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FRACP Shuyu > RPA Respiratory > Flashcards

RPA Respiratory Flashcards

1
Q

age onset of Aspirin-Exacerbated Respiratory Disease

A

adult acquired condition onset in 30s

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2
Q

clinical features of Aspirin-Exacerbated Respiratory Disease

A

symptoms after aspirin 30-90 min

mucosal swelling of sinuses and nasal membranes, formation of polyps and asthma

triggered by alcohol

upper and lower airway symptoms, hayfever symptoms

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3
Q

What has a high specificity in Aspirin-Exacerbated Respiratory Disease

A

normal sinus CT is a good rule out test

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4
Q

surgery and nasal polyps in Aspirin-Exacerbated Respiratory Disease

A

nasal polyps will recur

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5
Q

treatment for Aspirin-Exacerbated Respiratory Disease

A

ICS, leukotriene antagonists (monteleukasts), nasal steroids, antihistamines

definitive: desensitisation to aspirin then long term aspirin after debulking surgery

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6
Q

diagnositic test of Aspirin-Exacerbated Respiratory Disease

A

aspirin challenge test

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7
Q

who does the fleischner guidelines not apply to

A

under 35, known cancer, immunosuppressed

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8
Q

what kind of nodules should be monitored for a longer time as per Fleischner Guidelines

A

ground glass nodules:

adenocarcinoma in situ, slower growing

recommended for 5 years of monitoring (instead of the normal 2 years)

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9
Q

risk factors for pulmonary nodules

A
  • older age
  • smoking history 30 years and cessation within 15 years
  • larger nodle
  • spiculated
  • upper lobe location
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10
Q

classification of interstitial lung disease (7)

A
  1. idiopathic interstitial pneumonias
  2. Iatrogenic drug induced (bleomycin most severe; radiotherapy - gives a non anatomical straight line)
  3. Occpational/environmental
    1. Silicosis - jack hammers, stone masons, kitchen bench tops
    2. Hypersensitivity pneumonitis
  4. Granulomatous disease
  5. Collagen-vascular (scleroderma, lupus, sjgoren’s)
  6. Inherited (alpha-1-AT)
  7. Unique entities
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11
Q

3 lung manifestations of alpha-1- AT deficiency

A

emphysema

interstitial lung disease

bronchiectasis

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12
Q

What ILDs are associated with smoking?

A

Respiratory bronchiolitis-interstitial lung disease

desquamative interstitia pneumonia

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13
Q

what major idiopathic interstitial pneumonais are steroid insensitive

A

interstitial pulmonary fibrosis

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14
Q

onset of breathlessness of interstitial pulmonary fibrosis

A

months

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15
Q

what sign will all patients with symptomatic interstitial lung disease have

A

fine inspiratory crepitations

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16
Q

which condition relies on the distance for 6MWT vs hypoxia on 6MWT

A

PulHTN for distance for 6MWT, hypoxia for 6MWT

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17
Q

what is the first test to change in LFT in interstitial lung disease

A

DLCO (function of alveolar membrane)

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18
Q

What kind of films are required for HRCT for ILD

A

inspiratory/expiratory; prone/supine (differentiate between normal atelectasis changes due to gravity vs early IPF)

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19
Q

basal/lower lobe predominance in CXR ILD condition

A

interstitial pulmonary fibrosis

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20
Q

terminoogy w fibrosis vs ground glass

A

ground glass is no architectural distortion

fibrosis/honey has architectural distortion

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21
Q

key radiological featuers of IPD

A

lower lobe predominant

disease of architectural distortion

often prone film

predominantly subpleural

minimal ground glass

temporal heterogenity (pathognomonic) - on 1 scan, there is different ages of fibrotic disease; does not need biopsy

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22
Q

Diagnosis

A

Sjogren’s

cysts and ground glass (Lymphoid interstitial pneumonia)

pulmonary lymphomas

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23
Q

why have inspiratory and expiratory CTs

A

the black bits (with more air) should get smaller during expiration.

If the black bits get bigger, that’s gas trapping.

