Respiratory Flashcards

1
Q

What gender is idiopathic pulmonary fibrosis more common in?

A

Men (twice as likely).

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2
Q

What are the criteria for LTOT in COPD patients?

A
< 7.3 kPa or to those with a pO2 of 7.3 - 8 kPa and one of the following:
secondary polycythaemia
nocturnal hypoxaemia
peripheral oedema
pulmonary hypertension

ABGs results are based on 2 results, 3 week apart

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3
Q

What must be done before offering azithromycin in patients with COPD.

A

Only offered if having frequent exacerbations despite optimum therapy in patients who DO NOT SMOKE.

Should have CT to exclude bronchietasis.
Sputum cultures for TB and atypical infections e.g. mycoplasma.
LFTs and ECG (prolongs QTc)

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4
Q

What are the features of cor pulmonale?

A

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

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5
Q

What is the treatment of cor pulmonale?

A

Loop diuretics +/- LTOT

ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended.

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6
Q

What things improve survival in COPD

A

smoking cessation - the single most important intervention in patients who are still smoking
long term oxygen therapy in patients who fit criteria
lung volume reduction surgery in selected patients

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7
Q

What happens in ARDS?

A

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.

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8
Q

What are the causes of ARDS?

A
infection: sepsis, pneumonia
massive blood transfusion
trauma
smoke inhalation
acute pancreatitis
cardio-pulmonary bypass
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9
Q

What are the criteria for ARDS?

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)

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10
Q

What is the main role of alpha 1 antitrypsan

A

it is a protease inhibitor

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11
Q

Where is A1AT produced?

A

liver

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12
Q

What gene is A1AT deficiency located on

A

chromosome 14

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13
Q

What type of inheritance is A1AT deficiency

A

autosomal recessive

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14
Q

Outline the genotypes in alpha1 antitrypsan deficiecny

A

Normal = PiMM
PiSS (50 percent normal levels)
PiZZ (10 percent normal levels)

Patients who manifest the disease phenotypicall usually have PiZZ genotype

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15
Q

What does A1AT defiency result in

A

Emphysema
Liver cirrhosis
Hepatocellular carcinoma

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16
Q

What type of lung cancer is most commonly associated with cavitating lesions?

A

Squamous

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17
Q

What is the treatment of OSA

A

Weight loss
First line in moderate/severe is CPAP overnight
Intra oral devices can be uses if CPAP is not tolerated or in very mild cases

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18
Q

Outline the management of a primary pneumothorax

A

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

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19
Q

Outline the management of a secondary pneumothorax

A

if the patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.
otherwise aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater then 1cm) a chest drain should be inserted. All patients should be admitted for at least 24 hours
if the pneumothorax is less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours

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20
Q

What is the mechanism of varenicline?

A

Used to help smoking cessation.

Nicotinic receptor partial agonist.

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21
Q

How does sarcoidosis cause hypercalcaemia

A

Sarcoidosis mainly causes hypercalcaemia through forming increased concentrations of calcitriol, the active component of vitamin D. This is as a result of increased activity of 1α hydroxylase produced by the sarcoid macrophages.

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22
Q

What is sarcoidosis

A

multisystem disorder of unknown aetiology characterised by non-caseating granulomas. It is more common in young adults and in people of African descent

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23
Q

Name some characteristic features of sarcoidosis

A

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

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24
Q

What is Lofgrens syndrome

A

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

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25
Q

What is Mikulicz syndrome

A

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

26
Q

What is Heerfordt’s syndrome

A

parotid enlargement, fever and uveitis secondary to sarcoidosis

27
Q

What paraneoplastic syndromes are associated with small cell lung cancer

A
SIADH
Cushings syndrome (high ACTH)
Lambert Eaton (antibodies against presynaptic calcium channels at the NMJ)
28
Q

What paraneoplastic features are associated with squamous cell lung cancer

A

parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia
clubbing
hypertrophic pulmonary osteoarthropathy (HPOA)
hyperthyroidism due to ectopic TSH

29
Q

What paraneoplastic features are associated with adenocarcinoma of the lung?

