Respiratory Flashcards

(55 cards)

1
Q

COPD diagnosis

A

FEV1/FVC ratio <70% + symptoms of COPD

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2
Q

COPD severity

A

Based on FEV1

Gold 1: >80%
Gold 2: 50-79%
Gold 3: 30-49%
Gold 4: <30%

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3
Q

COPD therapy

A

For symptoms
LAMA mono therapy first line
LAMA/LABA 2nd line

Prevent exacerbations
ICS/LABA or LAMA/LABA first
Triple therapy

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4
Q

Factors that do not favour the use of ICS in COPD

A

Repeated pneumonias
Blood eosinophils <100cells/uL
History of mycobacterial infection

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5
Q

Patients who benefit most from triple therapy

A

If blood eosinophils >150

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6
Q

Pharmacotherapy for smoking cessation - MOAs and side effects

A

Vareniciline
-MOA: Nicotine receptor partial agonist, cholinergic agonist
-SE: Avoid if unstable psychiatric symptoms or S.I
Nausea, insomnia, abnormal dreams, nasopharyngitis

Buproprion
-MOA: Nicotine receptor antagonist and norepinephrine-dopamine re-uptake inhibitor
-Avoid in those with bipolar disorder
-SE: Dry mouth, nausea, constipation
Less effective than varenicicline

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7
Q

Asthma spirometry

A

May show obstruction
Reversibility: >12% AND >200mls. Large response 15-20% is particularly suggestive

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8
Q

Asthma bronchoprovocation testing
Direct and indirect

A

Direct: Metacholine = >20% fall in FEV1. Good NPV for excluding active asthma. False positives seen in allergic rhinitis, CF, HF, COPD

Indirect: Mannitol or hypertonic saline (4.5%) = 15% fall in FEV1. Better PPV for asthma than metacholine
Exercise or eucapnic voluntary hyperpnea

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9
Q

Other non-invasive tests for asthma

A

PEFR - variable PEFR consistent with asthma

FeNO - Increased in the presence of eosinophilic inflammation. Higher levels predict glucocorticoid response. Levels can be influenced by smoking (down), and atopy (up)

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10
Q

Asthma stepwise treatment

A
  1. PRN low dose ICS/formoterol
  2. Regular low dose ICS/formoterol + PRN
  3. Regular medium dose ICS/formoterol + PRN
  4. Add on LAMA, consider biologics
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11
Q

Asthma biologic - Anti IgE drug

A

Omelizumab
Binds free IgE and prevents binding to mast cells, basophils, eosinophils and T cells
SE: 1-2/1000 anaphylaxis
Give if increased IgE, atopy, asthma

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12
Q

Asthma biologics - Anti IL5 and IL5R

A

Mepolizumab = anti IL-5
Benralizumab = antil IL-5R

IL5 mediates eosinophil growth, differentiation, recruitment and activation
Need peripheral eosinophils >150 but ideally >300
Decreases oral steroid use

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13
Q

Asthma biologics - Anti IL4 and IL13

A

Dupilumab
Initially approved for atopic dermatitis
Need increased IgE or eosinophils to access

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14
Q

Asthma biologics - Anti thyme stromal lymphopoietin (TSLP)

A

Tezepelumab
TSLP is an epithelial cell derived cytokine, upstream of IL4/5/13 and IgE
Benefits regardless of eosinophil count

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15
Q

Nintedanib MOA and SE

A

MOA - inhibits multiple TKIs
SE: DIARRHOEA, nausea, LFT derangement

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16
Q

Pirfenidone MOA and SE

A

MOA - inhibits TGF-beta and fibroblast proliferation
Slows rate of FEV FVC decline but no differences in SOB

SE: Rash, nausea, diarrhoea

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17
Q

NSIP radiological features

A

Ground glass changes
Reticular opacities
Traction bronchiectasis
Diffuse - can have sub pleural sparing

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18
Q

UIP radiological features

A

Honeycombing
Traction bronchiectasis
Reticular opacities (peripheral and lower lobe predominant)
No atypical features

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19
Q

Causes of NSIP

A

CTD
HIV
Drugs (amiodarone, HIV, flecainide, nitrofurantoin)
Hypersensitivity pneumonitis

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20
Q

NSIP prognosis

A

Tends to be better than UIP and indicate potential for a response to immunosuppression

Pred –> Aza or MMF –> cyclo or ritux –> lung transplant

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21
Q

Causes of upper lobe ILD

A

A TEA SHOP

A- ABPA
T- Tb
E- Extrinsic allergic alveolitis
A- Ank spond
S- Sarcoid
H- Histocytosis
O- Occupational (silicosis, berylliosis)
P- Pneumoconiosis (coal workers)

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22
Q

Sarcoid investigations

A

Diagnosis of exclusion - requires biopsy unless clear syndrome e.g. Lofgren syndrome

Bronch: Increased CD4:CD8 ratio supportive
EBUS: positive in 80-90%

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23
Q

Indications for treatment in sarcoid

A

Progressive symptomatic pulmonary involvement
Progressive loss of lung function
Cardiac or neurological disease
Eye disease not responding to topical therapy
Symptomatic hypercalcaemia
Other symptomatic/progressive extra pulmonary disease