If the black bits get smaller, the grey bits are abnormal

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24
Q

ground glass definition

A

alveolitis

opposite of fibrosis

acute inflammatory change

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25
Q

who needs a biopsy in ILD

A

if clinical picture does not match radiological picture

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26
Q

first line treatment for sarcoidosis

A

prednisolone

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27
Q

treatment of IPF

A
  1. Antifibrotic drugs - slows the rate of decline; MDT required for diagnosis; works better earlier in disease progression
    1. Nintedanib
      1. Tyrosine kinase inhibition
    2. PIrfenidone
      1. Inhibition of TGF-beta production and downstream signaling, collagen synthesis, fibroblast proliferation
  2. lung transplant

Treatment of comorbidities: reflux; pulm HTN

Treatment criteria PBS:

  • FVC >50%
  • PEV1/FVC >0.5
  • DLCO >30%
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28
Q

which IPF drug causes hypersensitivity rashes

A

Pirfenidone

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29
Q

Which IPF drug causes diarrhoea

A

Nintedanib

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30
Q

definition of bronchiectasis

A

radiological definition

small airway that is bigger than the vessel that it runs with

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31
Q

classification of bronchiectasis

A

focal and diffuse

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32
Q

causes of focal bronchiectasis

A
  1. Luminal blockage: foreign body, slow growing cancer
  2. Extrinsic narrowing due to enlarged lymph node (middle lobe syndrome)
  3. Twisting or displacement of airway after a lobar resection

Presents with recurrent persistent lobar pneumonia

Next step is bronchoscopy

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33
Q

Patient presents with recurrent lobar pneumonia in the same area and CT shows bronchiectasis. WHat is the next step

A

bronchoscopy

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34
Q

Causes of diffuse bronchiectasis

A
  1. Infections (need pneumonitis from the disease that go on to develop bronchiectasis)
    1. TB most common cause worldwide
    2. Post-viral
    3. Severe bacterial infection
  2. Congenital conditions
  3. Immunodeficiency conditions
  4. Rheumatological conditions
  5. Toxins or drug exposure
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35
Q

Bronchiectasis in upper lobes cause

A

Cystic fibrosis (and Allergic bronchopulmonary aspergillosis)

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36
Q

Upper airway disease out of proportion to bronchiectasis

A

Primary ciliary dyskinesias

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37
Q

Primary ciliary dyskinesias genetics

A

autosomal recessive with variable penetrance

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38
Q

diagnosis of Primary ciliary dyskinesias

A

nasal swab biopsy w cilia studies

“ciliary studies”

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39
Q

Primary ciliary dyskinesias clinical symptoms

A

Bronchiectasis

CHornic sinusitis

agenesis of frontal sinuses

recurrent otitis media

some will have Kartagener’s syndrome (embrological consequence of severe back to ciliary things

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40
Q

proportion of RA w bronchietasis

A

30%

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41
Q

Management of bronchiectasis

A
  1. Sputum clearance
  2. Treat acute exacerbation (14 days)
  3. Prophylactic antibiotics (pseudomonas, who has >2 infections in a 12 mon period, who do not have non tuberculous mycobacterium)
    1. Macrolides; nebulised aminoglycosides
  4. Treatment of underlying conditions (e.g. IVIG for IgG def)
  5. Reduction of excessive inflammatory response (e.g. inhaled steroids)
  6. Contral of bronchial haemorrhage
  7. Surgical removal of segments/lobes
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42
Q

definition of difficult to treat asthma

A

symptoms despite high dose steroids

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43
Q

Common reasons for poor control

A

Puffer technique

Smoking

Upper respiratory tract infecitons

Medications (BB - note eye drops, NSAIDs, dustmites, molds)

Storms

Reflux

Upper airway disease

APBA

Churg Strauss (eosinophilic granulomatosis with polyangiitis)

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44
Q

definition of severe asthma

A

see slides

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45
Q

Which plant triggers thunderstorm asthma

A

Ryegrass

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46
Q

Other optiosn to add to high dose ICS/LABAB

A

tiopropium (only lama) - shown to increase lung funciton and time to first exacerbation

Macrolide

Leukotriene modifier

THeophylline (not commonly used and not on guidelines)

Oral steroids (not on guidelines)

then biologics

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47
Q

biologics for asthma

A
  1. omalizumab - subcutaneous injection into patients with moderate allergic asthma who have a raised IgE concentration and are already taking steroids
    1. forms complexes with free IgE to prevent it binding to mast cells
  2. mepolizumab
    1. Anti IL-5
  3. benzalizumab
    1. Anti IL-5
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48
Q

