Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MRCP > resp > Flashcards

resp Flashcards

1
Q

Features of life threatening asthma?

A
  • PEFR <33%
  • SpO2 <92%
  • Normal pCO2 (4.6-6.0)
  • Silent chest, cyanosis, feeble resp effort
  • Brady/ hypotension
  • exhaustion/ confusion/ coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Features of Severe Asthma?

A
  • PEFR 33-50%
  • can’t complete sentences
  • RR >25
  • HR >110
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Features of Moderate asthma?

A
  • PEFR 50-75%
  • speech normal
  • RR <25
  • HR <110
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Near-fatal asthma?

A

raised pCO2 -> requiring mechanical ventilation

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

CXR in asthma not routinely recommended unless…?

A
  • life threatening asthma
  • Suspected pneumothorax
  • failure to respond to treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When do BTS guidelines recommend ABG for asthma attacks?

A

oxygen sats <92%

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

Pathophysiology of Alpha-1 antitrypsin deficiency

A
  • A1AT protects against enzymes such as neutrophil elastase.

- lack of A1AT (protease inhibitor normally produced by liver) causes emphysema

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

Genetics of Alpha-1 antitrypsin deficiency

A
  • auto recessive

- chr 14

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

features of alpha-1 antitrypsin deficiency?

A
  • lungs: panacinar emphysema, most marked in lower lobes

- liver: cirrhosis/ HCC in adults, cholestasis in children

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

Ix of Alpha-1 antitrypsin deficiency?

A
  • A1AT concentrations

- spirometry - obstructive picture

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

Management of Alpha-1 antitrypsin deficiency?

A
  • no smoking
  • supportive: bronchodilators, physio
  • IV A1AT protein concentrates
  • Surgery: lung volume reduction surgery, lung transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Features of cryptogenic organizing pneumonia?

A
  • diffuse interstitial lung disease
  • not assoc w smoking
  • cough, SOB, fever, malaise
  • elevated ESR/ CRP
  • Bilateral patch/ ground glass opacities
  • TF reduced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment of cryptogenic organizing pneumonia?

A

watch and wait if mild, if severe -high dose oral steroids

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

most common organism isolated from patients with bronchiectasis?

A

haemophilus influenzae

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

Management of bronchiectasis: what is most important for long term control of symptoms?

A

inspiratory muscle training + postural drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Bronchoscopy showing “cherry red ball”

A

Lung Carcinoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

features of lung carcinoid?

A
  • typical age 40-50y
  • smoking not assoc
  • slow growing e.g long hx of cough, recurrent haemoptysis
  • often centrally located + not seen on CXR
  • cherry red ball often seen on bronchoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

management of lung carcinoid?

A

surgical resection

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

1st line for moderate or severe obstructive sleep apnoea?

A

CPAP

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

1st line mx of Chlamydia psittaci?

A

doxycycline

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

management of pleural plaques?

A
  • nothing, no follow up needed as pleural plaques are benign and do not undergo malignant change
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

asbestosis causes fibrosis in what part of the lung?

A

lower lobe fibrosis

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

Contraindications to lung surgery?

A
  • stage IIIb or IV (i.e. metastases present)
  • FEV1 < 1.5 litres (general cut off)
  • malignant pleural effusion
  • tumour near hilum
  • vocal cord paralysis
  • SVC obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Causes of lower zone pulmonary fibrosis?

A
  • idiopathic
  • most connective tissue disorders e.g. SLE
  • drug-induced: amiodarone, bleomycin, methotrexate
  • asbestosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Causes of Upper zone pulmonary fibrosis?

A

CHARTS:

C - Coal worker's pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

management of primary pneumothorax if rim of air >2cm OR SOB?

A

needle aspiration.

  • > if this fails, then chest drain
  • > advise STOP smoking!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

management of secondary pneumothorax if rim >2cm and/or SOB?

A
  • chest drain insertion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

management of secondary pneumothorax if rim of air is 1-2cm?

A

aspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

management of secondary pneumothorax if rim of air <1cm?

A

oxygen + admit for 24h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is KCO (transfer co-efficient of carbon monoxide) and how is it affected in lung disease?

A

KCO is a measure of the efficiency of gas exchange into the blood stream. It is reduced if the lungs are damaged and increased if there is additional blood in the lungs to remove carbon monoxide.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is TLCO (Transfer factor for carbon monoxide)?

