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RACP > Respiratory > Flashcards

Respiratory Flashcards

1
Q

How many airway generations are there?

A

23

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2
Q

At what airway generation is airway resistance maximal and minimal? When do you switch from the conducting zone to the respiratory zone?

A

Airway resistance peaks at gen 5
Airway resistance is negligible at general 15
Switch from conducting to respiratory zone at gen 15

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3
Q

How do you define asthma?

A

Symptoms consistent with asthma
+ airway obstruction that is either reversible/variable/inducible
+ bronchial hyper-responsiveness
+ airway inflammation

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4
Q

What investigations are available for diagnosis of asthma?

A
  • spirometry: significant reversibility if increase in FEV1 by 200ml AND > 12%
  • peak flow monitoring/variability measurement:
    highest PF - lowest PF/lowest PF = >20% is significant
  • lab confirmation of bronchial hyper-responsiveness
  • non-invasive assessment of airway inflammation: exhaled NO, blood eosinophil count
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5
Q

What is the indirect method of airway hyper responsiveness?

A
  • mannitol/hypertonic saline/adenosine, exercise challenge
  • activates mast cells to release histamine and other constrictor mediators.
  • reflects the inflammatory component of airway hyperresponsiveness
  • > 15% fall in FEV1 is significant
  • very specific test i.e. rule in
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6
Q

What is the direct method of airway hyperresponsiveness? What are the causes of false positives?

A
  • direct constriction of smooth muscle in the airway e.g. methacoline, histamine
  • reflects the persistent airway remodelling component of AHR
  • > 20% fall in FEV1 is significant
  • sensitive test i.e. rule out
  • causes of false positives: allergic rhinitis, CF, HF, COPD, bronchiectasis
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7
Q

Normal Spiro does not exclude asthma. What are the common reasons for lack of reversibility?

A
  • A normal baseline FEV1
  • recent bronchodilator use
  • airway inflammation and oedema (poorly controlled asthma) - reversibility may return after treatment
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8
Q

How do you define intermittent and persistent asthma?

A

Intermittent: Normal FEV1, symptoms/SABA <2x/weekm no limitations
Persistent:
2 or more course of OCS in 1 year
- Mild: normal FEV1, minor limitations, symptoms/SABA >2x/week
- Moderate: mildly abnormal FEV1, daily symptoms, some limitation or severe exacerbations requiring hospital presentation or admission
- Severe: FEV1 <60%, daily symptoms + nocturnal, limited function, ICU admission

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9
Q

What is thw 2019 GINA treatment strategy for asthma?

A

Step 1: PRN LABA/ICS
Step 2: Daily low dose ICS or PRN LABA/ICS
Step 3: Low dose ICS/LABA
Step 4: medium dose ICS/LABA
Step 5: high dose ICS/LABA
+ refer for phenotypic testing and consider add on therapy

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10
Q

What did the START study show?

A

Compared ICS vs placebo in mild, persistent asthma:

  • fewer exacerbations
  • more symptom free days, less OCS
  • Small but significant improvement in FEV1
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11
Q

How does intermittent ICS/LABA compare to regular ICS?

A
  • non-inferior
  • regular ICS better than intermittent ICS/LABA for symptom control
  • Once on a regular/intermittent ICS, more benefit from adding in LABA than increasing ICS
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12
Q

What add on therapies are available for asthma?

A
  • tiotropium if persistent airflow obstructing and hx of recurrent exacerbations
  • macrolide: reduces exacerbations, cough and sputum
  • Montelukast: for aspirin sensitive asthma
  • monoclonal abs for repeated exacerbations and some elevation of a type 2 biomarker
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13
Q

What biologicals are available for severe asthma?

A

Allergic asthma:

  • suggested if high level of exhaled NO:
  • target IgE, use omalizumab (binds Fc region of IgE)

Eosinophilic asthma:

  • indicated by raised serum eosinophil count >150-300 or sputum eosinophils >3%. Suggests TH2 mediated asthma.
  • target Il5 or Il5R: mepolizumab or benralizumab
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14
Q

How does benralizumab work? what outcome does it have the greatest impact on? What are Sesames and how does it effect your FEV1?

A
  • Depletes Il5 receptor bearing cells (eosinophils, basophils)
  • reduces exacerbation rate, corticosteroid sparing effect
  • SEs: pharyngitis, headaches
  • No effect on FEV1
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15
Q

What is dupilumab? In whom is it effective?

A

A human anti-Il-4 receptor MAB that blocks Il4 and Il13

  • effective for mod-severe asthma
  • greatest benefit for those with higher baseline level of eosinophils.
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16
Q

What is tezepelumab?

A

anti-thymic stromal lymphopoietin = epithelial derived cytokine critical to the development of type 2 allergic asthma

17
Q

What are the RFs for asthma exacerbations?

A 
Previous intubation
Uncontrolled asthma symptoms
1 or more exacerbations per year
Low FEV1
poor inhaler technique/adherence
Smoking
Elevated FeNO in adults with allergic asthma
Obesity
Pregnancy
Blood eosinophilia
18
Q

What are the RFs for fixed airflow limitation?

