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MRCP part 1 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Describe cystic fibrosis in lay terms

A

An inherited condition that causes sticky mucus to build up in the lungs and digestive system. Causes lung infections and problems with digesting food

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2
Q

Inheritance of cystic fibrosis

A

autosomal recessive

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3
Q

Gene implicated cystic fibrosis

A

CFTR

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4
Q

Describe key pathogenesis of cystic fibrosis

A

High sodium sweat: primary secretion of sweat duct is normal but CFTR does not absorb chloride ions, which remain in the lumen and prevent sodium absorption (therefore sweat testing used in diagnosis)

Pancreatic insufficiency: relative dehydration of pancreatic secretions, causing their stagnation in the pancreatic ducts.

Biliary disease: defective ion transfer across the bile duct causes reduced movement of water in the lumen so that bile becomes concentrated, causing plugging and local damage.

Gastrointestinal disease: low-volume secretions of increased viscosity, changes in fluid movement across both the small and large intestine and dehydrated biliary and pancreatic secretions cause intraluminal water deficiency.

Respiratory disease: dehydration of the airway surfaces reduces mucociliary clearance

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5
Q

What does CFTR gene do

A

Codes a cAMP-regulated chloride channel

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6
Q

Which chromosome most commonly affected in cystic fibrosis

A

Delta F508 on long arm of chromosome 7

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7
Q

Carrier rate cystic fibrosis

A

1 in 25

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8
Q

Why should those with CF minimise contact with each other (what bug(s))

A

Brukholderia cepacia complex and psudeomonas aeruginosa

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9
Q

Whats first line in those with pseudomonas aeruginosa who have failed eradication with antibiotics?

A

Nebulised colistimethate sodium

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10
Q

Contraindication to lung transplant in cystic fibrosis

A

Chronic infection with brukholderia cepacia

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11
Q

Drug used for those homozygous for delta F508 mutation (CF) - explain mechanism

A

Lumacaftor/Ivacaftor (Orkambi)

Lumacaftor increases the number of CFTR proteins that are transported to the cell surface

Ivacaftor is a potentiator of CFTR that is already at the cell surface, increasing the probability that the defective channel will be open and allow chloride ions to pass through the channel pore

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12
Q

Management COPD acute exacerbation

A

Pred 30mg
Ipratropium bromide 500mcg 5mg NEB
Salbutamol 5mg NEB

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13
Q

Ipratropium MOA

A

Blocks muscarinic acetylcholine receptors - relaxes bronchial smooth muscle. Tiotropium long acting

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14
Q

Theophylline MOA

A

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

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15
Q

Montelukast MOA

A

Block leukotriene receptors
(apparently useful in aspirin induced asthma) –> antiinflammatory and bronchodilatory properties

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16
Q

Features of eosinophilic granulomatosis (small - medium vessel vasculitis)

A

Asthma
Blood eosinophilia (e.g. > 10%)
pANCA positive in 60%
Mononeuritis multiplex

Sinusitis
Vasculitis
Dyspnoea

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17
Q

Precipitant of eosinophilic granulomatosis

A

LTRA

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18
Q

Features of granulomatosis with polyangitis

A

Renal failure
Epistaxis/haemoptysis
cANCA
Saddle shaped nose deformity

Sinusitis (+nasal crusting)
Vasculitis
Dyspnoea

also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions,
rapidly progressive glomerulonephritis (‘pauci-immune’, 80% of patients)

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19
Q

Is granulomatosis with polyangitis largely cANCA +ve or pANCA +ve?

A

cANCA

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20
Q

Renal biopsy granulomatosis with polyangitis

A

Epithelial crescents in bowman’s capsule

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21
Q

Management granulomatosis polyangitis

A

Steroids
Cyclophosphamide
Plasma exchange
Median survival 8-9 years

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22
Q

What is idiopathic pulmonary fibrosis?

A

Lung fibrosis when no underlying cause can be identified

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23
Q

Transfer factor IPF

A

Reduced

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24
Q

Gold standard investigation IPF

A

CT - honeycombing

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25
Q

Management IPF

A

Pulmonary rehab, some evidence for pirfenidone (antifibrotic)

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26
Q

What is kartageners?