A

TLCO = KCO x Alveolar volume
- The transfer factor describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Causes of raised TLCO (Transfer factor for carbon monoxide)? ie. increased rate of gas diffusion from alveoli into blood

A
  • asthma
  • pulmonary haemorrhage (Wegener’s, Goodpasture’s)
  • left-to-right cardiac shunts
  • polycythaemia
  • hyperkinetic states
  • male gender, exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Causes of reduced TLCO (Transfer factor for carbon monoxide)? ie. reduced rate of gas diffusion from alveoli into blood

A
  • pulmonary fibrosis
  • pneumonia
  • PE
  • pulmonary oedema
  • emphysema
  • anaemia
  • low cardiac output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Causes of conditions which increase KCO (increased efficiency of gas exchange) but have a normal/ reduced TLCO (ie. reduced rate of gas diffusion from alveoli into blood- due to reduced alveolar volume) ?

A
  • pneumonectomy/lobectomy
  • scoliosis/kyphosis
  • neuromuscular weakness
  • ankylosis of costovertebral joints e.g. ankylosing spondylitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Features of silicosis?

A
  • upper zone lung fibrosis

- ‘egg-shell’ calcification of the hilar lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

MOA of varenicline?

A

nicotinic receptor partial agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

MOA of bupropion?

A

a norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

CI for bupropion?

A

epilepsy (small risk of seizures), pregnancy, breast feeding, eating disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Smoking cessation for pregnancy women?

A

1st line: CBT

- nicotine replacement therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Diagnosistic test for obstructive sleep apnoea?

A

polysomnography (sleep studies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Lofgrens syndrome?

A

acute form of sarcoidosis characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Heerfordt’s syndrome (uveoparotid fever) ?

A

parotid enlargement, fever and uveitis secondary to sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Ix findings of extrinsic allergic alveolitis?

A
  • imaging: upper/mid-zone fibrosis
  • bronchoalveolar lavage: lymphocytosis
  • serologic assays for specific IgG antibodies
  • blood: NO eosinophilia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

hypercalcaemia in sarcoidosis?

A

macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

oxygen dissociation curve - shift to left =?

A

decreased oxygen delivery to tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

oxygen dissociation curve - shift to right =?

A

increased oxygen delivery to tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

factors causing oxygen dissociation curve to shift left?

A
  • everything that decreases oxygen delivery to tissues

HbF, methaemoglobin, carboxyhaemoglobin

Low [H+] (alkali)

Low pCO2

Low 2,3-DPG

Low temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

factors causing oxygen dissociation curve to shift right?

A
  • causing raised oxygen delivery

Raised [H+] (acidic)
Raised pCO2
Raised 2,3-DPG*
Raised temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

organism implicated in malt workers lung? (part of EAA)

A

Aspergillus clavatus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Organism implicated in farmers lung (part of EAA)?

A

spores of Saccharopolyspora rectivirgula from wet hay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

organism implicated in bird fanciers lung (part of EAA)?

A

avian proteins from bird droppings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

organism implicated in mushroom workers lung (part of EAA)?

A

thermophilic actinomycetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

paraneoplastic features of small cell lung ca?

A
  • ADH -> Hypona
  • ACTH -> Cushings
  • Lambert Eaton syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

paraneoplastic features of squamous cell lung ca?

A

PTH-related peptide, clubbing, hypertrophic pulmonary osteoarthropathy, ectopic TSH -> Hyperthyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

pleural effusion - pleural fluid showing low glucose assoc w?

A

rheumatoid arthritis, TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

pleural effusion - pleural fluid showing raised amylase assoc w?

A

pancreatitis, oesophageal perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

pleural effusion - pleural fluid showing heavy blood staining assoc w?

A

mesothelioma, Pulmonary embolism, TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Genetics of Cystic fibrosis?

A

Chr 7, auto recessive, CFTR gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

catamenial pneumothorax

A

cause of 3-6% of spontaneous pneumothoraces occurring in menstruating women. It is thought to be caused by endometriosis within the thorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Paraneoplastic features of lung adenocarcinoma?

A

gynaecomastia, Hypertrophic pulmonary osteoarthropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

1st line management of COPD?

A

SABA/ SAMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what features do NICE suggest to determine whether pt with suspected COPD has asthmatic/ steroid responsive features?

A
  • any previous diagnosis of asthma/ atopy
  • High eosinophil count in FBC
  • Peak flow: substantial diurnal variation in PEF (>/= 20%)
  • substantial variation in FEV1 over time (>400mL)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

management of COPD if no asthmatic features?

