Resp Quickfire Flashcards
Pleural analysis
a) Light’s criteria
b) Milky consistency
c) Straw coloured/ammonia smell
d) Empyema biochemistry
e) Causes of bloody tap
f) Cause of black pleural fluid
g) causes of low pH
h) If clinical history fits with transudates, should you still sample?
i) What would be suggestive of malignancy
a) Light’s criteria for exudate:
- Pleural protein > 0.5x serum protein
- Pleural LDH > 0.6x serum LDH or >2/3 ULN for serum LDH
b) Chylothorax - high pleural cholesterol
Pseudochylothorax - normal pleural cholesterol (e.g. caused by TB)
c) Urinothorax
d) Exudate, low pH, low glucose, high WCC, high LDH, purulent fluid
e) Trauma, malignancy, infection
f) Aspergillus niger, melanoma, other malignancy
g) pH < 7.2 is seen with empyema. Can also be low with tuberculosis, malignancy, collagen vascular disease or oesophageal rupture (Boerhaave’s)
h) - No, try treating cause and assess for improvement
- If no improvement, or if could be exudate - send pleural sample (always send 50mls for protein, cytology, LDH, gram stain, culture)
i) Exudative + high protein (>30) + bloody tap (consistently across multiple taps)
PE
a) treatment duration
b) thrombolysis indications
Provoked PE - 3 months if provoking factor no longer present and patient is stable
PE provoked by malignancy - 6 months
Unprovoked PE - review at 3 months risk/benefit, but likely to recommend continuing long-term
Recurrent PE - lifelong
b) Thrombolysis:
- Massive PE (circulatory collapse) - must be confirmed by bedside ECHO (right heart strain*) or CTPA if stable
- 50mg alteplase IV (+/- invasive thrombus fragementation)
*ECG findings:
- ST depression/TWI in V1-V3, and inferior leads (especially lead III)
- Right axis deviation
Asthma
a) 3 questions for assessing good control
b) adult treatment pathway
a) 1. Have you had symptoms during the day/ needed to use your SABA?
2. Has your asthma interfered with usual activities, including have you had to take time off work due?
3. Have you been waking up at night with coughing/wheezing?
b) Treatment pathway:
1. SABA for symptoms
2. Low-dose ICS (for anyone with daytime symptoms >3x per week or night-time symptoms 1x per week)
3. Leuko-TRI… Add LTRA (oral, take at night) - trial for 4-8 weeks
4. Add LABA (stop LRTA if no response)
5. Switch to MART* therapy (budesonide/formoterol or beclometasone/formoterol)
6. Increase steroid dose to moderate
7. 3 options:
- Add LAMA (triple therapy - Trelegy, Trimbow)
- Add theophylline
- Increase steroid dose to high
8. Oral steroids
*Maintenance and reliever therapy:
- Contains ICS + formoterol (which has LABA and SABA action)
- Hence can be used as maintenance and reliever
Eosinophilia
Allergy (including drug eruption)
Allergic bronchopulmonary aspergillosis
Asthma
Eosinophilic folliculitis
Parasite
Vasculitis - EGPA (Churg Strauss)
Transfer factor
a) What is DLCO (TLCO)? Equation for DLCO
b) Principles
c) What conditions increase, decrease and do not affect the DLCO?
d) Clinical use of DLCO
e) What effect does recent smoking, and high altitude have on DLCO?
a) DLCO = TLCO
DLCO: diffusion capacity of CO
TLCO: transfer capacity of CO
KCO: diffusion rate of CO
VA: ventilation surface area
DLCO = VA x KCO
b) CO is inhaled and due to high affinity for Hb, all of it should diffuse and end up on Hb. DLCO measures the ability of CO to diffuse into the blood and end up on Hb
Calculated as % predicted CO
c) DLCO reduced by:
- anything that reduces surface area for diffusion (e.g. emphysema, intrinsic restrictive lung disease i.e. fibrosis), or
- reduced perfusion (e.g. systolic HF, PAH, PE, anaemia, pulmonary AVM*)
*Pulmonary AVMs cause right-to-left shunting from PA to PV, bypassing the lung, hence reducing lung perfusion
DLCO increased by:
- anything that increases perfusion (e.g. left-to-right shunt, diastolic HF, exercise, polycythaemia, old pulmonary infarction* and haemorrhage)
- Also increased in pneumonectomy (if corrected for lung volumes)
- Perforated eardrum causes very high DLCO, as some of the administered CO enters the blood via perforation
*Due to increased blood flow to functional areas of the lung
DLCO is unaffected by:
- Asthma, bronchitis (but emphysema reduces it)
- Extrinsic restrictive lung disease
d) - Lung Ca: if DLCO <60%, pneumonectomy has poor prognosis; if <40%, pneumonectomy will not be offered
- PAH: isolated reduction in DLCO with normal lung volumes
- Intrinsic restrictive lung disease: DLCO is usually the first parameter to decrease, before lung volumes
- Particularly, patients on medications like amiodarone, bleomycin, methotrexate and nitrofurantoin should have DLCO monitoring
e) Recent smoking:
- Additional COHb so less capacity for CO binding on testing
- Hence, this reduces DLCO
(so patients told no smoking for 24h pre-test)
High altitude:
- Lower PaO2, so less oxygen competing for Hb
- Hence, increased capacity for CO to bind to Hb –> increased DLCO
Atraumatic pneumothorax management
a) Primary vs secondary pneumothorax - define
b) Management of secondary pneumothorax
c) Management of primary pneumothorax
d) If bilateral PTX or haemodynamically unstable…
e) Long term advice
a) Secondary:
- Age >50 and smoker, or
- Known underlying lung disease
Primary spontaneous:
- Most common in tall young men (basketballers, Marfan’s, etc.)
