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Medicine > Respiratory > Flashcards

Respiratory 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 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

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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

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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.

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54
Q

give 3 clinical features of bronchiectasis

A

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

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55
Q

give 2 possible complications of bronchiectasis

A

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

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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.

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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.

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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.

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59
Q

give 3 respiratory symptoms of CF

A

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

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60
Q

give 3 extrapulmonary features of CF

A

pancreatic insufficiency - DM, steatorrhoea. intestinal obstruction, gallstones, cirrhosis, male infertility, osteoporosis, arthritis, vasculitis, sinusitis.

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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.

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62
Q

how would CF be managed?

A

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

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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.

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64
Q

what is seen on transbronchial biopsy in sarcoidosis?

A

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

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65
Q

how does acute sarcoidosis present?

A

erythema nodosum ± polyarthralgia

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66
Q

give 3 pulmonary features of sarcoidosis?

A

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

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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

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68
Q

what are the features of sarcoidosis on CXR?

A

bilateral hilar lymphadenopathy ± pulmonary infiltrates/fibrosis

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69
Q

list some differential diagnoses for bilateral hilar lymphadenopathy

A

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

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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.

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71
Q

how would you treat sarcoidosis?

A

if symptomatic - corticosteroids (prednisolone). if severe - IV methylprednisolone or methotrexate.

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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.

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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.

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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.

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75
Q

what is the ultimate end treatment of idiopathic pulmonary fibrosis?

A

lung transplant

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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

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77
Q

define pulmonary hypertension

A

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

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78
Q

give 3 clinical features of pulmonary hypertension

A

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

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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

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80
Q

what is the eventual end treatment of primary pulmonary hypertension?

A

heart and lung transplant

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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

130
Q

what is Wegener’s granulomatosis also known as?

A

granulomatosis with polyangitis (GPA)

131
Q

what is the characteristic feature of Wegener’s granulomatosis?

A

necrotising granulomatous inflammation and vasculitis of small/medium vessels

132
Q

name 3 respiratory features of Wegener’s granulomatosis

A

cough, haemoptysis, pleuritis, sinusitis, saddle-nose deformity, epistaxis, nasal obstruction

133
Q

name 3 renal features of Wegener’s granulomatosis

A

proteinuria, haematuria, progressive glomerulonephritis

134
Q

name 3 features, other than respiratory/renal features, of Wegener’s granulomatosis

A

skin purpura, peripheral neuropathy, mononeuritis multiplex. eye involvement - keratitis, conjunctivitis, scleritis, episcleritis, uveitis.

135
Q

what would be the significant finding in the blood of Wegener’s granulomatosis patients?

A

ANCA +ve

136
Q

how would you treat Wegener’s granuomatosis?

A

corticosteroids + cyclophosphamide for remission induction. Azathioprine + methotrexate for maintenance.

137
Q

what prophylactic treatment would be given to Wegener’s granulomatosis patients? what does it protect against?

A

Co-trimoxazole. Pneumocystis jivorecii and staphylococcal colonisation.

138
Q

list the possible sources of an embolus

A

FATBAT Fat Air Thrombus Bacteria Amniotic fluid Tumours

139
Q

what is a likely cause of a PE?

A

DVT in pelvis/legs (iliofemoral veins)

140
Q

give 4 risk factors for a PE

A

recent surgery (esp abdo/pelvis or hip/knee replacement). thrombophilia. immobility. malignancy. pregnancy/pill/HRT. previous PE. DVT.

141
Q

list 3 steps taken to prevent PE in surgical patients

A

LMWH (e.g. dalteparin) given to all immobile patients. compression stockings. early mobilisation. stop HRT/Pill pre-op.

142
Q

give 3 symptoms of PE

A

sudden onset dyspnoea, pleuritic chest pain, haemoptysis, dizziness, syncope

143
Q

give 3 signs of PE

A

tachypnoea, pyrexia, cyanosis, tachycardia, hypotension, raised JVP, pleural rub

144
Q

what 2 investigations are carried out to confirm a diagnosis of PE?

A

D dimer - neg result excludes, +ve doesn’t mean it is PE. CTPA (CT pulmonary angiography)

145
Q

how would you manage a patient with a PE?

A

high flow oxygen, LMWH until INR 2-3, then start warfarin/stop heparin. massive PE - thrombolysis (alteplase)

146
Q

what is the usual cause of the common cold? how is this spread?

A

rhinovirus infection. spread by droplets and close personal contact.

147
Q

what 2 organisms usually cause sinusitis?

A

Strep pneumonia or H influenzae

148
Q

how would you treat sinusitis?

A

broad spectrum abx (e.g. co-amoxiclav). topical corticosteroids, steam inhalation.

149
Q

what is the surface of the influenza viruses coated with? what are these needed for?

