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Phase 2a - Systems > Respiratory 1 > Flashcards

Respiratory 1 Flashcards

1
Q

what two disease are included within the definition of COPD?

A

emphysema and chronic bronchitis

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2
Q

define chronic bronchitis

A

persistent cough for 3/12 for 2 consecutive years

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3
Q

list some features that would suggest it is more likely the patient has COPD than asthma

A

onset >35yo, smoking/pollution related, chronic dyspnoea (instead of attacks), sputum production, lack of diurnal FEV1 variation

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4
Q

give 2 causes of COPD

A

smoking, exposure to pollutants at work (mining, building, chemical), alpha-1 antitrypsin deficiency

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5
Q

what generally causes early-onset COPD?

A

alpha-1 antitrypsin deficiency

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6
Q

give 3 risk factors of COPD

A

smoking, pollutant exposure, frequent lower resp infections in childhood, age.

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7
Q

describe the pathology seen in chronic bronchitis

A

narrow airways. hypertrophy and hyperplasia of mucus secreting glands of the bronchial tree.
bronchial wall inflammation. mucosal oedema.
ulceration of epithelial layer - heals squamous instead of columnar (squamous metaplasia).

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8
Q

describe the pathology seen in emphysema

A

dilation and destruction of alveoli - leads to loss of elastic recoil - expiratory airflow limitation and air trapping

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9
Q

which disease is predominant in each of pink puffers and blue bloaters?

A

pink puffers = predominantly emphysema

blue boaters = predominantly chronic bronchitis

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10
Q

what are the features of a pink puffer?

A

increased alveolar ventilation - nearly normal PaO2 + normal/low PaCO2 - breathless but not cyanosed - may progress to type 1 resp failure

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11
Q

what are the features of a blue bloater?

A

decreased alveolar ventilation - low PaO2 and high PaCO2 - cyanosed but not breathless - poss. cor pulmonale - rely on hypoxic drive as respiratory centres are insensitive to CO2

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12
Q

what is cor pulmonale?

A

enlargement and failure of right side of the heart due to disease of lungs/pulmonary blood vessels - leads to oedema and raised JVP

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13
Q

explain how cigarette smoke causes COPD

A

causes mucous gland hypertrophy in larger airways - increase in neutrophils, macrophages and lymphocytes in airway walls - release of inflammatory mediators - inflammatory cells attracted - structural changes - break down of connective tissue

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14
Q

what is alpha1-antitrypsin?

A

a protease inhibitor - inactivated by cigarette smoke

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15
Q

give 3 symptoms of COPD

A

cough, sputum, dyspnoea, wheeze

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16
Q

give 3 signs of COPD

A

tachypnoea, use of accessory muscles of respiration, hyperinflation, decreased cricosternal distance, resonant/hyperresonant percussion, quiet breath sounds, wheeze, cyanosis, cor pulmonale

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17
Q

give 3 complications of COPD

A

acute exacerbations ± infection, polycythaemia, respiratory failure cor pulmonale, pneumothorax, lung carcinoma

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18
Q

give 3 differential diagnoses of COPD

A

asthma, bronchiectasis, pulmonary embolism, congestive heart failure, pneumothorax

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19
Q

what would be the results of a lung function test in a COPD patient?

A

reduced FEV1/FVC ratio, reduced PEFR.
raised TLC.
obstructive pattern.

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20
Q

what might you see on CXR in a COPD patient?

A

hyperinflation, flat hemidiaphragms, large central pulmonary arteries, decreased peripheral vascular markings, bullae.

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21
Q

how would you conduct a steroid trial in COPD? what information would it give you?

A

patient given oral prednisolone for 2 wks.

if FEV1 rises by >15% the COPD is steroid responsive - will benefit from long-term inhaled corticosteroids

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22
Q

how would you treat COPD?