A
  • add LABA/ LAMA

- if on SAMA, discontinue and switch to SABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

management of COPD if asthmatic features?

A
  • LABA + ICS
  • then Triple therapy ie. LAMA + LABA + ICS
  • if on SAMA, discontinue and switch to SABA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what investigations to do before starting oral prophylactic antibiotic therapy in COPD?

A
  • stop smoking
  • CT thorax to exclude bronchiectasis
  • sputum culture to exclude atypical infections/ TB
  • LFTs + ECG to exclude QT prolongation as azithromycin can prolong QT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

features of Loffler’s syndrome

A
  • thought to be due to parasites such as ascaris lumbricoides causing an alveolar reaction
  • transient CXR shadowing and blood eosinophilia
  • fever, cough, night sweats
  • generally self limiting, <2 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

mx of allergic bronchopulmonary aspergillosis

A

oral steroids.

2nd line - itraconazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Contraindications for varenicline?

A

pregnancy/ breast feeding.

caution- depression/ self harm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

features of Churg Strauss / eosinophilic granulomatosis with polyangiitis?

A

asthma, blood eosinophilia, paranasal sinusitis, mono neuritis multiplex, pANCA +

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what drug class might precipitate Churg Strauss?

A

Leukotriene receptor antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

genotype of homozygous A1AT deficiency leading to 50% and 10% normal A1AT levels?

A

50% of normal: piSS
10% of normal: PiZZ

Normal: PiMM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

features of Kartagener’s?

A
  • dextrocardia/ situs inversus
  • bronchiectasis
  • recurrent sinusitis
  • sub fertility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

most common chemical causing occupational asthma?

A

isocyanates

  • example occupations include spray painting and foam moulding using adhesives
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Investigation of choice for assessing compression of upper airway?

A

Flow volume loop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

factors associated with poor prognosis in sarcoidosis?

A
  • insidious onset, symptoms > 6 months
  • absence of erythema nodosum
  • extrapulmonary manifestations: e.g. lupus pernio, splenomegaly
  • CXR: stage III-IV features
  • black people
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

prophylaxis medication to prevent acute mountain sickness?

A

acetazolamide (a carbonic anhydrase inhibitor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Management of high altitude cerebral oedema?

A

descent, dexamethasone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Management of high altitude pulmonary oedema?

A

descent, oxygen if avail.
- nifedipine, dexamethasone, acetazoleamide, phosphodiesterase type V inhibitor* (all work by reducing systolic pulmonary artery pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what is a specific Cystic fibrosis contraindication to lung transplantation?

A

chronic infection with Bulrkholderia cepacia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Diet advice in Cystic fibrosis?

A

High calorie, high fat with pancreatic enzyme supplementation with every meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Lumacaftor/ Ivacaftor?

A
  • used to treat Cystic fibrosis
  • lumacaftor increases the number of CFTR proteins transported to cell surface
  • ivacaftor is a potentiator of CFTR, increasing the probability that the defective channel will be open
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Indication for steroid treatment in Sarcoidosis?

A
  • patients with chest x-ray stage 2 or 3 disease + symptomatic.
  • hypercalcaemia
  • eye, heart or neuro involvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

CXR findings in idiopathic pulmonary fibrosis?

A

bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ -> later progressing to ‘honeycombing’)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

CXR stages in Sarcoidosis?

A

stage 0 = normal
stage 1 = bilateral hilar lymphadenopathy (BHL)
stage 2 = BHL + interstitial infiltrates
stage 3 = diffuse interstitial infiltrates only
stage 4 = diffuse fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

How does silica lead to TB?

A

Silica is a Risk factor for developing TB as silica is toxic to macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what type of lung cancer would be most likely to cavitate?

A

squamous cell lung ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

causes of bilateral hilarity lymphadenopathy?

A

sarcoidosis, TB.

  • lymphoma/other malignancy
  • pneumoconiosis e.g. berylliosis
  • fungi e.g. histoplasmosis, coccidioidomycosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

which COPD patients should be assessed for long term oxygen therapy?

A
  • very severe airflow obstruction (FEV1 < 30% predicted). - - consider if FEV1 30-49%
  • cyanosis
  • polycythaemia
  • peripheral oedema
  • raised JVP
  • oxygen saturations = 92% RA
89
Q

when to offer LTOT to COPD patients?