A

haemaglutinin (H) and neuraminidase - needed for attachment to host respiratory epithelium.

150
Q

give 3 clinical features of influenza

A

abrupt onset fever, generalised aching of limbs, severe headache, sore throat and dry cough

151
Q

how would influenza be managed? what complication is the patient at risk of?

A

symptomatic - paracetamol, fluids, rest. pneumonia.

152
Q

name 3 organisms that can cause community acquired pneumonia

A

common - *strep pneumoniae, H influenzae, Mycoplasma pneumoniae. also - staph aureus, Legionella spp, Moraxella catarrhalis and Chlamydia.

153
Q

define nosocomial pneumonia

A

aka hospital-acquired. pneumonia acquired >48h after admission to hospital

154
Q

name some common causative organisms of hospital acquired pneumonia

A

Gram -ve enterobacteria or *Staph aureus. also - Pseudomonas, Klebsiella, Bacterioides, Clostridia.

155
Q

name 3 organisms that may cause pneumonia in immunocompromised patients

A

Strep pneumoniae, H influenzae, Staph aureus, M catarrhalis, M pneumonia, Gram -ve bacilli, Pneumocystic jivorecii.

156
Q

give 3 symptoms of pneumonia

A

fever, rigors, malaise, anorexia, dyspnoea, cough, purulent sputum, haemoptysis, pleuritic pain

157
Q

give 3 signs of pneumonia

A

pyrexia, cyanosis, confusion, tachypnoea, tachycardia, hypotension, signs of consolidation

158
Q

name 3 signs of lung consolidation you might find on examination

A

diminished expansion, dull percussion note, increased tactile vocal resonance, bronchial breathing + pleural rub

159
Q

list 3 differential diagnoses of pneumonia

A

PE, pulmonary oedema, pulmonary haemorrhage, bronchial carcinoma, hypersensitivity pneumonitis

160
Q

if a pneumonia patient was found to have a pleural effusion, what type would it be?

A

exudate - high protein

161
Q

what investigations might you perform in a case on pneumonia?

A

CXR - lobar infiltrates, cavitation or pleural effusion. blood tests and cultures. sputum MC&S. pleural fluid aspiration - MC&S.

162
Q

what are the components of the CURB-65 score?

A

Confusion Urea >7mmol/L Resp rate >30/min BP >65yo 0-1 home treatment 2 hospital treatment 3+ - severe mortality risk, consider ITU

163
Q

how would you treat a case of mild community acquired pneumonia? (CURB 1)

A

oral amoxicillin or erythromycin/clarithromycin if allergic.

164
Q

how would you treat a case of severe community-acquired pneumonia? (CURB >2)

A

IV cefuroxime / co-amoxiclav

165
Q

give 3 potential complications of pneumonia?

A

pleural effusion, empyema, lung abscess, respiratory failure, septicaemia, brain abscess, pericarditis, myocarditis, cholestatic jaundice

166
Q

which at risk groups are given the pneumococcal vaccine to protect against pneumonia? (apart from childhood imms)

A

>65yo. chronic heart/liver/renal/lung conditions. DM. immunosuppression. AIDS. those on chemo/prednisolone.

167
Q

name the causative organism of TB and how it can be transmitted

A

Mycobacterium tuberculosis/bovis. airborne - poor sanitation, overcrowding, coinfection with HIV

168
Q

how would you stain for the causative organisms on TB? what would they look like? what culture medium would be used?

A

Ziehl-Neelsen stain. Acid-fast bacilli (bright red). Lowenstein-Johnston medium.

169
Q

describe the typical granulomatous lesions of TB

A

central areas of CASEATION surrounded by epithelioid cells and Langhan’s giant cells

170
Q

give 3 features of pulmonary TB

A

cough, sputum, malaise, weight loss, night sweats, pleurisy, haemoptysis, pleural effusion

171
Q

what is miliary TB?

A

occurs following haematogenous dissemination of primary TB

172
Q

describe the features of miliary TB

A

nonspecific, overwhelming signs. nodular opacities on CXR. retinal disease. biopsies of lung/liver/lymph nodes or marrow show AFB or granuloma.

173
Q

give 3 GU features of TB

A

dysuria, frequency, loin pain, haematuria, sterile pyuria

174
Q

give 1 bone feature of TB

A

vertebral collapse. Pott’s vertebra.

175
Q

give 2 abdominal features of TB

A

peritonitis, GI upset.

176
Q

give 3 signs of TB seen on CXR

A

consolidation, cavitation, fibrosis, calcification

177
Q

describe 3 different methods of testing for TB

A

Mantoux test - tuberculin sensitivity skin test - identifies latent TB, active TB and BCG exposure. Quantiferon TB gold (IFN gamma test). MC&S for AFB of 3+ sputum samples (also pleural fluid, urine, pus ascites etc). PCR - for identifying drug resistance.

