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Phase 2a Medicine > Respiratory > Flashcards

Respiratory Flashcards

1
Q

COPD

A

A chronic lung condition characterised by breathlessness due to poorly reversible and progressive airflow obstruction.

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2
Q

epidemiology of COPD

A

Very common disease with a prevalence of 1-4% of the population
Mostly a disease of middle-aged to elderly adult smokers.

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3
Q

aetiology of COPD

A

85% of cases are caused by smoking
Most of the remainder are attributable to previous workplace exposure to dusts and fumes
A very small number are related to α1-antitrypsin deficiency

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4
Q

pathology of COPD

A

Inflammation and scarring of small bronchioles are thought to be the main source of airflow obstruction.
Imbalance of proteases and antiproteases causes destruction of the lung parenchyma with dilation of terminal airspaces (emphysema) and air trapping
Mucous gland hyperplasia and irritant effects of smoke causes productive cough (chronic bronchitis).

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5
Q

Clinical manifestations of COPD

A

Sudden onset of exertional breathlessness on a background of prolonged cough and sputum production
Dyspnoea
Wheeze
Spirometry shows lowered forced expiratory volume in FEV1 and FEV1/ forced vital capacity ratio
FEV1/FVC <70, FEV1 <80
Cyanosis
Cor pulmonale

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6
Q

Traditional division of COPD patients

A

Pink puffers and blue bloaters

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7
Q

pink puffer presentation

A

Have raised alveolar ventilation, a near normal PaO2 and a normal or low PaCO2.
They are breathless but are not cyanosed
They may progress to type I respiratory failure

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8
Q

blue bloaters presentation

A

Have lowered alveolar ventilation, with a low PaO2 and a high PaCO2.
They are cyanosed but not breathless and may go on to develop cor pulmonale.
Their respiratory centres are relatively insensitive to CO2 and they rely on hypoxic drive to maintain respiratory effort.

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9
Q

1st line investigations for COPD

A

Spirometry (FEV1/FVC < 0.7 = shows obstruction. Overall lung capacity is better than their ability to forcefully expire air quickly).
DLCO (diffusion capacity of CO across lung. COPD = low). Pulse oximetry (low O2)
Chest x-ray (hyperinflation, exclude lung cancer/other pathology)
ABG (type 2 respiratory failure – raised pCO2, low pO2).
FBC (chronic hypoxia > polycythaemia). BMI (weight loss - lung cancer). ECG. Serum alpha-1-antitrypsin levels. Sputum culture.

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10
Q

gold standard investigation for COPD

A

Clinical presentation + spirometry (FEV1/FVC <0.7 = obstruction. Bronchodilator irreversible = COPD. Bronchodilator reversible = asthma)

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11
Q

Features of Chronic bronchitis

A

clinical diagnosis. Daily productive cough for 3+ months, in at least 2 consecutive years. Hypertrophy and hyperplasia of mucous glands, chronic inflammation cells infiltrate bronchi > hypersecretion, ciliary dysfunction, luminal narrowing

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12
Q

Features of emphysema

A

pathological diagnosis. Permanent enlargement and destruction of airspaces distal to the terminal bronchiole. Destruction of elastin layer causes trapped air distal to blockage (large air sacs = bullae).

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13
Q

What is centriacinar emphysema

A

respiratory bronchioles only, smokers.

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14
Q

what is panacinar emphysema

A

A1AT deficiency.

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15
Q

What is the MRC dyspnoea scale

A

Grade 1: breathless on strenuous exercise
Grade 2: breathless walking up a hill
Grade 3: breathless that slows on the flat
Grade 4: stop to catch breath after 100m walking on flat
Grade 5: unable to leave house due to breathlessness

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16
Q

general management of COPD

A

stop smoking!! Pneumococcal vaccine, annual flu vaccine

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17
Q

1st line management of COPD

A

SABA short acting beta agonist (e.g., salbutamol or terbutaline) OR SAMA short acting muscarinic antagonist (e.g., ipratropium bromide)

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18
Q

2nd line COPD management

A

if no asthmatic/steroid response: LABA long-acting beta agonist (salmeterol), LAMA long-acting muscarinic antagonist (tiotropium). If asthmatic/steroid response: LABA long-acting beta agonist (salmeterol), ICS inhaled corticosteroids (budesonide)

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19
Q

3rd line management for COPD

A

LTOT long term oxygen therapy

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20
Q

Asthma

A

A chronic inflammatory disorder of large airways characterised by recurrent episodes of reversible airway narrowing.

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21
Q

aetiology of asthma

A

Hypersensitivity of the airways, triggered by: cold air, exercise, cigarette smoke, air pollution, allergens (pollen, cats, dogs, mould), time of day (early morning, night)

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22
Q

risk factors for asthma

A

Allergens, atopy, smoking, previous respiratory tract infection

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23
Q

pathophysiology of Asthma

A

Overexpressed TH2 cells in airways exposed to trigger > TH2 cytokine release, IgE production, eosinophil recruitment > IgE mast cell degranulation releasing histamines, leukotrienes, tryptase. Eosinophilia: release of toxic protein > bronchial constriction, mucus hypersecretion
Atopic triad: atopic rhinitis, eczema, asthma. Samter’s triad: asthma, aspirin allergy, nasal polyps

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24
Q

Presentations of asthma

A

Episodes of wheeze (widespread, polyphonic – multiple musical notes starting and ending at same time), breathlessness, chest tightness and dry cough.
Atopy (family/personal history of eczema/asthma/hayfever).
Diurnal variability (typically worse at night).

