough - major symptom, ↑ can ↑ QOL
      • Anti-tussives
      • Optimise Tx if GORD, seasonal rhinitis and post-nasal drip
      • Consider opioids for debilitating cough
      • Thalidomide - under respiratory consultant advice only
    • Immunosuppressants
    • Long-term oxygen therapy
  • Surgical
    • Transplant

median survival 2-4 years from diagnosis

131
Q

features of small cell lung cancer

A
  • 20-25%
  • Centrally located, proximal bronchi
  • Associated with smoking
  • Neuroendocrine tumour
  • Paraneoplastic syndromes
    • Ectopic ACTH
    • Lambert-Eaton syndrome
  • Associated with cerebellar degeneration
  • Highly malignant, metastases early → bone, adrenal, liver, brain
132
Q

features of SCC lung cancer

A
  • 30-50%
  • RF - M > F
  • Closely associated with smoking
  • Central tumours, may have cavitation
  • Bronchus obstruction → ↑ frequency and risk of infections
  • Associated with hypercalcaemia
    • PTH/PTHrP secreting → primary hyperparathyroidism
    • May secrete ectopic TSH (rare)
  • Local spread with late metastasis
  • Less responsive to chemotherapy
  • most common in smokers
133
Q

features of adenocarcinoma lung cancer

A
  • 20-30%
  • Now recognised as most common lung cancer
  • F, non-smokers
  • Malignancy epithelial tumour with glandular differentiation or mucin production
  • Peripherally located, metastases early (brain and bone)
  • most common in non-smokers
134
Q

features of large cell carcinoma lung CA?

A
  • 10-15%
  • Poorly differentiated malignancy epithelial tumour - large cells, large nuclei, prominent nucleoli
  • Poor prognosis
  • Can use beta-HCG to monitor
  • Early metastases
135
Q

features of carcinoid tumour

A
  • Non-small cell cancer
  • Rare
  • Release vasoactive substances → carcinoid syndrome
136
Q

what are the paraneoplastic syndromes associated with lung cancer

A
  • Associated paraneoplastic
    • Lambert Eaton - haemoptysis, weight loss, tired, bilateral ptosis, proximal weakness improving with testing (SCLC)
    • ADH → SIADH, hyponatraemia (SCLC)
    • ACTH → Cushing’s (SCLC)
    • PTH → primary hyperparathyroidism, ↑ Ca2+, bone pain (SCC)
    • Calcitonin → hypercalcaemia
    • Ectopic TSH → hyperthyroidism (SCC)
    • Serotonin → carcinoid syndrome: flushing, diarrhoea, bronchoconstriction
    • Bradykinin → cough
137
Q

assessment of suspected lung CA and 2WW rulse

A

2WW appointment:

  • CXR findings suggestive of lung cancer
  • > 40 with unexplained haemoptysis

Urgent CXR (within 2 weeks) if > 40 + 2 sx or ever smoked + 1 unexplained sx:

  • Cough
  • Fatigue
  • SOB
  • Chest pain
  • Weight loss
  • Appetite loss

Consider urgent CXR in > 40 with any of:

  • Persistent or recurrent infection
  • Clubbing
  • Supraclavicular LN ↑ or persistent cervical LN ↑
  • Chest signs of lung CA
  • Thrombocytosis
138
Q

management of lung cancer

A
  • conservative
    • MDT, smoking cessation
  • small cell lung CA
    • worse prognosis
    • surgical resection in early stage
    • later → combination cisplatin based chemotherapy
  • non small cell lung CA
    • surgical resection - 20% candidates, need FEV1 > 1.5L
    • radiotherapy
    • chemotherapy - platinum based regimes
    • biologics - TKI erlotinib, PD-1 antagonist nivolumab, EGFR cetiximab
139
Q

management of OSA

A
  • Conservative
    • Smoking cessation
    • Maintaining healthy weight
  • Medical
    • Concurrent nasal congestion/rhinitis - trial topical nasal corticosteroids (vasomotor, allergic) or antihistamines (allergic)
    • Home CPAP
      • May require mandibular advancement splint
  • Surgical
    • Tonsillectomy with large obstructive tonsils + BMI < 35
    • Refer for oropharyngeal surgery opinion if severe OSA and unable to tolerate CPAP or splint after few attempts
140
Q

definition of OSA

A

OSA is characterised by intermittent closure/collapse of the pharyngeal airway leading to apnoeic episodes during sleep which is terminated by partial arousal

  • Cessation of airflow is usually around 10 seconds
141
Q

what is pneumoconiosis and what are the types?

A

Pneumoconiosis refers to a group of pulmonary conditions which arise from inhalation and retention of mineral dusts resulting in fibrotic changes (fibrous interstitial lung disease)