- Usually due to rupture of apical blebs (gas balls)
b) Secondary pneumothorax management:
>2cm or breathless –> chest drain (8-14 Fr)
1-2cm –> aspirate no more than 2.5L –> once <1cm, admit for 24h observation and high flow oxygen*
<1cm –> admit for 24h observation and high flow oxygen*
*unless contraindicated - CO2 retainers
c) Primary pneumothorax management:
>2cm or breathless –> aspirate no more than 2.5L (16 or 18G cannula)
–> if fails, chest drain.
–> If successful (<2cm and not SOB), discharge and review in OPD 2-4 weeks.
<2cm and not breathless –> consider discharge and review in OPD 2-4 weeks.
d) Immediate chest drain (irrespective of primary/secondary)
e) - No smoking, no diving
- No flying for 2 weeks after full resolution
Long-term oxygen therapy
a) ABG samples to be taken when?
b) PaO2 threshold for considering LTOT (in COPD, but also in other respiratory disease)
c) Other criteria for considering at higher PaO2
d) How long should oxygen be given for generally?
e) Below what FEV1 level in COPD should assessment for LTOT be considered?
f) Absolute contraindication to LTOT
a) 2 samples, 3 weeks apart, during clinical stability
b) PaO2 < 7.3 kPa
c) PaO2 7.3 - 8.0 kPa in the context of 3 Ps:
- Polycythaemia (secondary)
- Peripheral oedema (cor Pulmonale)
- Pulmonary hypertension
- Or, overnight hypoxaemia (SpO2 <90% for 30% of the night)
d) At least 15 hours per day - mortality benefit seen
e) FEV1 < 30% predicted
f) Current smoker (offer smoking cessation interventions first)
COPD management
a) Treatment pathway, including add-on therapies
b) What are “asthmatic features”
c) Significant type/number of exacerbations
d) Who to consider rescue pack in
e) What is in a rescue pack
f) Advice for acute exacerbation
g) Pulmonary rehab
a) Management:
1. If breathless/exercise limitation: SABA or SAMA (Atrovent i.e. ipratropium)
- If continued SOB or exacerbations despite SABA:
- Combined LABA/LAMA if no asthmatic features (e.g. Ultibro)
- Combined LABA/ICS if asthmatic features present like reversibility/diurnal variation/eosionophilia/atopy (e.g. Fostair, Seretide, Symbicort - If continued symptoms affecting QoL or frequent exacerbations:
- TRiple therapy: LABA/LAMA/ICS (e.g. TRimbow, TRelegy)
- Note: if no asthmatic features, trial this inhaler for 3 months - if no response, go back to LABA/LAMA - If symptoms persisting, consider referral and add-on therapies, including:
- Mucolytics (e.g. carbocisteine)
- Slow-release theophylline
- Oral prednisolone
- Prophylactic antibiotics (e.g. azithromycin 500mg three times per week, trial for 6-12 months - must check LFTs and ECG at baseline and after 1 month)
- Phosphodiesterase-4 (PDE₄) inhibitors (e.g. roflumilast, cilomilast)
- Nebulised therapy
- LTOT
b) - Previous secure diagnosis of asthma or atopy
- Eosinophilia
- Substantial variation in FEV1 over time (at least 400 ml)
- Substantial diurnal variation in peak flow (at least 20%)
c) Two in a year, or one severe (requiring hospitalisation)
d) Those with 2+ exacerbations per year (know how to recognise an exacerbation)
e) Prednisolone 30mg (7 - 14 day supply)
- Amoxicillin 500mg TDS, or doxycycline 100mg OD, or clarithromycin 500mg BD, or antibiotic based on sputum culture (5 day supply)
f) In acute exacerbation:
- increase frequency of SABA/SAMA
- take steroids if more breathless
- take antibiotics if sputum changes colour or increases in thickness/volume
- notify GP
g) - For anyone who has significant breathlessness (usually MRC grade 3+)
- Contraindicated in unstable angina or recent ACS
Lung cancer differentiation
a) Location
b) Breakdown of different types (%)
c) Associated features
a) and b)
- Adenocarcinoma (40%) - more peripheral
- Squamous cell (30%) - more Sentral, intra-bronchial (earlier symptoms)
- Small cell (15%) - more Sentral (perihilar mass), more rapid progression and present late, poor prognosis
- Large cell (10%) - outer edge, grow rapidly and present late
- Carcinoid (5%)
c) Squamous cell
- commonly has hypercalcaemia from bone or mets or before metastasising as a result of PTH-rP production (endogenous PTH will be low)
- Gynaecomastia
- Hyperthyroidism
Small cell
- Ectopic ADH secretion causing SIADH and hyponatraemia
- Ectopic ACTH secretion causing Cushing’s syndrome
- Lambert-Eaton myasthenic syndrome - 60% have SCLC. Presents with gradual onset proximal muscle weakness, diminished reflexes and improvement in power with repeated movements. Caused by antibodies to voltage-gated calcium channels (pre-synaptic membrane
- Peripheral neuropathy
Adenocarcinoma
- HPOA most common in this subtype
- Also most associated with dermatomyositis
Carcinoid
- Not associated with smoking, younger patients
Mesothelioma
a) Chromosome abnormality commonly found
b) Risk of pleural drainage
a) Loss of tumour-suppressor material from Chromosome 22
b) Seeding of tumour along the track
Radiation lung injury
a) Early form - diagnosis and management
b) Late form
a) Radiation pneumonitis
- Occurs in the days-weeks following radiation
- Presents with pleurisy, SOB, mild inflammatory response (low-grade temp, mild leukocytosis, etc.), pleural rub
- CXR shows patchy infiltrates
- Rx: high dose steroids + PCP prophylaxis.