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25
Q

history for asthma

A

Episodes of wheeze (widespread, polyphonic – multiple musical notes starting and ending at same time), breathlessness, chest tightness and dry cough.
Atopy (family/personal history of eczema/asthma/hayfever).
Diurnal variability (typically worse at night).

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26
Q

gold standard investigations for asthma

A

Spirometry with reversibility testing. Obstructive pattern: FEV1 <80% of predicted normal, FEV1/FVC ratio <0.7. Bronchodilator reversible (>12% FEV1 improved).

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27
Q

Differential diagnoses for asthma

A

Cystic fibrosis, COPD, bronchiectasis, alpha-1-antitrypsin deficiency

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28
Q

general management of asthma

A

1st line – SABA short acting beta 2 adrenergic receptor agonists (salbutamol) – bronchodilation
2 – add ICS inhaled corticosteroids (budesonide) – reduce inflammation and reactivity of airways
3 – add LTRA leukotriene receptor antagonist (montelukast) – block leukotriene effects (inflammation, bronchoconstriction, mucus secretion)
4 – add LABA long-acting beta agonist (salmeterol)
5 – increase ICS dose

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29
Q

Exacerbations of asthma management

A

OSHITME: oxygen, SABA salbutamol, Hydrocortisone (ICS), Ipratropium bromide, Theophylline, MgSO4, escalate (ventilation – BiPAP bilevel positive airway pressure)

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30
Q

Respiratory failure

A

Defined as arterial PO2 <8kPa.

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31
Q

2 subtypes of respitatory failure

A

Type 1 is associated with a normal or low pCO2
Type 2 is associated with a raised pCO2

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32
Q

aetiology of type 1 resp failure

A

Severe pneumonia
Pulmonary embolism
Acute asthma
Pulmonary fibrosis
Acute LVF

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33
Q

aetiology of type 2 resp failure

A

COPD
Neuromuscular disorders impairing ventilation e.g. myasthenia gravis
Reduced respiratory drive e.g. sedative drugs

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34
Q

pathology of type 1 resp failure

A

a result of ventilation/ perfusion mismatching in areas of the lungs.
Increased ventilation removes any excess carbon dioxide but cannot compensate for the low pO2

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35
Q

pathology of type 2 resp failure

A

a result of a generalised alveolar hypoventilation.
Transfer of both oxygen and carbon dioxide is impaired, so pCO2 is raised, in addition to the low pO2

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36
Q

presentations of resp failure caused by hypercapnia

A

headache, change of behaviour, coma, warm extremities

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37
Q

presentations of resp failure caused by hypoxaemia

A

dyspnoea, confusion, tachypnoea, tachycardia, cyanosis, arrhythmia

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38
Q

1st line investigation of resp failure

A

Pulse oximetry (SpO2 <80%), chest x-ray, blood gas analysis, end-tidal carbon dioxide monitoring (capnometry)

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39
Q

gold standard investigations of resp failure

A

ABG (type 1: hypoxaemia without hypercapnia. Type 2: hypoxaemia with hypercapnia. pH <7.38)

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40
Q

Management of type 2 resp failure

A

Treat underlying cause
Give oxygen facemask
Assisted ventilation if PaO2 <8kPa despite 60% O2.

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41
Q

management of type 2 resp failure

A

The respiratory centre may be relatively insensitive to CO2 and respiration could be driven by hypoxia.
Treat underlying cause
Controlled oxygen therapy: start at 24% O2.
Oxygen therapy should be given with care
Recheck ABG after 20min. if PaCO2 is steady or lower, increase O2 concentration to 28%.
If this fails, consider intubation and ventilation, if appropriate.

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42
Q

What is hypersensitivity pneumonitis

A

An interstitial lung disease caused by an immunologic reaction to inhaled antigens.

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43
Q

aetiology of hypersensitivity pneumonitis

A

Thermophilic bacteria (mouldy hay, compost, air conditioner ducts)
Fungi (mouldy maple bark, barley or wood dust)
Avian proteins (bird droppings and feathers)

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44
Q

clinical manifestations of acute hypersensitivity pneumonitis

A

Acute disease follows exposure to large amounts of antigen and causes severe breathlessness, cough, and fever 4-6h after exposure. Resolution occurs within 12-18h after exposure ceases.
4-6hr post-exposure: fever, rigors, myalgia, dry cough, dyspnoea

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45
Q

Clinical manifestations of chronic hypersensitivity pneumonitis

A

Chronic disease results from prolonged exposure to small amounts of antigen with gradual onset of breathlessness, dry cough, and fatigue.
Chronic: finger clubbing, increasing dyspnoea, weight loss, exertional dyspnoea, type 1 RF