Types of asbestos related lung disease

A

pleural plaques

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49
Q

which type of asbestos is worst for mesotheliuoma

A

blue (crocidolite)

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50
Q

latency period of asbestos

A

30-40 years

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51
Q

which asbestos related lung disease is related to the highest amount of asbestos exposure

A

asbestosis

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52
Q

which asbestos related lung disease can occur from minimal (once-only) exposure

A

mesothelioma

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53
Q

pleural plaques CXR findings

A

benign

calcified

discrete plaques in the pleural

classically seen on diaghragm or cardiac line

number of plaques correlates to the exposure

monitor for 3 years

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54
Q

asbestos related pleural disease CT findings

A

benign, not pre-malignant

requires second most exposure after asbestosis

can present with pleural thickening or pleural exposure

diagnosis on CT - >25% of circumference of pleural disease OR rounded atelectasis - pleural is thickening and encroaches on normal lung; it is directly contiguous with the pleural; also has crow’s feet) also need other areas of asbestos related disease

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55
Q

asbestosis CT features

A

UIP pattern

nornally also need plaques

someone who has worked for decades

no treatment except for oxygen

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56
Q

mesothelioma clinical presentation

A

pleural effusion, with chest wall pain (dull ache keeps them awake at night) due to neural invasion

can be in peritoneum

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57
Q

diagnosis of mesothelioma

A

pleural biopsy (not just pleural fluid) - but be careful that mesol can seed the tract of the biopsy

CT has mediastinal reflection (unlike parapneumonic effusion)

58
Q

mesothelioma treatment

A

limited options

pleuropneumectomy (12% 5 year survival)

1st line pemetrexed+platinum based; 2nd line - gemcitabine

pain relief (neuropathic agents)

early pleuradiesis (usually at the same time as the VATs pleural biopsy)

59
Q

what other lung cancer is related to asbestos (not mesothelioma)

A

NSCLC

60
Q

acute exacerbation of IPF definition

A

ground glass

acutely hypoxia

exclude infection

mortality +++ (close to 100%); tx: corticosteroids but no evidence of mortality benefit

61
Q

diagnosis of restless legs syndromes

A

clinical diagnosis

diagnostic criteria: URGE

  1. urge to move limb
  2. rest (worse during rest)
  3. Getting up and moving or walking improves
  4. evening worsens or precipitates symptoms

non essential:

  1. family history
  2. response to dopaminergic therapy
  3. sleep disturbance
  4. PLMS (periodic leg movements 80%) or PLMW
62
Q

secondary causes of restless legs

A

iron def most common

ESRF, pregnancy, meds (antidepressants, antihistamines, lithium, D2receptor blockers) are other causes

63
Q

pathophysiology of restless legs

A

theories:

  • central dopamine dysfunction
  • reduced CNS iron stores
  • endogenous opiate system dysfunction (opioids and exercise improves RLS)
64
Q

treatment for restless legs

A
  • Non-pharmacological
    • replace iron aim ferritin >50
    • abstinence from caffeine, nicotine and alcohol
  • Pharmacological
    • First line
      • Dopaminergic agonists - pramipexol, sifero, ropinirole
        • SE: impulsive behaviours, augmentation (paradoxical worsening of RLS)
      • Alpha25delta ligands
        • Pregabalin
        • SE: suicide ideation and sleepiness
    • Second line
      • Opioids
65
Q

periodic limb movements in sleep definition

A

it’s a finding in a sleep study, not a disorder by itself

PSG findings:

  • 0.5-10 seconds
  • Amplitude > 8 uV above baseline
  • At least 4

There is a period limb movement disorder which is a rare condition - diagnosis of exclusion,

66
Q

parasomnia - when do they occur

A

sleep-wake transition disorders

or occasionally during slow wave sleep

REM sleep parasominias might be remembered

67
Q

NREM parasomnias pathogenesis

A

partial arousals from slow wave sleep

instability of sleep state

e.g. sleep walking, confusional arousals, sleep terrors

68
Q

REM sleep behavioural disorder diagnosis

A

usually requires sleep study for diagnosis

characterised loss of muscle atonia during REM

EMG during the normal sleep study during REM should be a flat line (aside from eye movements)