A 
No ICS treatment
Smoking
occupational exposure
mucous hyper secretion
blood eosinophilia
19
Q

What asthma variants do you need to be aware of and what are they?

A

Samter’s triad: asthma, asthma intolerance and nasal polyps

ABPA:

  • chronic asthma, recurrent pulmonary infiltrates, bronchiectasis
  • Very high total IgE (>1000)
  • evidence of aspergillum sensitivity

EGPA:

  • necrotising vasculitis, granulomas, tissue eosinophilia
  • asthma + eosinophila essential
  • evidence of multi system disease
  • some overlap with PAN but severe renal involvement uncommon
20
Q

How do you characterise REM sleep and what proportion of total sleep does it usually make up?

A

Makes up 20% of TST, mainly 2nd half of the night

Characterised by atone and tonic/phasic eye movements (EOG)

21
Q

How do you define an apnoea and a hypopnea?

A

apnoea: cessation of air flow for 10s +
- if with presence of respiratory effort = OSA
- if without presence of respiratory effort = central

hypopnea: reduction of airflow by at least 30% for 10+s followed by:
- 4% oxygen desaturation or
- EEG arousal

22
Q

What is a RERA?

A

Respiratory effort related arousal:

  • doesn’t meet criteria for a hypopnea
  • events of increased respiratory effort for 10s+ associated with an EEG arousal.
23
Q

What is AHI?

A

The number of apnoeas and hypopnoeas per hour.

24
Q

How do you define sleep hypoventilation?

A
  • Transcutanaeous CO2 (TcCO2) increases to >55mmHg for 10 mins + or
  • > 10mmHg increase during sleep compared to awake/supine to the value of 55mmHg for 10 mins
25
Q

What is Cheyne Stokes Respiration?

A

Recurrent central apnoeas/hypopnoeas alternating with a respiratory phase exhibiting a crescendo-decrescendo pattern of flow.
- long length cycle >40s
Associated with CCF/neurological disorders

26
Q

How do you define OSA?

A

Repetitive apnoeas/hypopnoeas due to partial or total collapse of the upper airways during sleep.

27
Q

What is the strongest RF for OSA?

A

obesity

28
Q

What is the pathogenesis of OSA?

A

onset of sleep causes relaxation of the upper airway muscles.
inspiration causes negative airway pressure and collapses the soft tissue causing obstruction.
Obstruction causes apnoea/hypopnea and then drop in O2 sats
This leads to increased sympathetic activity (increased CV risk)
Drop in O2 sats leads to arousal from sleep.
This increases upper airway tone again and cessation of the apnoea.

29
Q

What are the criteria for diagnosis of OSA?

A

AHI >5/hr + 1 symptom attributable to OSA

or just AHI >15/hr

30
Q

What is the treatment for central sleep apnoea?

A

Trial of CPAP
Treat the underlying cause
Consider ASV ventilator but avoid in patients with reduced EF as may increase mortality

31
Q

What are the complications of untreated OSA?

A
  • increased all cause mortality
  • Increased MVAs
  • HTN, MIs, CCF, arrhythmias, stroke
  • pulmonary HTN
  • metabolic dysregulation
32
Q

What does CPAP improve for OSA?

A

Eay time sleepiness, depression, cogs, QOL, blood pressure, reduces MVAs
No RCT evidence that it can reduce CV mortality

33
Q

How do you define OHS?

A
  • awake hypercapnia (>45)
  • BMI > 30
  • sleep disordered breathing when other causes of hypoventilation have been excluded.
34
Q

What is the pathophysiology of OHS?

A

Obesity causes increased mechanical load and leptin resistance (leptin is a potent respiratory stimulant centrally) causing a blunted ventilatory response.
Acute hypercapnia occurs during sleep which results in decreased compensatory hyperventilation and reduced HCO3- excretion.
The end result is chronic hypercapnia

35
Q

What is OHS associated with ?

A

How do you treat OHS and why is it important?
- if co-existing OSA, CPAP usually first choice
- If minimal OSA, usually NIV
OHS has a high association with CV disease.
weight loss and PAP improves survival.
RCT in 2019 showed no difference between CPAP and NIV

36
Q

How do you define narcolepsy?

A

Sleep latency < 8 mins associated with 2 sleep onset REM periods

37
Q

What is the pathogenesis of narcolepsy?

A

autoimmune destruction of hypothalamic neurons that produce hypocretin. Hypocretin regulates arousal and transition between wake and sleep.

38
Q

What are the 2 types of narcolepsy?

A

Type 1: excessive day time sleepiness for at least 3 months. + one of either cataplexy and positive MSLT or low CSF hypocretin
Type 2: EDS for 3 months, no cataplexy, positive SLT and normal CSF hypocretin.

39
Q

How do you treat narcolepsy?

A

stimulant therapy e.g. dexamphetamine or wake promoting agent such as armodafinil.
SSRI/SNRI for cataplexy

RACP (3 decks)

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