A

ipratropium - short-acting antimuscarinic
± short-acting beta2 agonist -salbutamol, terbutamine
± inhaled tiotropium bromide - long-acting antimuscarinic
± long-acting beta2 agonist - salmeterol, formoterol

Severe COPD:
combination LABA + corticosteroids - Symbicort (budesonide + formoterol).
OR - tiotropium + inhaled steroid + LABA

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23
Q

describe non-pharmacological treatment of COPD

A

pulmonary rehab programmes.
smoking cessation.
low BMI = diet advice ± supplements.
long-term oxygen therapy.

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24
Q

describe the features of the airway obstruction seen in asthma

A

reversible.
bronchial muscle constriction.
mucosal swelling/inflammation.
increased mucous production.

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25
Q

give 2 diseases associated with asthma

A

eczema, hay fever, any allergy - atopy

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26
Q

what is atopy?

A

ready development of IgE antibodies against common environmental antigens

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27
Q

explain the hygiene hypothesis

A

the idea that growing up in a clean environment may predispose towards IgE response, as there is no childhood exposure to allergens, bacteria etc

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28
Q

describe the pathology seen in the airways of someone with asthma

A

inflammation + remodelling:
increased inflammatory cells in bronchial wall, mucous membranes and secretions.
B cells producing IgE.
airway smooth muscle hypertrophy and hyperplasia. thickening of airway wall - smooth muscle + repair collagens.
loss of ciliated columnar cells into lumen + increase no. mucous secreting goblet cells in epithelium.

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29
Q

give 3 precipitants of an asthma attack

A

cold air, exercise, emotion, allergens, infection, smoking, pollution, NSAIDs, beta blockers

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30
Q

what investigations would you perform to diagnose asthma?

A

peak expiratory flow rate - diurnal variation, marked dip in PEFR in AM - variation of >15%.

also - increase in PEF/FEV1 ratio of >15% after salbutamol.

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31
Q

give the steps in the management of mild to severe asthma (BTS guidelines)

A

SILCO:

  1. Short-acting beta2 agonist (SABA) e.g. salbutamol PRN
    • Inhaled corticosteroid (e.g. beclamethasone) if using SABA >1/day
    • LABA e.g. salmeterol
  4. “Consider other options” = trial of leukotriene receptor agonist or oral theophylline
  5. add Oral prednisolone, refer to asthma clinic
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32
Q

how would you control an acute asthma attack?

A

100% O2 with facemask.
nebulisers of salbutamol and ipatropium bromide.
IV hydrocortisone/prednisolone.

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33
Q

how to beta 2 agonists work?

A

activate beta 2 receptors, inducing smooth muscle relaxtion in lungs.

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34
Q

describe what is happening in the lungs of a patient with extrinsic allergic alveolitis (hypersensitivity pneumonitis)

A

inhalation of allergens provokes a hypersensitivity reaction, with complement activation, granuloma formation and obliterative bronchiolitis.

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35
Q

give 2 causes of EAA (hypersensitivity pneumonitis)

A 
Farmer's lung.
Bird-fancier's lung - proteins in bird droppings.
Malt-worker's lung.
Bagassosis/Sugar worker's lung.
humidifier fever.
Mushroom workers.
Cheese washer's lung.
Wine maker's lung.
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36
Q

give 3 clinical features of EAA seen after exposure to the allergen

A

fevers, rigors, myalgia, dry cough, dyspnoea, crackles (no wheeze)

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37
Q

give 3 chronic features of EAA

A

increasing dyspnoea, weight loss, exertional dyspnoea, type I respiratory failure, cor pulmonale

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38
Q

what would been seen on CXR of a patient with EAA?

A

fibrosis/mottling of upper lobes and honeycomb lung

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39
Q

list some investigations that might be performed on a patient with EAA

A

bloods - neutrophilia, raised ESR
CXR.
lung function tests (reversible restrictive).
broncheoalveolar lavage.

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40
Q

how would you treat EAA in an acute and a chronic situation?

A

acute - remove allergen, give O2 + oral prednisolone.

chronic - avoid exposure (facemask), long-term steroids.

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41
Q

list 3 occupational lung diseases

A 
EAA (e.g. Farmer's lung).
Coal worker's pneumonconiosis.
Silicosis. 
Asbestosis.
Byssinosis.
Berylliosis.
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42
Q

what causes the fibrosis seen in coal worker’s pneumoconiosis?

