Title: Respiratory and Thoracic

Q: What proportion of asthmatics develop before age 10?
A: 50%

Q: What are the two major patterns of asthma presentation?
A: Acute severe asthma (90%) and hyperacute (10%) within 3 hours

Q: Cardiovascular effects of critical asthma
A: Critical negative intrapleural pressure leads to:
 - Increased venous return
 - RV failure
 - Impaired LV filling
 - Increased LV afterload
 - Impaired CO
 - Pulsus paradoxus

Q: Risk factors for death from asthma
A: Past history of severe exacerbation
2 or more hospitalisations in last 12 months
>3 ED visits in last 12 months
>2 canisters per month of SABA
Difficulty perceiving severity
Low SES
Illicit drug use
Psychiatric disease
Medical comorbidities

Q: Mild asthma
A: Dyspnoea with activity
Whole sentences
PEF >70% predicted

Q: Moderate asthma
A: Dyspnoea interferes with usual activity
PEF 40-70% predicted

Q: Severe asthma
A: Dyspnoea at rest
Speaks in words
PEF <40% predicted

Q: Life-threatening asthma
A: Cannot speak
Drowsy
Perspiring
Cyanotic
Desaturation
PEF <25% predicted

Q: DDx of critical asthma
A: CCF
Upper airway obstruction
Multiple PE
Tumor/mass endobronchial obstruction
Vocal cord dysfunction syndrome
Anaphylaxis

Q: Proportion of drug delivered with MDI and spacer to airways?
A: 20% max

Q: Salbutamol dosing
A: Mild/moderate - 6-12 puffs 100mcg MDI q20min for 3 doses then PRN with slow titration
Severe - 12 puffs 100mcg MDI or 5mg nebs q20min for 3 doses then 2.5-10mg every 1-4 hours as required
Life-threatening - 2x5mg nebs continuously until dyspnoea improved

Q: Ipratropium dosing
A: 500mcg neb or 8x18mcg MDI via spacer q20min for 3 doses then q4-6hr

Q: Steroid dose in acute asthma
A: Prednisone 50mg daily until PEFR >70% predicted or 5-10 days as outpatient
OR Hydrocortisone 100mg q6h if inpatient
OR Hydrocortisone 200mg q6h for 1-3 days weaned as able in ICU

Q: Which patients with asthma should receive inhaled corticosteroids?
A: Mild persistent and greater
Moderate/severe exacerbation

Q: Define status asthmaticus
A: Acute severe asthma that does not respond to usual doses of inhaled SABA and steroids

Q: Dose of Mg in severe asthma
A: 5-10mmol (1.2-2g) over 20 minutes
50mg/kg in children

Q: Ketamine dose in acute severe asthma
A: 0.2mg/kg IV bolus then 0.5mg/kg/hr infusion

Q: IV salbutamol dose in acute severe asthma
A: 250mcg bolus then 1-20mcg/min
In children 5mcg/kg/min for 1 hr then 1-2mcg/kg/min

Q: Benefits of NIV in acute severe asthma
A: Reduces intubation rates, clinical improvement and hospitalisation

Q: Absolute indications for intubation in asthma
A: Deteriorating consciousness
Severe exhaustion
Arrest

Q: pH target in respiratory acidosis from acute severe asthma
A: >7.2

Q: Target Pplat and iPEEP in acute severe asthma
A: Pplat <25 and iPEEP <12

Q: Management of pneumothorax in asthma
A: Reduce RR immediately to prevent PTX to other lung
Surgical ICC only

Q: Plan for post-intubation hypotension in asthma
A: Disconnect
Mechanically exhale
Slow RR
Fluid load + vasopressors
Auscultate for PTX
Check etCO2 and ECG
Urgent CXR
Treat cause
Consider ECMO/heliox

Q: Aminophylline dose for acute severe asthma
A: Aminophylline - 10mg/kg load over 60 min then 0.5mg/kg/hr (target level 30-80micromol/L)

Q: Risks of aminophylline
A: Arrhythmia
Seizures

Q: Discharge plan for asthma
A: Well
Salbutamol no more than 3 hourly
PEFR/FEV1 >70% predicted
No risk factors
Education re: spacer, ICS
Supply of appropriate meds
Asthma action plan
GP f/u
Good social situation

Q: Organisms in bronchitis
A: Viral - Influenza, Parainfluenza, RSV, coronavirus, adenovirus, rhinovirus
Atypical - Mycoplasma, Chlamydia, B. pertussis

Q: Influenza symptoms
A: Myalgia, weakness, cough, nasal congestion, SOB

Q: Incubation period of pertussis
A: 1-3 weeks

Q: Bronchitis presentation
A: Cough >5 days (URTI prior to this) +- bronchial hyperreactivity

Q: How to differentiate bronchitis and pneumonia clinically:
A: Need all 5 of:
HR <100
No focal chest crepitations
No fever
RR <24
Age <65

Q: When are antibiotics recommended for bronchitis?
A: If suspected Mycoplasma, B. pertussis or Chlamydia

Q: Benefits of oseltamivir?
A: Reduces symptoms by 1 day if treated with 48 hours
Can prevent pneumonia and hospitalisation

Q: Indications for oseltamivir
A: Suspected influenza in those with risk of complications or hospitalised

