respiratory 2

Question 1

NIV - key indications?

Answer 1

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
type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
cardiogenic pulmonary oedema unresponsive to CPAP
weaning from tracheal intubation

Question 2

Recommended intial setting for bi-level support in COPD?

Answer 2

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

Question 3

Asthma management algorithm?

Answer 3

Step 1 NICE
a low-dose inhaled corticosteroid (ICS)/formoterol combination inhaler to be taken as needed for symptom relief
this is termed anti-inflammatory reliever (AIR) therapy
if the patient presents highly symptomatic (for example, regular nocturnal waking) or with a severe exacerbation:
start treatment with low-dose MART (maintenance and reliever therapy, see below)
treat the acute symptoms as appropriate (e.g. a course of oral corticosteroids may be indicated)

Step 2 NICE
a low-dose MART
MART describes using an inhaled corticosteroid (ICS)/formoterol combination inhaler for daily maintenance therapy and the relief of symptoms as needed, i.e. regularly and as required

Step 3
a moderate-dose MART

Step 4
check the fractional exhaled nitric oxide (FeNO) level if available, and the blood eosinophil count NICE
if either of these is raised, refer to a specialist in asthma care
if neither FeNO nor eosinophil count is raised, consider a trial of either a leukotriene receptor antagonist (LTRA) or a long-acting muscarinic receptor antagonist (LAMA) used in addition to moderate-dose MART
if control has not improved, stop the LTRA or LAMA and start a trial of the alternative medicine (LTRA or LAMA)

Step 5
refer people to a specialist in asthma care when asthma is not controlled despite treatment with moderate-dose MART, and trials of an LTRA and a LAMA

Question 4

What type of bacteria is Klebsiella?

Answer 4

Klebsiella pneumoniae is a Gram-negative rod that is part of the normal gut flora. It can cause a number of infections in humans including pneumonia (typically following aspiration) and urinary tract infections.

Question 5

Features of Klebsiella?

Answer 5

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

Question 6

Prognosis in klebsiella pneumonia?

Answer 6

commonly causes lung abscess formation and empyema
mortality is 30-50%

Question 7

Most common organisms isolated from patients with bronchiectasis:

Answer 7

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

Question 8

What is Bronchiectasis?

Answer 8

Bronchiectasis describes a permanent dilatation of the airways secondary to chronic infection or inflammation.

Question 9

How is bronchiectasis managed?

Answer 9

physical training (e.g. inspiratory muscle training) - has a good evidence base for patients with non-cystic fibrosis bronchiectasis
postural drainage
antibiotics for exacerbations + long-term rotating antibiotics in severe cases
bronchodilators in selected cases
immunisations
surgery in selected cases (e.g. Localised disease)

Question 10

what causes CF?

Answer 10

In the UK 80% of CF cases are due to delta F508 on the long arm of chromosome 7. Cystic fibrosis affects 1 per 2500 births, and the carrier rate is c. 1 in 25

an autosomal recessive disorder causing increased viscosity of secretions (e.g. lungs and pancreas). It is due to a defect in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which codes a cAMP-regulated chloride channel

Question 11

What organisms may colonise CF patients?

Answer 11

Staphylococcus aureus
Pseudomonas aeruginosa
Burkholderia cepacia*
Aspergillus

Question 12

what would be seen on spirometry on restrictive lung disease?

Answer 12

reduced FVC and normal or increased FEV1/FVC ratio

Question 13

what is Bronchioitis obliterans?

Answer 13

Bronchiolitis obliterans (also known as obliterative bronchiolitis) is a rare complication of rheumatoid arthritis and is characterised by small airway inflammation and fibrosis, leading to airflow obstruction. This condition manifests as progressive dyspnoea and an obstructive spirometry pattern (reduced FEV1/FVC ratio)

progressive dyspnoea
obstructive pattern on spirometry
centrilobular nodules, bronchial wall thickening is seen on CT

Question 14

What respiratory problems may be seen in patients with Rheumatoid arthritis?

Answer 14

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 immunosupression

Question 15

What are the thre main types of altitude related disorders?

Answer 15

There are three main types of altitude-related disorders: acute mountain sickness (AMS), which may progress to high altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE).

Question 16

symptoms of acute montain sickness?