A

Primary ciliary dyskinesia, autosomal recessive problem with impaired mucocilliary clearance

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27
Q

Pathogenesis kartageners

A

Dynein arm defect results in immotile cilia

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28
Q

Features kartageners

A

Dextrocardia or complete situs inversus (quiet hear sounds, small volume complexes in lateral leads)
Bronchiectasis
Recurrent sinusitis
Subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)

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29
Q

Features of kelbsiella pneumonia

A

More common in alcoholic and diabetics
May occur following aspiration
‘Red-currant jelly’ sputum
Often affects upper lobes (abscesses, empyema)

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30
Q

Motelukast is associated with development of what syndrome?

A

Eosinophilic granulomatosis with polyangiitis

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31
Q

What is lofgren’s syndrome?

A

Acute form sarcoidosis

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32
Q

Characteristics of logren’s syndrome

A

Bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia

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33
Q

RF for lung abscess

A

Poor dental hygiene, prev stroke, reduced consciousness

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34
Q

Rarer causes lung abscess

A

Haematogenous spread eg 2ndary to IE, direct extension from empyema, bronchial obstruction eg lung tumour

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35
Q

Monomicrobial causes of lung abscess

A

Staphylococcus aureus
Klebsiella pneumonia
Pseudomonas aeruginosa

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36
Q

What is carcinoid lung ca?

A

NE tumours, arising from the amine precursor uptake and decarboxylation (APUD) system, like small cell tumour. Account for 1% of carcinoid tumours

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37
Q

Features lung carcinoid

A

Slow growing - long history. Often central and not seen on CXR. “Cherry red ball” often seen on bronchoscopy

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38
Q

What is carcinoid syndrome

A

Seen in those who have a carcinoid tumour when it spreads to the liver releasing serotonin - skin flushing, facial lesions, diarrhoea, dyspnoea, tachycardia

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39
Q

Contraindications to lung ca surgery

A

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

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40
Q

Small cell lung ca paraneoplastic features

A

ADH -> hypoN
ACTH - (cushings) not typical, hypertension, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc
Lambert-Eaton syndrome (antibodies to voltage gated calcium channels causing myasthenic like syndrome)

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41
Q

Squamous cell lung ca paraneoplastic features

A

Parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia
Clubbing
Hypertrophic pulmonary osteoarthropathy (HPOA)
Hyperthyroidism due to ectopic TSH

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42
Q

Adenocarcinoma lung ca paraneoplastic feautres

A

Gynaecomastia
Hypertrophic pulmonary osteoarthropathy (HPOA)

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43
Q

Is coal dust a RF for lung ca?

A

No

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44
Q

What cell type does small cell lung ca arrise from?

A

APUD cells
(Amine - high amine content
Precursor Uptake - high uptake of amine precursors
Decarboxylase - high content of the enzyme decarboxylase)

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45
Q

Fibrosis affecting upper zones

A

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

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46
Q

Fibrosis affecting lower zones

A

IPF
Most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
Drug-induced: amiodarone, bleomycin, methotrexate
Asbestosis

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47
Q

Microscopic polyangitis features (small vessel ANCA vasculitis)

A

renal impairment: raised creatinine, haematuria, proteinuria

fever

other systemic symptoms: lethargy, myalgia, weight loss

rash: palpable purpura

cough, dyspnoea, haemoptysis

mononeuritis multiplex

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48
Q

pANCA/cANCA microscopic polyangitis

A

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

cANCA (against PR3) - positive in 40%

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49
Q

What causes Middle East respiratory syndrome?

A

Betacoronavirus MERS-CoV

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50
Q

Risk factor for MERS-CoV

A

Contact with camels (including camel products such as milk)

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51
Q

Indications for non-invasive ventilation

A

COPD with respiratory acidosis pH 7.25-7.35
(pH<7.25 it can be used with increased monitoring, but lower threshold for intubation and ventilation)
Type 2 resp failure
Sleep apnoea
Cardiogenic pulmonary oedema unresponsive to CPAP
Weaning from tracheal intubation

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52
Q

Recommended initials settings for bi-level pressure support in COPD

A

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
back up rate: 15 breaths/min
back up inspiration:expiration ratio: 1:3

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53
Q

Predisposing factors sleep apnoea

A

Obesity
Macroglossia: acromegaly, hypothyroidism, amyloidosis
Large tonsils
Marfan’s syndrome

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54
Q

Consequences of sleep apnoea

A

Daytime somnolence
Compensated respiratory acidosis
hypertension

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55
Q

Management sleep apnoea

A

Weight loss
CPAP
Intra oral devices eg mandibular advancement
DVLA should be informed if excessive

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56
Q

What is olamizumab used for?