A

inhalation of coal dust particles - ingested by macrophages - these die and release their enzymes - fibrosis

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43
Q

what would a CXR show in coal worker’s pneumoconiosis?

A

round opacities in upper zone.

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44
Q

what causes progressive massive fibrosis? what are the features of this?

A

progression of coal worker’s pneumoconiosis.

progressive dyspnoea, fibrosis + eventual cor pulmonale.

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45
Q

give some examples of jobs at risk of silicosis

A

metal mining, stone quarrying, sand blasting, pottery/ceramic manufacture

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46
Q

what do investigations show in silicosis?

A

CXR - diffuse miliary/nodular pattern in upper and mid-zones + egg shell calcification of hilar nodes.
Spirometry - restrictive.

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47
Q

what disease are patients with silicosis at greater risk of?

A

TB

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48
Q

what are the clinical features of asbestosis?

A

progressive dyspnoea.

O/E - clubbing, fine end-inspiratory crackles, pleural plaques.

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49
Q

what two diseases are asbestosis patients at greater risk of?

A

bronchial adenocarcinoma and mesothelioma

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50
Q

in what industries might workers get byssinosis? and for berylliosis?

A

byssinosis - cotton mill workers.

berylliosis - beryllium-copper alloy used in aerospace industry, electronics, atomic reactors.

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51
Q

describe the pathogenesis of bronchiectasis

A

chronic infection of bronchi/bronchioles leads to inflamed, thickened and irreversibly damaged walls with permanent dilation.
mucociliary transport mechanism is impaired.

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52
Q

give 2 of the main organisms involved in bronchiectasis

A

H influenza, Strep pneumonia, Staph aureus, Pseudomonas aeruginosa

53
Q

give 3 possible causes of bronchiectasis

A

congenital - CF.
post-infection - measles, pertussis, pneumonia, TB, HIV.
Other - bronchial obstruction (tumour, foreign body), allergic bronchopulmonary aspergillosis (ABPA), hypogammaglobulinaemia, rheumatoid arthritis, UC.

54
Q

give 3 clinical features of bronchiectasis

A

persistent cough, copious purulent sputum, intermittent haemoptysis, finger clubbing, coarse inspiratory crepitations, wheeze

55
Q

give 2 possible complications of bronchiectasis

A

pneumonia, pleural effusion, pneumothorax, haemoptysis, cerebral abscess, amyloidosis

56
Q

name 3 investigations you would carry out in bronchiectasis and their results

A

*sputum culture.
*CT scan - shows the dilated airways.
CXR - cystic shadows, thickened bronchial walls.
spirometry - obstructive pattern.
broncoscopy - locate site of haemoptysis, exclude obstruction, obtain samples.

57
Q

how would you manage a patient with bronchiectasis?

A

physiotherapy - postural drainage.
Abx - flucloxacillin for staph, amoxicillin for strep, tazocin for pseudomonas.
bronchodilators - salbutamol nebulisers.
Oral/inhaled corticosteroids.

58
Q

what causes cystic fibrosis?

A

autosomal recessive mutation in the CF transmembrane conductase regulator gene on chromsome 7.
defective chloride secretion and increased sodium absorption over airway epithelium - produces very viscous and sticky mucous.

59
Q

give 3 respiratory symptoms of CF

A

cough, wheeze, recurrent infections, bronchiectasis, pneumothorax, haemoptysis, respiratory failure, cor pulmonale

60
Q

give 3 extrapulmonary features of CF

A

pancreatic insufficiency - DM, steatorrhoea.

intestinal obstruction, gallstones, cirrhosis, male infertility, osteoporosis, arthritis, vasculitis, sinusitis.

61
Q

name 3 investigations you would carry out in CF and their results

A

sweat test - increased sodium and chloride secretion in sweat.
faecal elastase - screens for pancreatic dysfunction.
genetic screening for CF mutations.
CXR - hyperinflation, bronchiectasis.

62
Q

how would CF be managed?

