General questions Flashcards
Someone will unilateral pneumonia. What do you do to improve their oxygenation?
Lie them on the side without pneumonia
To improve VQ mismatch
Perfusing the normal lung more on the dependent side - below the level of the right ventricle
What is considered MDR-TB?
Isoniazid and rifampicin resistance
Which TB drug resistance has the worst prognosis?
Resistance to fluoroquinolones has the worst prognosis because its used to treat MDR-TB
Smoking history
74M
CT chest bulky mediastinal lymphadenopathy
What is the most likely diagnosis? A) Lung adenocarcinoma B) HL C) Small cell lung cancer D) Germ cell tumour E) Thymic mass
Lung adenocarcinoma - peripheral mass
HL - younger patients with B symptoms
Small cell lung cancer - smoker, central mass
Germ cell tumour - younger patients (20-40 years), 2-4% anterior mediastinal mass
Thymic mass - anterior mediastinal mass; peak incidence 40-60yo
What’s Aa gradient?
Aa gradient assesses the ability of air to transfer from the lungs to the blood effectively. If Aa gradient is normal, argues against significant lung disease contributing to hypoxia or hypercapnia.
=PAO2 (alveolar) - PaO2 (arterial/ABG)
=Partial pressure of oxygen in alveolar - partial pressure of oxygen in artery
PAO2 = 150 - PaCO2/8 (at sea level, room air)
What does a normal or raised Aa gradient tell us?
Normal - argues against significant lung disease
Raised
- VQ mismatch
E.g. R to L shunt (intrapulmonary or intracardiac), diffusion defect (ILD)
What’s a normal Aa gradient?
Normal Aa gradient is 5-10mmHg
- Gradient varies with age and FiO2
- For every decade a person has lived, the Aa gradient is expected to increase by 1mmHg.
- Normal Aa gradient < (age/4) + 4
DDx of airway obstruction/stridor
VERY COLD DRAFT
V - vocal cord dysfunction C - conscious state D - dystonic reaction R - raging infection A - Anaphylaxis/angioedema F - FB T - trauma/burns
What type of Aa gradient does T1RF have?
Wide Aa gradient
Causes of T1RF
1) Alveolar problem - fluid, pus, destruction, collapse
2) Circulation problem - PE, shunt, destruction of capillaries
3) Interstitial problem - fibrosis, infiltration
4) Low Hb (high altitude)
What does FiO2 mean?
Fraction of air that is oxygen
RA = 21%
Definition of T1RF
PaO2 <60
Definition of T2RF
PaCO2 >45
What type of Aa gradient does T2RF have?
Normal
CO2 is great at diffusing across the membrane
Causes of T2RF
- Exac of COPD
- Neuromuscular/chest wall problem e.g. MND
- Central problem e.g. CNS depression
- OHS
- Progression of T1RF (fatigue of respiratory muscles, prior to respiratory arrest)
Which parts on an ABG suggests chronic T2RF?
Elevated PaCO2
Normal pH
Elevated HCO3 (if lower than 28, can exclude chronic T2RF)
Often found first in sleep. Nocturnal hypoventilation.
What is the difference between CPAP and BIPAP?
CPAP provides continuous pressure and a set level of airway support (usually 8-10cmH2O). Primarily used for OSA, APO, OHS.
BIPAP provides different inspiratory and expiratory pressure (e.g. 10/5). Can generate x number of breaths per minute or only initiate breaths when the patient doesnt.
Contraindications of NIV
GCS <9 Unable to protect own airway Upper airway trauma/burns/surgery Haemodynamic instability Extreme cardiorespiratory distress
Rx T2 respiratory failure associated with OHS +/- OSA
BiPAP
Coexisting OSA, use CPAP
List conditions that are less likely to benefit from NIV
- T1RF other than APO
- Pneumonia
- ARDS (most will require intubation)
- Asthma exacerbation (inconclusive data; short trial of NIV only, low threshold for intubation)
- Post-extubation respiratory failure
- Post-op respiratory failure
- Chest trauma-induced respiratory failure
When to initiate chronic NIV in chronic respiratory failure associated with neuromuscular disease e.g. MND?
