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MRCP Respiratory > MRCP2 > Flashcards

MRCP2 Flashcards

1
Q

Features of moderate asthma ?

A

PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm

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2
Q

Features of severe asthma?

A

PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm

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3
Q

Features of life threatening asthma?

A

PEFR < 33% best or predicted
Oxygen sats < 92%
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma

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4
Q

What is the difference in near fatal asthma?

A

Elevated CO2

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5
Q

When should you admit a person with severe asthma exacerbation?

A

When fail to respond to initial therapy

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6
Q

Treatment in life threatening / severe asthma?

A
  1. SABA
  2. Corticosteroid 40-50 mg prednioslone
  3. Ipratropium bromide
  4. IV magnesium
  5. Aminophyline with senior staff consultation
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7
Q

Treatment in life threatening / severe asthma?

A
  1. SABA
  2. Corticosteroid 40-50 mg prednioslone
  3. Ipratropium bromide
  4. IV magnesium
  5. Aminophyline with senior staff consultation
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8
Q

Criteria for discharge in asthma?

A

been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
inhaler technique checked and recorded
PEF >75% of best or predicted

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9
Q

Most common bacteria for COPD exacerbation?

A

Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis
account for around 30% of exacerbations

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10
Q

Most common viral exacerbation of COPD?

A

Rhinovirus

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11
Q

On acute review what should you aim saturations at in COPD

A

prior to the availability of blood gases, use a 28% Venturi mask at 4 l/min and aim for an oxygen saturation of 88-92% for patients with risk factors for hypercapnia but no prior history of respiratory acidosis
adjust target range to 94-98% if the pCO2 is normal

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12
Q

Management of severe COPD?

A

Nebulised bronchodilator
beta adrenergic agonist: e.g. salbutamol
muscarinic antagonists: e.g. ipratropium

Steroid therapy as above
IV hydrocortisone may sometimes be considered instead of oral prednisolone

IV theophylline
may be considered for patients not responding to nebulised bronchodilators

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13
Q

Indications for NIV?

A

typically used for COPD with respiratory acidosis pH 7.25-7.35
the BTS guidelines state that NIV can be used in patients who are more acidotic (i.e. pH < 7.25) but that a greater degree of monitoring is required (e.g. HDU) and a lower threshold for intubation and ventilation should be used

bilevel positive airway pressure (BiPaP) is typically used with initial settings:
Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O
Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O

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14
Q

Causes of acute respiratory distress syndrome?

A

infection: sepsis, pneumonia
massive blood transfusion
trauma
smoke inhalation
acute pancreatitis
Covid-19
cardio-pulmonary bypass

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15
Q

Criteria for acute respiratory distress syndrome?

A

acute onset (within 1 week of a known risk factor)
pulmonary oedema: bilateral infiltrates on chest x-ray (‘not fully explained by effusions, lobar/lung collapse or nodules)
non-cardiogenic (pulmonary artery wedge pressure needed if doubt)
pO2/FiO2 < 40kPa (300 mmHg)

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16
Q

Aetiology of allergic bronchopulmonary aspergillosis?

A

Allergy to aspergillis spores

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17
Q

Features of allergic bronchopulmonary aspergillosis?

A

bronchoconstriction: wheeze, cough, dyspnoea. Patients may have a previous label of asthma
PROXIMAL BRONCHIECTASAIS

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18
Q

Investigation findings of allergic bronchopulmonary aspergillosis?

A

eosinophilia
flitting CXR changes
positive radioallergosorbent (RAST) test to Aspergillus
positive IgG precipitins (not as positive as in aspergilloma)
raised IgE

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19
Q

Management of allergic bronchopulmonary aaspergillosis ?

A
  1. Steroids
  2. Itraconazole
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20
Q

Pathphysiology of alpha 1 antitrypsin disease ?

A

Lack of A1AT, lack of protease inhibitor - in non-smokers
Located on chromosome 14

Inherited by a autosomal co-dominant fashion

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21
Q

What is A1AT electrophoresis?

A

M - for normal
S - for slow
Z - very slow

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22
Q

What is the phenotypes of PiMZ?

A

if non-smoker low risk of developing emphsema but may pass on A1AT gene to children

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23
Q

What is the phenotype of PiSS?

A

50% normal levels A1AT

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24
Q

What is the phenotype of PiZZ?

A

10% normal level

These patients usually manifest disease
lungs: panacinar emphysema, most marked in lower lobes
liver: cirrhosis and hepatocellular carcinoma in adults, cholestasis in children

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25
Q

What are the investigation findings of A1At deficiency?

A

OBSTRUCTIVE PICTURE
Low A1At levels

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26
Q

Management of A1AT?

A

no smoking
supportive: bronchodilators, physiotherapy
intravenous alpha1-antitrypsin protein concentrates
surgery: lung volume reduction surgery, lung transplantation

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27
Q

What are the three altitude sicknesses?

A

Develop 2500 - 3000
Within 6-12 hours :
Acute mountain sickness
High altitude pulmonary oedema
High altitude cerebral oedema

Over 4000 meters - develope:
high altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE),
HACE presents with headache, ataxia, papilloedema

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28
Q

Management of acute mountain sickness?

A

Correlates to being more physically fit

Gain altitude at no more than 500 m per day

Acetazolamide (a carbonic anhydrase inhibitor) is widely used to prevent AMS and has a supporting evidence base
- it causes a primary metabolic acidosis and compensatory respiratory alkalosis which
- increases respiratory rate and improves oxygenation

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29
Q

How does acetazolamide prevent Acute mountain sickness?

A

Acetazolamide (a carbonic anhydrase inhibitor) is widely used to prevent AMS and has a supporting evidence base
- it causes a primary metabolic acidosis and compensatory respiratory alkalosis which
- increases respiratory rate and improves oxygenation

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30
Q

What is HACE?

A

High altitude cerebral oedema

HACE presents with headache, ataxia, papilloedema

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31
Q

Management of HACE?

A

descent
dexamethasone

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32
Q

Management of HAPE?

A

descent
nifedipine, dexamethasone, acetazolamide, phosphodiesterase type V inhibitors*
oxygen if available

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33
Q

How should aminophyline be given in COPD and asthma?

A

For patients not already treated with xanthines (theophylline or aminophylline) a loading dose is given:
dose: 5mg/kg
given by slow intravenous injection over at least 20 minutes

maintenance infusion 1g of aminophylline is added to 1 litre of normal saline to give a solution of 1 mg/ml.
dose: 500-700mcg/kg/hour. If elderly: 300mcg/kg/hour
plasma theophylline concentrations should be monitored

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34
Q

WHat does a respiratory picture look like on ABG?

