Respiratory Flashcards

1
Q

Expected findings in obstructive spirometry?

A

FEV1:FVC ratio <70% (below the 1.64 Z score)
FEV1 <80% predicted
FVC normal
Concave scooping of flow-volume loop

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

Expected findings in restrictive spirometry

A

Normal FEV1: FVC ratio
Low FVC

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

Expected findings in mixed restrictive and obstructive spirometry

A

Reduced FEV1:FVC
Low FEV1 and
Low FVC

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

Expected flow-volume loop in fixed central or upper airway obstruction

A

Box shaped

(eg subglottic stenosis or tracheal stenosis)

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

Expected flow-volume loop in variable extrathoracic airway obstruction?

A

Flattened inspiratory loop
(eg laryngeal paralysis or vocal cord dysfunction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Expected flow-volume loop with variable intrathoracic airway obstruction (Eg tracheomalacia)

A

Flattended expiratory loop with relatively normal inspiratory loop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causes of oxygen dissociation curve shift to the right (reduced affinity)?

A

Increased temp
Increased 2,3 DPG
Increased H+ (acidosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of oxygen dissociation curve shift to left (higher affinity of Hb for O2)

A

Carbon monoxide
Lower temp
Lower 2,3 DPG
Lower H+

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

Most common organism resulting in bronchiolitis obliterans?

A

Adenovirus (serotypes 3, 7, 21)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

CT findings in bronchiolitis obliterans

A

Mosaic attenuation
Gas trapping
Hyperinflation
Central bronchiectasis (tram tracks)

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

What is Idiopathic Pulmonary Haemosiderosis?

A

Accumulation of haemosiderin inside pulmonary macrophages that occurs after recurrent haemoptysis without a clear cause
- Managed with steroids or immunosuppression

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

Most common class of CFTR mutation?

A

Class II (delta F508)
- “trafficking” mutation due to missense (CFTR protein is misfolded, keeping it from moving to cell surface)

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

What class of mutation are G551D and S549N?

A

Class III mutation - “gating mutation”
- CFTR moves to the cell surface but the channel gate does not open properly

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

Which classes of CFTR mutation are usually associated with pancreatic insufficiency?

A

Class 1-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What defines CFPID?

A
  1. Sweat chloride <30 and 2 variants and at least 1 of unclear phenotype
  2. Sweat chloride 30-59 and 1 CF causing variant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What defines CF?

A
  1. Sweat chloride >60 OR
  2. Sweat chloride 30-59 with 2 CF causing variants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Causes of false positive sweat test

A

Adrenal insufficiency
Hypothyroidism and hypoparathyroidism
GSD
MPS
G6PD deficiency
Diabetes Insipidus

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

IV treatment of pseudomonas in CF?

A

IV tobramycin + ceftazidime or
IV meropenem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does Ivacaftor work?

A

partially corrects the Cl- channel defect, allowing Cl- transport - helpful for class III “gating” mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which classes of mutation can Trikafta be used for

A

Class 2-6 (incl class 2 - delta F508)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does trikafta work?

A

Contains corrector and potentiators”

Helps more protein reach the cell surface and to stay open for longer at the cell surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Side effects of Trikafta

A

*Rash incl SJS
*Liver dysfunction
*Headache
*Cataracts
* Mood disturbance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Benefits of Trikafta

A

Improved lung function
Reduced exacerbations
Improved BMI
Reduced sweat chloride
Reduced symptom scores

24
Q

How much creon per g of fat?

A

Creon 10 000 units for each 6-8g fat

25
Q

Poor prognostic factors in CF

A

Burkholderia cepacia
Pseudomonas
CFRD
Malnutrition
Frequent exacerbations
Female gender

26
Q

A mass of abnormal, non-functioning lung tissue isolated from normal functioning lung tissue and fed by systemic arteries, often found in left lower lobe

A

Pulmonary sequestration

27
Q

Stages of sleep

A

N1= transition to light sleep
N2= light sleep (k complexes and spindles)
N3= deep sleep - very hard to rouse
REM= decreased tone, rapid eye movement, vivid dreams

28
Q

Definition of apnoea

A

> /= 90% decrease in baseline flow for 2 or more respiratory cycles

Obstructive = continued effort
Central= absence of effort (no chest movement) + desaturated >3% or arousal

29
Q

Definition of hypopnoea

A

> /= 30% decrease in baseline flow for 2 or more respiratory cycles with desaturated or arousal

30
Q

Genetic mutation in congenital central hypoventilation syndrome?