178
Q

how would you treat TB?

A

isoniazid, rifampicin, pyrazinamide and ethambutol for 2mths. then isoniazid and rifampicin for 4 further months. DOTS - directly observed therapy to ensure compliance + avoid resistance.

179
Q

give 1 main side effect of each of the drugs used to treat TB

A

rifampicin - orange urine/tears, inactivation of Pill, flu symptoms. isoniazid - neuropathy, low WCC. ethambutol - optic neuritis. pyrazinamide - hepatitis, arthralgia.

180
Q

how do steroids work to help in an asthma attack?

A

corticosteroids inhibit phospholipase A2 - this inhibits the inflammatory cascade, so dampening down the inflammatory reaction that occurs in an asthma attack

181
Q

anti-muscarinics are used in severe asthma, what is their mechanism of action? what cardiac drug also works in a similar way?

A

blocks the muscarinic ACh receptors (competitive inhibition of ACh) - causes smooth muscle relaxation. atropine also acts on these receptors.

182
Q

why are beta-blockers CI in asthmatics?

A

beta-blockers can act on the beta2 receptors within the bronchi - blocking them induces bronchospasm, causing an asthma attack/worsening.

183
Q

why in type 2 respiratory failure do you not start the patient immediately on high flow O2? what respiratory disease is this common in?

A

common in COPD. px with type 2 resp failure is hypoxic but hypercapnic due to alveolar hypoventilation. due to chronic high CO2, body becomes desensitised to CO2 and so relies on hypoxic drive to breathe - if you raise their oxygen levels too quickly, they will lose this drive to breathe.

184
Q

how do antihistamines work?

A

block the H1 receptor, blocking the effects of excess histamine, which is usually released from mast cells in response to an antigen to induce features of immediate type 1 hypersensitivity.

185
Q

give 2 examples of antihistamines

A

cetirizine, loratadine, fexofenadine, chlorphenamine.

186
Q

give 2 examples of antimuscarinics used as bronchodilators

A

ipratropium, tiotropium, glycopyrronium

187
Q

give an example of a short-acting beta2 agonist and a long-acting beta2 agonist

A

SABA - salbutamol LABA - salmeterol, formoterol

188
Q

how do beta2 agonists work to improve asthma symptoms?

A

stimulate G protein coupled beta 2 receptors found in smooth muscle of bronchi and blood vessels - activates a signalling cascade leading to smooth muscle relaxation. airflow in constricted airways is improved.

189
Q

give some possible side effects of beta2 agonists

A

tachycardia, palpitations, tremor - activation of ‘fight or flight’ receptors

190
Q

give some examples of inhaled corticosteroids

A

beclometasone, budesonide, fluticasone

191
Q

how do inhaled corticosteroids work in COPD/asthma?

A

corticosteroids pass through the plasma membrane and interact with receptors in the cytoplasm. activated receptor passes into nucleus to modify transcription of lots of genes. downregulates pro inflammatory interleukins, cytokines and chemokines, upregulates anti inflammatory proteins. reduces mucosal inflammation, widens the airways, reduces mucus secretion.

192
Q

what class of drug is theophylline?

A

xanthine = non-selective phosphodiesterase inhibitors

193
Q

how does theophylline work?

A

a competitive non-selective phosphodiesterase inhibitor - inhibits leukotriene synthesis (major cause of bronchiole inflammation) - reduces inflammation and immunity

194
Q

give an example of a leukotriene receptor antagonist

A

montelukast, zafirlukast

195
Q

how do leukotriene receptor antagonists work to improve asthma symptoms?

A

block action of leukotrienes on the CsyLT1 receptor on bronchial smooth muscle cells and mast cells - blocks the effects of leukotrienes such as inflammation, mucous secretion, bronchoconstriction

196
Q

give some examples of indications for mucolytic inhalers/nebulisers

A

treatment of abnormal, sticky or thick mucous secretions - chronic emphysema, bronchitis, pneumonia, CF, COPD

197
Q

how do mucolytics work? name an example.

A

acetylcysteine. dissolve thick mucus by splitting disulphide chemical bonds between mucoproteins in secretions, and lowers viscosity by altering the mucin containing components.

198
Q

give 2 examples of obstructive lung diseases

A

COPD asthma

199
Q

give 2 examples of restrictive lung diseases

A

interstitial fibrosis sarcoidosis pneumoconiosis interstitial pneumonias connective tissue diseases pleural effusion obesity kyphoscoliosis neuromuscular problems

200
Q

how would you treat a case of hospital-acquired pneumonia?

A

gentamicin IV + antipseudomonal penicillin (e.g. piperacillin) IV or cefotaxime (3rd gen cephalosporins)

Medicine (14 decks)

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