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46
Q

1st line investigations for hypersensitivity pneumonitis

A

Serum IgG positive. Bronchoalveolar lavage: raised lymphocytes, mast cells.
Pulmonary function tests: restrictive in acute, mixed in sub-acute or chronic. DLCO reduced.
Chest x-ray: acute/sub-acute: patchy reticulonodular infiltrates. Chronic: fibrosis

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47
Q

Gold standard investigations for hypersensitivity pneumonitis

A

Exposure to allergen + high resolution chest CT: ground glass shadowing

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48
Q

management of hypersensitivity pneumonitis

A

Identify causative agent and avoid exposure.
Persistent exposure can lead to irreversible lung fibrosis and respiratory failure.
Acute:
Remove allergen and give O2, PO prednisolone, reducing course
Chronic:
Allergen avoidance or wear a facemask or +ve pressure helmet.
Long term steroids often achieve CXR and physiological improvement.

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49
Q

Coal workers pneumoconiosis (CWP)

A

A common dust disease in countries that have or have had underground coal-mines.
It results from inhalation of coal dust particles over 15-20yrs.
These are ingested by macrophages which die, releasing their enzymes and causing fibrosis.

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50
Q

clinical features of CWP

A

Asymptomatic but coexisting chronic bronchitis is common
CXR: many round opacities especially in upper zone

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51
Q

management of CWP

A

Avoid exposure to coal dust
Treat co-existing chronic bronchitis
Claim compensation

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52
Q

Progressive massive fibrosis (PMF)

A

Due to progression of CWP, which causes progressive dyspnoea, fibrosis and eventually cor pulmonale

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53
Q

CXR presentation of PMF

A

usually bilateral, upper-mid zone fibrotic masses develop from periphery towards hilum

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54
Q

management of PMF

A

Avoid exposure to coal dust
Claim compensation

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55
Q

caplans syndrome

A

The association between rheumatoid arthritis, pneumoconiosis, and pulmonary rheumatoid nodules.

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56
Q

Silicosis

A

Caused by inhalation of silica particles, which are very fibrogenic
A number of jobs may be associated with exposure e.g. metal mining, stone quarrying, and pottery/ ceramic manufacture

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57
Q
A
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58
Q

management of silicosis

A

Avoid exposure to silica
Claim compensation

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59
Q

asbestosis

A

Caused by inhalation of asbestos fibres.
Asbestos was commonly used in the building trade for fire proofing, pipe lagging, electrical wire insulation and roofing felt.
Degree of asbestos exposure is related to degree of pulmonary fibrosis

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60
Q

clinical features of asbestosis

A

Similar to other fibrotic lung diseases with progressive dyspnoea, clubbing and fine-end respiratory crackles
Also causes pleural plaques, increased risk of bronchial adenocarcinoma and mesothelioma

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61
Q

management of asbestosis

A

Symptomatic
Patients are often eligible for compensation

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62
Q

features of byssinosis

A

Cotton mill workers
Symptoms start on first day back at work then improve throughout week
Tightness in chest, cough and breathlessness in 1h of being in dusty areas of mill
Particularly in blowing and carding rooms – raw cotton cleaned, and fibres straightened
Most likely due to endotoxins in bacteria in the raw cotton – causes constriction of airways of lung
No CXR changes

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63
Q

Bronchiectasis

A

An abnormal permanent dilation of bronchi accompanied by inflammation in their walls and in adjacent lung parenchyma.

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64
Q

post infection causes of bronchiectasis

A

TB, pneumonia, H. influenzae, S. pneumoniae

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65
Q

non-post infection causes of bronchiectasis

A

cystic fibrosis, asthma, HIV, ABPA (allergic bronchopulmonary aspergillosis)

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66
Q

pathology of bronchiectasis

A

Thought to be the result of weakening in bronchial walls caused by recurrent inflammation
Scarring in the adjacent lung parenchyma places traction on the weakened bronchi, causing them to permanently dilate.
Permanent thinning of these airways.
Main organisms: H. influenzae, Strep. Pneumoniae, Staph. Aureus, Pseudomonas aeruginosa.

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67
Q

symptoms of bronchiectasis

A

Persistent cough
Copious purulent sputum
Intermittent haemoptysis

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68
Q

signs of bronchectasis

A

Finger clubbing
Coarse inspiratory crepitations
Wheeze

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69
Q

complications of bronchiectasis

A

Pulmonary hypertension and RVF
Pneumothorax
Deposition of serum amyloid A protein in β-pleated sheets in multiple organs (AA amyloidosis)

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70
Q

1st line investigations for bronchiectasis

A

Sputum culture (H. influenzae, S. pneumoniae, P. aeruginosa),
spirometry (obstructive FEV1:FVC <0.7),
chest x-ray (cystic shadows, thickened bronchial walls),
FBC (raised WCC), low serum immunoglobulins

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71
Q

gold standard investigations for bronchiectasis

A

High resolution chest CT (thickened, dilated bronchi – signet ring sign - and cysts at the end of bronchioles. Big broncho:arterial ratio)

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72
Q

management of bronchiectasis

A

Airway clearance techniques and mucolytics
Chest physiotherapy and devices such as flutter valve may aid sputum expectoration and mucus drainage
Antibiotics prescribed according to bacterial sensitivities
Bronchodilators: useful in patients in asthma e.g. nebulised salbutamol
Surgery: to control severe haemoptysis

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73
Q

Cystic fibrosis

A

An inherited disorder caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene.

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74
Q

genetics of CF

A

Inherited in an autosomal recessive manner
CFTR is on chromosome 7q and codes for a chloride ion channel
Over 1400 mutations have been described, though the most common is a deletion at position 508 that leads to loss of a phenylalanine amino acid

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75
Q

pathology of CF

A

The deletion of phenylalanine 508 (F508 mutation) causes abnormal folding of the CFTR protein and its subsequent degradation in the cell.
Other mutations may result in a correctly located protein, but abnormal function.
Lack of normal CFTR causes a defective electrolyte transfer across epithelial cell membranes, resulting in thick mucus secretions.

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76
Q

CF manifestations in Neonates

A

failure to thrive, meconium ileus, rectal prolapse

Bowel obstruction may occur in the neonatal period due to thick meconium (meconium ileus) or develop later in childhood

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77
Q

CF manifestations in children and young adults

A

Respiratory; cough, wheeze, recurrent infections
GI; pancreatic insufficiency (DM), gallstones, cirrhosis
Other; male infertility, osteoporosis, arthritis, vasculitis, nasal polyps
Liver disease develops late

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78
Q

first line investigations for CF

A

Liver disease develops late
Sweat test (>60mmol/L Cl-)
Chest x-ray (bronchiectasis, hyperinflation)
Faecal elastase decreased (normally elastase produced by pancreas and found in faeces – pancreatic exocrine insufficiency and bowel obstruction decreases it)
Genetic testing (CFTR mutation chromosome 7 – delta-F508) by amniocentesis or chorionic villous sampling

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79
Q

Gold standard investigations for CF

A

Sweat test (>60mmol/L Cl-): pilocarpine applied to skin, electrodes send small current causing sweat production, sweat is absorbed and sent to lab for chloride concentration. Diagnostic = over 60mmol/L

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80
Q

management of CF

A

Should be multidisciplinary e.g. physician, GP, physio, specialist nurse, dietician
Chest: physiotherapy (postural drainage, airway clearance techniques)
Antibiotics given for acute infective exacerbations and prophylactically
Bronchodilators
Gastrointestinal: pancreatic enzyme replacement, fat-soluble vitamin supplements
Other: treatment of CF-related diabetes, screening/treatment of osteoporosis

81
Q

treatment of advanced lung disease of CF

A

oxygen, diuretics, non-invasive ventilation, lung transplant

82
Q

pleural effusion

A

An accumulation of excess fluid within the pleural space.

83
Q

haemothorax

A

Blood in the pleural space

84
Q

empyema

A

Pus in the pleural space

85
Q

chylothorax

A

Chyle (lymph with fat) in the pleural space

86
Q

hemopneumothorax.

A

Both blood and air in the pleural space

87
Q

aetiology of transudate pleural effusion

A

due to increased hydrostatic pressure or low oncotic pressure. E.g., congestive heart failure, liver cirrhosis, nephrotic syndrome, hypalbuminaemia

88
Q

aetiology of exudate pleural effusion

A

due to inflammation causing increased vascular permeability. E.g., cancer, TB, pneumonia, rheumatoid arthritis

89
Q

division of pleural effusions

A

Exudate (protein >35g/L)
Transudate (protein <25g/L)

90
Q

pathology of pleural effusion

A

Increased pulmonary venous congestion (LVF), inflammation of the pleura (pneumonia, pulmonary embolism, autoimmune disease), infiltration of the pleura (malignancy)

91
Q

clinical manifestations of pleural effusions

A

Small effusions may be asymptomatic (though visible on imaging)
Large effusions cause breathlessness and pleuritic chest pain.
Signs;
Decreased expansion
Stony dull percussion note
Diminished breath sounds

92
Q

1st line investigations for pleural effusion

A

Chest x-ray (blunting of costophrenic angle), pleural ultrasound (pleural fluid), thoracocentesis (identifies underlying cause. Sample pleural fluid: protein, LDH, pH, lactate, microscopy, WCC. Transudate – translucent. Exudate - cloudy)

93
Q

Gold standard investigation for pleural effusion

A

Chest x-ray (decreased costophrenic angles – blunting. Excess fluid appears white. Fluid in lung fissures. Tracheal and mediastinal deviation)

94
Q

management of pleural effusion

A

Drainage: if the effusion is symptomatic, drain it, and repeat if necessary.
Pleurodesis: a procedure which involves putting a mildly irritant drug into the pleural space, to try to stick the lung to the wall of the chest to prevent a further collection of fluid.
Surgery: persistent collections and increasing pleural thickness (on ultrasound) requires surgery

95
Q

pneumothorax

A

The presence of air within the pleural space.

