Respiratory 1 Flashcards
1
Q
what two disease are included within the definition of COPD?
A
emphysema and chronic bronchitis
2
Q
define chronic bronchitis
A
persistent cough for 3/12 for 2 consecutive years
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
4
Q
give 2 causes of COPD
A
smoking, exposure to pollutants at work (mining, building, chemical), alpha-1 antitrypsin deficiency
5
Q
what generally causes early-onset COPD?
A
alpha-1 antitrypsin deficiency
6
Q
give 3 risk factors of COPD
A
smoking, pollutant exposure, frequent lower resp infections in childhood, age.
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).
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
9
Q
which disease is predominant in each of pink puffers and blue bloaters?
A
pink puffers = predominantly emphysema
blue boaters = predominantly chronic bronchitis
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
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
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
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
14
Q
what is alpha1-antitrypsin?
A
a protease inhibitor - inactivated by cigarette smoke
15
Q
give 3 symptoms of COPD
A
cough, sputum, dyspnoea, wheeze
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
17
Q
give 3 complications of COPD
A
acute exacerbations ± infection, polycythaemia, respiratory failure cor pulmonale, pneumothorax, lung carcinoma
18
Q
give 3 differential diagnoses of COPD
A
asthma, bronchiectasis, pulmonary embolism, congestive heart failure, pneumothorax
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.
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.
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
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
23
Q
describe non-pharmacological treatment of COPD
A
pulmonary rehab programmes.
smoking cessation.
low BMI = diet advice ± supplements.
long-term oxygen therapy.
24
Q
describe the features of the airway obstruction seen in asthma
A
reversible.
bronchial muscle constriction.
mucosal swelling/inflammation.
increased mucous production.
25
give 2 diseases associated with asthma
eczema, hay fever, any allergy - atopy
26
what is atopy?
ready development of IgE antibodies against common environmental antigens
27
explain the hygiene hypothesis
the idea that growing up in a clean environment may predispose towards IgE response, as there is no childhood exposure to allergens, bacteria etc
28
describe the pathology seen in the airways of someone with asthma
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.
29
give 3 precipitants of an asthma attack
cold air, exercise, emotion, allergens, infection, smoking, pollution, NSAIDs, beta blockers
30
what investigations would you perform to diagnose asthma?
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.
31
give the steps in the management of mild to severe asthma (BTS guidelines)
SILCO:
1. Short-acting beta2 agonist (SABA) e.g. salbutamol PRN
2. + Inhaled corticosteroid (e.g. beclamethasone) if using SABA >1/day
3. + LABA e.g. salmeterol
4. "Consider other options" = trial of leukotriene receptor agonist or oral theophylline
5. add Oral prednisolone, refer to asthma clinic
32
how would you control an acute asthma attack?
100% O2 with facemask.
nebulisers of salbutamol and ipatropium bromide.
IV hydrocortisone/prednisolone.
33
how to beta 2 agonists work?
activate beta 2 receptors, inducing smooth muscle relaxtion in lungs.
34
describe what is happening in the lungs of a patient with extrinsic allergic alveolitis (hypersensitivity pneumonitis)
inhalation of allergens provokes a hypersensitivity reaction, with complement activation, granuloma formation and obliterative bronchiolitis.
35
give 2 causes of EAA (hypersensitivity pneumonitis)
```
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.
```
36
give 3 clinical features of EAA seen after exposure to the allergen
fevers, rigors, myalgia, dry cough, dyspnoea, crackles (no wheeze)
37
give 3 chronic features of EAA
increasing dyspnoea, weight loss, exertional dyspnoea, type I respiratory failure, cor pulmonale
38
what would been seen on CXR of a patient with EAA?
fibrosis/mottling of upper lobes and honeycomb lung
39
list some investigations that might be performed on a patient with EAA
bloods - neutrophilia, raised ESR
CXR.
lung function tests (reversible restrictive).
broncheoalveolar lavage.
40
how would you treat EAA in an acute and a chronic situation?
acute - remove allergen, give O2 + oral prednisolone.
| chronic - avoid exposure (facemask), long-term steroids.
41
list 3 occupational lung diseases
```
EAA (e.g. Farmer's lung).
Coal worker's pneumonconiosis.
Silicosis.
Asbestosis.
Byssinosis.
Berylliosis.
```
42
what causes the fibrosis seen in coal worker's pneumoconiosis?
inhalation of coal dust particles - ingested by macrophages - these die and release their enzymes - fibrosis
43
what would a CXR show in coal worker's pneumoconiosis?
round opacities in upper zone.