A

Severe persistent confirmed allergic IgE-mediated asthma as an add on to optimised standard therapy in people aged 6 years and older:
who need continuous or frequent treatment with oral corticosteroids (defined as 4 or more courses in the previous year)a, given as an injection every 2 to 4 weeks

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57
Q

What type of drug is olamizumab?

A

Monoclonal antibody

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58
Q

Adverse effects olamizumab

A

Abdominal pain
Headache
Fever
Churg-Strauss syndrome: may present with eosinophilia, vasculitic rash, worsening respiratory symptoms and peripheral neuropathy

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59
Q

What is the oxygen dissociation curve?

A

Describes the relationship between the percentage of saturated haemoglobin and partial pressure of oxygen in the blood. It is not affected by haemoglobin concentration.

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60
Q

If oxygen dissociation curve shifts left what does this mean? What causes this?

A

For given oxygen tension there is increased saturation of Hb with oxygen i.e. decreased oxygen delivery to tissues.

Shifts to L → Lower oxygen delivery, caused by
Low [H+] (alkali)
Low pCO2
Low 2,3-DPG
Low temperature

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61
Q

If oxygen dissociation curve shifts right what does this mean? What causes this?

A

For given oxygen tension there is reduced saturation of Hb with oxygen i.e. enhanced oxygen delivery to tissues

‘CADET, face Right!’ for CO2, Acid, 2,3-DPG, Exercise and Temperature

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62
Q

Oxygen management in COPD patients

A

Prior to 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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63
Q

Transudate pleural effusion causes

A

Heart failure (most common transudate cause)
Hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption)
Hypothyroidism
Meigs’ syndrome

Transudate = failures of organs + meigs

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64
Q

Exudate pleural effusion

A

Infection: pneumonia (most common exudate cause), TB, subphrenic abscess
Connective tissue disease: RA, SLE
Neoplasia: lung cancer, mesothelioma, metastases
Pancreatitis
Pulmonary embolism
Dressler’s syndrome
Yellow nail syndrome

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65
Q

Pleural aspiration from pleural effusion - what is sent for?

A

pH, protein, lactate dehydrogenase (LDH), cytology and microbiology

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66
Q

What criteria differentiates transudate and exudate causes?

A

Exudates have a protein level of >30 g/L, transudates have a protein level of <30 g/L
If the protein level is between 25-35 g/L, Light’s criteria should be applied.

An exudate is likely if at least one of the following criteria are met:
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

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67
Q

Pleural fluid with low glucose might indicate

A

rheumatoid arthritis, tuberculosis

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68
Q

Pleural fluid with raised amylase might indicate

A

pancreatitis, oesophageal perforation

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69
Q

Pleural fluid with heavy blood staining might indicate

A

mesothelioma, pulmonary embolism, tuberculosis

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70
Q

When should a chest drain be placed pleural effusion?

A

If the fluid is purulent or turbid/cloudy a chest tube should be placed to allow drainage

If the fluid is clear but the pH is less than 7.2 in patients with suspected pleural infection a chest tube should be placed

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71
Q

Management options of recent pleural effusion

A

Recurrent aspiration
Pleurodesis
Indwelling pleural catheter
drug management to alleviate symptoms e.g. opioids to relieve dyspnoea

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72
Q

Describe CRB65 (primary care)

A

C: Confusion (abbreviated mental test score <= 8/10)
R: Respiration rate >= 30/min
B: Blood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg
65: Aged >= 65 years

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73
Q

What score of CRB 65 merits hospital admission

A

Considered if >2, Urgent if 3 or above

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74
Q

Management of severe CAP

A

Amox+macrolide dual therapy

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75
Q

What findings may block a person’s discharge with pneumonia

A

Temperature higher than 37.5°C
Respiratory rate 24 breaths per minute or more
Heart rate over 100 beats per minute
Systolic blood pressure 90 mmHg or less
Oxygen saturation under 90% on room air
Abnormal mental status
Inability to eat without assistance

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76
Q

Over what time periods should patients expect to feel better post pneumonia?