Answer 16

Acute mountain sickness is generally a self-limiting condition. 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

Question 17

Prevention of acute moutnain sickness ?

Answer 17

the risk of AMS may actually be positively correlated to physical fitness
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
treatment: descent

Question 18

What is High altitude pulmonary oedema ?

Answer 18

Happens above 4000m
HAPE
mechanism: hypobaric hypoxia → uneven hypoxic pulmonary vasoconstriction → uneven blood flow in the lungs → areas of the lung receiving more blood experience an increase in capillary pressure → more fluid leakage. Hypoxia may also directly increase capillary permeability, exacerbating fluid leakage into the alveolar space.
presents with classical pulmonary oedema features

Question 19

what is the mechanism of altitude cerebral oedema?

Answer 19

in contrast to the HAPE, cerebral vasodilation is the problem. Hypoxia → cerebral vasodilation → elevated cerebral blood volume
also, hypoxia → increase in the permeability of the blood-brain barrier → capillaries in the brain more leaky → leading to fluid accumulation in the extracellular spaces
both these factors → cerebral oedema
presents with headache, ataxia, papilloedema

Question 20

What is the management of HACE and HAPE

Answer 20

Management of HACE
descent
dexamethasone

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

*the relative merits of these different treatments has only been studied in small trials. All seem to work by reducing systolic pulmonary artery pressure

Question 21

First line investigations for asthma?

Answer 21

measure the eosinophil count OR fractional nitric oxide (FeNO)
diagnose asthma, without further investigations, if:
eosinophil is above the reference range
FeNO is ≥ 50 ppb

Question 22

If asthma is not conformed by the eosinophil count ot FeNO what investigations can be done?

Answer 22

measure bronchodilator reversibility (BDR) with spirometry
diagnose asthma if:
the FEV1 increase is ≥ 12% and 200 ml or more from the pre-bronchodilator measurement, or
the FEV1 increase is ≥ 10% of the predicted normal FEV1
if spirometry is not available or it is delayed, measure peak expiratory flow (PEF) twice daily for 2 weeks
diagnose asthma if:
PEF variability (expressed as amplitude percentage mean) is ≥ 20%

If asthma is not confirmed by eosinophil count, FeNO, BDR or PEF variability but still suspected on clinical grounds:
refer for consideration of a bronchial challenge test
diagnose asthma if bronchial hyper-responsiveness is present

Question 23

Investigations for asthma in children aged 5-16?

Answer 23

1st line - FeNO (diagnose asthma if FeNO is >35)

If the FeNO level is not raised, or if FeNO testing is not available:
measure bronchodilator reversibility (BDR) with spirometry
diagnose asthma if:
the FEV1 increase is ≥ 12% from the pre-bronchodilator measurement, or
the FEV1 increase is ≥ 10% of the predicted normal FEV1
if spirometry is not available or it is delayed, measure peak expiratory flow (PEF) twice daily for 2 weeks
diagnose asthma if:
PEF variability (expressed as amplitude percentage mean) is ≥ 20%

Question 23

How do eosinophils play a direct role in airway inflammation?

Answer 23

eosinophils play a direct role in airway inflammation by releasing granules containing cytotoxic proteins like eosinophil peroxidase and major basic protein, which damage epithelial cells and perpetuate inflammation. Additionally, eosinophils are activated by interleukin-5 (IL-5) and other cytokines in the type 2 pathway, distinguishing them from neutrophils or lymphocytes

Question 24

Why can Fractional exhaled nitric oxide (FeNO) be used to diagnose asthma?

Answer 24

Fractional exhaled nitric oxide (FeNO) reflects the level of nitric oxide produced by airway epithelial cells in response to eosinophilic inflammation, a hallmark of asthma. It is measured non-invasively by having the patient exhale steadily into a handheld device, which analyses nitric oxide concentration in parts per billion (ppb).

Question 25

Obstructive lung disease vs restrictive lung disease on pulmonary function tests ?

Answer 25

Question 26

causes of bilateral hilar lymphadenopathy?

Answer 26

The most common causes of bilateral hilar lymphadenopathy are sarcoidosis and tuberculosis. Other causes include: lymphoma/other malignancy pneumoconiosis e.g. berylliosis fungi e.g. histoplasmosis, coccidioidomycosis

Question 27

Causes of pulmonary eosinophila?