A

RO ME

Respiratory = Opposite
low pH + high PaCO2 i.e. acidosis, or
high pH + low PaCO2 i.e. alkalosis

PaCO2 > 6.0 kPa suggests a respiratory acidosis (or respiratory compensation for a metabolic alkalosis)
PaCO2 < 4.7 kPa suggests a respiratory alkalosis (or respiratory compensation for a metabolic acidosis)

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35
Q

What does a metabolic picture look like on ABG?

A

Metabolic = Equal
low pH + low bicarbonate i.e. acidosis, or
high pH + high bicarbonate i.e. akalosis

bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l) suggests a metabolic acidosis (or renal compensation for a respiratory alkalosis)
bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l) suggests a metabolic alkalosis (or renal compensation for a respiratory acidosis)

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36
Q

What does this show?

A

Pleural plaques

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37
Q

What are the asbestosis related damage?

A

Pleural plaques
Pleural thickening
Asbestosis
Mesothelioma

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38
Q

What are the features of asbestosis ?

A

latent period is typically 15-30 years.
Typically fibrosis of lower lobes

dyspnoea and reduced exercise tolerance
clubbing
bilateral end-inspiratory crackles
lung function tests show a restrictive pattern with reduced gas transfer

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39
Q

What spirometry pattern is there in asbestosis ?

A

Restrictive picture
Reduced gas transfer

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40
Q

How do you manage asbestosis ?

A

Conservatively

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41
Q

How do you manage asbestosis ?

A

Conservatively

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42
Q

What is the most dangerous form of asbestos?

A

Crocodile blue

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43
Q

What is the prognosis of mesothelioma?

A

8-14 months

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44
Q

What is the most common form of cancer from asbetos?

A

Lung cancer
Then Mesothelioma

Smoking has a synergistic effect with asbestos

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45
Q

What bacteria are typically implicated in aaspiration pneumonia?

A

Streptococcus pneumoniae
Staphylococcus aureus
Haemophilus influenzae
Pseudomonas aeruginosa
Klebsiella: often seen in aspiration lobar pneumonia in alcoholics

Bacteroides
Prevotella
Fusobacterium
Peptostreptococcus

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46
Q

How should asthma be diagnosed?

A

patients should be asked if their symptoms are better on days away from work/during holidays. If so, patients should be referred to a specialist as possible occupational asthma
all patients should have spirometry with a bronchodilator reversibility (BDR) test
all patients should have a FeNO test

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47
Q

WHat does a FeNO > 40 suggest?

A

in adults level of >= 40 parts per billion (ppb) is considered positive
in children a level of >= 35 parts per billion (ppb) is considered positive

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48
Q

What FEV1 and FVC is seen in asthma?

A

Obstructive picture

FEV1 reduced
FVC reduced, but not as much as FEV1

FEV1/FVC ratio: < 70% is OBSTRUCTIVE

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49
Q

What is considered positive reversibility test?

A

Adults: improvement in FEV1 of 12% or more and increase in volume of 200 ml or more

Children: positive test is indicated by an improvement in FEV1 of 12% or more

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50
Q

What is the treatment algorhythm for asthma?

A
  1. SABA
  2. SABA + ICS
  3. SABA + ICS + Leuotrine receptor antagonist
    (continue leukotrine receptor antagonist based on response)
  4. SABA + ICS + LABA
  5. SABA + Switch to MART (ICS/LABA)
  6. SABA + Medium MART
  7. SABA + High dose ICS ( not mart) + Theophylline
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51
Q

What is the mechanism of theophylline ?

A

Long term muscarinic antagonist

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52
Q

What is MART therapy?

A

Combination of ICS and LABA

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53
Q

What is the definitions of low, medium and high dose ICS?

A

<= 400 micrograms budesonide or equivalent = low dose
400 micrograms - 800 micrograms budesonide or equivalent = moderate dose
> 800 micrograms budesonide or equivalent= high dose.

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54
Q

Exposure to what is likely to cause occupational asthma?

A

isocyanates - the most common cause
example occupations include spray painting and foam moulding using adhesives
platinum salts
soldering flux resin
glutaraldehyde
flour
epoxy resins
proteolytic enzymes

Management: Refer to specialist

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55
Q

What is atelectasis ?

A

Airways obstructed from bronchial secretions

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56
Q

What are the features of atelectasis ? Management?

A

dyspnoea and hypoxaemia around 72 hours postoperatively

  1. Sit upright
  2. Breathing exercises
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57
Q

What are people who work in aerospace or fluorescent light bulbs/golf-club heads?

A

Beryliosis

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58
Q

Features of beryliosis?

A

lung fibrosis - Lower lobe fibrosis
bilateral hilar lymphadenopathy

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59
Q

What does tram track and signet rings suggest ?

A

Bronchiectasis

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60
Q

What is seen on this CT?

A

Bronchiectasis

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61
Q

What are the causes of bronchiectasis?

A

post-infective: tuberculosis, measles, pertussis, pneumonia
cystic fibrosis
bronchial obstruction e.g. lung cancer/foreign body
immune deficiency: selective IgA, hypogammaglobulinaemia
allergic bronchopulmonary aspergillosis (ABPA)
ciliary dyskinetic syndromes: Kartagener’s syndrome, Young’s syndrome
yellow nail syndrome

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62
Q

Indications for chest drain?

A

Pleural effusion
Pneumothorax not suitable for conservative management or aspiration
Empyema
Haemothorax
Haemopneumothorax
Chylothorax
In some cases of penetrating chest wall injury in ventilated patients

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63
Q

Contrainidcations to chest drain?

A

INR > 1.3
Platelet count < 75
Pulmonary bullae
Pleural adhesions

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64
Q

How to insert a chest drain?

A
  1. Position at 45 degrees
  2. 5’th intercostal space - mid axillary line
  3. Seldeinger technique
  4. Stitch drain in
  5. Ensure swinging and bubbling
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65
Q

Where is a chest drain inserted?

A

inserted into the pleural cavity which creates a one-way valve, allowing movement of air or liquid out of the cavity.

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66
Q

How to treat bronchiectasis?

A

Physical training
Antibiotics for exacerbation
Rotating antibiotics for severe cases
Immunisation
Consideration for surgery for localised cases

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67
Q

What bacteria as associated with bronchiectasis exacerbation ?

A

Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae

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68
Q

What is the most likely cause of bronchiolitis?

A

RSV

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69
Q

What is re-expansion pulmonary oedema? How is it prevented?

A

Rapid chest drain drainage

Do not allow more than 1.5 L to drain in first sitting
Drain 500 ml, then clamp for one hour. Then repeat

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70
Q

Indications for removing chest drain?

A

No output for > 24 hours

In pneumothorax: When drain no longer bubbling

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71
Q

Causes of caveatting lung lesion ?

A

abscess (Staph aureus, Klebsiella and Pseudomonas)
squamous cell lung cancer
tuberculosis
Wegener’s granulomatosis
pulmonary embolism
rheumatoid arthritis
aspergillosis, histoplasmosis, coccidioidomycosis

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72
Q

Causes of coin lesions?