A

1 week - fever should have resolved
4 weeks - chest pain and sputum production reduced
6 weeks - cough and breathlessness should have reduced
3 months - most symptoms should have resolved, may be fatigued
6 months - most back to normal

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77
Q

Following pneumonia when should a repeat CXR be done?

A

6 weeks after clinical resolution

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78
Q

RF for pneumothorax

A

Pre-existing lung disease (secondary)
Connective tissue disease
Ventilation including non invasive

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79
Q

What is a catamenial pneumothorax?

A

Cause of 3-6% of spontaneous pneumothorax, occurring in menstruating women

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80
Q

Management of primary penumothorax

A

If rim of air <2cm and patient not short of breath then consider discharge, otherwise aspiratino
If fails or >2cm chest drain insertion

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81
Q

Management of a secondary pneumothorax

A

Admit all
If >50 years old and rim of air is >2cm or SOB then chest drain
If rim of air 1-2cm then aspiration attempted
If <1cm O2

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82
Q

Management of iatrogenic pneumothorax

A

Most will resolve with observation, can aspirate if not
Ventilated and some with COPD may need chest drains

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83
Q

Lifestyle advice following pneumothorax

A

Avoid smoking to avoid risk of recurrence,
Fly 2 weeks after successful drainage/ 1 week post CXR
Can’t scuba dive

84
Q

Fever with history of bird contact you think of which type of pneumonia

A

Chlamydia psittaci

85
Q

Presentation with pneumonia and severe headache or organomegaly and failure to respond to penicillin-based antibiotics - which bug

A

Chlamydia psittaci

86
Q

Management of chlamydia psittaci pneumonia

A

1st-line: tetracyclines e.g. doxycycline
2nd-line: macrolides e.g. erythromycin

87
Q

Causes of pulmonary eosinophilia (conditions)

A

Churg-Strauss syndrome
Allergic bronchopulmonary aspergillosis (ABPA)
Loffler’s syndrome
Eosinophilic pneumonia
Hypereosinophilic syndrome
Tropical pulmonary eosinophilia
Less common: Wegener’s granulomatosis

88
Q

Causes of pulmonary eosinophilia (drugs)

A

Nitrofurantoin, sulphonamides 

89
Q

What is Loffler’s syndrome

A

A disease in which eosinophils accumulate in the lung in response to a parasitic infection (Ascaris lumbricoides). Generally self limiting

90
Q

Management eosinophilic pneumonia

A

Highly responsive to steroids

91
Q

What is tropical pulmonary eosinophilia caused by (typically)

A

Wuchereria bancrofti infection

92
Q

Obstructive lung disease on PFT

A

FEV1 - significantly reduced (<70)

FVC - reduced or normal 

FEV1% (FEV1/FVC) - reduced

93
Q

Examples obstructive lung disease

A

Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans

94
Q

Restrictive lung disease on PFT

A

FEV1 - reduced

FVC - significantly reduced

FEV1% (FEV1/FVC) - normal or increased

95
Q

Examples 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

96
Q

What is pulmonary hypertension (PAH)

A

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

97
Q

Group 1 pulmonary arterial hypertension (PAH

A
  • idiopathic
  • familial
  • associated conditions: collagen vascular disease, congenital heart disease with systemic to pulmonary shunts, HIV, drugs and toxins, sickle cell disease
  • persistent pulmonary hypertension of the newborn
98
Q

Group 2 pulmonary hypertension

A

With left heart disease
- left-sided atrial, ventricular or valvular disease such as left ventricular systolic and diastolic dysfunction, mitral stenosis and mitral regurgitation

99
Q

Group 3 pulmonary hypertension

A

Secondary to lung disease/hypoxia
- COPD
- interstitial lung disease
- sleep apnoea
- high altitude

100
Q

Group 4 pulmonary hypertension

A

Thromboembolic disease

101
Q

Group 5 pulmonary hypertension

A

Miscellaneous conditions
- lymphangiomatosis e.g. secondary to carcinomatosis or sarcoidosis

102
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

103
Q

Causes of respiratory alkalosis

A

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

*salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. 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

104
Q

What is tidal volume?

