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resp medicine > RESP royal college > Flashcards

RESP royal college Flashcards

1
Q

what does the diagnosis of asthma require ?

A
  1. Variable sx ( cough, chest tightness, dyspnea) which vary overtime and intensity
  2. Variable exam : confirmed variable expiratory flow limitation
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2
Q

what do you need diagnose asthma

A

need a spirometry

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3
Q

which subtype of asthma requires higher ICS ?

A

adult onset

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4
Q

which subtype of asthma is less responsive to ICS

A

non allergic type

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5
Q

which subtype of asthma could have paucigranulocytic inflammation

A

non allergic

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6
Q

which type of asthma is associated with little eosinophilic inflammation?

A

obesity

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7
Q

which type o fasthma is assocxaited with eosinophilic inflammation

A

both allergic and non allergic

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8
Q

how can variability be demonstrated via asthma testing ?

A
    • BD reversibility ( FEV1>12% and 200 ml post BD)
    • lung function w/ antiinflam x 4w ( FEV1>12% and 200 ml post BD)
  3. excessive FEV 1 variation in lung function between visits ( FEV1>12% and 200 ml post BD)
  4. peak flow variability ( average daily diurnal PEF variability >10% ; excessive variability in twice daily PEF over 2w)
    • bronchial challenge test or exercise challenge test ( methacholine challenge)
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9
Q

what if you have a normal spirometry ? does that rule out asthma

A

no

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10
Q

what can you do if your spirometry test is normal

A
  • test during sx
  • methacholine/exercise tes
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11
Q

what is a + methacholine test

A

basically if you have a drop in fev1 of 20% with 4 mg/ml of methacholine

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12
Q

what is a (-) methacholine test

A

if you have a drop of fev1 >20% if require 20 mg/ml of methacholine

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13
Q

what is a + exercise challenge

A

drop in fev1 >10% and >200ml from baselien

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14
Q

what are the 9 criterias required for asthma control in terms of
1. Daily sx
2. Nighttime sx
3. physical activity
4. exacerbation
5. absence from work/school bcs exacerbation
6. need a reliever ( saba/ bud-form)
7. FEV1 or PEF
8. PEF diurnal variation
9. Sputum eosnophils

A
  1. <2
  2. <1
  3. Normal
  4. Mild ( no steroids, no ED) + infrequent
  5. none
  6. <2
  7. > 90% of personal best
  8. <10-15%
  9. <2-3%
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15
Q

overuse of SABA is described as what ?

A

requiring use of 2 SABA inhalers ( bottles i guess) per year

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16
Q

what is a risk for severe exacerbation

A
  1. hx of previous severe asthma exacerbation ( systemic steroids/ed/hospit) 2. poorly controlled per criterias
  2. overuse of SABA ( used 2 in last year)
  3. current smoker
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17
Q

what is a severe asthma exacerbation vs mild

A

any asthma episode requiring
1. hospitalisation
2. ed visit
3. systemic steroids

mild= 0/3 criteria

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18
Q

so based on cts management graphic how do you go stepwise

A
  1. confirm dx
  2. enviro control/education/written action plan
  3. PRN Saba or PRN bud-form
  4. ICS ( 2nd line LTRA)
    5A. add LABA ( >12)
    5B . increase ICS ( 6-11)
    6A. add LTRA ( >12)
    6b . add LABA /LTRA ( 6-11)
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19
Q

Can use LABA in monotherapy? yes, no ? why

A

noooo
Increased risk of death

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20
Q

what’s the main difference between CTS and GINA

A

well gina seems to like combining ICS-LABA, prescrisely ICS-formoterol and basically incrase in dose
- start with PRN in step 1 and step 2
- then move to low dose maintenance in step 3
- medium dose maintenance as step 4
- step 5 : erquest phenotype assessment , LAMA, add on +/- anti IGE , anti IL5, anti IL4 , anti TSLP. consider high dose ICS forometerol

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21
Q

why do we love formeterol containing ICS compared to other LABAs?

A

bcs fast onset of action

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22
Q

compared to SABA alone, why is PRN ICS formoterol better ?