Q: How long should oseltamivir treatment be continued for?
A: 75mg BD for 7-10 days

Q: How long do CXR findings appear over in ARDS?
A: 12-24 hours

Q: Definition of mild ARDS
A: P:F 200-300

Q: Definition of moderate ARDS
A: P:F 100-200

Q: Definition of severe ARDS
A: P:F <100

Q: Mortality of mild ARDS
A: 27%

Q: Mortality of moderate ARDS
A: 32%

Q: Mortality of severe ARDS
A: 45%

Q: Risk factors for ARDS
A: Severe pulmonary sepsis
Severe non-pulmonary sepsis
Multitrauma
Aspiration
Blood transfusion
Drug overdose
Pancreatitis

Q: Benefits of BiPAP in ARDS
A: May prevent intubation and improve mortality in mild ARDS
Likely harmful in moderate/severe

Q: What did the ARDS-Network trial show?
A: Lung protective ventilation reduced mortality from 40% to 30%

Q: Pplat goal in ARDS
A: <30

Q: Benefits of PEEP
A: maximal recruitment of alveoli
Minimises cyclic atelectasis and shear trauma
Minimises de-nitrogenation atelectasis and oxygen toxicity (lower FiO2)

Q: Benefits of steroids in ARDS
A: Early use (<14 days) and prolonged (>7 days) reduces mortality and accelerates resolution

Q: Define bronchiectasis
A: Abnormal and permanent bronchial dilatation

Q: What proportion of bronchiectasis patients are women?
A: 2/3

Q: Causes of bronchiectasis
A: Pseudomonas, Haemophilus, S. aureus, Klebsiella, Anaerobes
Adenovirus, influenza
Bordatella pertussis
TB (developing)
Primary ciliary dyskinesia
CF

Q: Clinical presentation of bronchiectasis
A: Persistent sputum production, haemoptysis, fatigue, weight loss, clubbing

Q: CXR signs of bronchiectasis
A: Tram tracks, bronchial dilatation > vascular, ring shadows

Q: Treatment of acute exacerbations of bronchiectasis
A: Amoxicillin 1g QID PO (guided by previous colonisation/sensitivities)
If Pseudomonas colonised - Cipro or IV anti-pseudomonal

Q: Direct signs of lung collapse on CXR
A: Interlobar fissure displacement
Loss of aeration
Silhouette sign
Crowding of vessels/bronchi

Q: Indirect signs of collapse on CXR
A: Hemidiaphragm elevation
Mediastinal shift towards collapse
Hilar elevation or depression
Compensatory hyperinflation
Crowded ribs

Q: What suggests poor chronic asthma control?
A: Any night symptoms
Any limitation of activity
>2 times per week bronchodilator use
Daytime symptoms >2 times per week

Q: When are inhaled corticosteroids warranted in chronic asthma management?
A: Symptoms > twice per month despite SABA

Q: What proportion of asthmatics deteriorate with aspirin?
A: 1%

Q: Which asthmatics typically deteriorate with aspirin?
A: Perennial rhinitis, nasal polyps in non-atopic patients with late-onset asthma

Q: What proportion of asthmatic pregnant patients deteriorate/get better/stay the same?
A: 1/3 each

Q: How much does perinatal mortality increase with asthma?
A: 2x

Q: Which steroid should be used for asthma therapy in pregnant women?
A: Prednisolone (as foetal liver cannot convert to prednisone)

Q: What proportion of asthmatics smoke?
A: 20%

Q: What is bronchopulmonary aspergillosis?
A: Allergic response to spores of Aspergillus fumigatus

Q: How does BPA present?
A: Worsened asthma, haemoptysis, brown sputum, bronchiectasis

Q: Define chronic bronchitis
A: Chronic productive cough/sputum production for >3 months of 2 consecutive years

Q: What proportion of smokers will develop COAD?
A: 15%

Q: What proportion of COAD patients have co-existent asthma?
A: 27%

Q: Diagnostic threshold for COAD?
A: FEV1:FVC <0.7

Q: What is the best measure of COAD severity and prognosis?
A: % FEV1

Q: Define mild COAD
A: Breathless on moderate exertion
Little to no effect on daily activities
FEV1 60-80% predicted

Q: Define moderate COAD
A: Breathless on level ground
FEV1 40-59%

Q: Define severe COAD
A: Breathless on minimal exertion
Daily activities severely limited
FEV1 <40%

Q: Management of chronic COAD
A: Home O2 if qualifies
LABA + tiotropium +- ICS + PRN salbutamol
Smoking cessation
Pulmonary rehab
Pneumococcal and influenza vaccination

Q: What proportion of COAD patients benefit from long-term steroid use?
A: 20-30%

Q: Benefits of tiotropium in chronic COAD
A: Reduces exacerbations, improved lung function, dyspnoea and QoL

Q: Do LABA's improve mortality in COAD?
A: no

Q: At what duration do oral steroids need tapering?
A: 14 days

Q: Which chronic COAD patients warrant ICS therapy?
A: Frequent exacerbations despite LABA/LAMA therapy

Q: Which pneumococcal vaccine is preferred in the elderly?
A: 13-valent vs. polyvalent as is more immunogenic in the elderly

