Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Respiratory > General questions > Flashcards

General questions Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is considered MDR-TB?

A

Isoniazid and rifampicin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What type of Aa gradient does T1RF have?

A

Wide Aa gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does FiO2 mean?

A

Fraction of air that is oxygen

RA = 21%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Definition of T1RF

A

PaO2 <60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Definition of T2RF

A

PaCO2 >45

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What type of Aa gradient does T2RF have?

A

Normal

CO2 is great at diffusing across the membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Contraindications of NIV

A 
GCS <9
Unable to protect own airway
Upper airway trauma/burns/surgery
Haemodynamic instability
Extreme cardiorespiratory distress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Rx T2 respiratory failure associated with OHS +/- OSA

A

BiPAP

Coexisting OSA, use CPAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do you work out anion gap or what’s a “normal” anion gap?

A

In metabolic acidosis

(Na + K) - (Cl + HCO3) = 11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What causes a NAGMA?

A

Diarrhoea

Renal wasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What causes a HAGMA?

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How do you work out osmolal gap?

A

Osm (plasma) - Osm (calculated)

Osm calc = (2 x Na) + glucose + urea

Abnormal ≥10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

List causes of elevated osmolal gap

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How do you work out expected respiratory compensation in metabolic acidosis? (Winter’s formula)

A

Expected pCO2 = (1.5 x HCO3 + 8) +/- 2

Compare expected pCO2 with measured pCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Complications of bronchoscopy

A
  • Transient fever in 25-50% due to cytokine release
  • Bleeding - generally self limiting
  • Infection
  • Hypoxia
  • Arrhythmia
  • Injury to adjacent structures
  • PTX
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What’s a granuloma?

A

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
Q

What’s sarcoidosis?

A

Non-necrotising granulomas in multiple organs usually lungs and lymph nodes

Unknown aetiology

34
Q

Pathogenesis of sarcoidosis

A

Unknown aetiology

Unknown irritant –> T lymphocytes and macrophages come –> enclose the irritant by fusing to become multinucleated giant cells –> can develop fibrosis

35
Q

How does sarcoidosis cause hypercalcaemia?

A

Granulomas and macrophages cause increased production of calcitriol (1,25 vitamin D) –> hypercalcaemia

36
Q

Which organs does sarcoidosis typically affect?

A 
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
Q

Investigations in sarcoidosis

A

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
Q

What do you expect to see on CXR/HRCT in advanced sarcoidosis lung disease?

A 
Upper lobe predominance
Honeycombing 
Thickening of bronchovascular bundles
Ground glass changes
Parenchymal nodules
Traction bronchiectasis
39
Q

How do you stage sarcoidosis lung disease?

A

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
Q

Prognosis of sarcoidosis

A

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
Q

Rx sarcoidosis

A

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
Q

What’s the difference between primary and secondary PTX?

A

Primary: no lung disease
Secondary: underlying lung disease including significant smoking history

43
Q

Management of tension or haemodynamically unstable PTX

A

Decompress immediately with chest drain

44
Q

How do you manage a secondary PTX?

A

> 2cm or breathless = chest drain
1-2cm = aspirate 16-18G

None of the above = high flow oxygen, admit, observe for 24 hours

45
Q

How do you manage a primary PTX?

A

> 2cm or breathless = aspirate 16-18G

Otherwise, discharge and review in OPC 2-4/52

46
Q

What kind of imaging is best to evaluate an incidental lung nodule?

A

CT without contrast (thin 1mm sections)

47
Q

What features about an incidental lung nodule would make you suspicious of malignancy and should be evaluated with biopsy?

A
  • 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
Q

Incidental nodule <6mm

What’s your next step?

A

Generally do nothing. NO need for follow up.

49
Q

Incidental nodule 6-8cm

What’s your next step?

A

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
Q

Incidental nodule >8cm

What’s your next step?

A

Determine malignancy risk
If high or intermediate malignancy risk, do biopsy
If low suspicion - repeat CT chest in 3/12

51
Q

What is the first branching of the bronchial tree that has gas exchange?

A

Respiratory bronchioles

52
Q

Inspiration is due to obstruction … the thoracic inlet

Expiration is due to obstruction … the thoracic inlet

A

Above

Below

53
Q

DLCO =

A

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
Q

Significant reduction in DLCO and KCO

DDx

A

Pulmonary HTN

Emphysema

55
Q

Narcolepsy requires REM sleep within …

A

15 minutes

56
Q

What’s Klein Levine syndrome?

A

Episodic periods of hypersomnolence, during this time, some cognitive dysfunction including memory impairment, hypersexuality

57
Q

What’s pathognomonic of narcolepsy type 1?

A

Cataplexy

58
Q

SLE related ILD

Which antibodies?

A

High ANA titre, dsDNA positive (specific for SLE)

59
Q

NSIP pattern

A

Bilateral groundglass changes sparing the subpleural area

E.g. SLE

60
Q

Most likely ILD pattern in RA

A

UIP pattern - basal honeycombing, traction bronchiectasis

61
Q

Vast majority of EGPA have …

A

Eosinophilic asthma

62
Q

For a standard dissociation curve, decrease in which factor will cause a right shift in the curve?

A

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
Q

Hypoxia not improving with oxygen

2 DDx

A

Shunt (intrapulmonary or intracardiac)

Methaemoglobinemia

64
Q

What is Methaemoglobin?

A

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
Q

How does VQ change from apex to base?

A

Both ventilation and perfusion increase at the bases

But proportionally, VQ ratio decreases (more perfusion than ventilation increase) at the base

66
Q

How does pulmonary haemorrhage falsely elevate DLCO?

A

Already RBCs in the alveolar. Don’t need to travel through the alveolar basement membrane.
Hence falsely elevated DLCO in pulmonary haemorrhage

67
Q

Which lung function parameter has the greatest variability?

A

DLCO
Very difficult to do
Lots of variables in the measure

68
Q 
Which of the following decreases during a normal pregnancy?
A) Minute ventilation
B) Vital capacity
3) Serum HCO3
4) Arterial pH
A

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
Q

Aspirin associated respiratory disease presentation

A

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
Q

A normal sinus CT rules out aspirin associated respiratory disease
Yes or No

A

Yes

71
Q

Can you just excise the nasal polyps in aspirin associated respiratory disease?

A

No

They recur very soon after surgery

72
Q

Diagnostic test for aspirin associated respiratory disease

A

Aspirin challenge test

73
Q

Treatment aspirin associated respiratory disease

A

ICS
Leukotriene antagonist
Nasal steroids
Antihistamines

IL4 ab for dapilumab (new)

74
Q

Treatment aspirin associated respiratory disease

A

Aspirin desensitisation therapy

And lifelong aspirin 325mg daily

75
Q

What are the Fleischner guidelines?

A

Guidelines for monitoring of asymptomatic pulmonary nodules

Don’t apply to age <35, those with known cancer and those who are immunosuppressed

76
Q

Do we need to monitor groundglass nodules for as long as solid nodules?

A

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
Q

Risk factors for pulmonary nodules

A

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
Q

Pulmonary nodules <6mm. Follow up?

A

No

Respiratory (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions