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1 - Finals > Respiratory > Flashcards

Respiratory Flashcards

1
Q

what two types of disease are included within the definition of COPD?

A

emphysema and chronic bronchitis it’s chronic obstruction with *irreversible airflow obstruction –> air trapping and hyperinflation

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2
Q

define chronic bronchitis

A

narrowing of airways and mucosal oedema –> mucus hypersecretion –> cough + excessive mucus = persistent cough+mucus 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, occupational exposure (particles and gases) alpha-1 antitrypsin deficiency

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5
Q

what generally causes early-onset COPD?

A

alpha-1 antitrypsin deficiency - produced in liver.

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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

elastin breakdown –> dilation and destruction of alveoli - 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 they retain CO2 making it normal, will be old and thin, using accessory muscles

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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. peripheral oedema and overweight from RHF.

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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 Rx = LTOT + loop diuretic

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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, barrel chest, 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 (pneumococcal vaccine + yearly flu jab) cor pulmonale (RHF secondary to long standing lung disease/COPD) resp. failure *depression polycythaemia, 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? other Ix?

A

reduced FEV1/FVC ratio (obstruction = FEV1/FVC <0.7) - NON-reversible, reduced PEFR. raised TLC. obstructive pattern. CXR = see other card for findings FBC - ?polycythaemia sputum culture if ?IECOPD ABG - hypoxia ± hypercapnia

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20
Q

what might you see on CXR in a COPD patient?

A

flattened diaphragm increased intercostal spaces hyperlucent lungs increased AP diameter

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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

ALMOST DEFS NEW GUIDELINES HERE - LOOK UP + LEARN don’t forget lifestyle/education etc 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 (LTOT).

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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 - suppression of natural development of immune system

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28
Q

what is asthma? briefly explain the pathophysiology

A
  • chronic inflammatory airway disease with intermittent obstruction and hyperreactivity - inflammation –> constriction, oedema, mucus hypersecretion - chronically this –> airway remodelling, airway hyperresponsiveness - acute = bronchoconstriction, chronic = airway hyperresponsiveness, airway remodelling = persistent obstruction - linked to IgE and mast cells - allergen triggers release of histamine, leukotrienes and TNFa - increased vascular permeability + hypersecretion of mucus = airway oedema - increased airway tone + smooth muscle responsiveness - later it’s eosinophil mediated - increased goblet sells etc.
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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%. reversibility testing - increase in PEF or FEV1 >15% after salbutamol. spirometry = FEV1 <80% + FEV1/FVC = < 70% CXR = normal or hyperinflation skin prick test if want to test allergens

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31
Q

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

A

GUIDELINES HAVE ALMOST DEFINITELY CHANGED - LOOK UP AND LEARN THE NEW ONES aim for good control on minimal medication, FEV1 and PEFR >80% predicted 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 manage an acute asthma attack?

A

OSHITME O2 (aim 94-98% sats) Salbutamol nebs Hydrocortisone IV (or oral pred if mild) Ipatropium bromide nebs with senior help: Theophylline Magnesium Escalate/ITU

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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

dry cough, progressive dyspnoea. O/E - clubbing, diffuse, fine end-inspiratory crackles, pleural plaques. CT = ground glass opcaities.

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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 - reticular shadowing, decreased lung volume, bilateral lower zone HRCT = ground glass opacification, honeycombing if severe, reticular pattern. lung function tests - restrictive pattern, increased FEV1/FVC ratio. need a lung biopsy to diagnose **ask them about occupation!*

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75
Q

management of idiopathic pulmonary fibrosis

A

MDT! 6/12 assessment for pulmonary rehab. supportive = O2 therapy, physio, exercise/wt loss, vaccinations, smoking cessation. pirfenidone = antifibrotic drug, inhibits TGFB (transforming growth factor beta) collagen synthesis. acute exacerbation = admit, high dose pred ± cytotoxic, check for infective cause. lung transplant if extreme median survival only 2-5yrs!

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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

disease of small pulmonary arteries characterised by vascular proliferation and remodelling - progressive increase in pulmonary vascular resistance. elevated pulmonary artery pressure (mean pulmonary artery pressure >25mmHg at rest, pulmonary capillary wedge pressure <15mmHg) poor prognosis as most get secondary right ventricular failure (cor pulmonale) types = idiopathic, hertable, secondary.

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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. Graham Steel murmur = pulmonary regurg murmur (high pitched early diastolic) RHF signs (oedema, RV heave, ascites, pulsatile hepatomegaly, raised JVP)

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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 (pruning) ECG - RVH, P pulmonale (peaked P waves) transthoracic echo - RV dilation/hypertrophy r heart catheterisation (Swan-Ganz) - measures pressures.

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82
Q

how would you treat pulmonary hypertension?

A

CCB (nifedipine or amlodipine) or sildenafil (PDE5 inhibitor, augments pulmonary vascular response to nitric oxide) warfarin (target INR 21.5-2.5) - reduce thrombosis risk. furosemide/salt reduction - oedema. lifestyle - low level, graded exercise. supp. O2 if needed.

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83
Q

what is a haemothorax?

A

blood in the pleural space

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84
Q

what is a chylothorax?

A

chyle (lymph + fat) in the pleural space

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85
Q

what is an empyema?

A

pus in the plerual space

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86
Q

what is a pleural effusion? define transudates and exudates

A

excessive fluid in the pleural space (potential space between visceral and parietal pleura) transudates = low protein content (< 30g/L) exudates = high protein content (>30)

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87
Q

give 3 causes of a transudate pleural effusion

A

cardiac failure, constrictive pericarditis, fluid overload, cirrhosis, nephrotic syndrome, Meig’s synd (R pleural effusion + ovarian fibroma + ascites) increased venous pressure and fluid overload = disruption of hydrostatic and oncotic forces across pleural membranes (hypoproteinaemia can cause it too)

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88
Q

give 3 causes of an exudate pleural effusion

A

pneumonia, TB, rheumatoid arthritis, SLE, bronchogenic carcinoma, malignant metastases, lymphoma, mesothelioma, lymphangitis carcinomatosis. Dressler’s synd (comp. of MI) increased permeability of pleural capillaries secondary to infection, inflammation or malignancy.

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89
Q

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

A

on side of the effusion: unilateral reduced chest expansion, stony dull percussion note, diminished breath sounds. if really large effusion - trachea deviates away.

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90
Q

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

A

CXR - small effusions= blunted costophrenic angles. larger = water-dense shadows with concave upper borders. 200ml effusion visible on PA, 50ml on lateral view. diagnostic pleural aspiration/thoracocentesis (US guided) - send for clinical chemistry, bacteriology and cytology. (if unilateral and clinical picture suggests transudate just Rx cause instead of bothering with aspirating)

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91
Q

how would you treat a symptomatic pleural effusion?

A

pleural tap, repeat if necessary - up to 1.5l (otherwise fluid shift + pulmonary oedema). can use chest drain for controlled removal. don’t tap if transudates!!

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92
Q

how would you treat recurrent pleural effusion?

A

pleurodesis with tetracycline, bleomycine or talc. smoking cessation. recurrence is likely in malignancy.

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93
Q

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

A

young, thin men - usually traumatic. *marfan’s! smoking/FHx increases risk. secondary spontaneous PTX = pre-existing lung disease (COPD - bullae), CF, TB, PCP

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, can also get distended neck veins, resp/ distress)

98
Q

initial Rx of pneumothorax??

A

16-18G cannula in 2nd IC space, mid clavicular line!!!!! aim for just above a rib rather than just below to avoid neurovascular bundle! ± chest drain + admit after.

99
Q

give 3 risk factors for lung carcinoma

A

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

100
Q

which lung 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 lung carcinoma is most likely to cause an obstruction?

A

squamous cell carcinoma

103
Q

describe the features of a squamous cell lung carcinoma

A

20%. central airways. present as obstructive lesion ± leading to infection. local spread common, well differentiated cells. widespread metastases occur late.

104
Q

describe the features of an adenocarcinoma of the lung

A

40%. peripheral lung. most common lung cancer associated with asbestos exposure. more common in non-smokers. local invasion and distant metastases common (brain, adrenal bone). cancer of mucus cells in bronchial epithelium.

105
Q

what are the features of a large cell lung carcinoma?

A

10%. central airways. 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 lung cancer

A

cough + haemoptysis (new or persistent) + dyspnoea = requires imaging chest pain wt loss, fatigue etc.

108
Q

give 3 signs of lung cancer

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 lung cancer

A

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

110
Q

give 3 local complications of lung cancer

A

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

111
Q

give 3 neurological complications of lung cancer

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 lung adenocarcinomas most commonly metastasise to?

A

mediastinal lymph nodes, brain, bone, adrenals

114
Q

how would you investigate a possible lung cancer?

A

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

115
Q

list some possible features of a CXR of a patient with lung cancer

A

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

116
Q

what staging system is used for lung cancer?

A

TNM. T = tumour, N = nodes, M = distant metastases. converted into stage I-IV. ?? need to learn staging?

117
Q

how would you treat NSCLC?

A

peripheral tumours, stageI/II - surgical excision/lobar resection (lobectomy) or pneumonectomy + hilar/mediastinal LN sampling. pre-op cisplatin chemo. or, curative radiotherapy (stages 1-3). stage 3 or 4 = chemo ± radiotherapy (cisplatin based + bevacizumab)

118
Q

how would you treat small cell lung cancer?

A

may respond to chemo, but will relapse. no surgical option. chemo = cisplatin + etoposide for 4-6 cycles. ± radio ± prophylactic cranial irradiation.

119
Q

describe some features of supportive/palliative care given to patients with lung cancer

A

breathlessness = opiate obstruction = external beam radiotherapy pleural effusion = aspiration/drainage cough = opiate hoarseness = ENT SVCO = chemo + radio bony pain = radio Spinal cord compression = DEX! mouth care, pain killers etc 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 usually see it in men aged 60-90.

122
Q

what is mesothelioma?

A

aggressive epithelial neoplasm - of mesothelial cells, almost always pleural.

123
Q

investigations for mesothelioma?

A

CXR/CT - irregular pleural thickening/effusion, pleural plaques, unilateral pleural effusion. bloody pleural fluid. thoracocentesis - exudate with malignant cells. pleural biopsy - epithelioid mesothelioma clinical - dry cough, dyspnoea, digital clubbing + pleuritic chest pain = also recurrent pleural effusions. Hx of asbestos exposure.

124
Q

how would you treat mesothelioma?

A

operable (only curative if stage 1) = surgery + (neo)adjuvant chemo (cisplatin usually) ± radiotherapy. extrapleural pneumonectomy or pleurectomy can help pain/effusion, as can pleurodesis inoperable = chemoradiotherapy survival is usually only a year - entitled to compensation.

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

how does asthma present? what qus should you ask?

A

recurrent wheezing, breathlessness, chest tightness, coughing worse at night and early in morning wheeze = polyphonic + expiratory Fhx - atopy/nasal polyposis. in past 4 wks, how often have you: - felt SOB? - been woken from sleep? - used reliever - missed school/work etc? - how do you rate your asthma control? questionnaire = asthmas control questionnaire. *CHECK INHALER TECHNIQUE

131
Q

how do you classify an acute asthma exacerbation (severity)?

A

moderate = PEF 50-75%, increasing symptoms severe = any one of: PEF 33-50%, RR>25, HR>110, inability to complete sentences life threatening = any one of: PEF <33%, SpO2 <92%, PaO2<8kPa, silent chest, signs of exhaustion/poor resp effort, altered consciousness

132
Q

what is Wegener’s granulomatosis also known as?

A

granulomatosis with polyangitis (GPA)

133
Q

what is the characteristic feature of Wegener’s granulomatosis?

A

necrotising granulomatous inflammation and vasculitis of small/medium vessels

134
Q

name 3 respiratory features of Wegener’s granulomatosis

A

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

135
Q

name 3 renal features of Wegener’s granulomatosis

A

proteinuria, haematuria, progressive glomerulonephritis

136
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.

137
Q

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

A

ANCA +ve

138
Q

how would you treat Wegener’s granuomatosis?

A

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

139
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.

140
Q

list the possible sources of an embolus

A

FATBAT

Fat Air Thrombus Bacteria Amniotic fluid Tumours

141
Q

what is a likely cause of a PE?

A

DVT in pelvis/legs (iliofemoral veins)

142
Q

give 4 risk factors for a PE/DVT

A

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

143
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.

144
Q

how does PE present?

A

pleuritic chest pain, SOB, tachypnoeic, cough, can get fever

  • if massive can be shocked/collapsed/peri-arrest, acute RHF, sudden death
  • signs = pleural rub, tachypnoeic, tachycardic, elevated JVP, hypoxia, shock

DDx = ACS, aortic dissection (if you anticoag they’ll die!), PTX

145
Q

what investigations are carried out in PE?

A

D dimer - neg result excludes, +ve doesn’t mean it is PE (use Wells score)

CTPA (CT pulmonary angiography) = diagnostic, if available

CXR = decreased vascular markings, atelactasis, small pleural efusion, wedge shape infarction = late sign

ABG = reduced PaO2, high lactate

ECG = sinus tachy, S1Q3T3 (?), RBBB

146
Q

how would you manage a patient with a PE?

A

if CTPA available immediately do that

100% oxygen, IV access, morphine

anticoagulate (according to trust guidelines!)

haemodynamically stable = LMWH (dalteparin) or fondaparinus (10a inhibitor - give for 5 days or until INR > 2 for 24hrs if active cancer (whichever is longest); give LMWH for 6/12 for everyone else!

massive PE - thrombolysis (alteplase)

if can’t be on dalteparin for 6/12 then do 3/12 warfarin

147
Q

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

A

rhinovirus infection. spread by droplets and close personal contact.

148
Q

what 2 organisms usually cause sinusitis?

A

Strep pneumonia or H influenzae

149
Q

how would you treat sinusitis?

A

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

150
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.

151
Q

give 3 clinical features of influenza

A

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

152
Q

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

A

symptomatic - paracetamol, fluids, rest. pneumonia.

153
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.

154
Q

define nosocomial pneumonia

A

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

155
Q

name some common causative organisms of hospital acquired pneumonia

A

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

156
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.

157
Q

give 3 symptoms of pneumonia

A

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

158
Q

give 3 signs of pneumonia

A

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

159
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

160
Q

list 3 differential diagnoses of pneumonia

A

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

161
Q

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

A

exudate - high protein

162
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.

163
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

164
Q

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

A

oral amoxicillin or erythromycin/clarithromycin if allergic.

165
Q

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

A

IV cefuroxime / co-amoxiclav

166
Q

give 3 potential complications of pneumonia?

A

septic shock

ARDS - non-cardiogenic pulmonary oedema

pleural effusion (50%) or empyema

lung abscess, respiratory failure, brain abscess, pericarditis, myocarditis, cholestatic jaundice

167
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.

168
Q

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

A

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

169
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.

170
Q

describe the typical granulomatous lesions of TB

A

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

171
Q

give 3 features of pulmonary TB

A

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

172
Q

what is miliary TB?

A

occurs following haematogenous dissemination of primary TB

173
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.

174
Q

give 3 GU features of TB

A

dysuria, frequency, loin pain, haematuria, sterile pyuria

175
Q

give 1 bone feature of TB

A

vertebral collapse. Pott’s vertebra.

176
Q

give 2 abdominal features of TB

A

peritonitis, GI upset.

177
Q

give 3 signs of TB seen on CXR

A

consolidation, cavitation, fibrosis, calcification

178
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.

179
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.

180
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.

181
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

182
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.

183
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.

184
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.

185
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.

186
Q

give 2 examples of antihistamines

A

cetirizine, loratadine, fexofenadine, chlorphenamine.

187
Q

give 2 examples of antimuscarinics used as bronchodilators

A

ipratropium, tiotropium, glycopyrronium

188
Q

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

A

SABA - salbutamol LABA - salmeterol, formoterol

189
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.

190
Q

give some possible side effects of beta2 agonists

A

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

191
Q

give some examples of inhaled corticosteroids

A

beclometasone, budesonide, fluticasone

192
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.

193
Q

what class of drug is theophylline?

A

xanthine = non-selective phosphodiesterase inhibitors

194
Q

how does theophylline work?

A

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

195
Q

give an example of a leukotriene receptor antagonist

A

montelukast, zafirlukast

196
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

197
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

198
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.

199
Q

give 2 examples of obstructive lung diseases

A

COPD asthma

200
Q

give 2 examples of restrictive lung diseases

A

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

201
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)

202
Q

what genes are involved in asthma?

A

ADAM 33 = airway hyper-responsiveness

PHF 11 = IgE production (atopy)

203
Q

drug cautions for asthma?

A

beta blockers - blocking B2 receptors can cause airway constriction

NSAIDs/aspirin - block COX1 = decrease in prostaglandins + overproduction of pro-inflammatory leukotrienes

204
Q

what’s the difference between type 1 and type 2 resp. failure?

A

T1 = PaO2 < 8, normal CO2 = ventilation/perfusion mismatch

T2 = PaO2 < 8 + PaCO2 < 6 = alveolar hypoventilation

205
Q

outline the classification of COPD severity

A

mild: FEV1 > 80%
mod: FEV1 = 50-80%
severe: FEV1 = 30-50%
v. severe: FEV1 < 30%

206
Q

what organisms tend to be responsible for an IECOPD?

A

H. influenzae

S. pneumonia

M. catarrhalis

207
Q

management of an exacerbation of COPD?

A

SABA + SAMA nebs (salbutamol + ipratropium) + O2 (24% venturi aiming for 88-92%)

oral pred - prevents recurrence (ask how many hosp admissions/steroid courses when assessing severity of COPD!)

airway clearance - mucolytics/physio

?BIPAP if resp. insufficiency

Ix = blood/sputum culture

ABX:

community = amox or doxy

hosp = ?IV vancomycin or tazocin

extras = oral theophylline, mucolytics, LTOT, furosemide if HF

208
Q

learn spirometry graphs!!

A
210
Q

list some genetic risk factors for DVT/PE

A

factor V leiden

protein C deficiency

protein S deficiency

antithrombin deficiency

antiphospholipid

211
Q

what is Virchow’s triad?

A

the 3 things that –> thrombosis:

  • venous stasis
  • vessel injury
  • activation of clotting system (hypercoagulable state)
212
Q

how does DVT present? what clinical tool and what marker do we use in assessing them?

A

unilateral calf swelling + pain along deep venous system, asymmetric oedema, collateral superficial veins

marker = D-dimer (but not v. specific as also an acute phase protein)

Well’s score.

213
Q

what are the components of the Wells’ score?

A

clinical signs of DVT = 3

HR >100 = 1.5

recent surgery/immobilisation = 1.5

prev. PE or DVT = 1.5

haemoptysis = 1

malignancy = 1

alternative diagnosis more likely than PE = -3

(there’s lots of different versions though)

PE unlikely if <4

214
Q

what’s the algorithm for investigating DVT according to the Wells’ score?

A

(1) Wells 0 or 1 = do D-dimer, if +ve go to (2), if -ve DVT excluded
(2) Wells 2+ = do venous duplex USS if available within 4hrs, if not do D-dimer + 24hrs oral anticoagulation and go to (4)
(3) if venous USS +ve treat as DVT, if -ve repeat at 6-8 days
(4) do venous duplex USS in <24hrs, if +ve treat, if -ve and D-dimer -ve can exclude, if -ve but +ve D-dimer repeat at 6-8 days.

215
Q

what are the 4Ds for the presentation of pulmonary fibrosis?

A

dry cough, dyspnoea, digital clubbing, diffuse inspiratory crackles

216
Q

what is pulmonary fibrosis?

A

restrictive lung disease caused by interstitial lung damage and fibrosis leading to decreased compliance - part of the interstitial lung diseases

FVC low, FEV1/FVC high (>1)

interstitium = the area between the alveoli and the capillary basement membrane

217
Q

give some possible causes of pulmonary fibrosis

A
  • connective tissue diseases = RA, SLE, Sjogrens
  • occupational exposure = asbestos, coal dust, silica
  • drugs = amiodarone, bleomycin, MTX
  • inhalation of irritants = hypersensitivity pneumonitis, birds, mould
  • radiation

*idiopathic pulmonary fibrosis

218
Q

what are the mnemonics for causes of upper vs lower lung fibrosis?