A

PHOX2B (autosomal dominant)

31
Q

Conditions associated with congenital central hypoventilation syndrome?

A

Hirschsprung disease
Failure to develop fever when unwell
Neural crest tumours eg neuroblastoma
Iris problems
Cardiac arrhythmia

32
Q

Management of narcolepsy

A

Dexamphetamine or methylphenidate
2nd line = modafinil (with authority)

33
Q

Management of cataplexy

A

Fluoxetine or venlafaxine

BEST treatment is sodium oxybate (GHB) but safety concerns

34
Q

Tests for narcolepsy

A
  1. Multiple sleep latency test (MSLT): need abnormal latency (<8mins) and 2+ REM onsets
  2. HLA DR2, DRB1*0602
  3. Low Hypocretin1 levels in CSF (rarely done)
35
Q

What stage of sleep do night terrors occur in?

A

N3
More common in first part of night

36
Q

What is sleep onset association disorder?

A

A type of behavioural insomnia where child needs certain conditions to fall asleep eg being rocked or fed and can’t self-soothe. Unable to get back to sleep without same routine

37
Q

What is limit-setting sleep disorder?

A

A type of behavioural insomnia seen in young children where they protest and actively resist going to bed -> delayed sleep onset and inadequate sleep

38
Q

What is ‘delayed sleep phase’

A

Delay in going to sleep seen in adolescent due to decreased and delayed melatonin peak and exacerbated by after school sport/homework/texting, TV etc

39
Q

Difference between night terror and nightmare?

A

Night terror
- child unable to be comforted
- goes straight back to sleep
- cannot recall event
- occurs in Non-REM sleep (N3)

40
Q

Mild, moderate and severe OSA by OAHI

A

Mild: 1-5/hr
Moderate: 5-10/hr
Severe: >10/hr

41
Q

Which stage of sleep do sleep talking, bruxism and periodic leg movements occur?

A

Both REM and NREM sleep

42
Q

MOA of omalizumab?

A

Anti-IgE

43
Q

MOA of mepolizumab?

A

Anti- IL5

44
Q

MOA of dupilumab?

A

Anti-IL4 and IL13

45
Q

What would you expect the FeNO to be in asthma?

A

FeNO usually elevated (>25ppb) in asthma

46
Q

What is considered as positive bronchodilator response on spirometry?

A

Increase in FEV1 of >/= 12% and/or 200ml

47
Q

Low dose flixotide?

A

100microg /day

48
Q

Standard dose flixotide?

A

200-250microg/day

49
Q

Step up approach in a 5-11yr old with asthma?

A
  1. Low dose ICS
  2. Standard dose ICS/LABA eg Symbicort or breo
  3. Add montelukast if poor control
  4. High dose ICS/LABA and refer to respiratory (may need to consider biologic)
50
Q

Tests for primary ciliary dyskinesia

A
  • Nasal NO (low) - screening test
  • Electron microscopy of nasal or bronchial biopsy
  • Videomicroscopy analysis of nasal brush biopsy
  • Genetics (only identifies 50-60%)
51
Q

Features of Kartagener syndrome?

A
  1. PCD
  2. Situs inversus
  3. Chronic sinusitis
52
Q

4 features of chronic rinosinusitis?

A
  1. facial pain
  2. nasal obstruction
  3. nasal mucopurulent drainage
  4. cough
53
Q

Findings on pleural fluid analysis in empyema?

A

High protein
High LDH
Low glucose

54
Q

Difference between transudative and exudative (eg empyema) pleural effusions?

A

Exudative effusions will have high protein and LDH

55
Q
A