Q: What proportion of COAD exacerbations are infective?
A: 75%

Q: What proportion of COAD exacerbations are bacterial?
A: 50%

Q: Define hyperinflation on CXR
A: >10 ribs posteriorly
>6 ribs anteriorly
Flattened diaphragms

Q: Define right heart strain pattern
A: P pulmonale
RBBB
R wave dominance V1/2
ST depression/TWI V1-3

Q: What is BAP-65?
A: Classification of COAD exacerbations
 - BUN
 - ALOC
 - Pulse >109
 - Age over 65

Q: What proportion of COAD exacerbations without clear cause have a PE?
A: 25%

Q: Risk factors for hypercapnoeic respiratory failure
A: Chronic bronchitis
Obese
OSA
Sedatives

Q: Risk factors for normocapnoeic respiratory failure
A: Emphysema
Thin physique
Pursed lip breathing
Accessory muscle use
Hyperinflation

Q: Benefits of corticosteroids for acute exacerbations COAD
A: Reduces rate of return to ED

Q: MOA of theophylline
A: Phosphodiesterase inhibitor to improve mechanics of breathing and anti-inflammatory effect
Adenosine receptor blocker
Histone deacetylase activator

Q: Indications for NIV in COAD exacerbation
A: Increased WOB
T1 or T2RF
Most benefit if pH 7.25-7.30 rather than waiting until fatigued

Q: Relative CI to NIV use in COAD
A: Cardiovascular instability
Reduced LOC
Facial trauma
Recent facial or gastro-oesophageal surgery
Viscous/copious secretions

Q: Benefits of NIV in COAD exacerbations
A: Reduced intubation
Reduces short-term mortality
Symptomatic improvement
Reduced length of hospitalisation

Q: Inpatient mortality of COAD exacerbations requiring intubation
A: 25%

Q: 12 month mortality of hypercapnoeic COAD exacerbation
A: 50%

Q: Cystic fibrosis organ effects
A: Bronchiectasis
Chronic sinusitis
Infertility
Exocrine pancreatic failure
Intestinal dysfunction
Chronic cholelithiasis and cholecystitis
Sweat gland dysfunction

Q: Causes of empyema
A: Bacterial pneumonia
Chest surgery
Trauma
Oesophageal perforation
Complication of thoracocentesis
Extension of abdominal infection

Q: Diagnosis of empyema
A: Grossly purulent drainage + one of:
 - Positive Gram stain or culture
 - Glucose <2.2
 - pH <7.1
 - LDH >1000

Q: What is the utility of adenosine deaminase testing of thoracocentesis sample?
A: 99.9% rule out of TB if negative

Q: What are the three stages of empyema?
A: Exudative (<48 hours)
Fibrinopurulent (loculations arise)
Organisational (weeks of fibrosis)

Q: Antibiotic therapy for empyema
A: Ceftriaxone 1g BD + Metronidazole 500mg BD IV (+ consider MRSA/pseudomonas risk)

Q: Management of exudative empyema
A: Tube thoracostomy

Q: Management of fibrinopurulent empyema
A: Thoracic medicine fibrinolysis +- tube +- VATS

Q: Mangement of organisational empyema
A: Thoracic surgical removal of fibrous peel

Q: Causes of lung abscess
A: Aspiration pneumonia
Haematogenous seeding
Lung infarct
Penetrating lung trauma
Fungal abscess
Neoplasm
Wegener's granulomatosis
Sarcoidosis

Q: Mortality of primary lung abscess
A: 15%

Q: Mortality of secondary lung abscess (malignancy, immunosuppression, extrapulmonary infection, complication of surgery)
A: 50%

Q: How do community-acquired and hospital-acquired lung abscess differ?
A: Community-acquired typically anaerobic and lower mortality rate
Hospital-acquired usually aerobic, higher mortality and resistant

Q: Typical anaerobic bacteria in lung abscess
A: Prevotella, Bacteroides, Fusobacterium, peptostreptococcus

Q: What is Lemierre's syndrome?
A: Jugular vein thrombophlebitis from tonsillitis secondary to Fusobacterium necrophorum

Q: What proportion of patients with lung abscesses have cancer?
A: 15% (30% if over 45)

Q: What proportion of patients with lung abscesses suffer haemoptysis?
A: 25%

Q: DDx of cavitating lesions
A: Lung abscess
Infected bullae
TB
Fungal - Coccidioidomycosis, Histoplasmosis, Blastomycosis, Aspergillosis, Cryptococcus
Paraisitic - Amoebiasis, Echinococcus
Neoplastic - SCC, adenocarcinoma, metastatic, lymphoma, Hodgkin's
Wegener's
Sarcoidosis

Q: Empirical Ab for lung abscess
A: Ceftriaxone 1g BD + Metronidazole 500mg BD +- Vanc

Q: What proportion of lung abscesses require surgical intervention?
A: 10%

Q: Are mesotheliomas related to smoking?
A: No. Asbestosis is

Q: How do mesothelioma related pleural effusions present?
A: Do NOT show mediastinal shift away from side of effusion

Q: How does acute silicosis present on CXR?
A: Profuse miliary infiltration

Q: Chronic silicosis on CXR
A: Upper lobe small rounded opacities
Eggshell hilar node calcification