A

malignant tumour: lung cancer or metastases
benign tumour: hamartoma
infection: pneumonia, abscess, TB, hydatid cyst
AV malformation

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73
Q

Causes of lobar collapse?

A

lung cancer (the most common cause in older adults)

asthma (due to mucous plugging)

foreign body

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74
Q

Features of lobar collapse on chest X-ray?

A

Tracheal deviation towards the side of the collapse

Mediastinal shift towards the side of the collapse

Elevation of the hemidiaphragm

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75
Q

What cancers commonly metastasise to lung?

A

breast cancer
colorectal cancer
renal cell cancer
bladder cancer
prostate cancer

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76
Q

What cancers cause cannon ball metastasis?

A

Renal carcinoma
Prostatic cancer
Choriocarcinoma

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77
Q

Features of pulmonary oedema?

A

interstitial oedema
bat’s wing appearance
upper lobe diversion (increased blood flow to the superior parts of the lung)
Kerley B lines
pleural effusion
cardiomegaly may be seen if there is cardiogenic cause

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78
Q

What are these?

A

Kerley lines
Blue is Kerley B lies ( periphery) - seen in pulmonary oedema

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79
Q

What causes opacification on CXR?

A

consolidation
pleural effusion
collapse
pneumonectomy
specific lesions e.g. tumours
fluid e.g. pulmonary oedema

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80
Q

Causes of white out + trachea pulled towards?

A

Pneumonectomy

Complete lung collapse e.g. endobronchial intubation

Pulmonary hypoplasia

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81
Q

Causes of white out + trachea central?

A

Consolidation

Pulmonary oedema (usually bilateral)

Mesothelioma

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82
Q

Causes of white out + trachea pushed away?

A

Pleural effusion

Diaphragmatic hernia

Large thoracic mass

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83
Q

Causes of COPD?

A

Smoking!

Alpha-1 antitrypsin deficiency

Other causes
cadmium (used in smelting)
coal
cotton
cement
grain

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84
Q

Features of COPD?

A

Cough: often productive
Dyspnoea
Wheeze

In severe cases, right-sided heart failure may develop resulting in peripheral oedema

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85
Q

How is the severity of COPD worked out?

A

FEV1
(By definition will also have FEV1/FVC < 70%)

If the FEV1 is greater than 80% predicted but the post-bronchodilator FEV1/FVC is < 0.7 then this is classified as Stage 1 - mild

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86
Q

Who should be considered for LTOT?

A

Very severe airflow obstruction (FEV1 < 30% predicted).
Assessment should be ‘considered’ for patients with severe airflow obstruction (FEV1 30-49% predicted)
Cyanosis
Polycythaemia
Peripheral oedema
Raised jugular venous pressure
Oxygen saturations less than or equal to 92% on room air

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87
Q

What criteria should be met to offer

?

A

Offer LTOT to patients with a pO2 of < 7.3 kPa or to those with a pO2 of 7.3 - 8 kPa and one of the following:
- secondary polycythaemia
- peripheral oedema
- pulmonary hypertension

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88
Q

What general things should be done for management of COPD?

A

Pneumococcal vaccine
Influenza vaccine
Smoking cessation
Pulmonary rehab

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89
Q

First line management in stable COPD?

A
  1. SABA or SAMA
  2. Consider reversible asthma element

No asthma:LABA + LAMA
if already taking a SAMA, discontinue and switch to a SABA

Asthma component:
LABA + inhaled corticosteroid (ICS)
if patients remain breathless or have exacerbations offer triple therapy i.e. LAMA + LABA + ICS

  1. Oral theophylline
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90
Q

How to determine if COPD has a asthma component?

A

a higher blood eosinophil count - note that NICE recommend a full blood count for all patients as part of the work-up
substantial variation in FEV1 over time (at least 400 ml)
substantial diurnal variation in peak expiratory flow (at least 20%)

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91
Q

Who should be considered for prophylactic antibiotics in COPD?

A

Patients should not smoke, have optimised standard treatments and continue to have exacerbations

CT thorax (to exclude bronchiectasis) and sputum culture (to exclude atypical infections and tuberculosis)

LFTs and an ECG to exclude QT prolongation should also be done as azithromycin can prolong the QT interval

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92
Q

Management of COPD + Cor Pulmonale ?

A

Loop diuretic for oedema, consider long-term oxygen therapy

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93
Q

What are the features of Cor Pulmonale ?

A

Peripheral oedema
Raised jugular venous pressure,
Systolic parasternal heave
Loud P2

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94
Q

What improves COPD prognosis?

A

smoking cessation - the single most important intervention in patients who are still smoking

long term oxygen therapy in patients who fit criteria

lung volume reduction surgery in selected patients

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95
Q

What antibiotic should be considered for COPD prophylaxis?

A

Azithromycin

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96
Q

Side effect of azithormycin?

A

LFTs and an ECG to exclude QT prolongation should also be done as azithromycin can prolong the QT interval

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97
Q

Features of cystic fibrosis?

A

neonatal period (around 20%): meconium ileus, less commonly prolonged jaundice
recurrent chest infections (40%)
malabsorption (30%): steatorrhoea, failure to thrive
other features (10%): liver disease

short stature
diabetes mellitus
delayed puberty
rectal prolapse (due to bulky stools)
nasal polyps
male infertility, female subfertility

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98
Q

General management of cystic fibrosis?

A

High calorie diet
Prevent getting pseudomonas and Burkholderia
Vitamin supplements
Pancreatic enzyme

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99
Q

What is a strong contraindication to lung transplant in CF?

A

chronic infection with Burkholderia cepacia is an important CF-specific contraindication to lung transplantation

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100
Q

Treatment for F508 CF?

A

Lumacaftor/Ivacaftor (Orkambi)

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101
Q

What type of drug is theophylline?

A

Non-specific inhibitor of phosphodiesterase resulting in an increase in cAMP

Methylxanthine

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102
Q

What type of disease is eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)

A

pANCA
small-medium vessel vasculitis.

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103
Q

Features of Churg Strauss?

A

asthma
blood eosinophilia (e.g. > 10%)
paranasal sinusitis
mononeuritis multiplex
pANCA positive in 60%

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104
Q

What type of hypersensitivity reaction is extrinsic allergicic alveoli’s?

A

Type III hypersensitivity (mostly)

type 4 also has a part to play

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105
Q

Examples of extrinsic allergic alveoli’s?

A

Bird fanciers’ lung: avian proteins from bird droppings

Farmers lung: spores of Saccharopolyspora rectivirgula from wet hay (formerly Micropolyspora faeni)

Malt workers’ lung: Aspergillus clavatus

Mushroom workers’ lung: thermophilic actinomycetes*

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106
Q

Presentation of extrinsic allergic alevolitis?

A

acute (occurs 4-8 hrs after exposure)
- dyspnoea
- dry cough
- fever

chronic (occurs weeks-months after exposure)
- lethargy
- dyspnoea
- productive cough
- anorexia and weight loss

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107
Q

Where is the fibrosis in EAA?

A

Upper lobes

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108
Q

Investigation findings of EAA?

A

imaging: upper/mid-zone fibrosis
bronchoalveolar lavage: lymphocytosis
serologic assays for specific IgG antibodies
blood: NO eosinophilia

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109
Q

Is there an eosinophilia in EAA?

A

NO NO NO

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110
Q

Management of EAA?

A
  1. Glucocorticoidds
  2. Avoid precipitating factors
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111
Q

What are the features of granulomatosis polyangitis?

A

Upper respiratory tract: epistaxis, Sinusitis, nasal crusting
Lower respiratory tract: dyspnoea, Haemoptysis
rapidly progressive glomerulonephritis (‘pauci-immune’, 80% of patients)
saddle-shape nose deformity
also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions

cANCA

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112
Q

Investigating findings of Wegenrs?

A

cANCA positive in > 90%, pANCA positive in 25%
chest x-ray: wide variety of presentations, including cavitating lesions
renal biopsy: epithelial crescents in Bowman’s capsule

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113
Q

Management of Wegners?

A

steroids
cyclophosphamide (90% response)
plasma exchange
median survival = 8-9 years

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114
Q

What is histoplasmosis?

A

Histoplasma capsulatum. It is most commonly encountered in the Mississippi and Ohio River valleys.

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115
Q

Features of histoplasmosis?

A

URTI symptoms
retrosternal pain

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116
Q

Management of histoplasmosis?

A

amphotericin or itraconazole are the pharmacological agents of choice for histoplasmosis

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117
Q

Features of idiopathic pulmonary fibrosis?

A

progressive exertional dyspnoea
bibasal fine end-inspiratory crepitations on auscultation
dry cough
clubbing

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118
Q

What type of spirometry picture do you see in pulmonary fibrosis?

A

Restrictive picture
impaired gas exchange: reduced transfer factor (TLCO)

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119
Q

What imaging finding do you see in pulmonary fibrosis?

A

bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’) may be seen on a chest x-ray but high-resolution CT scanning is the investigation of choice and required to make a diagnosis of IPF

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120
Q

Management of pulmonary fibrosis?

A

pirfenidone (an antifibrotic agent)

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121
Q

Features of Kartenagers syndrome?

A

dextrocardia or complete situs inversus
bronchiectasis
recurrent sinusitis
subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)

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122
Q

What is the gram stain of Klebsielta?

A

Gram negative
- Typically following aspiration

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123
Q

Presentation of Klebsiella pneumonia?

A

more common in alcoholic and diabetics
may occur following aspiration
‘red-currant jelly’ sputum
often affects upper lobes

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124
Q

What is Lofgren’s syndrome ?

A

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

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125
Q

What is the most likely cause of lung abscess?

A

Secondary to aspiration pneumonia

Other causes:
direct extension e.g. from an empyema
bronchial obstruction e.g. secondary from a lung tumour

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126
Q

What on mono microbial cause of lung abscess?

A

Staphylococcus aureus
Klebsiella pneumonia
Pseudomonas aeruginosa

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127
Q

Signs of lung abscess?

A

Systemic symptoms of night sweats
Subacute onset
Possible finger clubbing
Foul smelling sputum

chest x-ray
fluid-filled space within an area of consolidation
an air-fluid level is typically seen
sputum and blood cultures should be obtained

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128
Q

What type of lung cancer gives you hoarseness?

A

Pancoast tumours

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129
Q

Paraneoplastic effect of a small cell lung cancer?

A

ADH

ACTH - not typical, hypertension, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc

Lambert-Eaton syndrome

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130
Q

Paraneoplastic effect of a squamous cell lung cancer?

A

Parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia

Clubbing

Hypertrophic pulmonary osteoarthropathy (HPOA)
hyperthyroidism due to ectopic TSH

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131
Q

Paraneoplastic effect of adenocarcinoma?

A

Gynaecomastia

Hypertrophic pulmonary osteoarthropathy (HPOA)

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132
Q

What blood changes can be seen FBC?

A

Thrombocytosis

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133
Q

Investigations for lung cancer?

A
  1. CXR
  2. CT thorax
  3. Bronchoscopy - biopsy
  4. PET scan
134
Q

What lung cancer should receive aPET scan?

A

Non- small cell lung cancer

135
Q

What are the types of non-small cell lung cancer?

A

Squamous
Adenocarcinoma
Large cell

136
Q

Management of non-small cell lung cancer?

A
  1. Lobectomy - in stage I and II cancer ( first line) curative intent
  2. Radiotherapy ( stage I - III) curative intent
  3. Chemotherapy non-curative

Complete resection: Offer chemotherapy adjuvant

Incomplete resection: Offer radiotherapy +/- chemotherapy

137
Q

What chemotherapy is used for non-small lung cancer?

A

Third-generation chemotherapy agent: e.g. docetaxel, paclitaxel or gemcitabine
Platinum agent: e.g. carboplatin or cisplatin

138
Q

Management of stage I-III NSLC, not fit for surgery?

A

Offer chemoradiotherapy

139
Q

What is considered extensive small cell lung cancer?

A

T 1-4, N 0-3, M1

140
Q

What is considered limited small cell lung cancer?

A

T 1-4, N 0-3, M0

141
Q

Treatment for limited small cell lung cancer?

A

4-6 cycles of Cisplatin-based combination chemotherapy

Concurrent or adjunct thoracic radiotherapy is only considered if there has been a good response to chemotherapy

142
Q

Treatment for extensive small cell lung cancer?

A

Platinum-based combination therapy where the patient is reassessed for a response after each cycle (up to a maximum of 6 cycles)

Concurrent or adjunct thoracic radiotherapy can be considered if there has been a good response to chemotherapy at both the primary and metastatic sites.

143
Q

How to treat relapse of small cell lung cancer?

A

Further chemotherapy (maximum 6 cycles)
Palliative radiotherapy to control local symptoms

144
Q

Local metastasis of lung cancer?

A

Nerve palsy; superior vena cava obstruction and pericarditis

145
Q

Metastatic sites for lung cancer?

A

Brain, spinal cord, bone, liver and adrenal glands are common sites

146
Q

Contraindications to surgery in lung cancer?

A

assess general health
stage IIIb or IV (i.e. metastases present)
FEV1 < 1.5 litres is considered a general cut-off point*
malignant pleural effusion
tumour near hilum
vocal cord paralysis
SVC obstruction

147
Q
A
148
Q

When should you offer a CXR for lung cancer?

A

40 and over if they have 2 or more of the following unexplained symptoms, or if they have ever smoked and have 1 or more of the following unexplained symptoms:

cough
fatigue
shortness of breath
chest pain
weight loss
appetite loss

149
Q

What cells does small cell lung cancer arise from?

A

APUD cells

Amine - high amine content
Precursor Uptake - high uptake of amine precursors
Decarboxylase - high content of the enzyme decarboxylase

150
Q

Features of small cell lung cancer?

A

ADH → hyponatraemia
ACTH → Cushing’s syndrome
ACTH secretion can cause bilateral adrenal hyperplasia, the high levels of cortisol can lead to hypokalaemic alkalosis
Lambert-Eaton syndrome: antibodies to voltage gated calcium channels causing myasthenic like syndrome

151
Q

Causes of upper zone fibrosis?

A

C - Coal worker’s pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis

152
Q

Causes of lower zone fibrosis?

A

idiopathic pulmonary fibrosis
most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis

153
Q

What type of cancer is a mesothelioma?

A

Cancer of the mesothelium of the pleura

154
Q

Features of mesothelioma?

A

Dyspnoea, weight loss, chest wall pain
Clubbing
30% present as painless pleural effusion
Only 20% have pre-existing asbestosis
History of asbestos exposure in 85-90%, latent period of 30-40 years

155
Q

What does mesothelioma look up on CXR?

A

Pleural thickening
Pleural effusion

156
Q

Features of microscopic polyangitis?

A

renal impairment: raised creatinine, haematuria, proteinuria
fever
other systemic symptoms: lethargy, myalgia, weight loss
rash: palpable purpura
cough, dyspnoea, haemoptysis
mononeuritis multiplex

157
Q

What is microscopic polyangitis?

A

pANCA (against MPO) - positive in 50-75%
cANCA (against PR3) - positive in 40%

158
Q

What is a microscopic polangitis?

A

small-vessel ANCA vasculitis.

159
Q

What causes Middle Eastern respiratory syndrome?

A

betacoronavirus MERS-CoV.

160
Q

Features of obesity hypoventilation syndrome?

A

Sleep apnoea
Morning headaches
Daytime sleepiness
Reduce exercise tolerance

161
Q

Risk factors for obesity hypoventilation syndrome?

A

obesity
macroglossia: acromegaly, hypothyroidism, amyloidosis
large tonsils
Marfan’s syndrome

Consequences: daytime somnolence
compensated respiratory acidosis
hypertension

162
Q

Assessment of sleepiness?

A

Epworth Sleepiness Scale - questionnaire completed by patient +/- partner

Multiple Sleep Latency Test (MSLT) - measures the time to fall asleep in a dark room (using EEG criteria)

163
Q

Diagnostic test for sleep apnoea ?

A

sleep studies (polysomnography) - ranging from monitoring of pulse oximetry at night to full polysomnography where a wide variety of physiological factors are measured including EEG, respiratory airflow, thoraco-abdominal movement, snoring and pulse oximetry

164
Q

Management of sleep apnoea?

A

weight loss
continuous positive airway pressure (CPAP) is first line for moderate or severe OSAHS
intra-oral devices (e.g. mandibular advancement) may be used if CPAP is not tolerated or for patients with mild OSAHS where there is no daytime sleepiness
the DVLA should be informed if OSAHS is causing excessive daytime sleepiness
limited evidence to support use of pharmacological agents

165
Q

What is considered an obstructive picture?

A

FEV1/FVC < 80%

166
Q

What is considered a restrictive picture?

A

FEV1/FVC > 80%

167
Q

Examples of obstructive pictures?

A

Chronic obstructive pulmonary disease
chronic bronchitis
emphysema: including alpha-1 antitrypsin deficiency

Asthma

Bronchiectasis

168
Q

Examples of restrictive pictures?

A

Intrapulmonary:
idiopathic pulmonary fibrosis
extrinsic allergic alveolitis
coal worker’s pneumoconiosis/progressive massive fibrosis
silicosis
sarcoidosis
histiocytosis
drug-induced fibrosis: amiodarone, bleomycin, methotrexate
asbestosis

Extrapulmonary:
neuromuscular disease: polio, myasthenia gravis
obesity
scoliosis

169
Q

Causes of transudate pleural effusion?

A

heart failure (most common transudate cause)
hypoalbuminaemia
- liver disease
- nephrotic syndrome
- malabsorption
hypothyroidism
Meigs’ syndrome

170
Q

Definition of exudates?

A

> 30

171
Q

Definition of transudates?

A

<30

172
Q

Light’s criteria should be applied when?

A

Protein level is 25-35

173
Q

What are the rules of Light’s criteria?

A

pleural fluid protein divided by serum protein >0.5
pleural fluid LDH divided by serum LDH >0.6
pleural fluid LDH more than two-thirds the upper limits of normal serum LDH

174
Q

Pleural effusions with a low glucose?

A

Rheumatoid arthritis
Tuberculosis

175
Q

Pleural effusions with raised amylase?

A

Pancreatitis
Oesophageal perforation

176
Q

Pleural effusions with heavy blood staining?

A

Mesothelioma
Pulmonary embolism
Tuberculosis

177
Q

When infection in expected in pleural effusion ? How is this managed?

A

pH < 7.2
Turbid colour

In such situation - insert chest drain

178
Q

Pneumonia + Herpes libilais ?

A

Strep pneumonia

179
Q

Pneumonia + COPD

A

Haemophilus

180
Q

Pneumonia + recent influenza infection?

A

Staph aureus

181
Q

Pneumonia + dry cough + autoimmune haemolytic anaemia + Erythema multiform ?

A

Mycoplasma

182
Q

Pneumonia + hyponatraemia +lymphopaenia

A

Legionella

183
Q

Pneumonia + alcoholic?

A

Klebsiella

184
Q

CURB 65

A

Confusion
Urea > 7
Respiratory rate > 30
Blood pressure < 90 mmHg
65

home-based care for patients with a CRB65 score of 0
oral amoxicillin is generally used first-line

hospital assessment for all other patients, particularly those with a CRB65 score of 2 or more.

GP practice remove the urea

185
Q

Resolution from pneumonia?

A

1 week Fever should have resolved
4 weeks Chest pain and sputum production should have substantially reduced
6 weeks Cough and breathlessness should have substantially reduced
3 months Most symptoms should have resolved but fatigue may still be present
6 months Most people will feel back to normal.

186
Q

For pneumonia, when should a CXR be repeated?

A

6 Weeks

187
Q

Risk factors for a pneumothorax?

A

Pre-existing lung disease
Non-invasive ventilation
Connective tissue disease: Marfans, rheumatoid arthritis

188
Q

Management of primary pneumothorax?

A

if the rim of air is < 2cm and the patient is not short of breath then discharge should be considered
otherwise, aspiration should be attempted
if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted

189
Q

Management of secondary pneumothorax?

A

if the patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.

otherwise aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater than 1cm) a chest drain should be inserted. All patients should be admitted for at least 24 hours

if the pneumothorax is less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours

190
Q

When can you fly post pneumothorax?

A

Yes - checked with CXR one week post

191
Q

Pulmonary function testing: obstructive?

A

FEV1 - significantly reduced
FVC - reduced or normal
FEV1% (FEV1/FVC) - reduced

192
Q

Pulmonary function testing: restrictive?

A

FEV1 - reduced
FVC - significantly reduced
FEV1% (FEV1/FVC) - normal or increased

193
Q

Obstructive lung disease?

A

Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans

194
Q

Restrictive lung disease?

A

Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis e.g. ankylosing spondylitis
Neuromuscular disorders
Severe obesity

195
Q

What is diagnostic if pulmonary hypertension?

A

pulmonary arterial pressure of greater than 25 mmHg at rest

196
Q

Group 1 pulmonary hypertension?

A

Group 1: Pulmonary arterial hypertension (PAH)

  • 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
197
Q

Group 2 pulmonary hypertension?

A

Group 2: Pulmonary hypertension with left heart disease

  • left-sided atrial, ventricular or valvular disease such as left ventricular systolic and diastolic dysfunction, mitral stenosis and mitral regurgitation
198
Q

Group 3 pulmonary hypertension?

A

Group 3: Pulmonary hypertension secondary to lung disease/hypoxia

  • COPD
  • interstitial lung disease
  • sleep apnoea
  • high altitude
199
Q

What is group 4 pulmonary hypertension?

A

Group 4: Pulmonary hypertension due to thromboembolic disease

200
Q

Causes of respiratory acidosis?

A

COPD
Decompensation in other respiratory conditions e.g. life-threatening asthma / Pulmonary oedema
Neuromuscular disease
Obesity hypoventilation syndrome
Sedative drugs: benzodiazepines, opiate overdose

201
Q

Causes of respiratory alkalosis?

A

Anxiety leading to hyperventilation
Pulmonary embolism
Salicylate poisoning*
CNS disorders: stroke, subarachnoid Haemorrhage, encephalitis
Altitude
Pregnancy

202
Q

Acidosis and alkalosis in salicylate overdose? - why?

A

Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis

203
Q

What is tidal volume?

A

volume inspired or expired with each breath at rest
500ml in males, 350ml in females

204
Q

What is inspiratory reserve volume?

A

Inspiratory reserve volume (IRV) = 2-3 L
maximum volume of air that can be inspired at the end of a normal tidal inspiration
inspiratory capacity = TV + IRV

205
Q

What is expiratory reserve volume?

A

Expiratory reserve volume (ERV) = 750ml
maximum volume of air that can be expired at the end of a normal tidal expiration

206
Q

What is residual reserve volume?

A

Residual volume (RV) = 1.2L
volume of air remaining after maximal expiration
increases with age
RV = FRC - ERV

207
Q

What is functional residual capacity?

A

Functional residual capacity (FRC)
the volume in the lungs at the end-expiratory position
FRC = ERV + RV

208
Q

What is vital capacity?

A

Vital capacity (VC) = 5L
maximum volume of air that can be expired after a maximal inspiration
4,500ml in males, 3,500 mls in females
decreases with age
VC = inspiratory capacity + ERV

209
Q

What is total lung capacity /

A

Total lung capacity (TLC) is the sum of the vital capacity + residual volume

210
Q

What are respiratory complications of rheumatoid?

A

Pulmonary fibrosis
Pleural effusion
Pulmonary nodules
Bronchiolitis obliterans
Complications of drug therapy e.g. Methotrexate pneumonitis
Pleurisy
Caplan’s syndrome - massive fibrotic nodules with occupational coal dust exposure
infection (possibly atypical) secondary to immunosuppression

211
Q

What is Caplan’s syndrome?

A

Caplan’s syndrome - massive fibrotic nodules with occupational coal dust exposure

212
Q

Features of sarcoidosis?

A

acute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgia
insidious: dyspnoea, non-productive cough, malaise, weight loss
skin: lupus pernio
hypercalcaemia: macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)

213
Q

What is lofgren’s syndrome ?

A

Lofgren’s syndrome is an acute form of the disease characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia. It usually carries an excellent prognosis

214
Q

What is Mikulicz syndrome?

A

enlargement of the parotid and lacrimal glands due to sarcoidosis, tuberculosis or lymphoma

215
Q

What is Heerfordt’s syndrome

A

(uveoparotid fever) there is parotid enlargement, fever and uveitis secondary to sarcoidosis

216
Q

Chest xray staging for sarcoid?

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

217
Q

Spirometry testing for sarcoid?

A

restrictive

218
Q

Investigation findings in sarcoid?

A

spirometry: may show a restrictive defect
tissue biopsy: non-caseating granulomas
gallium-67 scan - not used routinely
the Kveim test (where part of the spleen from a patient with known sarcoidosis is injected under the skin) is no longer performed due to concerns about cross-infection

219
Q

What are the indications of treatments in sarcoid?

A

patients with chest x-ray stage 2 or 3 disease who are symptomatic.
hypercalcaemia
eye, heart or neuro involvement

220
Q

What are the radiograph findings of silicosis?

A

upper zone fibrosing lung disease
‘egg-shell’ calcification of the hilar lymph nodes

221
Q

Guidance for a nodule < 5 mm?

A

clear benign features, or unsuitable for treatment: can be discharged

222
Q

Guidance for nodule > 8 mm and high risk features?

A

then CT-PET, and if CT-PET shows high uptake then biopsy

223
Q

Guidance for > 8mm and low risk features?

A

then CT surveillance

224
Q

Subglottic stenosis?

A

Subglottic stenosis may be defined as a narrowing of the airway below the vocal cords (subglottis) and above the trachea. It may be congenital or acquired.

225
Q

Mechanism of theophylline?

A

Xanthine

Mechanism uncertain

non-specific inhibitor of phosphodiesterase resulting in an increase in cAM

226
Q

Features of theophylline poisoning/

A

acidosis, hypokalaemia
vomiting
tachycardia, arrhythmias
seizures

227
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

228
Q

Conditions with raising TLCO / KCO (transfer factor)

A

asthma
pulmonary haemorrhage (Wegener’s, Goodpasture’s)
left-to-right cardiac shunts
polycythaemia
hyperkinetic states
male gender, exercise

229
Q

Conditions with low TLCO / KCO
(transfer factor)

A

pulmonary fibrosis
pneumonia
pulmonary emboli
pulmonary oedema
emphysema
anaemia
low cardiac output

230
Q

Most common lung cancer in adolescents?

A

Carcinoid tumour

231
Q

What causes hypertrophic pulmonary osteoarthropathy?

A

Squamous cell carcinoma
Causes symmetrical joint tenderness - e.g. wrists

232
Q

What one bacteria is the worst prognosis for CF?

A

Bukerholdia

233
Q

Presentation of Lymphangioleiomyomatosis (LAM) ?

A

Premenopausal women

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

Presentation is with dyspnoea due to progressive interstitial lung disease, pneumothorax or chylous pleural effusion.

234
Q

Management of Lymphangioleiomyomatosis (LAM) ?

A

Medroxyprogesterone is an anti-oestrogen

235
Q

How do you determine between pseudochylothroax vs chylothorax?

A

Triglyceride

236
Q

What monoclonal antibody can be used in asthma with an elevated eosinophilia?

A

Mepolizumab may be used for asthma with high eosinophils

Used at end of all other options

237
Q

Management of loeffler syndrome?

A

Mendazole

238
Q

Management of pulmonary fibrosis?

A

Pirfenidone ( antifibrotic agent)

very few medications have been shown to give any benefit in IPF. There is some evidence that pirfenidone (an antifibrotic agent) may be useful in selected patients

239
Q

When do you put a chest drain in a secondary pneumothorax?

A

If a secondary pneumothorax > 2cm and/or the patient is short of breath then patient should be treated with chest drain (not aspiration) as first-line

240
Q

Management of a primary pneumothorax?

A
  1. If the rim of air is < 2cm and the patient is not short of breath then discharge should be considered
    otherwise, aspiration should be attempted (regardless of size)
  2. if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted
241
Q

How do you manage a patient needing LTOT, who retains CO2?

A

LTOT with notruanl BIPAP

242
Q

Pleural effusion: exudate + low glucose + SOB?

A

Think cancer
Bronchial carcinoma

243
Q

Presentation of bronchopulmonary fistula?

A

Large right sided effusion
Constant bubbling in underwater seal
Pleural effusion and a suitable site is marked. A chest drain is inserted without complication and the drain yields frank pus

244
Q

How does theophylline poisoning affect the heart?

A

increased myocardial contractility

Other: hypokalaemia, hyperglycaemia, tachycardia and increased myocardial contractility

245
Q

What increases the risk of tuberculosis ?

A

Silicosis

246
Q

What can lead to excessive lacticaemia in asthma

A

Salbutamol type B lactic acidosis (that is not caused by tissue hypoperfusion or hypoxia resulting in anaerobic metabolism).

247
Q

Side effect of nicotine replacement therapy?

A

nausea & vomiting, headaches and flu-like symptom

248
Q

How should you prescribe nicotine replacement therapy?

A

Dual method
Patches + (gum lozenges, or another form )

249
Q

What is the mechanism of varenicline?

A

Partial nicotinic receptor antagonist
started 1 week before the patients target date to stop
recommended course of treatment is 12 weeks (but patients should be monitored regularly and treatment only continued if not smoking)

250
Q

Side effect of varenicline?

A

Nausea ( most common)

headache, insomnia, abnormal dreams

251
Q

When should varenicline be used with caution?

A

When has a history of depression / self harm

252
Q

Mechanism of buproprion?

A

norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist

253
Q

Contraindications for bupropion?

A

Epilepsy
Breast feeding
Pregnancy

254
Q

What is fist line smoking cessation in pregnancy?

A
  1. CBT
  2. Nicotine replacement therapy

as mentioned above, varenicline and bupropion are contraindicated

255
Q

When should Romuflast be used in COPD?

A

When trial of LAMA + ICS + LABA + SABA used

FEV1 < 50% of predicted

256
Q

What are the indications for LTOT therapy?

A
  1. Resting PaO2 ≤7.3 kPa
  2. Resting PaO2 ≤8 kPa with evidence of peripheral oedema, polycythaemia (haematocrit ≥55%) or pulmonary hypertension.
257
Q

What mechanism is mepolizumab and what it’s indication?

A

IL 5 antagonist

Used in asthma with eosinophilia

258
Q

When can you use a tyrosine kinase inhibitor in idiopathic pulmonary fibrosis?

A

a) The person has a forced vital capacity (FVC) between 50% and 80% of predicted
b) The company provides nintedanib with the discount agreed in the patient access scheme and
c) Treatment is stopped if the disease progresses (a confirmed decline in percent predicted FVC of 10% or more) in any 12month period.

259
Q

What drug prevents acute mountain sickness?

A

Acetazdolamiode

260
Q

What are contraindications to NIV?

A

Recent facial or upper airway surgery or facial injuries.
- Recent upper gastrointestinal surgery.
- Confusion/agitation.
- Bowel obstruction.
- Upper airway obstruction.
- Excessive upper airway secretions.
- Patient actively vomiting.

261
Q

When should omalizumab be used?

A

Ongoing frequent symptoms despite treatment, including a recent exacerbation
Symptoms are worse outdoors in the summer months
History of atopy
Elevated IgE levels

262
Q

When should omalizumab be used?

A

Ongoing frequent symptoms despite treatment, including a recent exacerbation
Symptoms are worse outdoors in the summer months
History of atopy
Elevated IgE levels

263
Q

COPD + reversible asthma component?

A

LABA + ICS

264
Q

What are Kelley B lines?

A

1-2 cm diagonal lines at the very periphery
Means pulmonary oedema

265
Q

Empyema vs abscess?

A

Empyema is an accumulation of pus in the pleural space, the cavity between the lungs and the inner surface of the chest wall

266
Q

How to determine if pleural aspirate if from an empyema?

A

If the pleural fluid is turbid or milky it should becentrifuged.

If the supernatant (liquid which lies above the sediment) is clear, the turbid fluid was due to cell debris and empyema is likely

267
Q

Tests that need to be done for LTOT?

A
  1. ABG
  2. ECHO - evidence of pulmonary hypertension
268
Q

Consolidation above horizontal fissure?

A

Upper lobe

269
Q

Consolidation below horizontal fissure?

A

Below lobe

270
Q

Beta D Glucan + Missippi ( or bats) + URTI symptoms
retrosternal pain or acute respiratory failure ?

A

Histoplasmosis

271
Q

What are the causes of bulging fissure sign?

A

Klebsiella pneumonia

272
Q

What is the mechanism of thunderstorm asthma?

A

Sudden pollen and spore release due to pressure changes

273
Q

What is a common P450 inducer in COPD patients?

A

Smoking

274
Q

What is see on this CXR ?

A

Pleural thickening

275
Q

Missippi ?

A

Think histoplasmosis

276
Q

Management of histoplasmosis ?

A

Itraconazole

277
Q

cANCA +ve
pANCA +ve
Crescentic renal stuff
No nose changes ?

A

Microscopic polangitis

278
Q

What type of ABG do you see in untreated OSA or obesity hypoventilation syndrome?

A

Compensated respiratory acidosis

279
Q

Difference between Wegners and Churg Strauss?

A

Renal failure –> Wegners
Epistaxis –> wegners
cANCA –> wegners
Asthma –> Churg strauss
pANCA –> Churg strauss
Eosinophillia –> Churg struass

280
Q

What medication may precipitate churg struass?

A

LTRA

281
Q

Symtomatic primary pneumothorax < 2cm - management?

A

As SOB pleural aspiration

282
Q

Acute complication of NIV?

A

pneuomothoax

283
Q

Management of weighers?

A

Cyclophosphamide + steroids

284
Q

COPD: >2 exacerbations per year + FEV1<50%? what medication to add?

A

Roflumilast

285
Q

parenchymal bands, traction bronchiectasis and honeycomb lung?

A

Asbestosis

286
Q

Causes of simple pulmonary eosinophilia?

A

Ascaris lumbricoides, Strongyloides, or Ancylostoma

287
Q

Causes of pulmonary eosinophilia?

A

roundworms Wuchereria bancrofti or Brugia malayi, common in the Asian Subcontinent and Africa

Spread by mosquito

can cause elephantiasis

paroxysmal nocturnal cough, wheeze, and breathlessness

288
Q

Management of tropical pulmonary eosinophilia?

A

diethylcarbamazine for diagnosis and, which is also the main treatment.

289
Q

Stable COPD treatment pathway?

A
290
Q

Prodrome of chlamydia psittaci?

A

diarrhoea
epistaxis
high fevers
Splenomegaly
Low white blood cell count are common

291
Q

What is the other name for extrinsic allergic alveolitis?

A

Hypersensitivity pneumonitis

292
Q

Pseudomonas eradication in CF patient?

A

IV ceftazidime + nebulised tobramycin

293
Q

What is the poor prognostic factor for asbestosis?

A

FINGER CLUBBING

294
Q

mononeuritis multiplex causes?

A

vasculitis
diabetes
AIDS
amyloidosis
rheumatoid arthritis.

295
Q

Treatment for small cell lung cancer ?

A
296
Q

What type of kidney damage is seen on charge Strauss?

A

pauci immune crescentic glomerulonephritis

297
Q

Most useful marker to determine if haemothorax?

A

If the haematocrit of the pleural fluid is more than half of the patient’s peripheral blood haematocrit, the patient has a haemothorax

298
Q

causes of exudate effusions?

A

infection
pneumonia (most common exudate cause),
tuberculosis
subphrenic abscess
connective tissue disease
rheumatoid arthritis
systemic lupus erythmatosus
neoplasia
lung cancer
mesothelioma
metastases
pancreatitis
pulmonary embolism
Dressler’s syndrome
yellow nail syndrome

299
Q

Difference between aspergilloma and invasive aspergillosis ?

A

aspergilloma fungus ball

Invasive aspergillosis - syndrome, invasion of fungi and invasive of vessel with blood in sputum

300
Q

What does this show?

A

g sub-pleural reticular opacities that increase from the apex to the bases of the lungs.

Pulmonary fibrosis

301
Q

Mechanism of Omalizumab?

A

Anti- IgE

302
Q

Pneumothorax diving advice?

A

Do not drive unless get pleurodesis

303
Q

Pneumothorax flying advice?

A

may travel 2 weeks after successful drainage if there is no residual air. The British Thoracic Society used to recommend not travelling by air for a period of 6 weeks but this has now been changed to 1 week post check x-ray

304
Q

Secondary pneumothorax <1 cm management?

A

Admit for 24 hours, oxygen and review

305
Q

What is this?

A

Mesothelioma

306
Q

Best diagnostic test for bronchiectasis ?

A

HRCT

307
Q

When should CXR repeat be done?

A

6 weeks

308
Q

What is suggestive of NSAID sensitive asthma?

A

Presence of nasal polyps

309
Q

Empyema + chest drain is bubbling. This bubbling is more significant when the patient is asked to cough.

A

Bronchopleural fistula

310
Q

Drugs that cause pleural effusions?

A

Nitrofurantoin
Amiodarone
Methotrexat

311
Q

What causes usual interstial pneumonia

A

UIP is scan finding not diagnosis

Idiopathic pulmonary fibrosis
Asbestosis
EAA

312
Q

Differentiating between EAA and idiopathic pulmonary fibrosis?

A

occurrence of episodic dyspnoea, cough, and flu-like symptoms in response to an environmental antigen is consistent with the acute presentation of hypersensitivity pneumonitis. Patients are well in between episodes and during the early phase of the disease examination and investigation can be normal.

313
Q

History of worsening asthma post intubation?

A

Think posterior supraglotic stenosis

314
Q

What does the PO2 have to be for consider LTOT?

A

<8

315
Q

How does wegners present on CT scan?

A

few well-defined regions of airspace opacification (as demonstrated by the grey-coloured, round lung markings) which can represent consolidation or pulmonary haemorrhag

316
Q

Complication of transjugular intrahepatic portosystemic shunt (TIPS)?

A

Pulmonary hypertension

317
Q

Test to determine prognosis of idiopathic pulmonary fibrosis?

A

Carbon moxoside transfer test

318
Q

Previous TB

A

Think aspergilloma

319
Q

Findings that suggest empyema on aspiration?

A

Turbid / pus
Micro-organisms seen
pH < 7.2

320
Q

Causes of lower zone fibrosis?

A

Causes of lower zone fibrosis: MAID
Most connective tissue diseases (e.g. rheumatoid arthritis)
Asbestosis
Idiopathic pulmonary fibrosis, infection
Drugs (e.g. methotrexate, amiodarone, bleomycin)

321
Q

What type of empysema is seen in alpha 1 antitrypsin disease?

A

Panacinar emphysema
Hasan assocaited low transfer factor

322
Q

Best management for anxiety on NIV?

A

Haloperidol

323
Q

Management of diabetes in CF?

A

High calorie diet and insulin

324
Q

Treatment of ARDS?

A

Low tidal volume ventilation

325
Q

After a reassuring aspirate from pleural effusion, what next test should be done to determine aetiology

A

CT thorax

326
Q

How does obestiy affect transfer factor ?>

A

It does not

327
Q

Pleural thickening best investigation?

A

VATS

328
Q

Management of someone who develops type 2 respiratory failure while on LTOT trial?

A

may have clinically unstable disease. These patients should undergo further medical optimisation and be reassessed after 4 weeks

329
Q

How to give nebulises on NIV?

A

Take off mask, then put back on

330
Q

Use of oxygen in pneumothorax management?

A

Exchange of nitrogen for oxygen allowing quicker resorption.

MRCP Respiratory (2 decks)

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