A 
physiotherapy.
Abx for exacerbations.
mucolytics - DNase (dornase alfa).
bronchodilators.
fat soluble vit supplements.
pancreatic enzyme replacement.
63
Q

what is sarcoidosis? what genes is it associated with?

A

multisystem granulomatous disorder of unknown cause.

associated with HLA-DRB1 and DQB1 alleles.

64
Q

what is seen on transbronchial biopsy in sarcoidosis?

A

infiltration of alveolar walls and interstitial spaces with mononuclear cells - later, granulomas

65
Q

how does acute sarcoidosis present?

A

erythema nodosum ± polyarthralgia

66
Q

give 3 pulmonary features of sarcoidosis?

A

dry cough, progressive dyspnoea, decreased exercise tolerance, chest pain.

67
Q

give 3 extra-pulmonary features of sarcoidosis

A

lymphadenopathy, hepatomegaly, splenomegaly, uveitis, conjunctivitis, glaucoma, Bell’s palsy, neuropathy, meningitis, brainstem and spinal syndromes, space occupying lesions, erythema nodosum, cardiomyopathy, arrhythmias, hypercalcaemia, renal stones, pituitary dysfunction

68
Q

what are the features of sarcoidosis on CXR?

A

bilateral hilar lymphadenopathy ± pulmonary infiltrates/fibrosis

69
Q

list some differential diagnoses for bilateral hilar lymphadenopathy

A

sarcoidosis, infection (TB, mycoplasma), malignancies, silicosis, EAA

70
Q

what investigations would you carry out, apart from CXR, in sarcoidosis, and what might they show?

A

SERUM ACE is raised.
lung function - restrictive pattern, reduced TLC, reduced FEV1/FVC ratio.
tissue biopsy - non-caseating granuloma.

71
Q

how would you treat sarcoidosis?

A

if symptomatic - corticosteroids (prednisolone).

if severe - IV methylprednisolone or methotrexate.

72
Q

what is the underlying pathology of idiopathic pulmonary fibrosis?

A

disruption of alveolar epithelium and basement membrane activates inflammation.
fibroblasts convert to myofibroblasts - synthesise collagen and aggregate to form fibrotic foci.

73
Q

give 3 symptoms and 3 signs of idiopathic pulmonary fibrosis

A

symptoms - dry cough, exertional dyspnoea, malaise, weight loss, arthralgia.
signs - cyanosis, finger clubbing, fine end-inspiratory crepitations.

74
Q

what investigations would you carry out in idiopathic pulmonary fibrosis? what do they show? which one is needed for diagnosis?

A

CXR - ground glass appearance, decreased lung volume, bilateral lower zone reticulo-nodular shadows - honeycombing if severe.
lung function tests - restrictive pattern, increased FEV1/FVC ratio.
need a lung biopsy.

75
Q

what is the ultimate end treatment of idiopathic pulmonary fibrosis?

A

lung transplant

76
Q

name 3 causes of pulmonary hypertension

A

hereditary, SLE, systemic sclerosis, rheumatoid arthritis, drugs, HIV, portal hypertension, schistosomiasis, chronic haemolytic anaemia, COPD, pulmonary fibrosis, mitral valve disease, sarcoidosis

77
Q

define pulmonary hypertension

A

elevated pulmonary artery pressure (>25mmHg at rest) and secondary right ventricular failure

78
Q

give 3 clinical features of pulmonary hypertension

A

exertional dyspnoea, lethary, peripheral oedema, loud pulmonary second sound, right parasternal heave

79
Q

give 3 signs that pulmonary hypertension has progressed to right heart failure (cor pulmonale)

A

elevated JVP, hepatomegaly, pulsatile liver, peripheral oedema, ascites, pleural effusion

80
Q

what is the eventual end treatment of primary pulmonary hypertension?

A

heart and lung transplant

81
Q

what 3 investigations would you carry out in pulmonary hypertension and what would they show?

A

CXR - enlarged proximal pulmonary arteries which taper distally.
ECG - RVH, P pulmonale (peaked P waves)
Echo - RV dilation/hypertrophy

82
Q

how would you treat pulmonary hypertension?