Q: DDx of eosinophilic pneumonia
A: ABPA
Parasitic infiltrations
Drug reactions
Idiopathic
Churg-Strauss
Hypereosinophilic syndrome

Q: Causes of drug-induced eosinophilic pneumonia
A: Nitrofurantoin
Sulfonamides
Penicillins
Thiazides
TCA
Hydralazine
Isoniazid
Indomethacin

Q: Define massive haemoptysis
A: >600mL in 24 hours

Q: Proportion of lung blood flow from bronchial circulation
A: 1%

Q: Proportion of haemoptysis from bronchial circulation?
A: 90%

Q: Causes of haemoptysis
A: Tracheobronchial disorders e.g. tracheitis, bronchitis, carcinoma, bronchiectasis, FB, fistula, trauma
Iatrogenic
Localised parenchymal disease e.g. pneumonia, PE, metastatic cancer, lung abscess
Diffuse parenchymal disease e.g. Viral pneumonitis, Scleroderma, Wegener's, SLE, Goodpasture's
Anticoagulants
Cardiac disease

Q: Important history in haemoptysis
A: Amount
Smoking hx
TB risk
PE risk
Systemic arthalgia/myalgia/fevers
Cyclical bleeding (catamenial)
Anticoagulants
Recent infective symptoms

Q: Which patients with haemoptysis can be discharged?
A: Mild haemoptysis, normal CXR, <40, smoker <40 pack years, duration of haemoptysis >1 week, discussed with respiratory team for follow-up +- bronchoscopy/CT

Q: What does RUL collapse and haemoptysis suggest?
A: Malignancy

Q: Management of mild haemoptysis with mass lesion on CXR?
A: FBC, UEC, Coags, urinalysis
Respiratory consult
Consider CT chest for staging in liaison with resp team
Bronchoscopy as per resp team

Q: Management of haemoptysis with parenchymal disease on CXR
A: FBC, UEC, Coags, urinalysis
Resp consult
Consider HRCT +- bronchoscopy if no specific diagnosis suggested in liaison with resp

Q: Do heart transplant patients respond to adrenergic agents?
A: Yes

Q: Do heart transplant patients suffer pain with ischaemia?
A: No

Q: Does the transplanted heart respond to atropine?
A: No

Q: Does the transplanted heart respond to adenosine?
A: Yes. 4-fold increase in response

Q: How may heart transplant rejection present?
A: Arrhythmias, SOB, weight gain, malaise, low-voltage ECG and echo evidence of declining function

Q: Signs of lung rejection
A: Cough, temperature change 0.28 degrees, hypoxaemia, FEV1 drop by 10%, new infiltrates

Q: Management of acute lung rejection
A: Increase immunosuppressive regime back to pre-rejection dose and add methylpred 15mg/kg IV daily for 3 days

Q: Survival post-heart transplant at 5 years
A: 70%

Q: Survival post heart-lung transplant at 5 years?
A: <50%

Q: Do patients suffer peripheral eosinophilia with hypersensitivity pneumonitis?
A: No

Q: How does chronic hypersensitivity pneumonitis present on CXR?
A: Diffuse reticulonodular infiltrate
Honeycombing
Apical sparing

Q: DDx of non-granulomatous interstitial lung disease
A: Asbestosis
Radiation pneumonitis
Aspiration pneumonia
Chronic ARDS
Idiopathic pulmonary fibrosis
Cryptogenic organising pneumonia
Goodpasture's

Q: DDx of granulomatous interstital lung disease
A: Hypersensitivity pneumonitis
Occupational lung disease e.g. silicosis
Sarcoidosis
Wegener's
Churg-Strauss

Q: Most common type of lung cancer
A: Adenocarcinoma

Q: What is more chemo-sensitive: Small cell or non-small cell?
A: Small cell initially but ultimately relapses

Q: What proportion of lung cancers occur in people who have smoked?
A: 85%

Q: What is the most common lung cancer in non-smokers?
A: Adenocarcinoma

Q: Which lung cancers are central?
A: Squamous cell carcinoma
Small cell lung cancer

Q: Which lung cancers tend to be peripheral?
A: Adenocarcinoma
Large cell cancer
*S = Sentral

Q: What is Pancoast syndrome?
A: Apical lung cancer with involvement of C8-T2 nerves presenting with shoulder pain and radiculopathy in ulnar distribution. Often get radiological destruction of 1st/2nd ribs

Q: What endocrine syndromes arise from small cell lung cancer?
A: SIADH
ACTH

Q: Which lung cancer releases PTHrP?
A: Squamous cell lung cancer

Q: How is non-small cell lung cancer staged?
A: TNM

Q: How is small cell lung cancer staged?
A: Limited (30%) - One hemithorax and regional nodes only
Extensive (70%)

Q: What proportion of solitary lung nodules are malignant?
A: 35%

Q: What proportion of solitary lung nodules are malignant in the under 30 non-smoker?
A: <1%

Q: Management of solid pulmonary nodule
A: If <6mm and low-risk patient - No F/u required
If >6mm or high-risk - Need CT f/u via GP

Q: Define low risk solid pulmonary nodule group
A: Younger, less smoking, non-upper lobe, small nodule, regular margins