Answer 27

Churg-Strauss syndrome allergic bronchopulmonary aspergillosis (ABPA) Loffler's syndrome eosinophilic pneumonia hypereosinophilic syndrome tropical pulmonary eosinophilia drugs: nitrofurantoin, sulphonamides less common: Wegener's granulomatosis ## Footnote Pulmonary eosinophilia describes a situation where there are increased numbers of eosinophils in the lung airways and parenchyma. This is generally associated with a blood eosinophilia.

Question 28

What is Loffler's syndrome?

Answer 28

transient CXR shadowing and blood eosinophilia thought to be due to parasites such as Ascaris lumbricoides causing an alveolar reaction presents with a fever, cough and night sweats which often last for less than 2 weeks. generally a self-limiting disease

Question 29

Is Extrinsic allergic alveolitis a pulmonary eosinophilia?

Answer 29

This condition, also known as hypersensitivity pneumonitis, is an immunologically mediated interstitial lung disease caused by repeated inhalation of a variety of antigens. The inflammatory response in extrinsic allergic alveolitis is primarily granulomatous and does not typically involve eosinophils

Question 30

What is Alpha-1 antitrypsin (A1AT) deficiency?

Answer 30

A common inherited condition caused by a lack of a protease inhibitor normally produced by the liver

Question 31

What is the primary role of A1AT?

Answer 31

To protect cells from enzymes such as neutrophil elastase

Question 32

What condition is classically caused by A1AT deficiency in young, non-smoking patients?

Answer 32

Emphysema (chronic obstructive pulmonary disease)

Question 33

On which chromosome is the A1AT gene located?

Answer 33

Chromosome 14

Question 34

How is A1AT inherited?

Answer 34

In an autosomal recessive / co-dominant fashion

Question 35

What liver conditions can occur in adults with A1AT deficiency?

Answer 35

* Cirrhosis * Hepatocellular carcinoma ## Footnote liver: cirrhosis and hepatocellular carcinoma in adults,

Question 36

What investigations are used for A1AT deficiency?

Answer 36

* A1AT concentrations * Spirometry: obstructive picture

Question 37

What is a key management strategy for A1AT deficiency?

Answer 37

No smoking Supportive measures * Bronchodilators * Physiotherapy Intravenous alpha1-antitrypsin protein concentrates Surgery - lung volume refuction surgery, lung transplant

Question 38

What is Tidal Volume?

Answer 38

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

Question 39

What is inspitatory reserve volume?

Answer 39

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

Question 40

Expiratory reserve volume?

Answer 40

maximum volume of air that can be expired at the end of a normal tidal expiration significantly reduced in obesity (increased abdominal fat mass pushes up against the diaphragm, reducing the volume of air that can be expelled)

Question 41

What is residual volume?

Answer 41

volume of air remaining after maximal expiration increases with age RV = FRC - ERV

Question 42

What is functional residual capacity ?

Answer 42

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

Question 43

What is vital capacity?

Answer 43

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

Question 44

What is the total lung capacity?

Answer 44

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

Question 45

What is the physiological dead space?

Answer 45

VD = tidal volume * (PaCO2 - PeCO2) / PaCO2 where PeCO2 = expired air CO

Question 46

What is Psitacosis?

Answer 46

Psittacosis is infection caused by Chlamydia psittaci. Chlamydia psittaci is an obligate intracellular bacteriu ## Footnote ransmission is typically from birds or bird secretions including urine and faeces, typically occurring after cleaning bird cages

Question 47

Features of Psittacosis?

Answer 47

sittacosis should be suspected in a combination of typical fever with a history of bird contact (reported in 84%) or a presentation with pneumonia and severe headache or organomegaly and failure to respond to penicillin-based antibiotics. Patients typically present with a subacute onset of: Flu-like symptoms (90%): fever, headache and myalgia Respiratory symptoms (82%): dyspnoea, dry cough and chest pain Signs: Chest: unilateral crepitations and vesicular breathing (common), evidence of pleural effusion (uncommon) Abdomen: hepatomegaly and splenomegaly (rare)

Question 48

Tratment for Psittacosis?