Patients with progressive disease should be monitored every 3-6 months with RFTs and ABGs
NIV should be started when:
- FVC <50% pred
- VC <60% pred or <1L or <15-20ml/kg
- Maximal inspiratory pressure
Is long-term NIV indicated in stable COPD?
Not usually. CO2 may be improved but no strong evidence to show benefit
Patients who require continuous NIV during an acute exacerbation may benefit from nocturnal NIV after discharge to home.
Stable patients with COPD and nocturnal desaturation despite the use of supplemental oxygen may benefit from NIV. Must exclude OSA.
When might long-term NIV be indicated?
Neuromuscular or chest wall disease - improve survival and QOL
OHS
Small portion of stable COPD patients
How much HCO3 is compensated for every 1mmol rise in PaCO2?
Acute and chronic setting
Acute setting: 1mmol HCO for every 1mmol rise in PaCO2
Chronic setting: 4mmol HCO for every 1mmol rise in PaCO2
How do you work out anion gap or what’s a “normal” anion gap?
In metabolic acidosis
(Na + K) - (Cl + HCO3) = 11
What causes a NAGMA?
Diarrhoea
Renal wasting
What causes a HAGMA?
Suggests the presence of an “umeasured” acid - e.g. lactic acid, uric acid, external toxin
MUDPILES
M - methanol U - uraemia D - DKA P - prophylene glycol I - infection, iron, isoniazid L - lactic acidosis E - ethylene glycol/ethanol S - salicylates
How do you work out osmolal gap?
Osm (plasma) - Osm (calculated)
Osm calc = (2 x Na) + glucose + urea
Abnormal ≥10
List causes of elevated osmolal gap
Presence of other osmotically active particles
PASCALA P - proteins A - alcohols (ETOH, ethylene, isopropyl, propylene, methanol, diethylene) S - sugars (mannitol, glycerol, sorbitol) C - contrast dye A - acidosis (lactic, ketoacidosis) L - lipids A - acetone
How do you work out expected respiratory compensation in metabolic acidosis? (Winter’s formula)
Expected pCO2 = (1.5 x HCO3 + 8) +/- 2
Compare expected pCO2 with measured pCO2
Complications of bronchoscopy
- Transient fever in 25-50% due to cytokine release
- Bleeding - generally self limiting
- Infection
- Hypoxia
- Arrhythmia
- Injury to adjacent structures
- PTX
What’s a granuloma?
A ball of histocytes/macrophages
Can be necrotising or non-necrotising
Necrotising (can be caseating - soft and cheesy) - TB, fungal infection, Wegner’s, rheumatoid nodules
Non-necrotising (usually non-infectious) - Sarcoid, hypersensitivity pneumonitis, drug reaction, leprosy, Beryllium
What’s sarcoidosis?
Non-necrotising granulomas in multiple organs usually lungs and lymph nodes
Unknown aetiology
Pathogenesis of sarcoidosis
Unknown aetiology
Unknown irritant –> T lymphocytes and macrophages come –> enclose the irritant by fusing to become multinucleated giant cells –> can develop fibrosis
How does sarcoidosis cause hypercalcaemia?
Granulomas and macrophages cause increased production of calcitriol (1,25 vitamin D) –> hypercalcaemia
Which organs does sarcoidosis typically affect?