44
what causes progressive massive fibrosis? what are the features of this?
progression of coal worker's pneumoconiosis.
| progressive dyspnoea, fibrosis + eventual cor pulmonale.
45
give some examples of jobs at risk of silicosis
metal mining, stone quarrying, sand blasting, pottery/ceramic manufacture
46
what do investigations show in silicosis?
CXR - diffuse miliary/nodular pattern in upper and mid-zones + egg shell calcification of hilar nodes.
Spirometry - restrictive.
47
what disease are patients with silicosis at greater risk of?
TB
48
what are the clinical features of asbestosis?
progressive dyspnoea.
| O/E - clubbing, fine end-inspiratory crackles, pleural plaques.
49
what two diseases are asbestosis patients at greater risk of?
bronchial adenocarcinoma and mesothelioma
50
in what industries might workers get byssinosis? and for berylliosis?
byssinosis - cotton mill workers.
| berylliosis - beryllium-copper alloy used in aerospace industry, electronics, atomic reactors.
51
describe the pathogenesis of bronchiectasis
chronic infection of bronchi/bronchioles leads to inflamed, thickened and irreversibly damaged walls with permanent dilation.
mucociliary transport mechanism is impaired.
52
give 2 of the main organisms involved in bronchiectasis
H influenza, Strep pneumonia, Staph aureus, Pseudomonas aeruginosa
53
give 3 possible causes of bronchiectasis
congenital - CF.
post-infection - measles, pertussis, pneumonia, TB, HIV.
Other - bronchial obstruction (tumour, foreign body), allergic bronchopulmonary aspergillosis (ABPA), hypogammaglobulinaemia, rheumatoid arthritis, UC.
54
give 3 clinical features of bronchiectasis
persistent cough, copious purulent sputum, intermittent haemoptysis, finger clubbing, coarse inspiratory crepitations, wheeze
55
give 2 possible complications of bronchiectasis
pneumonia, pleural effusion, pneumothorax, haemoptysis, cerebral abscess, amyloidosis
56
name 3 investigations you would carry out in bronchiectasis and their results
*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
how would you manage a patient with bronchiectasis?
physiotherapy - postural drainage.
Abx - flucloxacillin for staph, amoxicillin for strep, tazocin for pseudomonas.
bronchodilators - salbutamol nebulisers.
Oral/inhaled corticosteroids.
58
what causes cystic fibrosis?
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
give 3 respiratory symptoms of CF
cough, wheeze, recurrent infections, bronchiectasis, pneumothorax, haemoptysis, respiratory failure, cor pulmonale
60
give 3 extrapulmonary features of CF
pancreatic insufficiency - DM, steatorrhoea.
| intestinal obstruction, gallstones, cirrhosis, male infertility, osteoporosis, arthritis, vasculitis, sinusitis.
61
name 3 investigations you would carry out in CF and their results
sweat test - increased sodium and chloride secretion in sweat.
faecal elastase - screens for pancreatic dysfunction.
genetic screening for CF mutations.
CXR - hyperinflation, bronchiectasis.
62
how would CF be managed?
```
physiotherapy.
Abx for exacerbations.
mucolytics - DNase (dornase alfa).
bronchodilators.
fat soluble vit supplements.
pancreatic enzyme replacement.
```
63
what is sarcoidosis? what genes is it associated with?
multisystem granulomatous disorder of unknown cause.
| associated with HLA-DRB1 and DQB1 alleles.
64
what is seen on transbronchial biopsy in sarcoidosis?
infiltration of alveolar walls and interstitial spaces with mononuclear cells - later, granulomas
65
how does acute sarcoidosis present?
erythema nodosum ± polyarthralgia
66
give 3 pulmonary features of sarcoidosis?
dry cough, progressive dyspnoea, decreased exercise tolerance, chest pain.
67
give 3 extra-pulmonary features of sarcoidosis
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
what are the features of sarcoidosis on CXR?
bilateral hilar lymphadenopathy ± pulmonary infiltrates/fibrosis
69
list some differential diagnoses for bilateral hilar lymphadenopathy
sarcoidosis, infection (TB, mycoplasma), malignancies, silicosis, EAA
70
what investigations would you carry out, apart from CXR, in sarcoidosis, and what might they show?