Answer 48

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

Question 49

Why does pulmonary haemorrhage lead to increased TLCO?

Answer 49

In pulmonary haemorrhage, there is extravasation of blood into the alveolar spaces. This increases the amount of haemoglobin available in the alveoli for carbon monoxide binding, leading to an increased TLCO measurement. The presence of additional red blood cells in the alveolar space enhances the gas transfer capacity, as carbon monoxide has a high affinity for haemoglobin.

Question 50

Causes of Bronchiectasis?

Answer 50

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

Question 51

What is allergic broncopulmonary aspergillosis

Answer 51

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

Question 52

Features of allergic broncopulmonary aspergillosis ?

Answer 52

bronchoconstriction: wheeze, cough, dyspnoea. Patients may have a previous label of asthma bronchiectasis (proximal)

Question 53

diagnosis of allergic broncopulmonary aspergillosis ?

Answer 53

eosinophilia flitting CXR changes positive radioallergosorbent (RAST) test to Aspergillus positive IgG precipitins (not as positive as in aspergilloma) raised IgE ## Footnote Major criteria for the diagnosis are: Clinical features of asthma Proximal bronchiectasis Blood eosinophilia Immediate skin reactivity to Aspergillus antigen Increased serum IgE (>1000 IU/ml) Minor criteria: Fungal elements in sputum Brown flecks in sputum Delayed skin reactivity to fungal antigens

Question 54

Management of allergic bronocpulmonary aspergillosis?

Answer 54

oral glucocorticoids itraconazole is sometimes introduced as a second-line agent

Question 56

what is silicosis?

Answer 56

Silicosis is a fibrosing lung disease caused by the inhalation of fine particles of crystalline silicon dioxide (silica). It is a risk factor for developing tuberculosis (silica is toxic to macrophages).

Question 57

Occupations at risk of silicosis

Answer 57

mining slate works foundries potteries

Question 58

Features of Silicosis?

Answer 58

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

Question 59

What is Atelectasis?

Answer 59

Atelectasis is a common postoperative complication in which basal alveolar collapse can lead to respiratory difficulty. It is caused when airways become obstructed by bronchial secretions.

Question 60

What are the features of Atelectasis?

Answer 60

it should be suspected in the presentation of dyspnoea and hypoxaemia around 72 hours postoperatively

Question 61

What is the management of atelectasis?

Answer 61

positioning the patient upright chest physiotherapy: breathing exercises

Question 62

Paraneoplastic features of lung cancer? Small cell squamous cell adenocarcinoma

Answer 62

**Small cell **ADH ACTH - not typical, hypertension, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc Lambert-Eaton syndrome **Squamous cell **parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia clubbing hypertrophic pulmonary osteoarthropathy (HPOA) hyperthyroidism due to ectopic TSH **Adenocarcinoma **gynaecomastia hypertrophic pulmonary osteoarthropathy (HPOA)

Question 64

what may lead to respiratory alkalosis?

Answer 64

anxiety leading to hyperventilation pulmonary embolism salicylate poisoning* CNS disorders: stroke, subarachnoid haemorrhage, encephalitis altitude pregnancy

Question 65

Contraindications to surgical resection in lung cancer?

Answer 65

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

Question 66

presenting features in cystic fibrosis?

Answer 66

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 ## Footnote Other features of cystic fibrosis short stature diabetes mellitus delayed puberty rectal prolapse (due to bulky stools) nasal polyps male infertility, female subfertility

Question 67

What is the mechanism of action of Leukotriene receptor antagonists?

Answer 67

a class of drugs that block the action of leukotrienes, inflammatory mediators derived from arachidonic acid via the 5-lipoxygenase pathway. LTRAs, such as montelukast and zafirlukast, competitively block the CysLT1 receptor found in the airways, thereby reducing the effects of leukotrienes. ## Footnote Leukotrienes contribute to the pathophysiology of asthma by promoting bronchoconstriction, airway hyperresponsiveness, mucus secretion, and eosinophilic inflammation.

Question 68

What effect for LTRA have?

Answer 68

Decreased bronchoconstriction Reduced mucus production Attenuation of airway inflammation Improved airway calibre and reduced symptoms of asthma

Question 69

Adverse effects of LTRA?