A

upper = ESCHART (granulomatous diseases)

  • Extrinsic allergic alveolitis
  • Sarcoidosis/silicosis
  • Coal worker’s pneumoconiosis
  • Histiocytosis X
  • Ankylosing spondylitis
  • Radiotherapy
  • TB

lower = RASCO (systemic diseases)

  • RA
  • Asbestosis
  • Systemic sclerosis/SLE
  • Cryptogenic fibrosing alveolitis
  • Other (drugs)
219
Q

what proportion of people with a pleural effusion is due to malignancy? what cancers cause pleural effusion?

A

benign x2 more likely than malignant cause.

40% = lung mets, 25% = breast mets, 10% = malignant mesothelioma

220
Q

describe the appearance of pleural effusion aspirate related to different types of cause

what about what different pH and glucose levels imply?

A

clear/straw = transudate or exudate

turbid/yellow = empyema, parapneumonic

haemorrhagic = haemothorax - malignancy, PE, trauma.

pH - normal = 7.6, <7.2 = empyema, RA, SLE, TB, malignancy

glucose <3.3 = empyema, RA, SLE, TB, malignancy

221
Q

give some causes of bilateral hilar lymphadenopathy

A

TIMES

TB

Inorganic dust - silicosis, berylliosis

Malignancy - lymphoma, carcinoma, mediastinal

EAA e.g. bird fanciers’ lung

Sarcoidosis

222
Q

CXR findings for PTX/T-PTX?

A

should be clinical diagnosis!!!!

  • visceral pleural line identified, dark area with no lung markings ± evidence of causative process

for T-PTX = as above + increased intercostal space + contralateral mediastinal shift + depression of hemidiaphragm

223
Q

what is the “safe triangle” for chest drain insertion?

A

between lateral border pec major, ant. border lat. dorsi, and horizontal line at nipples.

place at mid-axillary line, IC space 4-6 - give pain relief!

224
Q

apart from needle thoracotomy/chest drain, how do you manage a PTX?

A

high flow oxygen.

± admit

if recurrent defs admit.

if/on discharge home - follow up OPD 2-4/52 for r/v - avoid strenuous exercise.

225
Q

list the DDx to consider in a pleuritic chest pain presentation

A

ACS, aortic dissection, PTX, PE, pneumonia, malignancy.

226
Q

what are the different types of lung cancer?

A

small cell (SCLC) - least common, 15%

non-small cell (NSCLC) = 85%:

  • adenocarcinoma
  • squamous cell carcinoma
  • large cell carcinoma

lung cancer = 1/3 of all cancer deaths!

227
Q

two week wait criteria for ?lung cancer?

A

>40yrs + 2 of:

  • cough, fatigue, SOB, chest pain, weight loss, appetatie loss

(or 1+smoker)

228
Q

what are “paraneoplastic features” and give examples of them for different types of lung cancer

A

= set of symps/signs that’s due to cancer but NOT due to mass effect.

Small cell = SIADH (hypoNa), ACTH (HTN, hyperglycaemia, hypoK), Lambert-Eaton Syndrome (muscle weakness that improves with muscle contraction - NMJ thing)

Squamous cell = PTH-rp secreation (bone pain + hyperCa2+), clubbing, hyperthyroidism

Adenocarcinoma - gynaecomastia

229
Q

what’s a Pancoast tumour?

A

local invasion of brachial plexus (in lung cancer) –> weakness, parasthesia, pain in C8-T1, shoulder pain.

230
Q

give some features of a lung cancer presentation that are due to local invasion etc

A

Pancoast tumour

Horner’s synd - invasion of sympathetic chain = ptosis, miosis, ipsilateral anydrosis

Hoarseness - invasion/mass effect on recurrent laryngeal nerve

mediastinal invasion/shift –> dysphagia, arrhythmia, facial swelling (SVC compression)

brain mets = seizures or N&V

231
Q

where do lung cancers usually metastasise to? also what lymph nodes are up in lung cancer?

A

liver, bones, brain, adrenals

LNs = hilar, mediastinal, supraclavicular

1 - Finals (15 decks)

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