A
  • less exacerb
  • less sx
  • less hospit
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23
Q

compared to ICS+SABA PRN, why is PRN ICS formoterol better ?

A
  • exacerbation is similar
  • less er visit
  • less hospit
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24
Q

meds to avoid in asthma

A
  • nsaid
  • bb
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25
Q

in what scenario is LTRA great in asthma

A
  • Aspirin induced
  • allergic rhinitis
  • exercise induced
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26
Q

LTRA vs ICS, in what way is LTRA less effective

A

less effective in preventing exacerbations

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27
Q

blackbox LTRA warning

A

increased suicidality

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28
Q

if you have samter’s triad, what should you try

A

LTRA

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29
Q

what’s samter’s triad again

A

ASA allergy
nasal polyp
asthma

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30
Q

when to consider AI investigation in asthma management

A
  • maintenance oral cortico
  • high dose ICS-LABA
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31
Q

if periph eo >0.3, what else should you do

A

consider non asthma dx, ie strongyloides, esp before corticosteroids systemic

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32
Q

if periph eo >1.5, what should consider

A

dx such as egpa

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33
Q

now , if have severe severe ashtma, what are the option considered in CTS 2017 ( and GINA 2024)

A
  1. tiotropium mist inhaler
  2. oral corticosteorid
  3. macrolides
  4. bronchial thermoplasty
  5. biologics
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34
Q

biological option if allergic asthma w/ high IgE

A

omalizumab ( anti IgE)

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35
Q

bio option if eo allergic asthma

A

all others
- IL5 ( i..e mepolizumab)
- IL4-IL13 (i.e. Dupilumab )

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36
Q

which ICS has most evidence in pregnancy

A

budesonide

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37
Q

asthma associated with what in pregnancy

A
  • preterm
  • preeclampsia
  • low birth weght
  • perinatal mortality
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38
Q

ABPA
- major criteria
- minor criteria

A

major :
- predispo condition : athnma, cf, copd, bronchiectasis
- serum ige >500 or a fumigatus specific ige >0.35

minor ( 2/3)
- periph eo >500
- + IgG against a fumigatus
- fleeting opactiies on CXR

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39
Q

tx of ABPA

A

pred +/- itraconazole

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40
Q

differentiate rads ( reactive airway dysfunction) from vocal cord dysfunctionm?

A

rads will have abN methacholine test

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41
Q

asthma exacerbation tx primary care

A

salbutamol , systemic corticosteroids, o2 supplementation

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42
Q

asthma exacerbation in ed/ er tx

A

saba,atrovent, o2, steroids
+/- mg
-/- high dose ICS ( methylprednisolone 125 mg IV)

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43
Q

when would lung volume reduction surgery might potentially be useful in COPD ?

A
  1. if fev1 <45% and significant gas trapping
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44
Q

Smoking cessation in COPD : how beneficial is it ?

A

increased survival for all , decreased rate of decline in fev 1

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44
Q

long term o2 therapy : survival benefit in who ?

A

those with severe resting hypoxemia

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45
Q

what does severe hypoxemia mean in terms of offering o2

A
  1. PaO2 <55
  2. PaO2 <60 w/ bilateral ankle edema , cor pulmonale or hct >56%
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46
Q

what does the NOTT trial 1980 say ? reduces what ???

A

those with copd and severe hypoxemia : continuous o2 reduces mortality compared to nocturnal o2 alone !!!!

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47
Q

what about giving LTOT in exercise ? what does the NEJM LOTT trial say ?

A

if stable copd and resting 89-93% or exercise induced desat –> LTOT did not result in longer time to death or first hospit comparefd to no LTOT

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48
Q

pulmo rehab : when does it decrease exacerbation ? what else does it increase ?