Q: Define non-low risk solid pulmonary nodule group
A: Older, heavier smoking, larger nodule size, irregular or spiculated margin or upper lobe nodule

Q: How much does NIV reduce intubation rates?
A: 25% overall

Q: How does CPAP reduce WOB?
A: Alveolar recruitment
Reduced negative pressure generation to match iPEEP
Reduces intrapulmonary shunt
Reduced LV transmural pressure gradient (afterload)
Reduced LV preload

Q: How much does NIV reduce mortality in COAD exacerbations?
A: 50%

Q: How much does NIV reduce intubation rates for COAD exacerbations?
A: 60^

Q: NNT to avoid intubation with NIV in COAD exacerbation
A: 4

Q: Clinical monitoring on NIV
A: Work of breathing
Mental status
Clearance of secretions
Air leaks
Respiratory rate
Tidal volume
Synchronicity

Q: What proportion of COAD exacerbations put on NIV suffer late failure >48 hours?
A: 10-20% with high mortality

Q: Complications of NIV
A: Aspiration
Hypotension
Sinus pain
Gastric insufflation
Pneumothorax
Pressure sores
Dryness
Failure

Q: Cochrane outcomes for NIV in asthma
A: Reduced hospital admission, length of ICU stay and length of hospital stay
No improvement in mortality or intubation rates

Q: Contraindications to HiFlow
A: Trauma/surgery to nasopharynx
Epistaxis
Base of skull fracture
Obvious need for intubation

Q: HiFlow settings for paediatrics
A: <10kg = 2L/kg/min
>10kg = 2L/kg/min for first 10 then 0.5L/kg/min above this

Q: HiFlow complications
A: Gastric distension
Pressure areas
Pneumothorax
Local trauma
Epistaxis
Delayed intubation and worse outcomes

Q: What did the FLORALI study show?
A: HFNP resulted in improved 90 day mortality without reducing intubation rates in adults with hypoxaemic respiratory failure

Q: Define community-acquired pneumonia
A: Not hospitalised or in care facility for 14 or more days

Q: Define hospital-acquired pneumonia?
A: New infection 48 hours or more after admission

Q: Define VAP
A: New pneumonia 48 hours or more after intubation

Q: Define healthcare-associated pneumonia
A: Hospitalised for 2 days or more in last 3/12
Nursing home/care facility resident
Home IV therapy
Dialysis patients
Chronic wound care
Chemotherapy patients
Immunosuppressed patients

Q: What proportion of patients with pneumonia show typical consolidation?
A: Only 25%

Q: What proportion of elderly patients with pneumonia have non-respiratory symptoms?
A: 50%

Q: Classic presentation of pneumococcal pneumonia
A: Sudden onset fever, rigors, pleurisy, rust-coloured sputum, lobar pneumonia

Q: Classic presentation of Staph aureus pneumonia
A: Gradual onset following viral infection. Patchy, multilobar +- empyema +- lung abscess

Q: Classic Klebsiella pneumoniae presentation
A: Sudden onset fevers, rigors, haemoptysis, brown-current jelly sputum, upper lobe infiltrates +- abscess
Especially alcoholics and nursing home residents

Q: In whom does Klebsiella pneumoniae pneumonia usually occur?
A: Alcoholics and nursing home residents

Q: How does pseudomonas pneumonia usually present?
A: Recently hospitalised, debilitated, immunocompromised patients with patchy infiltrate +- abscess

Q: Is Klebsiella Gram positive or Gram negative?
A: Gram-negative rod

Q: Is Pseudomonas Gram-pos or neg?
A: Gram-negative rod

Q: How does H. influenzae pneumonia present?
A: Gradual onset in elderly, COAD patients with patchy basilar infiltrate

Q: Is H. influenzae Gram pos or neg?
A: Gram-negative coccobacilli

Q: How does Legionella pneumonia present?
A: Fever, chills, headache, dry cough, GI symptoms

Q: How do anaerobic pneumonias present?
A: Putrid sputum in alcoholics with dependent lung consolidation +- abscess formation

Q: Which organisms most often cause cavitating lung pathology?
A: S. aureus, Fusobacterium, Bacteroides, E. coli, Klebsiella, Pseudomonas, Burkholderia cepacia, Burkholderia pseudomallei, TB, fungal

Q: Which organisms most often cause lung abscess?
A: S. aureus, Klebsiella, Pseudomonas

Q: Which organisms most often cause empyema?
A: S. aureus, Pseudomonas, Fusobacterium, Bacteroides

Q: What proportion of pneumococcal pneumonia have parapneumonic effusions?
A: 25%

Q: Risk factors for Pseudomonas pneumonia
A: Hospitalised
broad-spectrum antibiotic use
High-dose steroid use
Immunosuppressed
Structural lung disease e.g. CF/bronchiectasis
Nursing home residents

Q: When is Legionella most common?
A: No seasonality so is more prominent in summer when others are less common

Q: Risk factors for B. pseudomallei?
A: Diabetes
Alcohol abuse
CKD
Indigenous
Chronic lung disease
Immunosuppression

Q: How does Pneumocystis carinii present?
A: Dry cough, dyspnoea, fever, fatigue, weight loss and signs > CXR findings in immunosuppressed

Q: What sample is required for pertussis testing?
A: NPA (not just swab as need ciliated epithelium)

Q: Which pneumonia patients warrant BC?
A: All admitted patients as per eTG
Admitted ICU, leukopaenia, cavitary lesions, liver disease, alcoholic, asplenia or pleural effusions

Q: Which patients with pneumonia should have sputum sent?
A: All admitted patients

Q: What proportion of hospitalised CAP have positive BC?
A: 15%

Q: What proportion of hospitalised CAP have positive sputum culture?
A: 40%

Q: Which pneumonia patients warrant pneumococcal urinary antigen testing?
A: All severe cases

Q: Sensitivity of pneumococcal urinary antigen?
A: 50-80%

Q: Which pneumonia patients warrant Legionella urinary antigen testing?
A: All severe cases
Alcoholics
GI symptoms
2 week travel history

Q: Sensitivity and specificity of Legionella urinary antigen?
A: 95% for both

Q: What does Legionella urinary antigen test for?
A: Legionella pneumophila type 1 only

Q: Important bacteria in alcoholics with pneumonia
A: S. pneumonia, Klebsiella, H. influenzae

Q: Organisms in community-acquired aspiration pneumonia
A: S. pneumoniae
Oral commensal strep
Anaerobes
Enterobacteriaceae

Q: Organisms in hospital-acquired aspiration pneumonia
A: Pseudomonas
Gram-negatives

Q: Indications for antibiotics in suspected aspiration
A: Failure to improve with symptomatic therapy
Clinical deterioration
CXR suggestive of aspiration pneumonia
Aspiration of contaminated fluid e.g. bowel obstruction

Q: Diagnostic criteria for HAP
A: New infiltrate + Pathogenic organism on sputum + one of:
 - Fever >38.3
 - WCC >12
 - Sputum >2+ PMN and bacteria

Q: Why might a positive culture of tracheal aspirate not represent infection?
A: May be upper airway coloniser.
If pathogenic bacteria present, then highly unlikely to be in LRTI given microaspiration pathophysiology of HAP

Q: Which organisms, if identified on tracheal aspirate, are almost always pathogenic?
A: Legionella
Chlamydia
TB
Influenza
Para-influenza
RSV
Strongyloides
Toxoplasma
PCP
Histoplasma/Coccidioides/Blastomyces/Cryptococcus

Q: Diffuse infiltrates in immunosuppressed
A: CMV
Herpesvirus
PCP
Aspergillus
Bacterial
Cryptococcus

Q: Focal infiltrates in immunosuppressed
A: Gram-negative rods (Klebsiella, Pseudomonas)
S. aureus
Aspergillus
Cryptococcus
Nocardia
Mucormycosis
TB
Legionella

Q: What does SMART-COP predict?
A: ICU
Vasopressor support
Mortality

Q: What does PSI predict?
A: Mortality risk

Q: What does CURB-65 predict?
A: Mortality

Q: SMART-COP
A: Split into <50 and >50
SBP <90 (2)
Multilobar
Albumin <35
RR >25
Tachycardia >125
Confusion
O2 - PaO2 <70, SpO2 <93%, P/F <333 (2)
O2 - PaO2 <60, SpO2 <90%, P/F <250 if over 50 (2)
pH <7.35 (2)

Q: Is doxy/azithro effective against S. pneumoniae?
A: Sometimes. Increasing resistance means only suitable for mild CAP with early review

Q: Can penicillins be used for intermediate-penicillin resistant S. pneumoniae?
A: Yes. Must be given at adequate doses

Q: Empirical mild CAP therapy
A: Mild - Amoxicillin 1g PO q8h OR Doxycycline 200mg then 100mg BD
Early review to ensure improving on chosen therapy or use both if review not possible

Q: Empirical moderate CAP therapy (non-tropical)
A: BenPen 1.2g q6h IV + Doxycycline 100mg BD

Q: Empirical moderate CAP (tropical) therapy
A: BenPen 1.2g q6h +  Doxycycline 100mg BD
If risk factors for B. pseudomallei or Gram-negative bacilli on Gram stain
 - Ceftriaxone 1g BD + Gentamicin 5mg/kg IV +- Doxycycline 100mg BD/Azithro 500mg IV daily if atypical likely

Q: Is B. pseudomallei gram-pos or neg?
A: Gram-negative rod

Q: Empirical severe CAP therapy
A: BenPen 1.2g q4h +  Gent 5mg/kg (or Ceftriaxone 1g BD IV if penicillin allergic) + Azithromycin 500mg IV daily +- Vanc if MRSA suspected
If Gram-negative on Gram stain - Change Cef to PipTaz 4.5g QID and consider adding Gent

Q: How long should antibiotic course be for severe CAP?
A: 7 days
8 if Klebsiella
14 if S. aureus
15 if Pseudomonas or Acinetobacter

Q: Empirical treatment for tropical severe CAP
A: Meropenem 1g q8h IV (wet season)
PipTaz 4.5g q6h IV (dry season)
+ Azithromycin 500mg IV daily +- Vanc cover if MRSA likely

Q: Empirical therapy for community-acquired aspiration pneumonia
A: Amoxicillin 1g PO q8h

Q: Empirical therapy for community-acquired moderate aspiration pneumonia
A: BenPen 1.2g q6h + Metronidazole 500mg BD IV