A

Offer LTOT to patients with pO2 of < 7.3 kPa on 2 ABGs

OR

pO2 of 7.3 - 8 kPa + one of:

  • secondary polycythaemia
  • peripheral oedema
  • pulmonary hypertension
90
Q

diagnosis of asthma in adults?

A

FeNO test and spirometry with reversibility

91
Q

management of very early stage (T1-2a, N0, M0) small cell lung ca?

A

referral for surgery

92
Q

Which type of hypersensitivity reaction predominates in the acute phase of extrinsic allergic alveolitis?

93
Q

what is re-expansion pulmonary oedema?

A

a complication that can develop following over rapid aspiration / drainage of pneumothorax/effusion -> can lead to over-rapid re-expansion of the lung + oedema

94
Q

Risk factors for re-expansion pulmonary oedema?

A
  1. Longer duration of lung collapse
  2. Larger volume of lung collapse
  3. Rapid drainage of pleural fluid/air
  4. Application of negative pleural pressure (suction)
  5. Younger age of patient
95
Q

Calcification in lung metastases are usually seen in which type of tumours?

A

chondrosarcoma/ osteosarcoma

96
Q

most common organism isolated from patients with bronchiectasis?

A

haemophilus influenzae

97
Q

HLA association for bronchiectasis?

98
Q

approximate normal anatomical dead space in healthy adult?

A

approx 150ml

99
Q

patients on LTOT, what is the minimum length of time they should be on oxygen daily?

A

15 h/ day

preferably up to 18h/day

100
Q

What demonstrates eosinophilic inflammation in asthmatics?

A

One or more of:

  • sputum eosinophils >/= 3%
  • FENO: 50 ppb or >
  • Eosinophil count 0.3 x 10^9/L or >
  • prompt deterioration of asthma vontrol after a 25% or less reduction in inhaled corticosteroid dose
101
Q

Management of inadequately controlled eosinophilic asthma? Already on steroids

A

Anti IL5 therapy ie. Mepolizumab

  • particularly useful in patients on long term steroid therapy
    • can improve asthma to such an extent that may be able to cease oral steroids
102
Q

What is considered low/ moderate/ high dose Inhaled corticosteroids in adults?

A

<= 400 mcg budesonide low
400-800 moderate
>800 high

103
Q

Follow up for lung nodule <5 mm, or clear benign features, or unsuitable for treatment?

A

Can be discharged

104
Q

Follow up for lung nodule 5-6mm, or =>8mm and low risk of malignancy using Brock model?

A

CT thorax in 1 year if 5-6mm, or in 3 months if >=6mm

105
Q

Follow up of Lung nodule >= 8mm and high risk of malignancy using brock model?

A

CT-PET

+/- biopsy if CT PET shows high uptake

106
Q

What are some predictors of lung cancer in the Brock model?

A 
older age
female sex
family history of lung cancer
emphysema
larger size
upper lobe nodule location
part-solid nodule type
lower nodule count
spiculation
107
Q

Most common bacterial organisms causing COPD infective exacerbations?

A
  1. haemophilus influenzae
    - streptococcus pneumoniae
    - moraxella cararrhalis
108
Q

What are some drugs that cause pleural effusion as side effects?

A

Nitrofurantoin
Methotrexate
Amiodarone

109
Q

Respiratory follow up if pt on long term nitrofurantoin?

A

Spirometry every 3-6 months

  • acute: consolidation
  • chronic: fibrosis, effusions
110
Q

Non respi causes of exudative pleural effusion?

A 
Connective tissue disease: RA, SLE
Malignancy
Pancreatitis 
dresslers syndrome (2’ pericarditis)
Yellow nail syndrome: yellow nails, 1’ lymphoedema, respi problems
111
Q

Risk factor for MERS coronavirus

A

Contact with camels including camel products such as milk

112
Q

What medication can you give to anxious patient on NIV to calm them?

A

Haloperidol or morphine

113
Q

Definition of pulmonay hypertension?

A

Sustained elevation in mean pulmonary arterial pressure of > 25 mmHg at rest

114
Q

What causes increased DLCO? (Diffusing capacity of the lung for CO)

A

Pulmonary haemorrhage
Polycythaemia
L-> R carduac shunting

115
Q

Management of secondary pneumothorax If >50yo + rim of air >2cm +/- SOB

A

chest drain

116
Q

Management of secondary pneumothorax if <1cm?

A

Give oxygen and admit for 24h

117
Q

Management of secondary pneumothorax if rim of air is between 1-2cm?

A

Aspiration.
If fails-> for chest drain
Admit for 24h

118
Q

Pneumothorax + airplane rules?

A

Civil aviation authority: 2 weeks after CXR shows resolution

British thoracic society: 1 week post CXR check

119
Q

Diving and pneumothorax?

A

Should be permanently avoided unless pt has undergone bilateral surgical pleurectony and has normal lung function and chest CT post op

120
Q

Bubbling of chest drain continuously after chest drain inserted to drain empyema?

A

Suggestive of bronchopleural fistula

121
Q

Relative contraindications to chest drain insertion?

A

INR > 1.3
Plt <75
Pulmonary bullar
Pleural adhesions

122
Q

Management of re-expansion pulmonary oedema following chest drain insertion?

A
  • clamp chest drain

- urgent CXR

123
Q

How to reduce risk of reexpansion pulmonary oedema following chest drain insertion?

A

Drain tubing should be clamped regularly in the event of rapid fluid output

(Ie. Max 1L every 6h)

124
Q

When to remove chest drain of pleural effusion?

A

No output >24h + imaging shows resolution of fluid collection

125
Q

When to remove chest drain for pneumothorax?

A

When no longer bubbling spontaneously/ when coughing and ideally when imaging shows resolution of pneumothorax

126
Q

Renal manifestation of granulomatosis with polyangiitis?

A

Rapidly progressive GN

“Pauci immune”, 80% of pts

127
Q

Investigations in wegeners (GPA)?

A

cANCA + in > 90%
pANCA + in 25%
CXR: possibly cavitating lesions

128
Q

Renal biopsy findings in wegeners granulomatosis?

A

Epithelial crescents in Bowman’s capsule

129
Q

Management of wegeners granulomatosis?

A

Steroids
Cyclophosphamide (90% response)
Plasma exchange

Median survival 8-9 yrs

130
Q

Silicosis and TB?

A

Patients with silicosis are at higher risk of tuberculosis infection that is more severe and extensive than for other people = silicotuberculosis.

(silica is toxic to macrophages).

131
Q

which subtype of COPD has normal DLCO (Carbon monoxide diffusing capacity)

A

chronic bronchitis

132
Q

Ix for mesothelioma?

A

suspicion is normally raised by a chest x-ray showing either a pleural effusion or pleural thickening
->
the next step is normally a pleural CT

133
Q

diagnosis of mesothelioma?

A

cytology from pleural effusion
.
local anaesthetic thoracoscopy: high diagnostic yield in cytology negative exudative effusions
.
if an area of pleural nodularity is seen on CT -> image-guided pleural biopsy

134
Q

protein level of exudative pleural effusions?

A

protein >30g/L

135
Q

further ix in exudative pleural effusions?

A

contrast CT to investigate underlying cause

136
Q

Further management if persistent air leak or failure of lung to reexpand after draining a pneumothorax for 3-5 days?

A

seek a thoracic surgical opinion

as may need pleurectomy/ blebectomy/ pleurodesis

136
Q

management of cystic fibrosis patients who are homozygous for delta F508 mutation?

A

Lumacaftor/Ivacaftor (Orkambi)

  • lumacaftor increases no. of CFTR proteins transported to cell surface
  • Ivacaftor is a potentiator of CFTR
137
Q

contraindication to CF patients getting lung transplant?

A

chronic infection with Burkholderia cepacia

138
Q

Medication for symptomatic SOB in end stage COPD unresponsive to other medical tx?

A

1st line Opioids

- ie. short acting liquid morphine sulphate prn

139
Q

Eradication of pseudomonas aureginosa in CF patients?

A

IV anti-pseudomonal antibiotic plus inhaled aminoglycoside for 14 days (e.g IV Ceftazadime + Nebulised tobramycin)

OR

A prolonged course of oral Ciprofloxacin (e.g. 6 weeks)

140
Q

Next step of Diagnosis and staging of a lung mass with lymph node involvement (shown on scans)?

A

EBUS (endobronchial US) guided mediastinal LN sampling

-> aids in diagnosis and staging

141
Q

management of tropical pulmonary eosinophilia?

A

Diethylcarbamazine

142
Q

Causes of tropical pulmonary eosinophilia?

A

roundworms - Wucheria bancrofti, Brugia malayi

- spread by mosquitoes

143
Q

features of tropical pulmonary eosinophilia?