Types

  • Asbestosis - most common, can cause diffuse parenchymal fibrosis
  • Coal worker’s pneumoconiosis - 2nd most common
  • Silicosis - inhalation of silica
  • Berylliosis - inhalation of beryllium chronically
    • Aerospace, nucleur, telecommunications or electrical industries
  • Pulmonary siderosis - associated with inhalation of metallic particles e.g. metal grinding or welding, low long-term morbidity
142
Q

investigations for pneumoconiosis

A
  • Bedside
    • full occupation Hx
      • Sputum sample - exclude infective component
  • Bloods
    • CXR
      • Simple - nodular interstitial lung disease
      • Progressive massive fibrosis- evidence of massive fibrosis, large + nodular fibrotic masses
      • Upper lobe fibrosis - coal and silica
      • Staging
        • 1 - some opacities but normal lung markings visible
        • 2 - large number of opacities but normal lung markers visible
        • 3 - large number of opacities with normal lung not visible
    • High resolution CT - fibrosis
  • Imaging
  • Specialist or scoring
    • Lung function tests - normal (simple) or mixed obstructive + restrictive picture with ↓ lung volumes and gas transfer
    • Bronchoscopy: allows visualisation and bronchoalveolar lavage
    • Beryllium lymphocytes proliferation test: required to diagnose chronic beryllium disease. Positive result = diagnosis
143
Q

management of pneumoconiosis

A
  1. Avoidance of trigger
  2. Management by respiratory team
    • Pulmonary rehabilitation
    • Consider corticosteroids if chronic berylliosis
    • Bronchodilator if concurrent COPD
    • Consider home O2 if hypoxia
    • End stage respiratory failure consider if candidate for transplant
  3. Smoking cessation - if also smoking
  4. Notify authorities
144
Q

what are the typical pneumonia organisms?

A
  • Streptococcus pneumoniae (70% of CAP)
  • Haemophilus influenzae (2nd most common)
  • Morexalla catarrhalis
  • Group A streptococci
  • Klebsiella pneumoniae
  • Staphylococcus Aureus
145
Q

what are atypical pathogens of CAP?

A
  • Chlamydia pneumonia
  • Mycoplasma pneumoniae
  • Legionella
  • Chlamydia psittaci
  • C. burnetti (farm animals, hepatitis, travel)
  • B. pertussis (whooping cough in unvaccinated)
  • M. tuberculosis (see TB notes)
146
Q

features of strep. pneumoniae pneumonia

A
  • Rusty-coloured sputum
  • Lobar on CXR usually
  • Unvaccinated at risk
  • Associated with cold sores
  • +ve diplococci
  • Optochin sensitive
147
Q

features of haemophilus influenzae pneumonia

A
  • Associated with smoking and COPD
  • Gram -ve cocco-bacilli
148
Q

features of M. Cattarhalis pneumonia

A
  • Associated with smoking
  • Gram -ve cocci
149
Q

features of S. Aureus pneumonia

A
  • Associated with recent viral infection, often post-flu
  • May have cavitation on CXR
  • Gram +ve cocci (“grape-bunch clusters”
150
Q

features of Klebsiella pneumonia

A
  • Alcoholism
  • Elderly
  • Haemoptysis
  • Gram -ve rod
  • Enterobacteriaceae
151
Q

management of pneumonia (CAP)

A
  1. Place of care:
    • CURB score dependent - 1 → home, 2 → admission, 3+ → ITU
  2. Antimicrobial treatment
    • Typical CAP
      • Mild-moderate → 1st line - penicillin (amoxicillin) or macrolide (clarithromycin) for 5 days
      • Moderate-severe → penicillin + macrolide (co-amoxiclav + clarithromycin)
    • Atypical CAPs
      • General - macrolide or tetracycline e.g. clarithromycin or doxycycline
      • Legionella - macrolide + rifampicin
      • S. Aureus - flucloxacillin
  3. Supportive treatment
    • Oxygen, IV fluids, Analgesics
    • CPAP/BiPAP/mechanical ventilation as required
    • Surgical drainage of abscess or empyema
152
Q

Tx for aspiration pneumonia

A

cefuroxime + metronidazole (must have gram negative + anaerobic cover)

153
Q

treatment of HAP

A
  • General
    1. Ciprofloxacin + vancomycin
    2. Piptazobactam + vancomycin
  • Pseudomonas spp. - Piperacillin + tazobactam or ciprofloxacin + gentamicin
  • MRSA - vancomycin
154
Q

pneumothorax treatmetn

155
Q

TB investigations

A
  • Bedside
    • Sputum sample
      • MC&S with Ziehl Neelson or Auramine stain - require 3 +ve
        • Acid fast bacilli seen
        • Culture with Lowenstein-Jensen media
      • PCR - GeneXpert, resistance testing, paeds (paucibacillary)
  • Bloods
    • FBC, U&Es, LFTs, CRP
    • HIV test - prior to starting treatment
    • Hepatitis screen - prior to starting treatment
  • Imaging
    • CXR
      • Latent - Gohn focus in upper lobes
      • Primary - peripheral consolidation, hilar lymphadenopathy
      • Miliary - fine shadowing, diffuse, “millet-seeds” appearance
      • Post-primary - upper lobe shadowing, streaky fibrosis, cavitation, calcification, pleural effusion, hilar lymphadenopathy
    • Spinal x-ray - if concern about Pott’s disease
    • CT/MRI - if CNS involvement
  • Specialist or scoring
    • Mantoux/Heaf test - latent TB, offered after close contact, large wheel after 72hrs is +ve
      • +ve if had BCG
      • < 6 mm negative, 6-15mm hypersensitivity, > 15mm +ve likely infection
    • Interferon gamma (IGRA) - demonstrates exposure of host T cells to TB previously → interferon release
      • Cannot differentiate latent vs active
      • Less useful in young or immunosuppressed
      • Not affected by prior BCG
    • Lumbar puncture - suspicion of CNS infection
    • Non-pulmonary site biopsy
156
Q

Drug causes of fibrosis

A

BANS ME Bleomycin, busulfan Amiodarone Nitrofurantoin Sulfasalazine Methotrexate

IK6 - Exams (24 decks)

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