A

if started following recent <4 weeks AECOPD
Increased survival

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49
Q

other pharrm and non pharm tx with survival benefits since 2024

A
  1. NIV
  2. LAMA/LABA/ICS
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50
Q

what mrc dyspnea level is this : stops for breath after walking about 100 m or after a few min on the level

A

mmrc 3

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51
Q

what mmrc level is this : SOB breath when hurrying on level or walking up straight hill

A

1

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52
Q

what mmrc level is this : walks slower than people of same age on level b/c of breathlessness or has to stop for breath when walking at own pace on the level

A

2

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53
Q

what’s mild copd . what’s the tx

A

cat <10, mmrc 1
fev 1 >80
tx : lama or laba

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54
Q

whats the mod-severe tx if low aecopd risk ?

A

laba/lama –> laba/lama/ics

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55
Q

whats the mod-severe tx if high aercopd risk

A

laba/lama/ics –> + macrolide, pde4 inhb, mucolytic agents

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56
Q

high risk aecopd defined as what.

A

> 2 exacerbation or >1 requiring hospit

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57
Q

low risk of aecopd means what

A

<1 exacerbation, no ed/hospit

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58
Q

what does cts recommend downstepping back to lama-laba once start lama-laba-ics in a mod-severe high risk aecopd ?

A

bcs withdrawing ics could lower health status and lung function

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59
Q

what’s the benefit of adding macrolid to severe risk aecopd

A

decrease aecopd

60
Q

risk of macrolide (3)

A
  • hearing impairment
  • qt prolongation
  • atb resistanced
61
Q

when do you consider adding roflumilat or n acetyl cystein ?

A

chronic bronchitis phenotype

62
Q

can theophylline help in preventing acute exacerbation in copd ? what about asthma ?

A
  1. copd no
  2. asthma no
63
Q

what are the 3 required criteria for ACO

A
  1. COPD dx ( hx, spirometry, risk factors)
  2. Asthma hx ( past hx, dignoasis, sx consistent, physio confirmed with spirometry)
  3. fixed post BD FEV1/FVC <0.7
64
Q

how to treat ACO

A

Per GOLD - treat as asthma

1st line is LABA-ICS and can progress to adding LAMA if needed

65
Q

NIV in stable copd with hypercapnea, imp0roves what per multiple trials ?

A

mortality benefit

66
Q

paco2 level to initiate NIV even in stable COPD

A

52

67
Q

in whom does lung volume reduction surgery increase survival ( type of copd) per nett trial ?

A

emphysema (severe) with upper lobe predominant disease and low post rehab exercise capacity

68
Q

1 year mortalty after aecopd compared to MI ?
what’s the FEV 1 loss that you get with it ?

A

30% vs 23%
8ml/year

69
Q

aecopd tx

A
  1. o2
  2. SABD + LABD stat
  3. steroids
  4. atb
    5.NIV
70
Q

what does steroid reduce when given ina ecopd

A

recovery and hospit duration

71
Q

what the atb duration in aecopd as outpatient ?

A

<5days as shown by meta analysis

72
Q

per gold 2024, benefit of BIPAP/NIV

A

mortality benefit and reduced reintubation rate

73
Q

when to BIPAP/NIV per GOLD 2024

A
  1. paco2 >45 + ph <7.35
  2. severe dyspnea (impeding resp failure)
  3. hypoxemia despite supp o2
74
Q

is hfnc recommended in aecopd

A

nope

75
Q

what smoking cessation tx is superior to nicotine patch

A

varenicline

76
Q

bronchiectasis definition

A

clinical syndrome with cough, sputum production and bronchial infection w/ radiological evidence of permanent + abN dilatation of bronchi

77
Q

what pattern pfts expected with bronchiectasis ?

A

obstruction

78
Q

most common cause of bronchiectasis ?

A
  • postinfectious
  • idiopathic
79
Q

mournier kuhn, a congenital disease, can be associated with what ?

A

bronchiectasis

80
Q

how can you test for primary ciliary dyskinesia ?