96
Q

aetiology of pneumothorax

A

Spontaneous pneumothorax typically occurs in thin, tall young men due to the rupture of small delicate apical blebs of lung tissue which result from stretching of the lungs.
Underlying lung disease e.g. COPD, asthma, pneumonia
Trauma e.g. penetrating chest wound, rib fractures
Iatrogenic e.g. subclavian vein cannulation, lung biopsy

97
Q

pathology of pneumothorax

A

Air leaks out of the damaged lung into the pleural space until the pressures equalize
The lung collapses to a variable degree, depending on the size of the pneumothorax
Rare: tissues near the lung defect and act as a one-way valve, preventing the equalization of pressure. The continuous build-up of pressure and volume in the pleural space displaces the mediastinal structures, causing cardiorespiratory arrest (tension pneumothorax).

98
Q

clinical manifestations of pneumothorax

A

Sudden onset of unilateral pleuritic chest pain
Breathlessness (depends on size of pneumothorax)
Patients with asthma or COPD may present with sudden deterioration

99
Q

1st line investigations for pneumothorax

A

Erect chest x-ray (reduced/absent lung markings between lung margin and chest wall. Visible rim between lung margin and chest wall)
Bloods – clotting abnormalities. Chest USS. CT chest. ABG is stats <92% on room air.

100
Q

gold standard investigation for pneumothorax

A

Chest x-ray (excess air appears black. Tracheal deviation to contralateral side. Reduced/absent lung markings between lung margin and chest wall. Visible rim between lung margin and chest wall)

101
Q

management of Small primary spontaneous pneumothorax (visible rim <2cm) and not SOB

A

self-healing, consider discharge and follow-up chest x-ray.

102
Q

management of Large primary spontaneous pneumothorax (visible rim >2cm) and/or SOB

A

needle aspiration and remove air with syringe, if not <2cm on repeat chest x-ray insert chest drain and supplemental O2 if needed. Chest drain triangle of safety: 5th intercostal space, midaxillary line, anterior axillary line.

103
Q

management of tension PTX

A

cardiac arrest call, high flow O2, immediate decompression. Unless due to trauma: insert large bore cannula into pleural space through 2nd intercostal space at midclavicular line. Hiss sound confirms diagnosis.

104
Q

non-small cell lung cancer

A

Any type of epithelial lung cancer other than small cell lung cancer. Most common types: adenocarcinoma (40%), squamous cell carcinoma (20%), large cell carcinoma (10%), carcinoid tumour.

105
Q

risk factors for non-small cell lung cancer

A

Cigarette smoking, asbestos, coal, radon exposure, pulmonary fibrosis, COPD, genetics

106
Q

key presentations of non-small cell lung cancer

A

Persistent cough, shortness of breath, haemoptysis, weight loss, chest pain, wheeze, recurrent infections

107
Q

1st line investigations of non-small cell lung cancer

A

Chest x-ray (pulmonary nodules, mass, pleural effusion, lung collapse)
CT chest, abdomen, pelvis (lymphadenopathy, mediastinal invasion, staging)
Sputum culture (malignant cells in sputum)

108
Q

gold standard investigations for non-small call lung cancer

A

Bronchoscopy and biopsy (endobronchial lesions, histological diagnosis)

109
Q

management of non-small cell lung cancer

A

1st line - surgical excision (e.g., lobectomy, segmentectomy/wedge resection, pneumonectomy.) Metastasised = chemotherapy and radiotherapy.
Palliative (radiotherapy, SVC stent, tracheal stent, pain relief)

110
Q

small cell lung cancer

A

Lung cancer arising from cells lining the lower respiratory tract. The tumour cells are small and densely packed, with scant cytoplasm, finely granular nuclear chromatin, and absence of nucleoli.

111
Q

aeitology of small cell lung cancers

A

Exclusively cigarette smokers, 15% of bronchial carcinomas

112
Q

pathophysiology of small cell lung cancers

A

SCLC cells contain neurosecretory granules that can release neuroendocrine hormones. This makes SCLC responsible for multiple paraneoplastic effects.
Secondary lung tumours are more common because all blood passes through the lungs so there is a higher risk of metastases

113
Q

key presentations of SCLC

A

Persistent cough, shortness of breath, haemoptysis, chest pain, wheeze, recurrent infections

114
Q

1st line investigations of SCLC

A

Chest x-ray (central mass, hilar lymphadenopathy, pleural effusion)
CT chest, abdomen, pelvis (lymphadenopathy, mediastinal invasion, staging)
Sputum culture (malignant cells in sputum)

115
Q

Gold standard investigations for SCLC

A

Bronchoscopy and biopsy (endobronchial lesions, malignant cells, high nuclear to cytoplasm ratio)

116
Q

management of SCLC

A

1st line – if early = chemotherapy and radiotherapy. Often metastasised at presentation so may response to chemo but will relapse = palliative (radiotherapy, SVC stent, tracheal stent, pain relief)

117
Q

mesothelioma

A

A malignant tumour arising in the pleura from mesothelial cells and showing a diffuse pattern of growth over the pleural surfaces.

118
Q

pathology of mesothelioma

A

Inhaled asbestos fibres become permanently entrapped in the lung
Most do not cause a tissue reaction and these are probably the ones responsible for the carcinogenic effects.
A minority become coated with iron, forming asbestos bodies

119
Q

clinical manifestations of mesothelioma

A

Breathlessness, often due to a large pleural effusion
Chest pain
Weight loss and malaise are often profound

120
Q

investigations for mesothelioma

A

CXR/ CT: pleural thickening/ effusion. Bloody pleural fluid
Diagnosis made on histology, usually following a thoracoscopy. Often the diagnosis is only made post-mortem.

121
Q

management of mesothelioma

A

Pemetrexed + cisplatin chemotherapy can improve survival.
Surgery is hard to evaluate (few RCTs).
Radiotherapy is controversial.
Pleurodesis and indwelling intra-pleural drain may help.

122
Q

pulmonary hypertension

A

A mean pulmonary artery pressure >25mmHg at rest or >30mmHg during exercise.

123
Q

subtypes of pulmonary hypertension

A

Secondary pulmonary hypertension is a complication of chronic lung or cardiac disease
Primary pulmonary hypertension occurs in the absence of chronic lung or heart disease

124
Q

aetiology of pulmonary hypertension

A

Common causes of secondary hypertension include COPD, interstitial lung disease, LVF, and chronic pulmonary thromboemboli
Primary pulmonary hypertension may be idiopathic or associated with certain drugs, HIV infection, collagen vascular disease, and congenital systemic-to-pulmonary shunts.

125
Q

pathology of pulmonary hypertension

A

Chronic hypoxia and obliterative pulmonary fibrosis both lead to the development of raised pressure in the pulmonary arterial circulation.

126
Q

clinical manifestations of pulmonary hypertension

A

Secondary pulmonary hypertension causes worsening of the symptoms of the pre-existing condition with increasing breathlessness.
Primary pulmonary hypertension presents with exertional dyspnoea and fatigue.
Dizziness
Syncope

127
Q

investigations for pulmonary hypertenstion

A

CXR: enlarged proximal pulmonary arteries which taper distally
ECG: RVH, and P pulmonale (peaked P waves)
Echo: right ventricular dilation/ hypertrophy

128
Q

management of pulmonary hypertension

A

Oxygen
Warfarin due to high risk of intrapulmonary thrombosis
Diuretics for oedema
Oral CCBs – pulmonary vasodilators
Treat underlying cause

129
Q

Tuberculosis

A

Infectious granulomatous caseating disease caused by mycobacterium tuberculosis bacteria

130
Q

4 TB causing mycobacteirae

A

M. tuberculosis, M. africanum, M. microtis, M. bovis

131
Q

pathophysiology of TB

A

Aerobic, non-motile, non-sporing slightly curved bacilli with a thick waxy mycolic acid capsule. Acid-fast bacilli – stains red/pink with Ziehl Neelsen stain. Slow growing. Resistant to phagolysosomal killing and able to remain dormant by granuloma formation.
TB spreads via respiratory droplets. TB phagocytosed but resists phagolysosomal killing and forms caseating granuloma > T cells recruited and central region of granuloma undergoes caseating necrosis to form Ghon focus in upper lungs > Ghon focus spreads to nearby lymph nodes forming Ghon complex > if TB spreads systemically = miliary TB, if infection in containing within granulomas (dormant, asymptomatic) it is latent TB.

132
Q

key presentations of TB

A

Productive cough (sputum), cough > 3 weeks, haemoptysis, breathlessness, chest pain, lymphadenopathy
Weight loss, low grade fever, anorexia, night sweats, malaise, pyrexia

133
Q

signs of TB

A

Signs of bronchial breathing, dullness on percussion, decreased breathing, fever, crackles.
Extrapulmonary: meningitis, skin changes (erythema nodosum), TB pericarditis symptoms, joint pain (spinal TB – Pott’s disease of spine)

134
Q

1st line investigations for TB

A

Chest x-ray (fibronodular opacities on upper lobes), sputum acid-fast bacilli smear 3x (Ziehl Neelsen stains red/pink), biopsy (shows caseating granuloma), sputum culture (positive), FBC (raised WBCs), NAAT (positive for M. tuberculosis)
Diagnosing latent TB: tuberculin skin test ‘Mantoux’ (tuberculin injected in skin and look for induration – thickening/hardening - of 5mm or more), interferon gamma release assay (mixing blood with TB antigens, if a person has already had TB, their WBCs will release interferon gamma)

135
Q

Gold standard for TB

A

Sputum culture (positive)

136
Q

management of TB

A
  • R: rifampicin – 6 months, bactericidal > blocks protein synthesis, SE: red urine, hepatitis
  • I: isoniazid – 6 months, bactericidal > blocks cell wall synthesis, SE: neuropathy, hepatitis
  • P: pyrazinamide – 2 months, bactericidal initially, less effective after, SE: gout, arthralgia, rash, hepatitis
  • E: ethambutol – 2 months, bacteriostatic > blocks cell wall synthesis, SE: optic neuritis
137
Q

pneumonia

A

An infection of the lung parenchyma caused by bacterial organisms.