69
Q

REM sleep behavioural disorder clinical features

A

violent dreams

the next day there is a recollection of the dreams (differentiating feature with NREM sleep disorders)

pathophysiology - alpha-synucleinopathies (Parkinson’s LBD MSA)

50% of patients don’t have an underlying alpha-synucleopathy (but within 15 years 80% of these patients will develop clinical alpha-synucleonopathy

70
Q

Management of REM sleep disorders

A

Safe home environment

Clonazepam

Melatonin (controversial)

Avoid changes in sleep routine

Avoid antidepressants

Neurology

71
Q

definition of narcolepsy

A

sleep state dissociation - poor quality and fragmented sleep

demonstrated on sleep study

NT type 1

  • with cataplexy
  • low CSF hypocretin

NT type 2

  • without cataplexy
72
Q

symptoms and features of narcolepsy

A

irresistable urge to fall asleep

cataplexy (emotion driven loss of muscle tone) as a manifestation of REM sleep manifestation

links with other parasomnias

metabolic syndrome

73
Q

type 1 narcolepsy genetic and phenotypes

A

HLA-DQB1*06:02 (sensitive but not specific)

LP shows low or no hypocretin

No hypocretin in hypothalamus

Chronic

74
Q

Type 2 narcolepsy phenotype

A

some may improve without treatment

No or atypical cataplexy

diagnosed by multiple sleep latency test (mean sleep latency <8min and Sleep Onset REM periods - going into REM in the first 15 min)

75
Q

Narcolepsy treatment

A

Non-pharmacological (schedule naps, work/school/driving)

Pharmacological

  • nodafinil, amphetamine

Cataplexy

  • antidepressant, sodium oxybate
76
Q

Treatment of insomnia

A

CBT is the mainstay

pharmacology: benzo, zolpidem

77
Q

Health conditions associated with OSA

A

AF highest OR (4.0)

78
Q

CPAP evidence in OSA

A

SAVE study NEJM 2017

secondary prevention study

mod to severe OSA, CPAP use 3.3hr

No difference in mortality or other primary endpoints

but results may be confounded by CPAP duration use

79
Q

Obesity hypoventilation syndrome definition

A

high CO2

obesity BMI >30

Hypoventilation during wakefulness

80
Q

obesity hypoventilation syndrome pathophysiology

A

OSA is major phenotype

apnoeas is prolonged and they don’t resaturate (which happens in normal OSA); hence chemoreceptors reset to cause resting hypercapniea

10% of OHS do not have OSA - they have a more pure hypoventilation phenotype

These patients need BIPAP

81
Q

Obesity hypoventilation treatment

A

OSA phenotype - CPAP

Hypoventilation phenotype - BIPAP

82
Q

first branching of the bronchial tree that has gas exchanging capabilities

A

respiratory bronchioles

83
Q

dynamic collapse

A

during forced expiration

there is increased pleural pressure onto the alveolar and respiratory tract. As you move proximally, there is decreased pressure in the respiratory tract, which creates an equal pressure point” where the pleural pressure equals the airway pressure. The airway proximal to that has “dynamic collapse”.

In obstructive lung disease,the equal pressure point moves peripherally

84
Q

FEF 25-75 reduction

A

early obstructive disease

FEF 25-75 is not dependent on effort

85
Q

Respiratory physiology changes with age

A

More compliance but less elasticity

change in elastic properties:

  • decrease in elastic fibres increaase in type 3 collage, changes in cross-linking and fibre orientation

Change in surface properties

  • Decrease in number of alveoli
  • Increase int he size of alveolar ducts
  • Decrease in surface to volume ratio
86
Q

effect of

1) venous congestion on lung compliance
2) emphysema on lung compliance

A

heart failure/venous congestion - decreased lung compliance

emphysema more compiant

87
Q

gas trapping effects on spirometry

A

decreaed FVC

decreased FEV1

88
Q

features of fixed airway obstruction on flow volume diagream

A

where the insoiratory and expiratory are both effected

e.g. subglottic stenosis

89
Q

largyneal malacia vs tracheomalacia on flow volume loop

A

laryngeal malacia is reducd expiratory

tracheomalacia is deduced inspiration

90
Q

how much does functional residual capacity take up

A

30%

91
Q
A
92
Q

layers for gas exchange in lungs

A
93
Q

what causes reduced DLCO

A
  • decrased membrane for gas transfer
  • dodgy alveolar membranes
  • decreased chest expansion
  • lobectomy, pneumonectomy
  • pulmonary fibrosis
  • emphysema
  • decreased blood in pulmonary capillaries
  • volulme of capillary Hb (eg decreased cardiac output)
  • less capillaries (emphysema, pulmonary fib)
  • less blood (heart failure, pulmonary HTN)
94
Q