Q: Empirical management of mild HAP
A: Augmentin 875/125 BD

Q: Empirical therapy of severe HAP
A: Ceftriaxone 1g BD IV or
PipTaz 4.5g QID IV if high risk ward >5 days

Q: CURB-65 score allowing outpatient therapy
A: <2

Q: CURB-65 features
A: Confusion
Urea >7
RR >30
BP <90
Age >65
Score 0-1 = 1.5% mortality = outpatient
Score 2 = 9.2% mortality = Either
Score 3 or more = 22% mortality

Q: What to consider if pneumonia fails to respond?
A: Correct diagnosis
Correct antibiotic
Obstructed bronchus
Empyema
BOOP
Organisms resistance
Drug fever

Q: Which pneumonia patients need a f/u CXR at 6 weeks?
A: Smokers
Those over 50yo
(those at risk of lung cancer)

Q: Classification of PTX
A: Spontaneous primary
Spontaneous secondary
Traumatic

Q: Risk factors for primary spontaneous PTX
A: Smoking
Male
Mitral valve prolapse
Marfan's
Changes in ambient temperature
Familial patterns

Q: Causes of secondary spontaneous PTX
A: Asthma
COAD
Pneumonia
Cystic fibrosis
ILD
HIV
PCP
TB
Scleroderma
Lung cancer
Catamenial

Q: What proportion of spontaneous secondary PTX suffer haemothorax?
A: 5%

Q: Sensitivity of CXR for PTX?
A: 75%

Q: Define a small PTX
A: <2cm from apex
<2cm between lung edge and chest wall (BTS)

Q: Size cannula for emergent decompression of tension PTX?
A: 14G adults (18G children)

Q: Baseline rate of resorption of PTX
A: 1.25% per day

Q: Which patients can be discharged with a PTX?
A: Spontaneous primary PTX, small, stable, comfortable, no comorbidities, improved on repeat CXR at 4 hours

Q: Management of small secondary spontaneous PTX
A: Small catheter or aspiration and admission

Q: Which patients are at risk of re-expansion lung injury?
A: PTX >72 hours, large PTX, rapid re-expansion and wall suction >20cmH20

Q: When is pleurodesis indicated?
A: First spontaneous PTX with ongoing air leak
Second ipsilateral spontaeous PTX
First contralateral PTX
Bilateral spontaneous PTX
First episode of secondary PTX
Recurrent flying/diving

Q: Risk of pneumothorax with subclavian line insertion?
A: 0.5-3%

Q: DDx of diffuse alveolar opacification
A: ARDS
APO
Diffuse alveolar haemorrhage
Wegener's
Pneumocystis carinii
Viral or bacterial pneumonia
Sarcoidosis

Q: Obstructive lung function tests
A: Reduced FEV1:FVC
Reduced vital capacity
Increased TLC
Increased residual volume

Q: Restrictive lung function tests
A: Reduced TLC
Reduced residual lung volume
Increased FEV1:FVC ratio

Q: FiO2 of 2L NP
A: 0.28

Q: FiO2 of 4L NP
A: 0.36

Q: Minimum flow-rate for Hudson mask
A: 6L/min

Q: FiO2 of HM on 6L/min
A: 0.45

Q: FiO2 of HM on 8L/min
A: 0.55

Q: FiO2 of HM on 10L/min
A: 0.65

Q: Maximum FiO2 with NRBM?
A: 0.60-0.80

Q: Minimum flow for NRBM
A: 10L/min

Q: Complications of O2 therapy
A: Denitrogenation atelectasis
Reperfusion injury
CO2 retention
ARDS
Retinopathy of prematurity
Bleomycin/paraquat poisoning progression

Q: What factors are useful in differentiating CCF from pulmonary disease?
A: S3, interstitial lung markings, pulmonary venous congestion, raised JVP
NOTE: Wheeze, dyspnoea on exertion, orthopnoea, PND and peripheral oedema are NOT helpful

Q: Differentials of hypoxia
A: Hypoventilation
VQ mismatch
Shunt
Diffusion abnormality
Low atmospheric O2

Q: Treatment of cough paroxysms in ED
A: Nebulised lignocaine 4mL of 1% lignocaine

Q: DDx of chronic cough
A: Post-nasal drip
Chronic bronchitis
Asthma
ACEi
GORD

Q: What proportion of patients on ACEi or ARB suffer dry cough?
A: 10-12%

Q: When does ACEi cough arise?
A: 1 week to 1 year after initiation

Q: Management of chronic cough
A: Reduce exposure to irritants/ACEi/ARB/beta-blockers
Treat for post-nasal discharge e.g. antihistamines, decongestants, IN steroid
Evaluate for asthma
Chest and sinus imaging
Evalute and treat GORD
Refer for respiratory f/u (CT +- bronchoscopy)

Q: DDx of chronic, persistent, intractable hiccups
A: Hair on TM (LOOK)
CNS lesion
Uraemia

Q: Management of intractable hiccups
A: Check TM for hair
CXR for intrathoracic pathology
Full neuro exam
CT head +- MRI
Swallow teaspoon of dried sugar
Chlorpromazine or metoclopramide take 30 minutes to work

Q: SpO2 in methaemoglobinaemia
A: 80-85% regardless of actual arterial oxygen content