SERUM ACE is raised.
lung function - restrictive pattern, reduced TLC, reduced FEV1/FVC ratio.
tissue biopsy - non-caseating granuloma.
71
how would you treat sarcoidosis?
if symptomatic - corticosteroids (prednisolone).
| if severe - IV methylprednisolone or methotrexate.
72
what is the underlying pathology of idiopathic pulmonary fibrosis?
disruption of alveolar epithelium and basement membrane activates inflammation.
fibroblasts convert to myofibroblasts - synthesise collagen and aggregate to form fibrotic foci.
73
give 3 symptoms and 3 signs of idiopathic pulmonary fibrosis
symptoms - dry cough, exertional dyspnoea, malaise, weight loss, arthralgia.
signs - cyanosis, finger clubbing, fine end-inspiratory crepitations.
74
what investigations would you carry out in idiopathic pulmonary fibrosis? what do they show? which one is needed for diagnosis?
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
what is the ultimate end treatment of idiopathic pulmonary fibrosis?
lung transplant
76
name 3 causes of pulmonary hypertension
hereditary, SLE, systemic sclerosis, rheumatoid arthritis, drugs, HIV, portal hypertension, schistosomiasis, chronic haemolytic anaemia, COPD, pulmonary fibrosis, mitral valve disease, sarcoidosis
77
define pulmonary hypertension
elevated pulmonary artery pressure (>25mmHg at rest) and secondary right ventricular failure
78
give 3 clinical features of pulmonary hypertension
exertional dyspnoea, lethary, peripheral oedema, loud pulmonary second sound, right parasternal heave
79
give 3 signs that pulmonary hypertension has progressed to right heart failure (cor pulmonale)
elevated JVP, hepatomegaly, pulsatile liver, peripheral oedema, ascites, pleural effusion
80
what is the eventual end treatment of primary pulmonary hypertension?
heart and lung transplant
81
what 3 investigations would you carry out in pulmonary hypertension and what would they show?
CXR - enlarged proximal pulmonary arteries which taper distally.
ECG - RVH, P pulmonale (peaked P waves)
Echo - RV dilation/hypertrophy
82
how would you treat pulmonary hypertension?
warfarin - reduce thrombosis risk.
diuretics - oedema.
oral CCBs - pulmonary vasodilators
sidenafil (PDE5 inhibitor) for primary pulmonary hypertension
83
what is a haemothorax?
blood in the pleural space
84
what is a chylothorax?
chyle (lymph + fat) in the pleural space
85
what is an empyema?
pus in the plerual space
86
what is a pleural effusion? define transudates and exudates
fluid in the pleural space
transudates = low protein content
exudates = high protein content
87
give 3 causes of a transudate pleural effusion
cardiac failure, constrictive pericarditis, fluid overload, cirrhosis, nephrotic syndrome, malabsorption, hypothyroidism.
increased venous pressure and fluid overload.
88
give 3 causes of an exudate pleural effusion
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
what would you hear on auscultation of a patient with a pleural effusion?
on side of the effusion:
| decreased expansion, stony dull percussion note, diminished breath sounds.
90
what investigations would you perform to diagnose a pleural effusion? what would they show?
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
how would you treat a symptomatic pleural effusion?
drain it, repeat if necessary
92
how would you treat recurrent pleural effusion?
pleurodesis with tetracycline, bleomycine or talc.
| smoking cessation.
93
what group of people are most likely to have a spontaneous pneumothorax?
young, thin men - rupture of sub-pleural bulla
94
what is a pneumothorax?
air in pleural space, leading to partial or complete collapse of the lung
95
what is a tension pneumothorax? how does it present?
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
give 3 causes of a pneumothorax
spontaneous, chest trauma, asthma, COPD, TB, pneumonia, lung abscess, carcinoma, cystic fibrosis, lung fibrosis, sarcoidosis, connective tissue disorders (Marfan's, Ehler-Danos)
97
give 3 signs of a pneumothorax
reduced expansion, hyper-resonance to percussion, diminished breath sounds on affected side.
(in tension pneumothorax, trachea deviates away from the affected side)
98
how would you manage a pneumothorax?
chest drain - urgent.