how is DLCO measured

A

helium is used as it is not difused

the delium is diluted by the air in the lungs

that allows for the calculation of the alveolar volume (based on the assumption for homogenous gas mixing which is not true in obstruction or increased resistence in airways). ALveolar volume is compared with TLC (should be within 10%). If there is poor gas mixing, the TLCO will be underestimated.

The rate of diffusion is KCO (rate of carbon monoxide uptake)

DLCO = KCO x VA

95
Q

what is assos w an increase in KCO

A
  1. when there is less lung, there is increased blood to lung ratio and the sink for carbon monoxide uptake is greater
  2. RBC in the airways (outside of capillaries) will also take up carbon monoxide. Of note, DLCO can be used to detect pulmonary haemorrhage withouth haemoptysis
  3. Obesity - cardiac output is increased in obesity
  4. Asthma - very large swings in intrathoracic pressure, there is more blood in the pulmonary circulation

essentially more blood in lungs will increase KCO

96
Q

A-a gradient calculation

A

PAO2 = FiO2 x [Patm - PH20]-(PaCO2 / R)

= 150 - PaCO2/0.8

97
Q

hypoventilation in hypoxaemia

A

PaCO2 >45 mmHg

98
Q

Causes of elevated A-a gradient

A

R-> L shunt - cardiac, pulmonary

VQ mismatch - Most common cause of hypoxia in disease states

Diffusion limitation (rare)

99
Q

most common cause of hypoxaemia in ILD

A

still VQ mismatch although diffusion limitation plays a small role

100
Q

predominant physiological echanism for a normal A-a gradient (of 15 mmHg)

A

VQ inequality

101
Q

bronchial provocation challenge

A

direct challenge

  • histamine and metachonline
  • sensitive but not specific
  • >20% drop in FEV1

Indirect challenge - detect the presence of inflammatory cells in the airways and are more indication of current asthma

  • Hypertonic saline, exercis and manitol
  • Positive when >15% reduction FEV1 to stimulus
  • More false negatives (specific)
102
Q

what happens to VO2Max and heart rate with fitness

A

the curve does not shift but athletic peopleare able to reacher higher VO2Max

However, the heart rate relationship shifts as people can achieve higher VO2s with lower heart rates

103
Q

Upper lobe fibrosis Ddx

A

see slides

104
Q

pulmonary disease distribution associated with:

RA

mixed connective tissue

diffuse systemic sclerosis

Ankylosing spond

A

RA - can have either a UIP (slightly more common 8) or NSIP pattern

mixed connective tissue - an interstitial pneumonitis: 20-65%; pulmonary fibrosis: 20-65%

diffuse systemic sclerosis -

Ankylosing spond - unilateral/bilateral cystic changes with upper lobe distribution

105
Q

criteria for reversibility in LFT

A

12% and 200mL improvement post bronchodilator

106
Q

aspirin overdose

A

resp alkalosis

+/- raised anion gap

107
Q

ABG in PEs

A

high variability

can even have normal A-a gradient

108
Q

distribution of adenocarcinonas and pathological features

A

peripheral and spiculated - distinguises primary lung cancer with metastases

metastases early

109
Q

squamous cell carcinoma location and pathology features

A

central

thick walled with large air fluid levels

“march” from parachyma to node to mets

assoc hypercalcaemia

110
Q

relationship of vascular resistance and lung volume

A

at low volumes - atelectasis and distortion of vessels

at high volumes, the vessels are stretched - becomes longer but radius decreases

vascular resistance lowest at FRC

111
Q

V:Q in different parts of the lungs

A

low V:Q ratio in bottom

high V:Q in top of the lungs

112
Q

by which method does CPAP work in cardiogenic pulmonary pedema

A

CPAP restores FRC by alveolar recruitment, reducing right to left intrapulmonary shunt and improving oxygenation and lung mechanics

113
Q

what cells are important in sarcoid

A

T-cells

pathogenesis: some antigen binds to a toll-like receptor, triggering a cascade of events leading to granulomas. T cells drive the disease to recruit macrophages and form granulomas (non-caseating)

