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General questions Flashcards

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1
Q

Someone will unilateral pneumonia. What do you do to improve their oxygenation?

A

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

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2
Q

What is considered MDR-TB?

A

Isoniazid and rifampicin resistance

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3
Q

Which TB drug resistance has the worst prognosis?

A

Resistance to fluoroquinolones has the worst prognosis because its used to treat MDR-TB

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4
Q

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
A

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

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5
Q

What’s Aa gradient?

A

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)

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6
Q

What does a normal or raised Aa gradient tell us?

A

Normal - argues against significant lung disease

Raised
- VQ mismatch
E.g. R to L shunt (intrapulmonary or intracardiac), diffusion defect (ILD)

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7
Q

What’s a normal Aa gradient?

A

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
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8
Q

DDx of airway obstruction/stridor

A

VERY COLD DRAFT

V - vocal cord dysfunction
C - conscious state
D - dystonic reaction
R - raging infection
A - Anaphylaxis/angioedema
F - FB
T - trauma/burns
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9
Q

What type of Aa gradient does T1RF have?

A

Wide Aa gradient

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10
Q

Causes of T1RF

A

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)

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11
Q

What does FiO2 mean?

A

Fraction of air that is oxygen

RA = 21%

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12
Q

Definition of T1RF

A

PaO2 <60

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13
Q

Definition of T2RF

A

PaCO2 >45

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14
Q

What type of Aa gradient does T2RF have?

A

Normal

CO2 is great at diffusing across the membrane

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15
Q

Causes of T2RF

A
  • 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)
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16
Q

Which parts on an ABG suggests chronic T2RF?

A

Elevated PaCO2
Normal pH
Elevated HCO3 (if lower than 28, can exclude chronic T2RF)

Often found first in sleep. Nocturnal hypoventilation.

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17
Q

What is the difference between CPAP and BIPAP?

A

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.

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18
Q

Contraindications of NIV

A 
GCS <9
Unable to protect own airway
Upper airway trauma/burns/surgery
Haemodynamic instability
Extreme cardiorespiratory distress
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19
Q

Rx T2 respiratory failure associated with OHS +/- OSA

A

BiPAP

Coexisting OSA, use CPAP

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20
Q

List conditions that are less likely to benefit from NIV

A
  • 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
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21
Q

When to initiate chronic NIV in chronic respiratory failure associated with neuromuscular disease e.g. MND?

A

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
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22
Q

Is long-term NIV indicated in stable COPD?

A

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.

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23
Q

When might long-term NIV be indicated?

A

Neuromuscular or chest wall disease - improve survival and QOL

OHS

Small portion of stable COPD patients

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24
Q

How much HCO3 is compensated for every 1mmol rise in PaCO2?

Acute and chronic setting

A

Acute setting: 1mmol HCO for every 1mmol rise in PaCO2

Chronic setting: 4mmol HCO for every 1mmol rise in PaCO2

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25
How do you work out anion gap or what's a "normal" anion gap?
In metabolic acidosis (Na + K) - (Cl + HCO3) = 11
26
What causes a NAGMA?
Diarrhoea | Renal wasting
27
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 ```
28
How do you work out osmolal gap?
Osm (plasma) - Osm (calculated) Osm calc = (2 x Na) + glucose + urea Abnormal ≥10
29
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 ```
30
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
31
Complications of bronchoscopy
- Transient fever in 25-50% due to cytokine release - Bleeding - generally self limiting - Infection - Hypoxia - Arrhythmia - Injury to adjacent structures - PTX
32
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
33
What's sarcoidosis?
Non-necrotising granulomas in multiple organs usually lungs and lymph nodes Unknown aetiology
34
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
35
How does sarcoidosis cause hypercalcaemia?
Granulomas and macrophages cause increased production of calcitriol (1,25 vitamin D) --> hypercalcaemia
36
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
37
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
38
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 ```
39
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) ```
40
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
41
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
42
What's the difference between primary and secondary PTX?
Primary: no lung disease Secondary: underlying lung disease including significant smoking history
43
Management of tension or haemodynamically unstable PTX
Decompress immediately with chest drain
44
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
45
How do you manage a primary PTX?
>2cm or breathless = aspirate 16-18G Otherwise, discharge and review in OPC 2-4/52
46
What kind of imaging is best to evaluate an incidental lung nodule?
CT without contrast (thin 1mm sections)
47
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)
48
Incidental nodule <6mm | What's your next step?
Generally do nothing. NO need for follow up.
49
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
50
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
51
What is the first branching of the bronchial tree that has gas exchange?
Respiratory bronchioles
52
Inspiration is due to obstruction ... the thoracic inlet | Expiration is due to obstruction ... the thoracic inlet
Above | Below
53
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
54
Significant reduction in DLCO and KCO | DDx
Pulmonary HTN | Emphysema
55
Narcolepsy requires REM sleep within ...
15 minutes
56
What's Klein Levine syndrome?
Episodic periods of hypersomnolence, during this time, some cognitive dysfunction including memory impairment, hypersexuality
57
What's pathognomonic of narcolepsy type 1?
Cataplexy
58
SLE related ILD | Which antibodies?
High ANA titre, dsDNA positive (specific for SLE)
59
NSIP pattern
Bilateral groundglass changes sparing the subpleural area E.g. SLE
60
Most likely ILD pattern in RA
UIP pattern - basal honeycombing, traction bronchiectasis
61
Vast majority of EGPA have ...
Eosinophilic asthma
62
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)
63
Hypoxia not improving with oxygen | 2 DDx
Shunt (intrapulmonary or intracardiac) | Methaemoglobinemia
64
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
65
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
66
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
67
Which lung function parameter has the greatest variability?
DLCO Very difficult to do Lots of variables in the measure
68
``` 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
69
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
70
A normal sinus CT rules out aspirin associated respiratory disease Yes or No
Yes
71
Can you just excise the nasal polyps in aspirin associated respiratory disease?
No | They recur very soon after surgery
72
Diagnostic test for aspirin associated respiratory disease
Aspirin challenge test
73
Treatment aspirin associated respiratory disease
ICS Leukotriene antagonist Nasal steroids Antihistamines IL4 ab for dapilumab (new)
74
Treatment aspirin associated respiratory disease
Aspirin desensitisation therapy | And lifelong aspirin 325mg daily
75
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
76
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)
77
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)
78
Pulmonary nodules <6mm. Follow up?
No

Respiratory (7 decks)

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