Lung Skin - erythema nodosum, lupus pernio Eye - anterior uveitis Lymph nodes Liver - hepatomegaly Spleen/BM - anaemia, leukopenia Neurologic - facial palsy, headache, seizures, pituitary lesions Cardiac - arrhythmias, cardiomyopathy, PAH
Others - fatigue, weight loss, low grade fever, arthralgia
Investigations in sarcoidosis
FBC - anaemia, leukopenia
CRP/ESR raised
High 1,25 vitamin D + Hypercalcaemia + low PTH
ALP raised in hepatic involvement
ACE raised - secreted by granulomas
CXR - bilateral hilar lymphadenopathy, lung infiltrates, honeycombing/fibrosis in advanced disease
HRCT - high sensitivity compared to CXR, upper lobe predominance
PFTs - restrictive (classic) or obstructive or mixed, mild reduced DLCO (most sensitive), airway hyper-reactivity to metacholine challenge
Transbronchial biopsy - required for diagnosis
Slit lamp opthal exam
Skin biopsy
What do you expect to see on CXR/HRCT in advanced sarcoidosis lung disease?
Upper lobe predominance Honeycombing Thickening of bronchovascular bundles Ground glass changes Parenchymal nodules Traction bronchiectasis
How do you stage sarcoidosis lung disease?
Based on CXR
Stage 0 to 4
0 - normal CXR 1 - bilateral hilar lymphadenopathy 2 - bilateral hilar lymphadenopathy + infiltrates 3 - lung infiltrates alone without LN 4 - pulmonary fibrosis (honeycombing)
Prognosis of sarcoidosis
65% spontaneous remission. Highly variable.
Mortality <5% if untreated, due to respiratory failure, right HF, AMI, CNS involvement
Early stages are more likely to remit
Acute presentations are more likely to remit, while chronic presentations tend to progress
Rx sarcoidosis
Not always required as sarcoidosis can remit spontaneously
Treat symptomatically with NSAIDs
Indications for immunosuppressants:
- Worsening symptoms or reduced ET
- Significant lung infiltrates
- Significantly abnormal PFTs
- Disabling skin or joint disease
- Myocardial, neuro, hepatic, renal, ocular involvement
1st line: prednisolone +/- topical steroids for skin/eyes
2nd line: MTX
3rd line: azathioprine, hydroxychloroquine, chlorambucil, infliximab, cyclosporin
Last line: lung transplant but disease can reoccur
What’s the difference between primary and secondary PTX?
Primary: no lung disease
Secondary: underlying lung disease including significant smoking history
Management of tension or haemodynamically unstable PTX
Decompress immediately with chest drain
How do you manage a secondary PTX?
> 2cm or breathless = chest drain
1-2cm = aspirate 16-18G
None of the above = high flow oxygen, admit, observe for 24 hours
How do you manage a primary PTX?
> 2cm or breathless = aspirate 16-18G
Otherwise, discharge and review in OPC 2-4/52
What kind of imaging is best to evaluate an incidental lung nodule?
CT without contrast (thin 1mm sections)
What features about an incidental lung nodule would make you suspicious of malignancy and should be evaluated with biopsy?
- Nodule is >8mm
> Low suspicion for Cancer - CT surveillance
> Intermediate/High suspicion - biopsy - Growth of the nodule - increased attenuation or size (>2mm) or development of a solid component
- Lack of benign features - fat (hamartoma) or characteristic calcification pattern (granuloma, hamartoma)
Incidental nodule <6mm
What’s your next step?
Generally do nothing. NO need for follow up.
Incidental nodule 6-8cm
What’s your next step?
Monitor with CT in 6-12 months
If growing then need biopsy
If unchanged, determine malignancy risk, and repeat chest CT at 18-24 months if high or intermediate malignancy risk, no further follow up if low malignancy risk
Incidental nodule >8cm
What’s your next step?
Determine malignancy risk
If high or intermediate malignancy risk, do biopsy
If low suspicion - repeat CT chest in 3/12
What is the first branching of the bronchial tree that has gas exchange?
Respiratory bronchioles
Inspiration is due to obstruction … the thoracic inlet
Expiration is due to obstruction … the thoracic inlet
Above
Below
DLCO =
KCO (how well CO diffuses across membrane) x VA (alveolar volume)
KCO is affected by membrane (thickness, surface area) and amount of Hb available for diffusion
Significant reduction in DLCO and KCO
DDx
Pulmonary HTN
Emphysema
Narcolepsy requires REM sleep within …
15 minutes
What’s Klein Levine syndrome?