A

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

105
Q

What is inspiratory reserve volume?

A

Maximum volume of air that can be inspired at the end of a normal tidal inspiration
inspiratory capacity = TV + IRV

106
Q

What is expiatory reserve volume?

A

Maximum volume of air that can be expired at the end of a normal tidal expiration

107
Q

What is residual volume?

A

Volume of air remaining after maximal expiration
Increases with age
RV = FRC - ERV

108
Q

What is functional residual capacity?

A

The volume in the lungs at the end-expiratory position
FRC = ERV + RV

109
Q

What is vital capacity?

A

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

110
Q

What is total lung capacity?

A

The sum of the vital capacity + residual volume

111
Q

What is caplan’s syndrome?

A

Combination of rheumatoid arthritis (RA) and pneumoconiosis - massive fibrotic nodules with occupational coal dust exposure

112
Q

What respiratory conditions are associated with rheumatoid?

A

Pulmonary fibrosis
Pleural effusion
Pulmonary nodules
Bronchiolitis obliterans
Complications of drug therapy e.g. methotrexate pneumonitis
Pleurisy
Caplan’s syndrome
Infection (possibly atypical) secondary to immunosuppression

113
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 (malar rash)

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

114
Q

What is Lofgren’s syndrome

A

Acute form of sarcoidosis characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia. It usually carries an excellent prognosis

115
Q

What is Mikulicz syndrome

A

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

116
Q

What is Heerfordt’s syndrome

A

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

117
Q

Diagnostic tests sarcoidosis

A

ACE levels (monitoring rather than diagnosis)
CXR:
1 - BHL
2 - BHL + interstitial infiltrates
3 - Diffuse interstitial infiltrates
4 - Diffuse fibrosis

118
Q

Indication for steroids in sarcoidosis

A

CXR stage 2 or 3 with symptoms
Hypercalcaemia
Eye, heart or near involvement

PUNCH
parenchymal lung involvement
Uveitis
Neuro involvement
Cardio involvement
Hypercalcaemia

119
Q

Prognosis of sarcoidosis

A

Remits in around 2/3 without treamtent

120
Q

Signs of poor prognosis sarcoidosis

A

Insidious onset, symptoms > 6 months
Absence of erythema nodosum
Extrapulmonary manifestations: e.g. lupus pernio, splenomegaly
CXR: stage III-IV features
black people

121
Q

What is silicosis?

A

Fibrosing lung disease caused by the inhalation of fine particles of crystalline silicon dioxide (silica)

122
Q

Features of sarcoidosis on cxr

A

Egg-shell calcification of the hilarity lymph nodes

123
Q

How long should smoking cessation be prescribed for?

A

2 weeks after the target stop date. If unsuccessful not to offer a repeat prescription within 6 months unless special circumstances

124
Q

Adverse effects nicotine replacement therapy?

A

Nausea & vomiting, headaches and flu-like symptoms

125
Q

What is varenicline?

A

A nicotinic receptor partial agonist, shown to more effective that bupropion

126
Q

How long is a typical course varenicline?

A

12 weeks

127
Q

SE varenicline?

A

Nausea, headache, insomnia, abnormal dreams. Use with caution in those with history of depression and self harm. CI in pregnancy and breast feeding

128
Q

What is bupropion?

A

A norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist

129
Q

SE bupropion

A

Small risk of seizures

130
Q

Contraindications to bupropion

A

Contraindicated in epilepsy, pregnancy and breast feeding. Having an eating disorder is a relative contraindication

131
Q

Management of smoking cessation pregnant women

A

Apparently all tested with CO detectors!
CBT, motivational interviewing, self help
Can use NRT

132
Q

What is transfer factor?

A

The rate at which a gas will diffuse from alveoli into blood

133
Q

Whats the difference between TLCO and KCO?

A

Results may be given as the total gas transfer (TLCO) or that corrected for lung volume (transfer coefficient, KCO)

134
Q

Causes of raised TLCO?