114
Q

Allergic bronchopulmonary aspergillosis clinical features

A

predisposing conditions: hypersensitivity to aspergillosis, total IgE levels (>1000), condidtent pulmonary opacities - fleeting pulmonary infiltrates relating to mucoid impact. They could simulate hilar lymphadenopathy.

cough, expectoration, wheezing, haemoptysis, fever, nasal symptoms

gold brown nasal plugs

diagnosis via

115
Q

biggest cause of pulmonary hypertension

A

left heart disease (70%)

lung disease/hypoxia (15-20%)

pulmonary arterial hypertension (4%)

116
Q

HOw to differential pre or post capillary causes for PH

A

If PCWP >15 it’s left heart disease or left vein aetiology

117
Q

osteoarthritis pathogenesis

A

metalloproteinasa and TIMPs

catabolic cytokines - increased Il-1 in synovium and SF TNF in synovium

Anabolic cytokines - increased IGF-1 correlates with osteophyes

118
Q

what type of OA is assoc w CV disease

A

knee>hand

symptomatic >asymptomatic

119
Q

what is the most important modifiable risk factor for OA

A

knee injury

(but age carries the greatest risk overall)

120
Q

what gender with XR change of OA are more likely to get pain

A

women

121
Q

stratification of osteoarthritis

A
  1. knee only vs muti joint OA
  2. whether there are other comorbidities
122
Q

Management of OA

A
123
Q

which bisphosphonates are useful in OA

A

IV ones

124
Q

what antidepressants are useful in OA

A

duloxetine

125
Q

Intra-articular injections in OA

A

PRP has some improved funcitonal scores

126
Q

genetics of RA

A

DR1, DR4 most important HLA that confers risk

PTPN22 (regulates activities for T and B cells) gain of function mutations

127
Q

citrullination in RA

A

the conversion of the amino acid arginine in a protein into the amino acid citrulline

can be genetic and environment (e.g. smoking

128
Q

what is the only biologic that is better than methotrexate as monotherapy

what biologic in combo with methotrexate is better than adalimumab and methotrexate?

A

tocilizumab (IL-6)

probably the go to drug in people who fail a TNF inhibitor

baricitinib in combo with methotrexate is better than ada and methotrexate. SE thrombosis

129
Q

tofacitinib SE

A

elevated transaminitis

elevted creatinine

elevated lipids

neutropenia

increased risk of zoster

130
Q

biologics and surgery

A

miss 1-2 cycles for surgery

can continue in minor surgery

131
Q

biologics and pregnancy

A

TNF: remain on until falling pregnant then stop

certoluzimab is a very large molecule that probbaly does not cross the placementa

one of the big problems is that in the 3rd trimester, it will intefere with giving live vaccines to the baby

Class C: rituximab, abatacept, tociluzimab

132
Q

solid malignancy <5 years and RA treatment

A

rituximab

>5 years any malignancy

133
Q

where is urate reabsorbed

A

proximal tubule (URAT1 and OAT4)

134
Q

what is the most important interleukin in gout

A

IL-1beta

that leads to the release of TNF, IL-6, neutrophil chemotactants

135
Q

dosing of colchicine for acute gout

A

1mg stat, 500microg 1 hour later

Renal impairement

CrCl <80 mL/minute or hepatic impairment, do not use for acute attack if using colchicine for prophylaxis:

CrCl <30 mL/minute or severe hepatic impairment, dosage as above; do not repeat the course within 2 weeks.

Dialysis, oral 500 micrograms single dose, do not repeat within 2 weeks.

136
Q

risk factoers for severe allopurinol hypersensitivity

A

renal impairement, increased age

thiazide use

initial high erdose

HLA-B*58:01 (test in Han Chinese; Thai; Korean)

137
Q

what urate lowering therapy should not be used in cardiovascular disease

A

febuxostat

138
Q

how is febuxostat metabolised

A

liver

139
Q

where are uric acid crystals formed

A

in the urinary tract

(in tissue - monosodium urate monohydrate crystals)

140
Q

what to do when there is ongoing frequent gout attacks despite being on urate acid lowering for 12 months and achieving satisfactory uric acid levels

A

add colchicine to control inflammation

FRACP Shuyu (65 decks)

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