Episodic periods of hypersomnolence, during this time, some cognitive dysfunction including memory impairment, hypersexuality
What’s pathognomonic of narcolepsy type 1?
Cataplexy
SLE related ILD
Which antibodies?
High ANA titre, dsDNA positive (specific for SLE)
NSIP pattern
Bilateral groundglass changes sparing the subpleural area
E.g. SLE
Most likely ILD pattern in RA
UIP pattern - basal honeycombing, traction bronchiectasis
Vast majority of EGPA have …
Eosinophilic asthma
For a standard dissociation curve, decrease in which factor will cause a right shift in the curve?
Decrease Hb saturation to oxygen
Think about a working muscle…
Increase hydrogen ions (acid = lactic acid)
Increase CO2
Increase temperature
Increase ,2,3 DPG (red cell metabolic byproduct)
Hypoxia not improving with oxygen
2 DDx
Shunt (intrapulmonary or intracardiac)
Methaemoglobinemia
What is Methaemoglobin?
Doesn’t carry oxygen
But allows the remaining Hb to bind to oxygen more tightly –> can’t be delivered to organs
Standard pulse oximetry cannot detect Hb-Fe3+ (methhaemoglobin) = typically measured at SpO2 85%
Can turn blue
How does VQ change from apex to base?
Both ventilation and perfusion increase at the bases
But proportionally, VQ ratio decreases (more perfusion than ventilation increase) at the base
How does pulmonary haemorrhage falsely elevate DLCO?
Already RBCs in the alveolar. Don’t need to travel through the alveolar basement membrane.
Hence falsely elevated DLCO in pulmonary haemorrhage
Which lung function parameter has the greatest variability?
DLCO
Very difficult to do
Lots of variables in the measure
Which of the following decreases during a normal pregnancy? A) Minute ventilation B) Vital capacity 3) Serum HCO3 4) Arterial pH
Serum HCO3
During pregnancy, increased MV and O2 uptake mainly driven by increase in tidal volume
Ve = RR x TV (main increase)
Increased RR = metabolic alkalosis in late pregnancy
Aspirin associated respiratory disease presentation
Mucosal swelling of sinuses and nasal membranes, formation of nasal polyps and asthma
Symptoms after ingesting aspirin/NSAIDs, ETOH
Upper airway symptoms and lower respiratory tract symptoms (laryngospasm, cough, wheeze)
GI and skin manifestation
A normal sinus CT rules out aspirin associated respiratory disease
Yes or No
Yes
Can you just excise the nasal polyps in aspirin associated respiratory disease?
No
They recur very soon after surgery
Diagnostic test for aspirin associated respiratory disease
Aspirin challenge test
Treatment aspirin associated respiratory disease
ICS
Leukotriene antagonist
Nasal steroids
Antihistamines
IL4 ab for dapilumab (new)
Treatment aspirin associated respiratory disease
Aspirin desensitisation therapy
And lifelong aspirin 325mg daily
What are the Fleischner guidelines?
Guidelines for monitoring of asymptomatic pulmonary nodules
Don’t apply to age <35, those with known cancer and those who are immunosuppressed
Do we need to monitor groundglass nodules for as long as solid nodules?
Groundglass nodules need to be followed for longer due to their slow growth - now recommended 5 years (solid nodules are usually monitored for 2 years)
Risk factors for pulmonary nodules
Nodule
- Size - >2cm extremely high risk; <6mm extremely low risk
- Margins - spiculated
- Location - upper lobes more likely cancer
- Number of nodules - lower risk with >5 nodules
Patient factors
- Age - >50 is higher risk
- Smoking status - 30pyh and quitting within 15 years
- Presence of emphysema and fibrosis (adenocarcinomas can develop in scars)
Pulmonary nodules <6mm. Follow up?
No