A

Asthma - due to hyperinflation
Pulmonary haemorrhage (Wegener’s, Goodpasture’s)
Left-to-right cardiac shunts
Polycythaemia
Hyperkinetic states
male gender, exercise

135
Q

Cause of lower TLCO

A

Pulmonary fibrosis
Pneumonia
Pulmonary emboli
Pulmonary oedema
Emphysema
Anaemia
Low cardiac output

136
Q

Conditions that may lead to increased KCO with normal/reduced TLCO

A

Pneumonectomy/lobectomy
Scoliosis/kyphosis
Neuromuscular weakness
ankylosis of costovertebral joints e.g. ankylosing spondylitis

137
Q

What is allergic bronchopulmonary aspergillosis?

A

Allergic bronchopulmonary aspergillosis results from an allergy to Aspergillus spores.
In the exam questions often give a history of bronchiectasis and eosinophilia.

138
Q

Investigations allergic bronchopulmonary aspergillosis?

A

Flitting CXR changes, positive radioallergosorbent (RAST) test to Aspergillus, positive IgG precipitins (not as positive as in aspergilloma. - aspergilloma being a fungus ball), raised IgE

139
Q

Management bronchopulmonary aspergillosis

A

Oral glucocorticoids
Itraconazole is sometimes introduced as a second-line agent (a triazole)

140
Q

Criteria for life threatening asthma

A

PEFR < 33%
Oxygen sats < 92%
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma
Normal pCO2 (exhaustion)

141
Q

Indications CXR acute asthma

A

Life-threatening asthma
Suspected pneumothorax
failure to respond to treatment

142
Q

Indication ABG acute asthma

A

Sats <92%

143
Q

Management acute asthama

A

Oxygen, nebuliser salbutamol, pred 40mg, if no response to this ipratropium bromide

144
Q

Criteria for discharge acute 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

145
Q

Most common bacterial organisms COPD exacerbation

A

Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis

146
Q

What’s ARDS

A

Caused by the increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli, i.e. non-cardiogenic pulmonary oedema.

147
Q

Causes of ARDS

A

Infection: sepsis, pneumonia
Massive blood transfusion
Trauma
Smoke inhalation
Acute pancreatitis
Cardio-pulmonary bypass

148
Q

Criteria for ARDS diagnosis

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 (200 mmHg)

149
Q

What’s pulmonary artery wedge pressure?

A

pulmonary artery wedge pressure gives an indirect estimate of left arterial pressure. Measured by putting a catheter in a peripheral vein and advancing to RA->RV->PA->branch of PA

150
Q

What is alpha 1 antitrypsin deficiency?

A

Caused by a lack of a protease inhibitor (Pi) normally produced by the liver.
The role of A1AT is to protect cells from enzymes such as neutrophil elastase.
Classically causes emphysema (i.e. chronic obstructive pulmonary disease) in patients who are young and non-smokers.

151
Q

A1AT what chromosome?

A

14

152
Q

Inheritance of A1AT

A

Autosomal recessive / co-dominant fashion*

153
Q

Describe genotypes for A1AT?

A

Alleles classified by their electrophoretic mobility - M for normal, S for slow, and Z for very slow

normal: PiMM

heterozygous: PiMZ
homozygous PiSS: 50% normal A1AT levels
homozygous PiZZ: 10% normal A1AT levels

154
Q

Which genotype of A1AT typically manifests disease?

A

PiZZ genotype, paracinar emphysema

155
Q

What are the three types of altitude related disorder?

A

Acute mountain sickness (AMS), which may progress to…
High altitude pulmonary oedema (HAPE) or
High altitude cerebral oedema (HACE)

156
Q

Features of acute mountain sickness?