A
  • common in Asian subcontinent and Africa
  • nocturnal cough, wheeze and SOB
  • diagnosis aided by clinical response to diethylcarbamazine (the main tx)
144
Q

most likely causative organism in Loefflers syndrome (eosinophilic pneumonia)?

A

Ascaris lumbricoides (roundworm)

145
Q

Management of Loeffler’s syndrome (eosinophilic pneumonia)?

A

generally self limiting

- tx with mebendazole for 3 days might help

146
Q

Flash pulmonary oedema after ACEi initiation?

A

Renal artery stenosis

-> ix with MRA

147
Q

Tx of choice for allergic bronchopulmonary aspergillosis?

A

oral steroids

148
Q

most common lung cancer in adolescents?

A

bronchial carcinoid

  • often presents with recurrent pneumonia
  • assoc w smoking
149
Q

1st line management of DM in CF patients?

A

insulin + high calorie diet

150
Q

what management is available for those with allergic asthma and elevated IgE levels not controlled with normal therapies?

A

Anti-IgE therapy: Omalizumab

-> s/c monoclonal antibody that binds to free IgE and prevents activation of mast cells by the antigen

150
Q

what medication is indicated in idiopathic pulmonary fibrosis?

A

pirfenidone (antifibrotic agent)

- may be useful in selected patients

151
Q

Recommended threshold of FEV1 for pneumonectomy to be offered to lung cancer patients?

152
Q

recommended threshold for lobectomy for lung cancer patients?

153
Q

What management is advised prior to surgery if surgery is indicated in Non small cell lung cancer?

A

Mediastinoscopy

- as CT does not always show LN involvement

154
Q

Contraindications to surgery in lung cancer?

A 
Stage IIIb or IV (mets present)
FEV1 <1.5L
malignant pleural effusion
tumour near hilum
vocal cord paralysis
SVCO
155
Q

what is the TLCO cut off for surgery to be recommended in lung cancer?

A

TLCO recommended to be >40% prior to resective surgery

156
Q

what ventilation decreases overall mortality of ARDS?

A

maintaining low tidal volume ventilation

157
Q

When to offer LTOT to COPD patients based on ABG results?

A
  1. if pO2 <7.3 on 2 separate ABGs 3/52 apart

2. pO2 7.3 -8 kPa with 2’ polycythaemia, peripheral oedema, nocturnal hypoxaemia or pulm HTN

157
Q

features of eosinphilic GPA (Churg strauss)

A

ANCA assoc- small-medium vessel vasculitis

  • asthma
  • eosinophilia
  • sinusitis
  • mononeuritis multiplex
  • pANCA+
158
Q

Restrictive lung disease

- Low DLCO but HIGH KCO?

A

Low Diffusion capacity (DLCO), high rate of CO uptake (KCO)

  • > extra pulmonary cause of restrictive lung disease
    e. g. obesity
159
Q

lung cancer + intermittent aching and swelling in the wrists and ankles

A

hypertrophic pulmonary osteoarthropathy

160
Q

rheumatoid arthritis + melanoptysis (coughing up of black sputum) ?

A

Coal workers pneumoconiosis

-> severe progressive fibrosis with massive fibrotic nodules (Caplans syndrome)

161
Q

what may you see on CXR/ HRCT in non tuberculous mycobacterial lung infection?

A

Chest X-ray or HRCT demonstrating cavities, bronchiectasis +/- nodules

161
Q

diagnosis of pulmonary hypertension secondary to chronic thromboembolic disease?

A

right heart catheterization

to assess pulmonary pressures

162
Q

indication for nocturnal BIPAP along with LTOT in COPD patients?

A

if pt develops respiratory acidosis +/- rise in PaCO2 of >1kPa during LTOT assessment

163
Q

Pneumonia + splenomegaly + diarrhoea + epistaxis

A

Psittacosis

- chlamydia psittaci

164
Q

features of combined pulmonary fibrosis and emphysema?

A

SOBOE, UL emphysema and LL fibrosis

  • preserved lung volume
  • severely reduced capacity of gas exchange
165
Q

Low glucose in pleural fluid sample?

A

Rheumatoid arthritis
TB
If coupled with likely malignancy: bronchial carcinoma

166
Q

Omalizumab =?

A

Anti igE monoclonal antibody

- used in severe allergic asthma

167
Q

Long term management for COPD patients with >/=2 exacerbations despite triple therapy (LABA, LAMA + ICS) + FEV1<50%?