A

gynaecomastia

hypertrophic pulmonary osteoarthropathy (HPOA)

30
Q

Describe the chest x ray stages in sarcoidosis

A

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

31
Q

What is the most common cause of occupational asthma?

A

Isocyanates

32
Q

what is loffler’s syndrome

A

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

33
Q

What HLA is associated with bronchietasis

A

DR1

34
Q

Which HLA is associated with SLE

A

DR2

35
Q

What is HLA-DR3 associated with

A

autoimmune hepatitis, primary Sjogren syndrome, type 1 diabetes Mellitus, SLE

36
Q

what is associated with HLA DR4

A

rheumatoid arthritis, type 1 diabetes Mellitus

37
Q

What is associated with HLa-B27

A

ankylosing spondylitis, postgonococcal arthritis, acute anterior uveitis

38
Q

give causes of bronchietasis

A

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

39
Q

what features can be associated with mycoplasma pneumonia

A

erythema mutiforme

autoimmune haemolytic anaemia

40
Q

what type of pneumonia classically occurs after flu

A

staph aureus

41
Q

what pneumonia is classically caused by aspiration

A

klebsiella

42
Q

what features are ‘classic’ of klebsiella pneumonia

A

cavitating

red currant jelly sputum

43
Q

what lung causes fibrosis in the lower zone

A

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

44
Q

what lung fibrosis occurs in the upper zone

A

hypersensitivity pneumonitis (also known as extrinsic allergic alveolitis)
coal worker’s pneumoconiosis/progressive massive fibrosis
silicosis
sarcoidosis
ankylosing spondylitis (rare)
histiocytosis
tuberculosis

45
Q

what medication can precipitate Churg strauss

A

montelukast

46
Q

at what pH of fluid would you insert a chest drain

A

7.2

47
Q

what is the mechanism of action of montelukast

A

leukotriene receptor antagonist

48
Q

what is allergic bronchopulmonary aspergillosis

A

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

49
Q

what are the major diagnostic criteria for allergic bronchopulmoanry aspergillosis

A
Clinical features of asthma
Proximal bronchiectasis
Blood eosinophilia
Immediate skin reactivity to Aspergillus antigen
Increased serum IgE (>1000 IU/ml)
50
Q

what are the minor diagnotic criteria for allergic bronchopulmonary aspergillosis

A

Fungal elements in sputum
Brown flecks in sputum
Delayed skin reactivity to fungal antigens

51
Q

what causes raised TLCO

A
asthma
pulmonary haemorrhage (Wegener's, Goodpasture's)
left-to-right cardiac shunts
polycythaemia
hyperkinetic states
male gender, exercise
52
Q

what causes lower TLCO

A
pulmonary fibrosis
pneumonia
pulmonary emboli
pulmonary oedema
emphysema
anaemia
low cardiac output
53
Q

what is KCO

A

transfer coeffient of gas exchange corrected for lung volume

54
Q

What conditions may cause an increased KCO with a normal or reduced TLCO

A

pneumonectomy/lobectomy
scoliosis/kyphosis
neuromuscular weakness
ankylosis of costovertebral joints e.g. ankylosing spondylitis

55
Q

what classically causes ‘egg shell calcification’ on CT

A

silicosis

56
Q

exposure to what material increases your risk of TB

A

silicosis

57
Q

what is the most common side effect of varenciline

A

nausea

58
Q

what is normal pulmonary arterial pressure?

A

less than 25 at rest, 30 if exercising

59
Q

give some skin disorders associated with TB

A

lupus vulgaris (accounts for 50% of cases)
erythema nodosum
scarring alopecia
scrofuloderma: breakdown of skin overlying a tuberculous focus
verrucosa cutis
gumma

60
Q

what cell secrete surfactant

A

type 2 pneumocytes