A

via nitric oxide

81
Q

antimicrobial for bronchiectasis

A
  1. colistin/gentamicin inhaled for psA colonbization
  2. chronic azithro if recurrent exacerbations ( w/ or w/o PSA colonization)
82
Q

what do you want to rule out prior to starting chronic azithro in bronchiectasis

A

NTM

83
Q

what should not be offered routinely in bronchiectasis

A
  1. ICS, PDE4i, oral steroids
84
Q

tx bronchiectasis exacerbation and during of atb

A
  • atb (IV ideally)
  • if hemoptysis : atb, txa, embolization

atb for 14 days especially if PSA colonized. shorter course if mld bronchiectasis

85
Q

what’s the most common IIP

A

IPF

86
Q

type of radiological pattern seen in IPF

A

it’s UIP ( usual interstitial pneumonia pattern)
1. honeycombining
2. subpleural, basal predominal
3. reticular changes
4. No presense of anything suggestive of an alternate dx
-cysts
-predominant GGO
-nodules/centrolobular nodules
-profuse micronodules
-consolidation
- mosaic attenuation
- predominant distribution : peribronchovascular/perilymphatic/upper-midlung

87
Q

antifibrinolytic meds? what do they reduce ?

A
  1. Nintendanib
  2. Pirfenidone

FVC decline by 50%

88
Q

NIntendanib beneficial in what way

A

Per INPULSIS 1/2 trials
- reduced fvc decline
- trend to reduced mortality

89
Q

Pirfenidone beneficial in what way

A

Per the Ascend/Capacity trials
- reduced FVC decline
- reduced 6MWTD decline
- improved survival

90
Q

role for corticosteroids chronically or immunosup in IPF ?

A

NO ( PANTHER-IPF) , incrased mortality

91
Q

role chronic atb in ipf

A

no ( Cleaup-IPF)

92
Q

tx for acute exacerbation in IPF

A
  • high dose steroids and empiric atb
93
Q

in who should you consider immunosuppression in context of ILD

A

non IPF

94
Q

how does hypersensitivity pneumonitis
- cause
- location
- tx

A
  • cause : organic
  • location : upper lobe
  • tx : remove trigger, steroids, mmf/aza sometimes
95
Q

pneumoniosis
- cause
- location
- tx

A
  • inorganic ( i.e. silica)
  • location ( variable, silica upper lobe)
  • tx supportive care , transplant
96
Q

CTD associated ILD
- tx

A
  • steroids ( short term)
  • MMF prefered
  • ritux/aza
  • toci for scleroderma
97
Q

scleroderma ILD , what do you give as tx

A

tocilizumab

98
Q

drugs that can cause ILD

A
  • mtx
  • amio
  • bleo
  • nitrofurantoine
  • vap
99
Q

how to traet drug induced ild

A

steroids

100
Q

Per chest guideline - if have parapneumonic effusion, when can you forego sampling and follow radiographically ?

A

<1cm

101
Q

what imaging for exudate nyd ?

A

ct chest

102
Q

what are lights criteria ?

A

LDH >2/3
LDH >0.6 ( fluid : serum)
proten >0.5 ( fluid : serum)

103
Q

1 cause of chytlothorax

A

malignancy ( lymphoma)

104
Q

causes of pleural fluid eosinophilia

A

asbestos, infection, pe, drugs ( nitrofurantoin) , EGPA

105
Q

if you have low glucose in pleural fluid
- <1 : ?
- 1-3

A
  • RA & empyema
  • SLE, TB, malignancy
106
Q

high lymphoytosis in pleural fluid, what’s you dx

A

tb vs lympohoma

107
Q

chest tube insertion for parapneumotic effusion

A

PH <7.2
PH 7.2-7.4 w/ LDH >300
no pH but glucose < 3.3

108
Q

other causes of low glucose in pleural fluid

A

tb
ra

109
Q

how long tx parapneumotic efffusion

A

5-7D IV + long course
long course usually around 3 weeks ( BTS says about 2-6 weeks)

110
Q

antibiotics for pleural infection
1. community |
2. hosp

A
  1. 2/3 gen cephao + anaerobe : ctx+ mtx
  2. gram neg + mra : tazo+vanco
111
Q

risk factors for primary spont pneumothorax

A
  1. smoker, marfan,thoracic endometriosis , fam hx
112
Q

if symptomatic primary spont pneumothorax - what do you look for ?

what do you do ?