A

Add roflumilast

- long acting imhibitor of phosphodiesterase-4 enzyme

168
Q

Nintedanib used in?

A

Idiopathic pulmonary fibrosis
- small molecule tyrosine kinase inhibitor including the receptors PDGFR (platelet derived growth factor) and FGFR 1-3 (fibroblast derived growth factor) and VEGFR 1-3

169
Q

What to monitor with aminophylline loading?

A

Cardiac monitoring

- aminophylline can induce tachyarrhythmias

170
Q

Aminophylline infusion: what blood tests Should be monitored?

A

RP: hypoK

LFTs

171
Q

US for pleural effusion aspiration - what indicates likelihood of failure?

A

Septation density on US

- indicates various pockets so even if u drain one you might not drain all the effusion

172
Q

Lower zone pulmonary fibrosis causes?

A

Idiopathic
Connective tissue disorders: e.g. SLE
Drugs: amiodarone, bleomycin, methotrexate
Asbestosis

173
Q

Upper zone pulmonary fibrosis causes?

A

CHARTS

C- coal workers pneumoconiosis
H- Histiocytosis/ hypersensitivity pneumonitis (EAA) 
A- ankylosing spondylitis
R- radiation
T- TB
S- silicosis/ sarcoidosis
174
Q

Ix in microscopic polyangiitis?

A

pANCA (against MPO) - positive in 50-75%

cANCA (against PR3) - positive in 40%

175
Q

What is the benefit of oxygen In the treatment of a pneumothorax?

A

exchange of nitrogen for oxygen allowing quicker resorption of the pneumothorax

176
Q

Recommended treatment in small cell lung cancer Early stage (T1-2a,N0,M0)?

177
Q

Recommended treatment in small cell lung cancer with spread to nodes?

Early stage (T1-2a,N0,M0)-Limited disease (T1-4,N0-3,M0)

A

4-6 cycles cisplatin based chemotherapy

carboplatin if poor renal function/poor performance status +/- radiotherapy

178
Q

Recommended treatment in small cell lung cancer?

Extensive disease (T1-4, N0-3, M1a/b)

A

6 cycles platinum based combination chemotherapy + thoracic radiotherapy if good response

179
Q

Average life expectancy of idiopathic pulmonary fibrosis?

180
Q

Appropriate treatment of Pseudomonas positive bronchiectasis failing to respond to oral ciprofloxacin ?

A

Change to IV tazocin, ceftazidime, aztreonam or meropenem

181
Q

Appropriate treatment of Pseudomonas positive bronchiectasis failing to respond to oral ciprofloxacin ?

A

Change to IV tazocin, ceftazidime, aztreonam or meropenem

182
Q

What investigation would aid in distinguishing chylothorax from pseudochylothorax?

A

chylothorax is high in triglycerides and chylomicrons

pseudochylothorax would be high in cholesterol.

183
Q

Chylothorax?

A

Chylothorax = the accumulation of lymph in the pleural space. This can occur following damage to the thoracic duct in surgery or in malignant melanoma.

184
Q

Pseudochylothorax?

A

A pseudochylothorax occurs with longstanding fibrotic pleura.
- milky white fluid, high in cholesterol

185
Q

What is Lymphangioleiomyomatosis?

A

affects premenopausal women causing proliferation of atypical smooth muscle cells in the lungs, lymphatics and uterus, most likely caused by oestrogens

186
Q

What is associated with Lymphangioleiomyomatosis?

A

tuberous sclerosis, renal angiomyolipomas.

187
Q

Presentation of Lymphangioleiomyomatosis?

A

SOB due to progressive ILD, pneumothorax or chylous pleural effusion

Lung damage is similar to emphysema with:

  • reduced FVC, TLCO and KCO
  • increased TLC.
188
Q

Management / medication to delay disease progression in lymphangioleiomyomatosis?

A

Medroxyprogesterone

- anti-oestrogen used to delay disease progression.

189
Q

Chest x-ray shows bat wings + diagnosis confirmed with bronchoalveolar lavage (milky fluid, PAS positive material).

A

Alveolar proteinosis
- accumulation of lipoproteinaceous material in alveolar spaces

  • most commonly affects males
  • can be 2’ insecticides, silica, HIV
190
Q

oculocutaneous albinism, abnormal platelet function and interstitial lung disease

A

Hermansky Pudlak syndrome

191
Q

Chest x-ray shows bat wings + diagnosis confirmed with bronchoalveolar lavage (milky fluid, PAS positive material).