138
Q

classification of pneumonia

A

Community-acquired
Hospital-acquired
Aspiration
Immunosuppression

139
Q

microbiology of pneumonia

A

Community-acquired: streptococcus pneumoniae, mycoplasma pneumoniae, Haemophilus influenzae, Legionella pneumophila.
Hospital-acquired: gram-negative bacteria, e.g. Klebsiella, Escherichia coli, Pseudomonas
Aspiration: mixed aerobic and anaerobic bacteria
Immunosuppression: all the previously mentioned possible (as well as viral, mycobacteria, and Pneumocystic).

140
Q

clinical manifestations of pneumonia

A

Productive cough
Breathlessness
Chest pain
Fever
Haemoptysis

141
Q

5 signs of pneumonia

A

Pyrexia
Cyanosis
Confusion
Tachypnoea, tachycardia

142
Q

1st line investiogations of pneumonia

A

FBC (raised WCC), CRP raised, pulse oximetry/ABG (low arterial O2), U&Es (raised urea), blood culture (organism growth), sputum culture and gram stain (growth),
Chest x-ray (consolidation, multi-lobar: s. pneumoniae, s. aureus. Multiple abscesses: s. aureus)

143
Q

Gold standard investigations for pneumonia

A

Chest x-ray shows consolidation: air that fills lung airways is replaced with something with. Air bronchogram – fluid filled alveoli.
* Pneumonic lesions: multi-lobar – s. pneumonia, s. aureus, legionella.
* Multiple abscesses: s. aureus.
* Upper lobe: Klebsiella but exclude TB first

144
Q

CURB-65 score

A

to assess severity of pneumonia , 1 point for each
* Confusion (abbreviated mental test score <8)
* Urea > 7
* Respiratory rate > 30
* BP < 90 systolic AND/OR <60 diastolic
* Age > 65

145
Q

results of CURB-65 score

A

0-1 (outpatient treatment), 2 (short-stay inpatient treatment OR hospital-supervised outpatient treatment), 3-5 (manage as high-severity pneumonia)

146
Q

CURB-65 guided pneumonia treatment

A

0-1: oral amoxicillin at home
2: consider hospitalising, amoxicillin (IV or oral) + macrolide (clarithromycin, erythromycin)
3+: consider ITU, IV co-amoxiclav + macrolide (clarithromycin + erythromycin)

147
Q

general and atypical pneumonia treatment

A

Maintaining O2 saturation between 94-98% (88-92% in COPD patients), analgesia (NSAIDs or paracetamol), IV fluids
1st line – clarithromycin. Pneumocystis jirovecii pneumonia – co-trimoxazole (trimethoprim/sulfamethoxazole)

148
Q

complications of pneumonia

A

Respiratory failure
Hypotension
Atrial fibrillation
Pleural effusion
Empyema
Lung abscess
Septicaemia

149
Q

features of common cold

A

Usually caused by rhinovirus infection
Spread by droplets and close personal contact
Incubation period = 12h to 5d

150
Q

symptoms of common cold

A

Malaise
Slight pyrexia
Sore throat
Watery nasal discharge – becomes mucopurulent after a few days

151
Q

sinusitis

A

Infection of paranasal sinuses
Complicates allergic rhinitis or an URTI – caused by mucosal oedema and blockage of ostium

152
Q

causes of sinusitis

A

Strep pneumoniae or H. influenzae

153
Q

symptoms of sinusitis

A

Frontal headache
Facial pain and tenderness
Nasal discharge

154
Q

treatment of sinusitis

A

Broad-spectrum abx e.g. co-amoxiclav
Topical corticosteroids – e.g. fluticasone propionate nasal spray to reduce local mucosal swelling
Steam inhalations

155
Q

features of rhinitis

A

Sneezing attacks, nasal discharge or blockage occurring for more than 1h for most days;
For a limited period of the year (seasonal rhinitis)
Throughout the whole year (perennial or persistent rhinitis)

156
Q

seasonal rhinitis

A

Allergy to grass and tree pollen, and a variety of mould spores which grow on cultivated plants
Nasal symptoms + itching of eyes and soft palate

157
Q

perennial rhinitis

A

May be allergic – allergens similar to those of asthma
Or non-allergic – triggered by cold air, smoke and perfume
Symptoms rarely affect eyes or soft palate
Nasal polyps may develop – nasal obstruction

158
Q

diagnosis of rhinitis

A

Clinical
Skin-prick testing and RAST tests (measuring serum IgE antibody against the antigen) to identify causal agents

159
Q

management of rhinitis

A

Avoid allergens
Antihistamines e.g. cetirizine or loratadine tablets
Decongestants, topical steroids e.g. beclomethasone spray twice daily