Answer 69

neuropsychiatric effects associated with montelukast, including agitation, sleep disturbances, depression, and, rarely, suicidal ideation. Patients should be monitored for these symptoms, and the drug should be discontinued if they occur. Hepatic dysfunction: Zafirlukast has been associated with hepatic impairment, and liver function should be monitored during therapy. Churg-Strauss syndrome: As mentioned, caution is advised when tapering corticosteroids in patients starting LTRAs, as CSS may be unmasked.

Question 70

COPD severity staging?

Answer 70

The severity of COPD is categorised using the FEV1*: ## Footnote *note that the grading system has changed following the 2010 NICE guidelines. 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

Question 71

High risk characteristics indicating insertion of chest darin in pneumothroax?

Answer 71

haemodynamic compromise (suggesting a tension pneumothorax) significant hypoxia bilateral pneumothorax underlying lung disease ≥ 50 years of age with significant smoking history haemothorax

Question 72

What is Eosinophilic granulomatosis with polyangiitis (EGPA)?

Answer 72

Eosinophilic granulomatosis with polyangiitis (EGPA) is now the preferred term for Churg-Strauss syndrome. It is an ANCA associated small-medium vessel vasculitis.

Question 73

What are the features of Eosinophilic granulomatosis with polyangiitis (EGPA)?

Answer 73

asthma blood eosinophilia (e.g. > 10%) paranasal sinusitis mononeuritis multiplex renal involvement occurs in around 20% pANCA positive in 60%

Question 74

What may precipitate Eosinophilic granulomatosis with polyangiitis?

Answer 74

Leukotriene receptor antagonists may precipitate the disease.

Question 75

Causes of pulmonary fibrosis predominately affecting the upper zones?

Answer 75

hypersensitivity pneumonitis (also known as extrinsic allergic alveolitis) coal worker's pneumoconiosis/progressive massive fibrosis silicosis sarcoidosis ankylosing spondylitis (rare) histiocytosis tuberculosis radiation-induced pulmonary fibrosis may develop following radiotherapy for breast or lung cancer typically seen between 6 and 12 months following completion of radiotherapy course ## Footnote Acronym for causes of upper zone fibrosis: CHARTS C - Coal worker's pneumoconiosis H - Histiocytosis/ hypersensitivity pneumonitis A - Ankylosing spondylitis R - Radiation T - Tuberculosis S - Silicosis/sarcoidosis

Question 76

Causes of fibrosis predominately affecting the lower zones?

Answer 76

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

Question 77

What is Extrinsic allegic alveolitis?

Answer 77

Extrinsic allergic alveolitis (EAA, also known as hypersensitivity pneumonitis) is a condition caused by hypersensitivity induced lung damage due to a variety of inhaled organic particles.

Question 78

What type of hypersensitivity reactions occure in extrinsic allergic alveolitis?

Answer 78

It is thought to be largely caused by immune-complex mediated tissue damage (type III hypersensitivity) although delayed hypersensitivity (type IV) is also thought to play a role in EAA, especially in the chronic phase.

Question 79

Examples of extrinsic allergic alveolitis?

Answer 79

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*

Question 80

How does extrinsic allergic alveolitis present?

Answer 80

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

Question 81

Investigations and management for Extrinsic allergic alveolitis?

Answer 81

Investigation imaging: upper/mid-zone fibrosis bronchoalveolar lavage: lymphocytosis serologic assays for specific IgG antibodies blood: NO eosinophilia Management avoid precipitating factors oral glucocorticoids

Question 82

Paraneoplastic features of lung cancer?

Answer 82

Paraneoplastic features of lung cancer squamous cell: PTHrp, clubbing, HPOA small cell: ADH, ACTH, Lambert-Eaton syndrome

Question 83

what type of lung cancer is PTH related peptide secretion seen in?

Answer 83

Squamous cell lung cancer

Question 84

What is a contraindication to lung transplantation in cystic fibrosis?

Answer 84

chronic infection with Burkholderia cepacia is an important CF-specific contraindication to lung transplantation ## Footnote Chronic infection with Burkholderia cepacia is an important CF-specific contraindication to lung transplantation. Patients with Burkholderia cepacia complex, particularly the Burkholderia cenocepacia species, have an increased risk of mortality due to recurrent disease after transplantation. Burkholderia cepacia typically causes a more rapid progression of disease associated with a deterioration in lung function and FEV1. It is also responsible for an often fatal necrotizing pneumonia known as the 'cepacia syndrome.'