24
Q

Sarcoid treatment

A

Oral steroids first line
Steroid sparing agents: MTX/HCQ/Aza

Inhaled steroids can help with cough

25
Lofgren syndrome
Acute sarcoid presentation Triad of: 1. Erythema nodosum 2. Fever 3. Bilateral hilar lymphadenopathy
26
Causes of bronchiectasis
Idiopathic 40% Post infectious 30% Immunodeficiency 5% COPD/CTD/ABPA 5% each
27
Macrolides in bronchiectasis
Useful for frequent exacerbations (>= 3 per year) Decreases exacerbation frequency No change in QOL or FEV1
28
Pseudomonas in bronchiectasis
Independent risk factor for mortality
29
ABPA epidemiology, presentation and investigations
Almost exclusively in asthma or CF patients Chronic asthma, recurrent pulmonary infiltrates, bronchiectasis Have very high total IgE (>10iu/mL) Evidence of aspergillus sensitivity (positive skin test for A fumigates or positive apergillus IgG precipitins)
30
ABPA treatment
Oral steroids +/- itraconazole Itraconazole may increase risk of adrenal insufficiency in CF patients
31
ABPA exacerbation definition
Doubling of serum IgE New infiltrates (upper and mid zones) May be asymptomatic in 20-30% Treat exacerbations with steroids - slight increase risk in invasive aspergillus
32
CFTR function
Responsible for transmembrane transport of Na and Cl- in the ciliary epithelium
33
CF investigations
Present with symptoms or positive newborn screening test Then do sweat chloride If <29mmol = not CF if >60mmol = CF diagnosis if 20-59mmol = genetic analysis
34
Pseudomonas in CF Phenotypes
Mucoid phenotype (biofilm formation) associated with worse lung function and hard to eradicate After initial isolation of pseudomonas (non-mucoid phenotype) try to prevent colonisation with aggressive Abx
35
Azithro in CF
3x/week Increases FEV1 Decreases exacerbations by 40% Do not use in pt with NTM due to risk of resistance developing
36
Specific bacteria to know in CF
Burkholderia cepacia complex -Decreases lung function and survival -Usually MDR -Worse outcomes with lung transplant Non-tuberuclous mycobacterium -Not associated with worse transplant outcomes -M abscessus - decreases lung function and increases transplant complications Only treat NTM if symptoms, decreased lung function, nodular infiltrates/cavitary disease
37
CF medications
Ivacaftor - potentiator Tezacaftor/elexacaftor/lumacaftor = correctors
38
Ivacaftor in CF
Not effective in delta f508 mutants Causes weight gain
39
Delta F508 mutation
Class II mutant -CFTR is created but misfolded, keeping it from reaching the cell surface
40
Elexacaftor/texacaftor/ivacaftor triple therapy
Improves FEV1 Improved sweat chloride and QOL
41
Indications for pre-transplant assessment in CF
FEV1 <30% predicted Rapid decline in FEV1 despite therapy Malnutrition and DM Frequent exacerbations Recurrent massive haemoptysis Relapsing or complicated pneumothorax ICU admission
42
Relative contraindications to transplant in CF
Age >65 Critical/unstable Seriously limited functional status without potential for rehab Colonisation with burkholderia or M abscessus Disease not optimally treated e.g. PH, DM
43
OSA phenotype that responds best to PAP therapy
Sleepy phenotype
44
Narcolepsy subtypes
Type 1: daytime sleepiness for at least 3 months, and one of definitive cataplexy and positive MSLT, or low CSF hypocretin (orexin) Type 2: narcolepsy without catoplexy -Positive MSLT but normal CSF hypocretin
45
Sleep in narcolepsy patients
Fall asleep quickly and reach REM sleep quickly
46
Orexins function
Excitatory effect - promote wakefulness during the day
47
5 key symptoms of narcolepsy
1. Daily sleepiness 2. Catoplexy 3. Inability to move at the start or end of sleep 4. Vivid hallucinations 5. Fragmented sleep
48
Narcolepsy management
Stimulants (dexamphetamine) or wake promoting agents like armodafnil SSRI/SNRI for catoplexy
49
Kartagners syndrome
Triad of 1. Situs inversus 2. Chronic sinusitis 3. Bronchiectasis
50
Mycobacterium tuberculosis features
Rod-shaped Need O2 (strict aerobes) Waxy cell wall from mycelia acid Can survive on dry surfaces for months at a time
51
TB meds and side effects
Isoniazide: hepatotoxicity, peripheral neuropathy (give Vit B6) Rifampicin: red/orange urine and sweat, drug interactions (P450 induction) Ethambutol: optic neuritis, red/green colour vision loss, decreased visual acuity Pyrizinamide: Gout (increased uric acid), polyarthralgia
52
TB length of treatment
Guided by sputum AFB at 2 months and presence of cavitatory disease on CXR
53
When to commence treatment in HIV and TB co-infection
Based on CD4 count CD4 count <50: start early ART (< 2 weeks). Except in TB meningitis - early treatment does not improve outcomes. CD4 count >50: start ART by 8 weeks after starting TB treatment
54
Timing and treatment of TB paradoxical reaction
Occurs 20-150 days (usually 2-3 months) post commencement of therapy Presents with fever, respiratory failure, lymphadenopathy, neuro deterioration, sinus formation Treat with steroids, aspiration of pus, excision, CONTINUE TB TREATMENT, anti-TNF if severe
55
TB meningitis
Moxiflox better CNS penetration than ethambutol 9-12 months total treatment Dexamethasone decreases mortality