A
  1. tension
  2. bilat
  3. hemopneumo
  4. > 50
  5. smoker
  6. significant hypoxia

admit and chest drain insertion

113
Q

secondary spont pneumothorax. most common etiology?

A

COPD

114
Q

chances of secondary spontaneous pneumothorax to spontaneously resolve ?

A

unlikely

115
Q

follow up pneumothorax if conservative

A

2-4 days and then 2-4 weeks

116
Q

sarcoid involvement

A
  • 90% lungs
  • about 30% extrapulmonary : cardiac, cns, eyes !!! ( and then rest liver, spleen, msk, kidney)
117
Q

2 syndromes in sarcoid

A
  1. lofgren
  2. heerfordt
118
Q

lofgren syndrome involves what

A

bilat hilar adnp
eryhthema nodosum
migratory polyarthralgia
fever
women&raquo_space;>

spont remission often

119
Q

heerford syndrome

A

anterior uveitis
parotid enlargement
fever (uveoparotid fever)
Facial palsy

120
Q

pft w/ sarcoid looks like what?

A

anything !!!!!

normal, restriction, obstruction, or both (+/- reduced DLCO)

121
Q

pulmo htn in sarcoid?

A

rarely

122
Q

fibrosis s what state of sarcod ?

A

stage 4

123
Q

another cutaneous sarcoidosis finding other than erythema nodosum ?

A

yes . lupus pernio

124
Q

most common neuro finding of sarcoidosis ?

A

cranial nerve palsy

125
Q

most common ocular sarcoidosis finding

A

anterior uveitis

126
Q

how do you screen for abN in cardiac sarcoidosis

A

ekg for heart block +/- echo
cardiac mri
pet if concern

127
Q

finding on cbc about sarcoidosis ?

A

lymphopenia

128
Q

why ask alp in sarcoidosis ?

A

to screen for hep sarcoid

129
Q

when steroid indicated in sarcoidosis ?

A

enhd organ failure from granulomatous inflammation

130
Q

if skin disease refractory to steroids in sarcoid, what do you give ?

A

infliximab

131
Q

if relapse on steroids while tx sarcoidosis, what other regimen to consider

A

mtx

132
Q

fatigue in sarcoidosis, what to do ?

A

pulmo rehab

133
Q

erythema nodosum in sarcoidosis, what to give ?

A

nsaids alone

134
Q

definition of pulmonary htn ?

A

mean PAP >20 and PVR > 2WU

135
Q

what on pft makes you sus about phtn

A

isolated low DLCO

136
Q

tx of groupe 1 htn

A

endothelin r antagonist
prostanoid
pde5i

137
Q

main cardiac dyhfct seen in groupe 2 pulmo htn

A
  1. l heart dysfunction
  2. diastolic dysfunction precisely
138
Q

what is one widened A-a gradient condition which doesn’t improve with 100% fio2

A

Shunts

139
Q

if you have a young non smoker with hemoptysis and lung collapse, what are you suspecting and what should do for work up up

A

carcinoid ( endobronchial tumors)

TTE to rule out carcinoid heart ( TR)

140
Q

single solid nodule . if <6 mm , but high risk, when to follow

A

ct in 12 months

141
Q

single solid nodule. low risk. but 7 mm. when to follow ?

A

CT at 6-12 mos then consider 18-24mos

142
Q

single solid high risk but 7.5 mm . when to follow?

A

CT at 6-12 mos, AND CT at 18-24 mos.

143
Q

now single solid nodule , but >8mm. what to do ?

A

Consider CT at 3 mos, PET – CT or biopsy

144
Q

multple solid nodules. 4 mm. what to do in low risk vs high riks

A
  • low risk : nothing
  • high risk : ct (optional) 12 months
145
Q

now let’s say >6mm multple solid nodules. they seem low risk. what to do.

A

CT at 3-6 mos, then consider CT at 18-24 mos*

146
Q

let’s say >6mm multple solid nodules. they seem high risk . what to do.

A

CT at 3-6 mos, and CT at 18-24 mos

147
Q
A

resp medicine (1 decks)

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