A

warfarin - reduce thrombosis risk.
diuretics - oedema.
oral CCBs - pulmonary vasodilators

sidenafil (PDE5 inhibitor) for primary pulmonary hypertension

83
Q

what is a haemothorax?

A

blood in the pleural space

84
Q

what is a chylothorax?

A

chyle (lymph + fat) in the pleural space

85
Q

what is an empyema?

A

pus in the plerual space

86
Q

what is a pleural effusion? define transudates and exudates

A

fluid in the pleural space
transudates = low protein content
exudates = high protein content

87
Q

give 3 causes of a transudate pleural effusion

A

cardiac failure, constrictive pericarditis, fluid overload, cirrhosis, nephrotic syndrome, malabsorption, hypothyroidism.

increased venous pressure and fluid overload.

88
Q

give 3 causes of an exudate pleural effusion

A

pneumonia, TB, rheumatoid arthritis, SLE, bronchogenic carcinoma, malignant metastases, lymphoma, mesothelioma, lymphangitis carcinomatosis.

increased leakiness of pleural capillaries secondary to infection, inflammation or malignancy.

89
Q

what would you hear on auscultation of a patient with a pleural effusion?

A

on side of the effusion:

decreased expansion, stony dull percussion note, diminished breath sounds.

90
Q

what investigations would you perform to diagnose a pleural effusion? what would they show?

A

CXR - small effusions blunt the costophrenic angles. larger = water-dense shadows with concave upper borders.
diagnostic pleural aspiration (US guided) - send for clinical chemistry, bacteriology and cytology.

91
Q

how would you treat a symptomatic pleural effusion?

A

drain it, repeat if necessary

92
Q

how would you treat recurrent pleural effusion?

A

pleurodesis with tetracycline, bleomycine or talc.

smoking cessation.

93
Q

what group of people are most likely to have a spontaneous pneumothorax?

A

young, thin men - rupture of sub-pleural bulla

94
Q

what is a pneumothorax?

A

air in pleural space, leading to partial or complete collapse of the lung

95
Q

what is a tension pneumothorax? how does it present?

A

pleural tear acts as a one way valve - air passes through during inspiration but is unable to exit during expiration.

presents in patient on mechanical ventilation - unilateral increase in pleural pressure with increasing respiratory distress - then shock - then cardiorespiratory arrest

96
Q

give 3 causes of a pneumothorax

A

spontaneous, chest trauma, asthma, COPD, TB, pneumonia, lung abscess, carcinoma, cystic fibrosis, lung fibrosis, sarcoidosis, connective tissue disorders (Marfan’s, Ehler-Danos)

97
Q

give 3 signs of a pneumothorax

A

reduced expansion, hyper-resonance to percussion, diminished breath sounds on affected side.

(in tension pneumothorax, trachea deviates away from the affected side)

98
Q

how would you manage a pneumothorax?

A

chest drain - urgent.

99
Q

give 3 risk factors for bronchus carcinoma

A

smoking, asbestos, chromium, arsenic, iron oxides, radiation (radon gas)

100
Q

which bronchial carcinoma is more common in non-smokers?

A

adenocarcinoma

101
Q

what cells do small cell lung cancers arise from? what can be the side effects of this?

A

endocrine cells (enterochromaffin cells) - carcinoid syndrome - flushing, diarrhoea, hyponatraemia

102
Q

which type of bronchial carcinoma is most likely to cause an obstruction?

A

squamous cell carcinoma

103
Q

describe the features of a squamous cell bronchial carcinoma

A

35%.
mostly present as obstructive lesion leading to infection.
occasionally cavitates. local spread common.
widespread metastases occur late.

104
Q

describe the features of an adenocarcinoma of the bronchus

A 
27%.
most common lung cancer associated with asbestos exposure. 
more common in non-smokers.
usually occurs peripherally.
local and distant metastases.
105
Q

what are the features of a large cell bronchial carcinoma?

A

10%.

poorly differentiated tumour, metastasizes early.