Question 85

How many hours a day should COPD patients with LTOT wear their oxygen ?

Answer 85

15 hours

Question 86

When should LTOT be given to patients with COPD?

Answer 86

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

Question 87

What are the features of cor pulmonale?

Answer 87

features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2

Question 88

Normal genes seen for alpha 1 antitripsin and what is seen in defiency?

Answer 88

normal: PiMM heterozygous: PiMZ evidence base is conflicting re: risk of emphsema however, if non-smoker low risk of developing emphsema but may pass on A1AT gene to children homozygous PiSS: 50% normal A1AT levels homozygous PiZZ: 10% normal A1AT levels

Question 89

Staging of sarcoidosis on CXR?

Answer 89

A chest x-ray may show the following changes: stage 0 = normal stage 1 = bilateral hilar lymphadenopathy (BHL) stage 2 = BHL + interstitial infiltrates stage 3 = diffuse interstitial infiltrates only stage 4 = diffuse fibrosis

Question 90

What bacteria is responsible for malt workers lung?

Answer 90

Aspergillus clavatus causes malt workers' lung, a type of EAA

Question 91

what is responsible for bird fanciers' lung?

Answer 91

avian proteins from bird droppings

Question 92

What is responsible for farmers lung?

Answer 92

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

Question 93

features of eosinophilc granulomatosis with polyangitis?

Answer 93

Features asthma blood eosinophilia (e.g. > 10%) paranasal sinusitis mononeuritis multiplex renal involvement occurs in around 20% pANCA positive in 60%

Question 94

Granulomatosis with polyangitis (wegener's) vs eosinophilic granulomatosis with polyangitis (churg strauss)

Answer 94

Question 95

Pre-disposing factors to OSA?

Answer 95

Predisposing factors obesity macroglossia: acromegaly, hypothyroidism, amyloidosis large tonsils Marfan's syndrome

Question 96

Diagnostic tests for obstructive sleep apnoea?

Answer 96

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

Question 97

Management of OSA?

Answer 97

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

Question 98

What is Varenicline? When should it be started What is the course length Saide effects Contraindications

Answer 98

a nicotinic receptor partial agonist should be started 1 week before the patients target date to stop the recommended course of treatment is 12 weeks (but patients should be monitored regularly and treatment only continued if not smoking) has been shown in studies to be more effective than bupropion nausea is the most common adverse effect. Other common problems include headache, insomnia, abnormal dreams varenicline should be used with caution in patients with a history of depression or self-harm. There are ongoing studies looking at the risk of suicidal behaviour in patients taking varenicline contraindicated in pregnancy and breastfeeding

Question 98

How should secondaru spontanous pneumothorax be managed?

Answer 98

Patients with a secondary spontaneous pneumothorax that is managed conservatively should be monitored as an inpatient

Question 99

What is Bupropion? When should it be started Side effects and contraindicaitons ?

Answer 99

a norepinephrine-dopamine reuptake inhibitor and nicotinic antagonist unlike many antidepressants it has a minimal effect on serotonin should be started 1 to 2 weeks before the patient's target date to stop small risk of seizures (1 in 1,000) contraindicated in epilepsy, pregnancy and breast feeding. Having an eating disorder is a relative contraindication

Question 100

What is idiopathic pulmonary fibrosis?

Answer 100

Idiopathic pulmonary fibrosis (IPF, previously termed cryptogenic fibrosing alveolitis) is a chronic lung condition characterised by progressive fibrosis of the interstitium of the lungs. Whilst there are many causes of lung fibrosis (e.g. medications, connective tissue disease, asbestos) the term IPF is reserved when no underlying cause exists.

Question 101

In what age group is idopathic pulmonary fibrosis seen ?

Answer 101

50-70 years and is twice as common in men.

Question 102

What are the features of idiopathic pulmonary fibrosis?

Answer 102

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

Question 103

How is idiopathic pulmonary fibrosis diagnosed?