If ARDS or failing to respond - IV methylpred + broad spectrum ABx
b) Radiation fibrosis
- Occurs after around 6 months post-radiation
Surgical treatment of lung Ca
a) Functional criteria for pneumonectomy (FEV1, FVC, PaCO2, DLCO)
b) Mediastinal lymph nodes
a) FEV1 > 2L and FVC >1.5L
Normal PaCO2 at rest
DLCO >60% generally (if <40% definitely not for surgery)
b) If <1mm, unlikely to be malignant, PET scan is best way of differentiating inflammatory vs malignant
FeNO testing
a) What is it?
b) Positive test value, and confounding factors
c) Indications for FeNO testing
d) Alternatives for asthma diagnosis
a) Fraction of exhaled nitric oxide
- surrogate marker of airways inflammation (thought to be due to eosinophil mediated inflammation)
b) Age 5-16: FeNO level of ≥35 ppb
Age 17+ : FeNO >40
Factors that may increase FeNO: male, high nitrate diet, current infection/rhinitis/allergen exposure
Factors that may decrease FeNO: children, smoking, treatment with ICS/oral steroid/LTRA
c) Symptoms suggestive of asthma, but negative spirometry and/or negative peak flow variability:
- If FeNO positive, asthma can be diagnosed
d) Spirometry + reversibility
Peak flow diary
Bronchial challenge e.g. histamine, mannitol –> test for sensitivity of airways
Serum eosinophils, serum IgE, skin prick testing
Flow-volume loops
a) Obstructive lung disease (and effect of SABA)
b) Restrictive lung disease
c) Upper airway obstruction (e.g. laryngeal tumour, tracheal stenosis, goitre)
d) Variable extra-thoracic obstruction
e) Variable intra-thoracic obstruction
a) Obstructive (asthma/COPD):
- Reduced PEFR
- Normal inspiration with coving of expiration curve (looks like church with steeple)
- Increased residual volumes (due to hyper-expansion)
SABA leads to increased PEFR and reduced coving if good reversibility (i.e. asthma)
b) Restrictive:
- Reduced lung volumes (including residual volume)
- Reduced PEFR
- No coving, normal expiration
c) UA obstruction:
- Flattening of inspiration and expiration curves
- Increased residual volumes
d) Variable extra-thoracic obstruction:
- Restricted inspiratory phase
e) Variable intra-thoracic obstruction
- Restricted expiratory phase
Sarcoidosis
a) Typical features
b) CXR findings
c) Diagnosis
d) Staging
e) Treatment
a) - Cough, SOB, erythema nodosum, hypercalcaemia
- May have general unwellness
- Most common in African middle-aged people
- Lofgren syndrome: triad of bilateral hilar LN, arthralgia and erythema nodosum
- Ocular involvement common: dry eyes, uveitis
- CNS involvement in 2%
b) Hilar lymphadenopathy, upper lobe granulomas
c) - Initially CXR, then CT chest to demonstrate granulomas/ alveolitis
- May do a biopsy - skin (if lesions present) or transbronchial biopsy (via bronchoscopy) for non-caseating granulomas
- Raised serum ACE in 60%
d) - Stage 0: clear CXR
- Stage 1: Bilateral hilar LN
- Stage 2: Bilateral hilar LN and interstitial infiltrates
- Stage 3: diffuse interstitial disease
- Stage 4: advanced fibrosis
e) - Pulmonary - Treat if symptomatic or stage 2 or above
- Also treat if hypercalcaemia
Or if there is ocular, CNS or cardiac involvement
- Steroids, then steroid sparing agents