106
Q

which type of bronchial carcinoma generally has a worse prognosis, NSLC or SCLC?

A

small cell

107
Q

give 3 symptoms of bronchial carcinoma

A

cough, haemoptysis, dyspnoea, chest pain

108
Q

give 3 signs of bronchial carcinoma

A

cachexia, anaemia, clubbing, HPOA (hypertrophic pulmonary osteoarthropathy), supraclavicular or axillary nodes.
chest signs - none, or consolidation/collapse/pleural effusion

109
Q

give 3 examples of signs that there are distant mets in bronchial carcinoma

A

bone tenderness, hepatomegaly, confusion, fits, focal CNS signs, cerebellar syndrome, proximal myopathy, peripheral neuropathy

110
Q

give 3 local complications of bronchial carcinoma

A

recurrent laryngeal nerve palsy, phrenic nerve palsy, SVC obstruction, Horner’s syndrome, rib erosion, pericarditis, AF

111
Q

give 3 neurological complications of bronchial carcinoma

A

confusion, fits, cerebellar syndrome, proximal myopathy, neuropathy, polymyositis

112
Q

list the differential diagnoses of a nodule on the lung seen on CXR

A

malignancy, primary or secondary; abscesses, granuloma, carcinoid tumour, pulmonary hamartoma, arterio-venous malformation, encysted effusion (fluid, blood, pus), cyst, foreign body, skin tumour

113
Q

where do bronchial adenocarcinomas most commonly metastasise to?

A

mediastinal lymph nodes, brain, bone, adrenals

114
Q

how would you investigate a possible bronchial carcinoma?

A

sputum and pleural fluid samples for cytology.
CXR.
fine needle aspiration or biopsy.
bronchoscopy, CT, PET.

115
Q

list some possible features of a CXR of a patient with bronchial carcinoma

A

peripheral nodule, hilar enlargement, consolidation, lung collapse, pleural effusions, bony secondaries (e.g. ribs).

116
Q

what staging system is used for bronchial carcinomas?

A

TNM.
T = tumour, N = nodes, M = distant metastases.
converted into stage I-IV.

117
Q

how would you treat NSCLC?

A

peripheral tumours, stageI/II - surgical excision.
or, curative radiotherapy.
more advanced disease = chemo ± radiotherapy

118
Q

how would you treat small cell lung cancer?

A

may respond to chemo, but will relapse.
cyclophosphamide + doxorubicin + vincristine + etoposide.
OR cisplatin ± radiotherapy.

119
Q

describe some features of palliative care given to patients with bronchial carcinoma

A

radiotherapy - bronchial obstruction, haemoptysis, bone pain, cerebral mets.
SVC stent + radio - SVC obstruction.
pleural drainage.
analgesia, steroids, antiemetics, codeine for cough etc.

120
Q

name two benign lung cancers

A

bronchial adenoma, hamartoma

benign mesothelioma

121
Q

what is the biggest cause of mesothelioma?

A

occupational ASBESTOS exposure

122
Q

what is mesothelioma?

A

tumour of mesothelial cells that usually occurs in the pleura

123
Q

how would you diagnose mesothelioma?

A

CXR/CT - pleural thickening/effusion.
bloody pleural fluid.
histology following thoracoscopy - often only diagnosed postmortem.

124
Q

how would you treat mesothelioma?

A

chemo - cisplatin + premetrexed

125
Q

what are the two main features of Goodpasture’s disease?

A

acute glomerulonephritis + lung symptoms

126
Q

what are the pulmonary features of Goodpasture’s disease?

A

cough, intermittent haemoptysis, anaemia, upper respiratory tract infecions

127
Q

what investigation would you need to confirm a diagnosis of Goodpasture’s disease?

A

kidney biopsy - crescenteric glomerulonephritis

128
Q

how would you treat Goodpasture’s disease?

A

immunosuppression (corticosteroids) + plasmapheresis to remove antibodies

129
Q

what causes the features of Goodpasture’s disease?

A

anti-glomerular basement membrane antibodies - bind to kidney basement membrane and alveolar membrane

Phase 2a - Systems (18 decks)

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