A

Features of AMS start to occur above 2,500 - 3,000m, developing gradually over 6-12 hours and potentially last a number of days:

headache
nausea
fatigue

157
Q

Prevention of acute mountain sickness

A

Ascend no more than 500m per day, acetazolamide (a carbonic anhydrase inhibitor) (it causes a primary metabolic acidosis and compensatory respiratory alkalosis which increases respiratory rate and improves oxygenation)

158
Q

Presentation and management of High altitude pulmonary oedema (HAPE)

A

Pulmonary oedema features

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

159
Q

Presentation and management of high altitude cerebral oedema (HACE)

A

headache, ataxia, papilloedema

descent and dexamethasone

160
Q

Most dangerous form asbestos

A

Crocidolite (blue)

161
Q

Types of asbestos disease

A

Pleural plaques (benign), pleural thickening, asbestosis (lower lobe fibrosis), mesothelioma

162
Q

New asthma diagnosis test

A

Emphasis on fractional exhaled nitric oxide (FeNO).
Nitric oxide is produced by 3 types of nitric oxide synthases (NOS).
One of the types is inducible (iNOS) and levels tend to rise in inflammatory cells, particularly eosinophils.
Levels of NO therefore typically correlate with levels of inflammation.

163
Q

What is considered a positive FeNO test?

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

164
Q

Considered positive for asthma in reversibility testing

A

In adults, a positive test is indicated by an improvement In FEV1 of 12% or more and increase in volume of 200 ml or more

165
Q

Management asthma - steps

A
  1. SABA
  2. SABA + ICS
  3. SABA + ICS + LTRA
  4. SABA + low-dose ICS + long-acting beta agonist (LABA), Continue LTRA depending on patient’s response to LTRA
  5. SABA +/- LTRA, Switch ICS/LABA for a maintenance and reliever therapy (MART), that includes a low-dose ICS
  6. SABA +/- LTRA + medium-dose ICS MART, OR consider changing back to a fixed-dose of a moderate-dose ICS and a separate LABA
  7. SABA +/- LTRA + one of the following options:
    Increase ICS to high-dose (only as part of a fixed-dose regime, not as a MART)
    A trial of an additional drug (for example, a long-acting muscarinic receptor antagonist or theophylline)
    seeking advice from a healthcare professional with expertise in asthma
166
Q

What is MART

A

A form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required
MART is only available for ICS and LABA combinations in which the LABA has a fast-acting component (for example, formoterol)

167
Q

What are the doses of low, medium and high corticosteroid doses asthma

A

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

168
Q

Most common cause occupational asthma

A

Isocyanates eg spray painting and foam moulding using adhesives
GF at PEPSI factory
Platinum salt
Epoxy resins
Proteiolytic enzymes
Solodering flux resins
Isocynayes

169
Q

Whats atelectasis?

A

Common postoperative complication in which basal alveolar collapse can lead to respiratory difficulty. It is caused when airways become obstructed by bronchial secretions. Within 72hrs

170
Q

Causes of bilateral hilarity lymphadenopathy

A

The most common causes are sarcoidosis and tuberculosis.

Other causes include:
* lymphoma/other malignancy
* pneumoconiosis e.g. berylliosis (a form of metal posioning - berillyium)
fungi e.g. histoplasmosis (bad/bird droppings), coccidioidomycosis (“valley fever” - southwest america and mexico)

171
Q

What is bronchiectasis?

A

Permanent dilatation of the airways secondary to chronic infection or inflammation.

172
Q

Triad of Youngs syndrome

A

Male infertility, sinusitis, bronchiectasis

173
Q

Triad of yellow nail syndrome

A

Yellow nail discolouration, lymphoedema, bronchiectasis

174
Q

What’s bronchiolitis

A

Acute bronchiolar inflammation, most common cause of a serious lower respiratory tract infection in < 1yr olds (90% are 1-9 months, with a peak incidence of 3-6 months). Maternal IgG provides protection to newborns against RSV.

175
Q

Contraindications chest drain insertion

A

INR > 1.3
Platelet count < 75
Pulmonary bullae - focal regions of emphysema
Pleural adhesions

176
Q

What intercostal space is a chest drain inserted

A

5th

177
Q

Complication chest drain insertion

A

Failure of insertion - the drain may be leaning on the apical pleura
Bleeding
Infection
Penetration of the lung
Re-expansion pulmonary oedema

178
Q

Whats re-expansion pulmonary oedema?

A

When a lung re-expands quickly. May be preceded by the onset of a cough and/or shortness of breath. Chest drain should be clamped and an urgent chest x-ray should be obtained. To avoid re-expansion pulmonary oedema, it is recommended that the drain tubing should be clamped regularly in the event of rapid fluid output i.e. drain output should not exceed 1L of fluid over a short period of time (less than 6 hours)

179
Q

When should chest drain be removed?

A

Fluid drainage - no output for > 24 hours and imaging shows resolution of the fluid collection.

Pneumothorax - when drain no longer bubbling spontaneously or when the patient coughs and ideally when imaging shows resolution of the pneumothorax.

Drains inserted in cases of penetrating chest injury should be reviewed by the specialist to confirm an appropriate time for removal.

180
Q

CXR signs COPD

A

hyperinflation, bullae, flat hemidiaphragm (lungs push against the diaphragm puhsing it downwards)

181
Q

Severity of COPD stages

A

Stage 1 - FEV1 >80%
Stage 2 - FEV1 50-79%
Stage 3 - 30-49%
Stage - <30%

182
Q

Criteria for LTOT?

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

Assess if stage 3

183
Q

How frequent are gases for LTOT assessment?

A

Measuring arterial blood gases on 2 occasions at least 3 weeks apart in patients with stable COPD on optimal management

184
Q

Management COPD if no asthmatic features or features suggesting steroid responsiveness

A

SABA or SAMA
No asthmatic features/features suggesting steroid responsiveness:
-add a LABA + LAMA
-if already taking a SAMA, discontinue and switch to a SABA

185
Q

What drugs should not be given alongside theophylline

A

Macrolide or fluroquinones

186
Q

Who qualifies for prophylactic antibiotic therapy in COPD

A

Azithromycin for those who don’t smoke, optimised treatment, exacerbations (need CT and sputum culture). Not can prolong QT

187
Q

Features fo cor pulmonale

A

Peripheral oedema, raised JVP, systolic parasternal heave, loud P2

188
Q

Management cor pulmonale

A

Use a loop diuretic for oedema, consider long-term oxygen therapy

189
Q

Whats cryptogenic organising pneumonia?

A

Diffuse interstitial lung disease that affects the distal bronchioles, respiratory bronchioles, alveolar ducts and alveolar walls. Aetiology unknown

190
Q

Presentation of cryptogenic organising pneumonia

A

Cough, shortness of breath, fever and malaise. With no response to abx

Bloods show a leukocytosis and an elevated ESR and CRP.
Imaging typically shows bilateral patchy or diffuse consolidative or ground glass opacities. Transfer factor reduced

191
Q

Which lung ca most likely in a smoker

A

Squamous - caviating and associated with hypercalcaemia

192
Q

Which lung ca most likely in a non smoker

A

Adeonocarcioma

193
Q

Typical presentation alveolar cell lung ca

A

Productive cough with copious sputum and fluffy infiltrates on chest x-ray

194
Q

Presentation small cell carcinomas

A

Fast growing, may well be mets

195
Q

Presentation small cell carcinomas

A

Fast growing, may well be mets

196
Q

Most common organisms bronchiectasis

A

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

197
Q

Most suitable way of assessing compression of upper airway

A

Flow volume loop

198
Q

How much does smoking increase risk of lung ca by

A

Factor of 10

199
Q

How much does asbestos increase risk of lung ca by

A

Factor of 5

200
Q

COPD management when asthmatic features/steroid responsiveness

A

Asthmatic features/features suggesting steroid responsiveness:
LABA + ICS
- if patients remain breathless or have exacerbations offer triple therapy i.e. LAMA + LABA + ICS (if already taking a SAMA, discontinue and switch to a SABA)

201
Q

How is asthma/steroid responsiveness features assessed in COPD?

A

Prev diagnosis of asthma or atopy
Higher blood eosinophil count
Substantial variation in FEV1 over time (at least 400ml)
Substantial diurnal variation in peak exploratory flow

202
Q

Gene association bronchiectasis

A

HLA-DR1

203
Q

Gene association SLE

A

HLA DR2

204
Q

Gene association autoimmune hepatitis, sjogre, T1DM, SLE

A

HLA DR3

205
Q

Gene association rheumatoid arthritis, T1DM

A

HLA DR4

206
Q

Gene association ankylosing spondylitis, post gonococcal arthritis, acute anterior uveitis

A

HLA B27

207
Q

A good prognostic factor in sarcoidosis

A

Erythema nodosum

MRCP part 1 (3 decks)

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