Answer 103

spirometry: classically a restrictive picture (FEV1 normal/decreased, FVC decreased, FEV1/FVC increased) impaired gas exchange: reduced transfer factor (TLCO) imaging: 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 ANA positive in 30%, rheumatoid factor positive in 10% but this does not necessarily mean that the fibrosis is secondary to a connective tissue disease. Titres are usually low

Question 104

How is idiopathic pulmonary fibrosis managed ?

Answer 104

Management pulmonary rehabilitation 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 (see NICE guidelines) many patients will require supplementary oxygen and eventually a lung transplant Prognosis poor, average life expectancy is around 3-4 years

Question 105

What is Kartagener's syndrome?

Answer 105

Kartagener's syndrome (also known as primary ciliary dyskinesia) was first described in 1933 and most frequently occurs in examinations due to its association with dextrocardia (e.g. 'quiet heart sounds', 'small volume complexes in lateral leads') Pathogenesis dynein arm defect results in immotile cilia

Question 106

Features of Kartagener's syndrome?

Answer 106

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

Question 107

when is calcificaion in lung mets seen ?

Answer 107

Calcification in lung metastases is uncommon except in the case of chondrosarcoma or osteosarcoma.

Question 108

What is the bronchial challenge test?

Answer 108

The bronchial challenge test assesses airway hyperresponsiveness, a characteristic feature of asthma, by measuring the airway's response to a provocative agent such as methacholine or histamine. In asthma, heightened bronchial smooth muscle reactivity and inflammation lead to excessive narrowing of the airways when exposed to these agents, resulting in a significant decline in FEV1

Question 109

If asthma is not confirmed by eosinophil count, FeNO, BDR or PEF variability but still suspected then refer for consideration of....

Answer 109

bronchial challenge test

Question 110

What is ARDS?

Answer 110

Acute respiratory distress syndrome (ARDS) is caused by the increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli, i.e. non-cardiogenic pulmonary oedema. It is a serious condition that has a mortality of around 40% and is associated with significant morbidity in those who survive.

Question 111

Causes of acute respiratory distress syndrome?

Answer 111

infection: sepsis, pneumonia massive blood transfusion trauma smoke inhalation acute pancreatitis Covid-19 cardio-pulmonary bypass Clinical features? dyspnoea elevated respiratory rate bilateral lung crackles low oxygen saturations

Question 112

Diagnosis of ARDS?

Answer 112

A chest x-ray and arterial blood gases are the key investigations. Criteria (American-European Consensus Conference) 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)

Question 113

Management of ARDS?

Answer 113

due to the severity of the condition patients are generally managed in ITU oxygenation/ventilation to treat the hypoxaemia general organ support e.g. vasopressors as needed treatment of the underlying cause e.g. antibiotics for sepsis certain strategies such as prone positioning and muscle relaxation have been shown to improve outcome in ARDS

Question 114

what is the normal vital capacity ?

Answer 114

4,500ml in males, 3,500 mls in females

Question 115

CURB 65

Answer 115

Question 116

Management of CAP?

Answer 116

**Management of low-severity community acquired pneumonia** amoxicillin is first-line if penicillin allergic then use a macrolide or tetracycline NICE now recommend a 5 day course of antibiotics for patients with low severity community acquired pneumonia **Management of moderate and high-severity community acquired pneumonia** 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 community acquired pneumonia

Question 117

Discharge criteria and advice post-discharge CAP

Answer 117

NICE recommend that patients are not routinely discharged if in the past 24 hours they have had 2 or more of the following findings: 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.

Question 118

what is seen on spirometry of an obese patient?

Answer 118

. A reduced FEV1 and FVC with a normal FEV1/FVC ratio, and reduced expiratory reserve volume may be observed in cases of obesity

Question 119

COPD causes?

Answer 119

Smoking! Alpha-1 antitrypsin deficiency Other causes cadmium (used in smelting) coal cotton cement grain

Question 120

What is Kartagener's syndrome

Answer 120

Kartagener's syndrome (also known as primary ciliary dyskinesia) was first described in 1933 and most frequently occurs in examinations due to its association with dextrocardia (e.g. 'quiet heart sounds', 'small volume complexes in lateral leads') Pathogenesis dynein arm defect results in immotile cilia

Question 121

Features of Kartagener's syndrome?

Answer 121

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