99
give 3 risk factors for bronchus carcinoma
smoking, asbestos, chromium, arsenic, iron oxides, radiation (radon gas)
100
which bronchial carcinoma is more common in non-smokers?
adenocarcinoma
101
what cells do small cell lung cancers arise from? what can be the side effects of this?
endocrine cells (enterochromaffin cells) - carcinoid syndrome - flushing, diarrhoea, hyponatraemia
102
which type of bronchial carcinoma is most likely to cause an obstruction?
squamous cell carcinoma
103
describe the features of a squamous cell bronchial carcinoma
35%.
mostly present as obstructive lesion leading to infection.
occasionally cavitates. local spread common.
widespread metastases occur late.
104
describe the features of an adenocarcinoma of the bronchus
```
27%.
most common lung cancer associated with asbestos exposure.
more common in non-smokers.
usually occurs peripherally.
local and distant metastases.
```
105
what are the features of a large cell bronchial carcinoma?
10%.
| poorly differentiated tumour, metastasizes early.
106
which type of bronchial carcinoma generally has a worse prognosis, NSLC or SCLC?
small cell
107
give 3 symptoms of bronchial carcinoma
cough, haemoptysis, dyspnoea, chest pain
108
give 3 signs of bronchial carcinoma
cachexia, anaemia, clubbing, HPOA (hypertrophic pulmonary osteoarthropathy), supraclavicular or axillary nodes.
chest signs - none, or consolidation/collapse/pleural effusion
109
give 3 examples of signs that there are distant mets in bronchial carcinoma
bone tenderness, hepatomegaly, confusion, fits, focal CNS signs, cerebellar syndrome, proximal myopathy, peripheral neuropathy
110
give 3 local complications of bronchial carcinoma
recurrent laryngeal nerve palsy, phrenic nerve palsy, SVC obstruction, Horner's syndrome, rib erosion, pericarditis, AF
111
give 3 neurological complications of bronchial carcinoma
confusion, fits, cerebellar syndrome, proximal myopathy, neuropathy, polymyositis
112
list the differential diagnoses of a nodule on the lung seen on CXR
malignancy, primary or secondary; abscesses, granuloma, carcinoid tumour, pulmonary hamartoma, arterio-venous malformation, encysted effusion (fluid, blood, pus), cyst, foreign body, skin tumour
113
where do bronchial adenocarcinomas most commonly metastasise to?
mediastinal lymph nodes, brain, bone, adrenals
114
how would you investigate a possible bronchial carcinoma?
sputum and pleural fluid samples for cytology.
CXR.
fine needle aspiration or biopsy.
bronchoscopy, CT, PET.
115
list some possible features of a CXR of a patient with bronchial carcinoma
peripheral nodule, hilar enlargement, consolidation, lung collapse, pleural effusions, bony secondaries (e.g. ribs).
116
what staging system is used for bronchial carcinomas?
TNM.
T = tumour, N = nodes, M = distant metastases.
converted into stage I-IV.
117
how would you treat NSCLC?
peripheral tumours, stageI/II - surgical excision.
or, curative radiotherapy.
more advanced disease = chemo ± radiotherapy
118
how would you treat small cell lung cancer?
may respond to chemo, but will relapse.
cyclophosphamide + doxorubicin + vincristine + etoposide.
OR cisplatin ± radiotherapy.
119
describe some features of palliative care given to patients with bronchial carcinoma
radiotherapy - bronchial obstruction, haemoptysis, bone pain, cerebral mets.
SVC stent + radio - SVC obstruction.
pleural drainage.
analgesia, steroids, antiemetics, codeine for cough etc.
120
name two benign lung cancers
bronchial adenoma, hamartoma
| benign mesothelioma
121
what is the biggest cause of mesothelioma?
occupational ASBESTOS exposure
122
what is mesothelioma?
tumour of mesothelial cells that usually occurs in the pleura
123
how would you diagnose mesothelioma?
CXR/CT - pleural thickening/effusion.
bloody pleural fluid.
histology following thoracoscopy - often only diagnosed postmortem.
124
how would you treat mesothelioma?
chemo - cisplatin + premetrexed
125
what are the two main features of Goodpasture's disease?
acute glomerulonephritis + lung symptoms
126
what are the pulmonary features of Goodpasture's disease?
cough, intermittent haemoptysis, anaemia, upper respiratory tract infecions
127
what investigation would you need to confirm a diagnosis of Goodpasture's disease?
kidney biopsy - crescenteric glomerulonephritis
128
how would you treat Goodpasture's disease?
immunosuppression (corticosteroids) + plasmapheresis to remove antibodies
129
what causes the features of Goodpasture's disease?
anti-glomerular basement membrane antibodies - bind to kidney basement membrane and alveolar membrane