A

Alveolar proteinosis
- accumulation of lipoproteinaceous material in the alveolar spaces

  • most commonly affects males
  • can be 2’ to insecticides, silica, HIV.
192
Q

Apical lung fibrosis
+

Work in aerospace industry
Or
manufacture of fluorescent light bulbs/golf-club heads

A

Berylliosis

  • caused by inhalation of the fumes of molten beryllium
  • causes lung fibrosis + BL hilar lymphadenopathy
193
Q

What is the most useful pleural fluid marker to make a diagnosis of a haemothorax?

A

Haematocrit

-If the Hct of the pleural fluid is >
1/2 of peripheral blood Hct, the patient has a haemothorax.

194
Q

What test is most useful in determining prognosis of idiopathic pulmonary fibrosis?

A

impaired gas exchange: reduced transfer factor (TLCO)

195
Q

Management of theophylline poisoning?

A
  • consider gastric lavage if <1 hour prior to ingestion
  • activated charcoal
  • whole-bowel irrigation can be performed if theophylline is sustained release form
  • charcoal haemoperfusion is preferable to haemodialysis
196
Q

Emphysema pts: who are likely unsuitable candidates for lung volume reduction surgery?

A
  1. non-upper lobe emphysema + high exercise capacity.

2. FEV1<20% + homogenous distribution of emphysema OR TLCO < 20%

197
Q

Treatment of histoplasmosis?

A

amphotericin or itraconazole

198
Q

Ferritin target for CKD patients on ferrous fumarate replacement?

A

~500

should be below <800

199
Q

Hyperventilation syndrome: what questionnaire can you use?

A

Nijmegen questionnaire

- score of >23/64 is diagnostic of HVS

200
Q

Aetiology of Group I pulmonary Hypertension?

A

A for Pulmonary Arterial Hypertension

201
Q

Causes of Group i pulmonary hypertension?

A
  • idiopathic*
  • familial
  • associated conditions: collagen vascular disease, congenital heart disease with systemic to pulmonary shunts, HIV**, drugs and toxins, sickle cell disease
  • persistent pulmonary hypertension of the newborn
202
Q

Aetiology of group 2 pulmonary hypertension?

A

pulmonary hypertension secondary to left heart disease

B for BARDIAC

203
Q

Causes of Group 2: Pulmonary hypertension with left heart disease?

A
  • left-sided atrial, ventricular or valvular disease such as LV systolic/ diastolic dysfunction, mitral stenosis and mitral regurgitation
204
Q

Aetiology of group 3 pulmonary hypertension?

A

pulmonary hypertension secondary to lung disease

C for Chronic Lung stuff

205
Q

Causes of Group 3: Pulmonary hypertension secondary to lung disease/hypoxia?

A
  • COPD
  • interstitial lung disease
  • sleep apnoea
  • high altitude
206
Q

Aetiology of group 4 pulmonary hypertension?

A

IV pulmonary hypertension secondary to chronic thromboembolic disease

D for D DIMER HIGH

207
Q

Aetiology of group 5 pulmonary hypertension?

A

V pulmonary hypertension with unclear causes

E for everything else (basically unsure)

208
Q

Causes of group V pulmonary hypertension?

A

Miscellaneous conditions

- lymphangiomatosis e.g. secondary to carcinomatosis or sarcoidosis

209
Q

Features of histoplasmosis?

A

Due to the fungus Histoplasma capsulatum

  • URTI
  • retrosternal pain
210
Q

What medication may be indicated in COPD patients still symptomatic on triple therapy with LABA ICS/LAMA/SABA?

A

Roflumilast
- phosphodiesterase inhibitor

If:
1. FEV1 after bronchodilator <50%

AND

  1. 2 or more exacerbations in the previous 12 months
211
Q

Occupational risk factors for berylliosis?

A
  • inhalation of fumes of molten beryllium

> aerospace industry
manufacture of fluorescent light bulbs/ golf club heads

212
Q

Most useful pleural fluid marker to diagnoses haemothorax?

A

Haematocrit

> if Hct is more than half of pts peripheral blood Hct, the pt has haemothorax

213
Q

Management of non small cell lung ca if not for surgery

A

Radiotherapy

  • response to chemo is poor
214
Q

What is the primary form of treatment for ARDS?

A

invasive mechanical ventilation with low tidal volumes*
+ high positive end-expiratory pressures

*low tidal vol avoids alveolar hyperinflation

MRCP (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions