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MRCP Part 1 > Resp > Flashcards

Resp Flashcards

1
Q

typically central

associated with PTHrP secretion → hypercalcaemia

strongly associated with finger clubbing

cavitating lesions are more common than other types

hypertrophic pulmonary osteoarthropathy (HPOA)

Which is the type of lung cancer ?

A

Non small cell
Squamous cell cancer

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2
Q

typically peripheral

most common type of lung cancer in non-smokers

What type of lung cancer?

A

Non small cell
Adenocarcinoma

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3
Q
  1. typically peripheral
  2. anaplastic, poorly differentiated tumours with a poor prognosis
  3. may secrete β-hCG

What type of lung cancer?

A

Non small cell
Large cell lung carcinoma

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4
Q
  1. central
  2. arise from APUD* cells
  3. associated with ectopic ADH, ACTH secretion
  4. ADH → hyponatraemia
  5. ACTH → Cushing’s syndrome
  6. ACTH secretion can cause bilateral adrenal hyperplasia, the high levels of cortisol can lead to hypokalaemic alkalosis
  7. Lambert-Eaton syndrome: antibodies to voltage gated calcium channels causing myasthenic like syndrome

What type of lung cancer?

A

Small cell lung cancer

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5
Q

Management of small cell

A

very early stage disease (T1-2a, N0, M0) are now considered for surgery.

however, most patients with limited disease receive a combination of chemotherapy and radiotherapy

palliative chemotherapy for more extensive disease

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6
Q

Management of Non small cell

A

only 20% suitable for surgery

mediastinoscopy performed prior to surgery as CT does not always show mediastinal lymph node involvement

curative or palliative radiotherapy

poor response to chemotherapy

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7
Q

Non small cell lung cancer sugery contraindications (7)

A
  1. assess general health
  2. stage IIIb or IV (i.e. metastases present)
  3. FEV1 < 1.5 L
  4. malignant pleural effusion
  5. tumour near hilum
  6. vocal cord paralysis
  7. SVC obstruction
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8
Q

In non small cell lung cancer
1. Lobectomy if FEV1…….

  1. Pneumonectomy if FEV1 ……
A
  1. < 1.5 L
  2. < 2.5 L
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9
Q

Lung cancer: 8 risk factors

A
  1. Smoking - increases risk of lung ca by a factor of 10
  2. asbestos - increases risk of lung ca by a factor of 5
  3. arsenic
  4. aromatic hydrocarbon
  5. chromate
  6. cryptogenic fibrosing alveolitis
  7. radon
  8. nickel
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10
Q

Management of Lung cancer: carcinoid

A

surgical resection

if no metastases then 90% survival at 5 years

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11
Q
  1. typical age = 40-50 years
  2. smoking not risk factor
  3. slow growing: e.g. long history of cough, recurrent haemoptysis
  4. often centrally located and not seen on CXR
  5. ‘cherry red ball’ often seen on bronchoscopy
  6. rare associated with liver metastases

Features of ………….

A

Lung carcinoid features

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12
Q

Lung cancer: paraneoplastic features of small cell (3)

A
  1. ADH
  2. ACTH - not typical, hypertension, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc
  3. Lambert Eaton syndrome
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13
Q

Lung cancer: paraneoplastic features of squamous cell (4)

A
  1. PTHrP secretion causing hypercalcemia
  2. Hyperthyroidism due to ectopic TSH
  3. Clubbing
  4. Hypertrophic pulmonary osteoarthropathy
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14
Q

Lung cancer: paraneoplastic features of Adenocarcinoma (2)

A
  1. gynaecomastia
  2. hypertrophic pulmonary osteoarthropathy (HPOA)
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15
Q

Lung metastases are seen with a wide variety of cancers including:

A

breast cancer

colorectal cancer

renal cell cancer

bladder cancer

prostate cancer

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16
Q

Calcification in lung metastases is uncommon except in the case of

A
  1. chondrosarcoma
  2. osteosarcoma
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17
Q

” cannonball metastases” are most commonly seen with…..

A
  1. renal cell cancer

may also occur secondary to

  1. choriocarcinoma
  2. prostate cancer.
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18
Q

Chest x-ray: cavitating lung lesion (9)

A
  1. abscess (Staph aureus, Klebsiella andPseudomonas)
  2. squamous cell lung cancer
  3. TB
  4. Wegener’s granulomatosis
  5. PE
  6. rheumatoid arthritis
  7. aspergillosis,
  8. histoplasmosis,
  9. coccidioidomycosis
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19
Q

Causes of Respiratory acidosis (5)

A
  1. COPD
  2. Decompensation in other respiratory conditions: BA , pulmonary oedema
  3. OHS
  4. Neuromuscular disease
  5. sedative drugs:benzodiazepines,opiate overdose
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20
Q

Causes of Respiratory alkalosis (6)

A
  1. Hyperventilation
  2. PE
  3. Pregnancy
  4. CNS disorders: stroke, subarachnoid hemorrhage, encephalitis
  5. Altitude
  6. Salicylate poisoning: Early stimulation of the respiratory centre leads to a respiratory alkalosiswhilst later the direct acid effects of salicylates (combined with AKI) may lead to an acidosis
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21
Q

Recommended initial settings for BIPAP in COPD

  1. IPAP:
  2. EPAP:
  3. Back up rate :
  4. I:E ratio :
A
  1. IPAP: RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O
  2. EPAP: 4-5 cm H2O
  3. back up rate: 15 breaths/min
  4. I:E ratio: 1:3
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22
Q

Non-invasive ventilation - key indications (4)

A
  1. COPD with respiratory acidosis pH 7.25-7.35
  2. T2 RF secondary to chest wall deformity, neuromuscular disease or OSA
  3. cardiogenic pulmonary oedema unresponsive to CPAP
  4. weaning from tracheal intubation
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23
Q

Acute mountain sickness is

A

a self-limiting condition.

start to occur above 2,500 - 3,000m,
developing gradually over 6-12 hours

headache

nausea

fatigue

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24
Q

Prevention and treatment of Acute mountain sickness

A
  1. gain altitude at no more than 500 m per day
  2. acetazolamide (a carbonic anhydrase inhibitor)is widely used to prevent AMS
    - it causes a primary metabolic acidosis and compensatory respiratory alkalosis which increases respiratory rate and improves oxygenation
  3. treatment: descent
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25
Q

Management of high altitude cerebral oedema HACE

A

descent

dexamethasone

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26
Q

Management of high altitude pulmonary oedema HAPE

A
  1. descent
  2. nifedipine, dexamethasone, acetazolamide, phosphodiesterase type V inhibitors*
  3. oxygen if available
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27
Q

Causes of decreased lung compliance (4)

A

3PK
1. Pulmonary oedema

  1. Pulmonary fibrosis
  2. Pneumonectomy
  3. Kyphosis
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28
Q

Causes of increased lung compliance (2)

A
  1. Age
  2. Emphysema - this is due to loss alveolar walls and associated elastic tissue
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29
Q

Oxygen dissociation curve

Shifts to Right = Raised oxygen delivery

(5)

A
  1. Raised [H+] (acidic)
  2. Raised pCO2
  3. Raised 2,3-DPG*
  4. Raised temperature
  5. Exercise
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30
Q

Oxygen dissociation curve

Shifts to Left = Lower oxygen delivery

(5)

A
  1. Low [H+] (alkali)
  2. Low pCO2
  3. Low 2,3-DPG
  4. Low temperature
  5. HbF,methaemoglobin,carboxyhaemoglobin
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31
Q

the most suitable way of assessing compression of the upper airway

A

Flow volume loops

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32
Q

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

A

Obstructive lung disease

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33
Q

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

A

Restrictive lung disease

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34
Q

7 Causes of a raised TLCO

A
  1. asthma
  2. pulmonary haemorrhage(e.g. granulomatosis with polyangiitis, Goodpasture’s)
  3. left-to-right cardiac shunts
  4. polycythaemia
  5. hyperkinetic states
  6. male gender,
  7. exercise

“A Happy Life Promotes Healthy Men’s Exercise”

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35
Q

7 Causes of a lower TLCO

A

4P ACE

  1. pulmonary fibrosis
  2. pneumonia
  3. pulmonary emboli
  4. pulmonary oedema
  5. anaemia
  6. low cardiac output
  7. emphysema
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36
Q

4 Causes of increased KCO with normal or reduced TLCO

A
  1. pneumonectomy/lobectomy
  2. scoliosis/kyphosis
  3. neuromuscular weakness
  4. ankylosis of costovertebral joints e.g. ankylosing spondylitis
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37
Q

Hypoxia leads to

A

vasoconstriction of the pulmonary arteries. This allows blood to be diverted to better aerated areas of the lung and improves the efficiency of gaseous exchange

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38
Q

Control of respiration

A
  1. central regulatory centres
  2. central and peripheral chemoreceptors
  3. pulmonary receptors
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39
Q

Central regulatory centres

A
  1. medullary respiratory centre
  2. apneustic centre (lower pons)
  3. pneumotaxic centre (upper pons)
  • MAP = central regulatory centers
  • (p)neuroma is = u(pp)er
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40
Q

Central and peripheral chemoreceptors

A
  1. central: raised [H+] in ECF stimulates respiration
  2. peripheral: carotid + aortic bodies, respond to raised pCO2 & [H+], lesser extent low pO2

*low PH
*high pCo2
*low O2

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41
Q

Pulmonary receptors

A
  1. stretch receptors, lung distension causes slowing of respiratory rate (Hering-Bruer reflex)
  2. irritant receptor, leading to bronchoconstriction
  3. juxtacapillary receptors, stimulated by stretching of the microvasculature
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42
Q

Haldane effect

A

increase pO2 means CO2 binds less well to Hb

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43
Q

Bohr effect

A

increasing acidity (or pCO2) means O2 binds less well to Hb

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44
Q

Chloride shift

A
  • CO2 diffuses into RBCs
  • CO2 + H20 —- carbonic anhydrase -→
  • HCO3- + H+
  • H+ combines with Hb
  • HCO3- diffuses out of cell,- Cl- replaces it
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45
Q

Mechanism of action

Methylxanthines (e.g. theophylline)

A

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

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46
Q

FeNO: is considered positive

A
  • in adults level of >= 40
  • in children a level of >= 35
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47
Q

Reversibility testing considers a positive test if

A

in adults
- improvement in FEV1 of > 12% and increase in volume of > 200 ml

in children
- improvement in FEV1 of > 12%

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48
Q

chemicals is associated with occupational asthma:

A
  1. isocyanates
  2. glutaraldehyde
  3. platinum salts
  4. proteolytic enzymes
  5. soldering flux resin
  6. epoxy resins
  7. flour

*I G 2p SEF

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49
Q

Adverse effects of Omalizumab

A

abdominal pain

headache

fever

Churg-Strauss syndrome

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50
Q

Drugs associated with the development of Churg-Strauss syndrome

A
  1. Leukotriene receptor antagonists
  2. Omalizumab
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51
Q

Life-threatening of acute asthma

A
  1. PEFR < 33 %
  2. SPO2 < 92 %
  3. Bradycardia, dysrthmia
  4. Hypotension
  5. Silent chest, cyanosis or feeble respiratory effort
  6. Exhaustion, confusion or coma
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52
Q

Severe acute asthma

A
  1. PEFR 33-50%
  2. RR > 25
  3. HR > 110
  4. Can’t complete sentences
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53
Q

Moderate acute asthma

A
  1. PEFR 50 - 75 %
  2. RR < 25
  3. HR < 110
  4. normal speech
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54
Q

In acute asthma, chest x-ray is not routinely recommended, unless

A
  1. life-threatening asthma
  2. suspected pneumothorax
  3. failure to respond to treatment
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55
Q

Criteria for discharge, patient with acute asthma

A
  1. beenstable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
  2. inhaler technique checked and recorded
  3. PEF >75%
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56
Q

COPD: causes

A
  • Smoking!
  • Alpha-1 antitrypsin deficiency
  • Other causes
  1. cadmium (used in smelting)
  2. coal
  3. cotton
  4. cement
  5. grain

COPD = 4C G

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57
Q

The severity of COPD is categorised using theFEV1

A

4 stages

  • mild FEV1 > 80 %
  • moderat FEV1 50 - 79 %
  • severe FEV1 30 - 49 %
  • very severe FEV1 < 30 %
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58
Q

LTOT INDICATED IN

A
  1. very severe airflow obstruction (FEV1 < 30%
  2. cyanosis
  3. polycythaemia
  4. peripheral oedema
  5. raised jugular venous pressure
  6. SPO2 < 92 %
  7. PO2 < 7.3 kpa
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59
Q

criteria NICE suggest to determine whether a patient has asthmatic/steroid responsive features:

A
  1. any previous, secure diagnosis of asthma or of atopy
  2. a higher blood eosinophil count - note that NICE recommend a CBC for all patients as part of the work-up
  3. substantial variation in FEV1 over time (at least 400 ml)
  4. substantial diurnal variation in peak expiratory flow (at least 20%)
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60
Q

Phosphodiesterase-4 (PDE-4) inhibitors
oral as roflumilast reduce the risk of COPD exacerbations

Recommend if

A
  1. FEV1 < 50
  2. Had > 1 exacerbation in the previous 12 months despite triple therapy LAMA, LA A and ICS.
61
Q

Bronchiectasis: causes

A
  1. post-infective: TB, measles, pertussis, pneumonia
  2. cystic fibrosis
  3. bronchial obstruction e.g. lung cancer/foreign body
  4. immune deficiency: selective IgA, hypogammaglobulinaemia
  5. allergic bronchopulmonary aspergillosis (ABPA)
  6. ciliary dyskinetic syndromes: Kartagener’s syndrome, Young’s syndrome
  7. yellow nail syndrome
62
Q

Most common organisms isolated from patients with bronchiectasis:

A

Haemophilus influenzae(most common)

Pseudomonasaeruginosa

Klebsiella spp.

Streptococcuspneumoniae

63
Q

dynein arm defect results in immotile cilia

A

Kartagener’s syndrome

64
Q

Predisposing factors of Obstructive sleep apnoea/hypopnoea syndrome

A
  1. obesity
  2. macroglossia: acromegaly,hypothyroidism, amyloidosis
  3. large tonsils
  4. Marfan’s syndrome
65
Q

Cystic fibrosis, due to a defect in ….

A

cystic fibrosis transmembrane conductance regulator gene (CFTR), which codes a cAMP-regulated chloride channel

66
Q

In the UK 80% of Cystic fibrosis cases are due to delta ….. on the long arm of chromosome ………

A

due to (delta F508) on the long arm of chromosome (7)

67
Q

Organisms which may colonise CF patients

A

Staphylococcus aureus

Pseudomonas aeruginosa

Burkholderia cepacia*

Aspergillus

68
Q

features of cystic fibrosis

A
  1. short stature
  2. DM
  3. delayed puberty
  4. rectal prolapse(due to bulky stools)
  5. nasal polyps
  6. male infertility, female subfertility
  7. recurrent chest infections
  8. malabsorption

9.liver disease

69
Q

Cystic fibrosis: management

A
  1. regular (at least twice daily) chest physiotherapy and postural drainage
  2. high calorie diet, including high fat intake
  3. vitamin supplementation
  4. pancreatic enzyme supplements taken with meals
  5. lung transplantion

chronic infection withBurkholderia cepaciais an important CF-specific contraindication to lung transplantation

  1. Lumacaftor/Ivacaftor (Orkambi)

is used to treat cystic fibrosis patients who arehomozygous for the delta F508 mutation

70
Q

Criteria of ARDS (American-European Consensus Conference)

A
  1. acute onset (within 1 week of a known risk factor)
  2. pulmonary oedema: bilateral infiltrates on chest x-ray (‘not fully explained by effusions, lobar/lung collapse or nodules)
  3. non-cardiogenic (pulmonary artery wedge pressure needed if doubt)
  4. pO2/FiO2 < 40kPa (300 mmHg)
71
Q

Allergic bronchopulmonary aspergillosis results from an allergy to

A

Aspergillus spores

72
Q

Allergic bronchopulmonary aspergillosis

Investigations

A

eosinophilia

flitting CXR changes

positive radioallergosorbent (RAST) test to Aspergillus

positive IgG precipitins (not as positive as in aspergilloma)

raised IgE

73
Q

Management of Allergic bronchopulmonary aspergillosis

A
  1. oral glucocorticoids
  2. itraconazole is sometimes introduced as a second-line agent
74
Q

Alpha-1 antitrypsin deficiency is caused by a lack of …1…. normally produced by …..2…..

A
  1. a protease inhibitor (Pi)
  2. the liver
75
Q

Alpha-1 antitrypsin deficiency

Genetics
located on chromosome

A

chromosome 14

76
Q

Features of Alpha-1 antitrypsin deficiency

A

lungs: panacinar emphysema, most marked inlower lobes

liver: cirrhosis andhepatocellular carcinomain adults, cholestasis in children

77
Q

Managment of Alpha-1 antitrypsin deficiency

A

no smoking

supportive: bronchodilators, physiotherapy

Iv alpha1-antitrypsin protein concentrates

surgery:lung volume reduction surgery, lung transplantation

78
Q

PiMM =

PiMS =

PiMZ =

PiSS =

PiSZ =

PiZZ =

A

PiMM =100 % normal A1AT levels

PiMS = 80% normal A1AT levels

PiMZ = 60% normal A1AT levels

PiSS = 50 % normal A1AT levels

PiSZ = 40% normal A1AT levels

PiZZ = 10 % normal A1AT levels

79
Q

What is the most common pathogen in Bronchiolitis

A

Respiratory syncytial virus (RSV)

80
Q

Maternal IgG provides protection to newborns against …..

A

RSV

81
Q

Varenicline is

A

nicotinic receptor partial agonist

82
Q

the recommended course of Varenicline is ….

A

12 weeks (but patients should be monitored regularly and treatment only continued if not smoking)

83
Q

Varenicline is contraindicated in

A
  1. pregnancy
  2. breast feeding
84
Q

Bupropion is

A

norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist

85
Q

Bupropion should be started ………. before the patients target date to stop

A

1 to 2 weeks

86
Q

Bupropion is contraindicated in

A
  1. epilepsy,
  2. pregnancy
  3. breast feeding.
  4. Having an eating disorder is a relative contraindication
87
Q

all pregnant women should be tested for smoking using…….

A

carbon monoxide detectors

All women who smoke, or have stopped smoking within the last 2 weeks, or those with a CO reading of 》7 ppm should be referred to NHS Stop Smoking Services.

88
Q

the first-line interventions of smoking cessation in pregnancy should be …

A

1.cognitive behaviour therapy,

  1. motivational interviewing
  2. structured self-help
  3. support from NHS Stop Smoking Services
89
Q

Transudate pleural effusion if protein level …

What are the causes?

A
  • if protein < 30g/L
  1. heart failure (most common transudate cause)
  2. hypoalbuminaemia
    - liver disease
    - nephrotic syndrome
    - malabsorption
  3. hypothyroidism
  4. Meigs’ syndrome
90
Q

Exudatepleural effusion if protein level …

What are the causes?

A
  • protein > 30g/L
  1. infection
    - pneumonia (most common exudate cause),
    - tuberculosis
    - subphrenic abscess
  2. connective tissue disease
    - rheumatoid arthritis
    - SLE
  3. neoplasia
    - lung cancer
    - mesothelioma
    - metastases
  4. pancreatitis
  5. PE
  6. Dressler’s syndrome
  7. yellow nail syndrome
91
Q

Light’s criteria should be used if the protein level is between …..

A

25-35 g/L,

92
Q

In Light’s criteria
exudate is likely if at least one of the following criteria are met:

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

93
Q

Other characteristic pleural fluid findings:

low glucose:

raised amylase:

heavy blood staining:

A

low glucose: rheumatoid arthritis, TB

raised amylase: pancreatitis,oesophageal perforation

heavy blood staining: mesothelioma, PE , TB

94
Q

Chest tube indicated in pleural effusion if

A
  1. the fluid is purulent or turbid/cloudy
  2. fluid is clear but thepH is < 7.2
95
Q

Management of recurrent pleural effusion

A
  1. recurrent aspiration
  2. pleurodesis
  3. indwelling pleural catheter
  4. drug management to alleviate symptoms e.g. opioids to relieve dyspnoea
96
Q

Management of low-severity community acquired pneumonia

A
  1. amoxicillin is first-line
  2. if penicillin allergic then use a macrolide or tetracycline
  • For 5 day course of antibiotics
97
Q

Management of moderate and high-severity community acquired pneumonia

A
  1. dual antibiotic therapy is recommended with amoxicillin and a macrolide

a 7-10 day course is recommended

NICE recommend considering a beta-lactamase stable penicillin such as co-amoxiclav, ceftriaxone or piperacillin with tazobactam and a macrolide in high-severity CAP

98
Q

Features of Klebsiella pneumonia (6)

A
  1. more common inalcoholic and diabetics
  2. may occur following aspiration
  3. ‘red-currant jelly’ sputum
  4. often affects upper lobes
  5. commonly causes lung abscess formation andempyema
  6. mortality is 30-50%
99
Q

Management of Lung abscess

A
  1. intravenous antibiotics
  2. percutaneous drainage if not resolving
  3. surgical resection in very rare cases surgical resection
100
Q

monomicrobial causes of lung abscess include:

A
  1. Staphylococcus aureus
  2. Klebsiella pneumonia
  3. Pseudomonas aeruginosa
101
Q

What is the cause of 3-6% of spontaneous pneumothoraces occurring in menstruating women ?
It is thought to be caused by ………..?

A
  • Catamenial pneumothorax
  • endometriosis within the thorax
102
Q

Management of 1ry pneumothorax

A
  • chest drain if > 2 cm or SOB
  • discharge if < 2 cm & asymptomatic
103
Q

Management of 2ry pneumothorax

A
  • O2 & admission for 24 hrs if < 1 cm
  • Aspiration if 1-2 cm
  • chest drain if
    1. Age >50
    2. SoB
    3. >2 cm
    4. Failed Aspiration with 1- 2 cm
104
Q

Management of Iatrogenic pneumothorax

A

majority will resolve with observation, if treatment is required then aspiration should be used

ventilated patients need chest drains, as may some patients with COPD

105
Q

Management of Persistentent / recurrent pneumothorax

A

video-assisted thoracoscopic surgery (VATS)should be considered to allow for mechanical/chemical pleurodesis +/- bullectomy.

106
Q

Post pneumothorax

  1. Fitness to fly
  2. Scuba diving
A
  1. 2 weeks after successful drainage if there is no residual air
  2. Diving should be permanently avoided unless the patient has undergone bilateral surgical pleurectomy and has normal lung function and chest CT scan postoperatively.’
107
Q

Psittacosis is infection caused by

A

Chlamydia psittaci

108
Q

Psittacosis should be suspected in a combination of …

A
  1. typical fever with ahistory of bird contact.

or

  1. presentation with pneumonia and severe headache or organomegaly and failure to respond to penicillin-based antibiotics.
109
Q

Treatment of Psittacosis

A

1st-line: tetracyclines e.g. doxycycline

2nd-line: macrolides e.g. erythromycin

110
Q

causes of bilateral hilar lymphadenopathy

A
  1. sarcoidosis
  2. tuberculosis.
  3. lymphoma/other malignancy
  4. pneumoconiosis e.g. berylliosis
  5. fungi e.g. histoplasmosis, coccidioidomycosis
111
Q

chest drain is contraindicated in patients with any of the following:

A
  1. INR > 1.3
  2. Platelet count < 75
  3. Pulmonary bullae
  4. Pleural adhesions
112
Q

Causes of pulmonary eosinophilia

A
  1. Churg-Strauss syndrome
  2. allergic bronchopulmonary aspergillosis (ABPA)
  3. eosinophilic pneumonia
  4. hypereosinophilic syndrome
  5. tropical pulmonary eosinophilia
  6. Loffler’s syndrome
  7. drugs:nitrofurantoin, sulphonamides
  8. less common: Wegener’s granulomatosis
113
Q

Loffler’s syndrome due to parasites such as

A

Ascaris lumbricoides

114
Q

Tropical pulmonary eosinophilia associated with

A

Wuchereria bancroftiinfection

115
Q

Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)

Features (5)

A
  1. asthma
  2. bloodeosinophilia(e.g. > 10%)
  3. paranasalsinusitis
  4. mononeuritis multiplex
  5. pANCApositive in 60%
116
Q

Churg-Strauss syndrome may precipitated by …

A

Leukotriene receptor antagonists

117
Q

Granulomatosis with polyangiitis (Wegener’s granulomatosis)
Features

A
  1. upper respiratory tract: epistaxis,sinusitis, nasal crusting
  2. lower respiratory tract: dyspnoea,haemoptysis
  3. rapidly progressive glomerulonephritis(‘pauci-immune’, 80% of patients)
  4. saddle-shape nose deformity
  5. also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions
118
Q

Granulomatosis with polyangiitis (Wegener’s granulomatosis)

Investigations

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

119
Q

Granulomatosis with polyangiitis (Wegener’s granulomatosis)
Treatment

A

steroids

cyclophosphamide (90% response)

plasma exchange

median survival = 8-9 years

120
Q

Microscopic polyangiitis
Features

A

renal impairment: raised creatinine, haematuria, proteinuria

fever

other systemic symptoms: lethargy, myalgia, weight loss

rash: palpable purpura

cough, dyspnoea, haemoptysis

mononeuritis multiplex

121
Q

Microscopic polyangiitis

A

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

cANCA (against PR3) - positive in 40%

122
Q

mushroom workers’ lung

A

thermophilic actinomycetes

123
Q

malt workers’ lung

A

Aspergillus clavatus

124
Q

farmers lung

A

spores of Saccharopolyspora rectivirgulafrom wet hay (formerlyMicropolyspora faeni)

125
Q

imaging:upper/mid-zone fibrosis

bronchoalveolar lavage: lymphocytosis

serologic assays for specific IgG antibodies

blood: NO eosinophilia

Diagnosis?

A

Extrinsic allergic alveolitis ( hypersensitivity pneumonitis)

126
Q

Management of Extrinsic allergic alveolitis ( hypersensitivity pneumonitis)

A

avoid precipitating factors

oral glucocorticoids

127
Q

Features of acute sarcoidosis

A

acute:
1. erythema nodosum,

  1. bilateral hilar lymphadenopathy,
  2. swinging fever,
  3. polyarthralgia
128
Q

Mechanism of hypercalcemia in sarcoidosis

A

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

129
Q

Mikulicz syndrome

A

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

130
Q

Heerfordt’s syndrome (3)

A
  1. parotid enlargement,
  2. fever
  3. uveitis

secondary to sarcoidosis

131
Q

Lofgren’s syndrome

A

acute form sarcoidosis characterised by

  1. bilateral hilar lymphadenopathy (BHL),
  2. erythema nodosum,
  3. fever and
  4. polyarthralgia.

It typically occurs in young females and carries an excellent prognosis.

132
Q

Stages of 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

133
Q

Indications for steroids in sarcoidosis

A
  1. patients with chest x-ray stage 2 or 3 disease who are symptomatic. Patients with asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatment
  2. hypercalcaemia
  3. eye, heart or neuro involvement
134
Q

Factors associated with poor prognosis in sarcoidosis

A
  1. insidious onset, symptoms > 6 months
  2. absence of erythema nodosum
  3. extrapulmonary manifestations: e.g. lupus pernio, splenomegaly
  4. CXR: stage III-IV features
  5. black African or African–Caribbean ethnicity
135
Q

respiratory problems may be seen in patients with rheumatoid arthritis:(8)

A
  1. pulmonary fibrosis
  2. pleural effusion
  3. pulmonary nodules
  4. pleurisy
  5. bronchiolitis obliterans
  6. complications of drug therapy e.g. methotrexate pneumonitis
  7. Caplan’s syndrome - massive fibrotic nodules with occupational coal dust exposure
  8. infection (possibly atypical) secondary to immunosuppression
136
Q

most common form of asbestos-related lung disease

A

Pleural plaques arebenign and do not undergo malignant change. They, therefore don’t require any follow-up

137
Q

Treatment of Asbestosis

A

treated conservatively- no interventions offer a significant benefit.

138
Q

Which asbestos is the most dangerous form ?

A

Crocidolite (blue) asbestos

139
Q

Treatment of Mesothelioma

A

palliative chemotherapy and

there is also a limited role for surgery and radiotherapy.

Unfortunately, the prognosis is very poor, with a median survival from diagnosis of 8-14 months.

140
Q

Occupations at risk of silicosis

A
  1. mining
  2. slate works
  3. foundries
  4. potteries
141
Q

Features of silicosis

A
  1. upper zone fibrosing lung disease
  2. ‘egg-shell’ calcification of the hilar lymph nodes
  3. It is a risk factor for developingtuberculosis
142
Q

causes of upper zone fibrosis

A

CHARTS

C -Coal worker’s pneumoconiosis

H -Histiocytosis/hypersensitivity pneumonitis

A -Ankylosing spondylitis

R - Radiation

T -Tuberculosis

S -Silicosis/sarcoidosis

143
Q

Fibrosis predominately affecting the lower zones

A

idiopathic pulmonary fibrosis

most connective tissue disorders (except ankylosing spondylitis) e.g.SLE

drug-induced:amiodarone,bleomycin,methotrexate

asbestosis

144
Q

Treatment of IPF

A
  1. pulmonary rehabilitation

2.pirfenidone (an antifibrotic agent) may be useful in selected patients

  1. many patients will require supplementary oxygen and eventually a lung transplant
145
Q

Prognosis of IPF

A

poor, average life expectancy is around 3-4 years

146
Q

Cryptogenic organizing pneumonia

A
  • not associated with smoking
  • history of non-response to antibiotics
147
Q

Treatment of Cryptogenic organizing pneumonia

A

Treatment is watch and wait if mild or high dose oral steroids if severe.

148
Q

Lung carcinoid is associated with……metastasis

A

Liver metastasis

MRCP Part 1 (15 decks)

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