Q: How much pleural fluid is required to produce signs on erect CXR in adult?
A: 150-200mL

Q: When should pleural effusions in the setting of CCF be drained?
A: If fails to improve with 3-4 days of therapy OR if diagnosis uncertain

Q: Tests to send for pleural fluid analysis
A: Gram stain
MCS
Cell count
Glucose
LDH
Cytology
pH
Amylase
Ziehll-Nielsen
Fungal stains
TB PCR
ADenosine deaminase
IFN-gamma

Q: PaO2 at SpO2 90%
A: 60mmHg

Q: PaO2 at SpO2 98%
A: 100mmHg

Q: Normal P50
A: PaO2 27mmHg

Q: How much does O2 therapy enhance PTX resorption?
A: 3-4 fold

Q: How is re-expansion pulmonary oedema managed?
A: Aggressive fluid resuscitation if in shock
Supportive ventilation

Q: How much fluid should be drained from pleural space at a time?
A: 1.5L as per BTS

Q: DDx of exudative pleural effusion
A: Parapneumonic
Malignancy
TB
PE
RA
SLE
Pancreatitis
Liver abscess
Ruptured oesophagus

Q: DDx of transudate pleural effusion
A: CCF
Ascites
CKD
PE
Nephrotic syndrome

Q: What proportion of patients suffering droplet exposure to TB suffer infection?
A: 30%

Q: What controls initial TB infection?
A: Cell-mediated immunity - Tubercles at hilar nodes + Ghon focus = Ghon complex

Q: Where does TB lie latent?
A: Apical upper or superior lower lobes
Renal cortex
Meninges
Epiphyses of long bones
Vertebrae

Q: How can latent TB be diagnosed?
A: Positive tuberculin skin test

Q: What proportion of healthy individuals with latent TB go on to suffer post-primary disease?
A: 10%

Q: What proportion of children and patients with HIV suffer post-primary disease with TB?
A: 20%

Q: What is the risk of TB reactivation per year if a patient has HIV?
A: 5-10%

Q: Risk factors for TB reactivation
A: Increasing age
HIV
Solid organ cancer
Leukaemia
Transplant immunosuppression
TNF-alpha antagonists
Corticosteroids
Diabetes
Haemodialysis

Q: Presentation of reactivation TB
A: Haemoptysis, pneumonia, weight loss, night sweats, fevers, pleurisy + extrapulmonary manifestations

Q: Extrapulmonary manifestations of reactivation TB
A: Painless lymphadenopathy
Peritoneal TB
Hepatosplenomegaly
Prostatitis
Adrenal insufficiency
Osteomyelitis
Pott's disease
Meningitis
Pericarditis

Q: What proportion of reactivation TB suffer extrapulmonary manifestations?
A: 20%

Q: Benefit of quantiferon gold
A: More specific for M. tuberculosis
Cannot differentiate past exposure (latent) vs. reactivation

Q: What proportion of microscopy of sputum samples is positive in active pulmonary TB?
A: 50%

Q: How sensitive is GeneXpert for TB
A: Equal to solid culture (80%) and detects rifampicin resistance

Q: Define latent TB?
A: Positive Mantoux or Quantiferon Gold with negative GeneXpert/sputum smear/Ziehl-Nielsen stain.

Q: Benefits of treatment of latent TB
A: Reduces progression to reactivation by 60-90% and prevents transmission

Q: Side effects of isoniazid?
A: Hepatotoxicity
Peripheral neuropathy

Q: Side effects of rifampicin
A: Hepatitis
Orange secretions
Thrombocytopaenia
GI symptoms

Q: Side effects of ethambutol
A: Retrobulbar optic neuritis
Peripheral neuropathy

Q: How does tuberculous meningitis present?
A: Subacute fever, headache, cognitive impairment without classic meningism
May have focal neurology

Q: When is augmentin indicated in CAP?
A: If patient fails to improve or Gram-negative on sputum Gram stain

Q: What is Pemberton's sign?
A: Triad of facial plethora, dyspnoea and cyanosis with lifting arms above head due to SVC obstruction

Q: Well's score for DVT
A: Previous DVT
Recent immobilisation of leg
Bedridden >3 days or major surgery within 4 weeks
Calf swelling >3cm
Pitting oedema
Entire leg swollen
Localised tenderness along deep venous system
Alternative Dx more likely (-2)
Active malignancy
>1= High risk

Q: Well's score for PE
A: Clinical signs and symptoms of DVT (3)
PE most likely diagnosis(3)
HR >100(1.5)
Immobilisation or surgery in last 4 weeks(1.5)
Past history of DVT/PE(1.5)
Haemoptysis
Active malignancy
Score 5 or more = Likely
Score 4 or less = Unlikely

Q: PERC rule
A: Low risk Well's/Gestalt?
Age >=50
HR >100
Prior hx of VTE
Recent trauma or surgery
Haemoptysis
Exogenous oestrogen
Unilateral leg swelling
Yes to any one precludes use

Q: Stable spontaneous PTX definition
A: No dyspnoea at rest
RR <24
HR 60-120
SpO2 >90% RA
Normal BP
No haemothorax

Q: Aminophylline or theophylline in acute severe asthma?
A: Aminophylline as per RCH