160
Q

features of acute pharyngitis

A

Usually viral – adenoviruses
Sore throat and fever – self-limiting, rarely require symptomatic treatment

161
Q

what does more persistent and severe pharyngitis indicate

A

bacterial infection – haemolytic Strep, Haemophilus influenzae, staphylococcus aureus

162
Q

treatment of persisitent acute pharyngitis

A

penicillin IV four times a day for 10d
Erythromycin if allergic

163
Q

Croup

A

Acute laryngotracheobronchitis
Infection with a parainfluenza virus or measles virus
Symptoms are most severe when <3yo

164
Q

symptoms of croup

A

Inflammatory oedema involving larynx = hoarse voice, barking cough (croup) and stridor
Tracheitis = burning retrosternal pain

165
Q

treatment of croup

A

Oxygen therapy
Oral/ IM corticosteroids
Nebulized adrenaline

166
Q

influenza

A

Two main forms of the influenza virus = A and B
Surface of virion is coated with haemagglutinin (H) and neuraminidase (N) – both are necessary for attachment to the host respiratory epithelium
Human immunity develops against the H and N antigens
Influenza A has the capacity to undergo antigenic shift and major changes in the H and N antigens are associated with pandemic infections

167
Q

features of seasonal influenza

A

Acute viral infection of lungs and airways
Rapid person-to-person spread by aerosolised droplets and contact
Infectivity from 1d prior – 7d after symptoms
Includes three subtypes of virus: A, B and C.
Seasonal epidemics peak during the winter in temperate countries.

168
Q

presentation of influenza

A

Incubation 1-4d
Fever, dry cough, sore throat, coryzal symptoms, headache, malaise, myalgia, conjunctivitis, eye pain, photophobia.

169
Q

diagnosis of influenza

A

Clinical: acute onset + cough + fever has positive predictive value.
Testing limited to outbreaks, and public health surveillance.
Includes viral PCR, rapid antigen testing, viral culture of clinical samples

170
Q

high risk influenza patients

A

Chronic disease: lung, heart, kidney, liver, DM
Immunosuppression: immunodeficiency
Pregnancy
BMI>40, <6months old, >65yr

171
Q

treatment of uncomplicated influenza

A

symptomatic treatment e.g paracetamol
Antivirals only if high risk

172
Q

complicated influenza

A

lower respiratory tract infection, exacerbation of any underlying medical condition, all needing hospital admission.

173
Q

treatment of influenza neuraminidase

A

Antiviral inhibitors:
Oseltamivir
Zanamivir

174
Q

prevention of flu

A

Post-exposure prophylaxis: if high risk and not protected by vaccination: oseltamivir PO OD for 10d.
Annual vaccination in UK: all high risk, children >2 yrs, healthcare workers

175
Q

pulmonary embolism

A

Occlusion of a pulmonary artery by an embolic thrombus.

176
Q

aetiology of PE

A

As pulmonary emboli originate from deep vein thromboses, the risk factors are the same as for that condition i.e.
Immobility
Acute medical illness
Recent surgery
Malignancy
Pregnancy
Congenital and acquired thrombotic disorders.

177
Q

pathology of PE

A

A fragment of a detached thrombus from a deep vein thrombosis embolises via the right side of the heart into the pulmonary arterial circulation and lodges in a pulmonary artery.

178
Q

Clinical manifestations of PE

A

Blockage of a major pulmonary artery usually may cause instant death due to a sudden huge rise in pulmonary arterial pressure, acute RVF, and cardiac arrest
Blockage of medium-sized arteries causes an area of ventilation/ perfusion mismatch in the lungs with breathlessness
Smaller pulmonary emboli may lead to subtle symptoms of breathlessness, chest pain, and dizziness – these can easily go undiagnosed

179
Q

investigations of PE

A

FBC, U&E, baseline clotting, D-dimers
ABG may show lowered PaO2 and PaCO2
Imaging: CXR may be normal, or show oligaemia of affected segment
ECG: sinus tachycardia

180
Q

management of PE

A

Oxygen if hypoxic
Aspirin
Morphine IV with anti-emetic if the patient is in pain or very distressed
If haemodynamically unstable - thrombolyse for massive PE (IV alteplase)
Haemodynamically stable – start LMWH or unfractionated heparin if underlying renal impairment

181
Q

prevention of PE

A

Give heparin to all immobile patients.
Stop HRT and the combined contraceptive pill pre-op

182
Q

Sarcoidosis

A

A multisystem disease of unknown cause in which tissues are infiltrated by granulomas.

183
Q

pathology of sarcoidosis

A

Presumably the granulomatous inflammation is a reaction to an as yet unidentified antigen

184
Q

clinical manifestations of sarcoidosis

A

Virtually any organ may be involved, but the most common sites are lymph nodes, lungs and skin
Acute sarcoidosis tends to present suddenly with manifestations such as erythema nodosum
Chronic sarcoidosis is more insidious and is characterised by lupus pernio, pulmonary fibrosis, and posterior uveitis.

185
Q

pulmonary manifestations of sarcoidosis

A

Dry cough
Progressive dyspnoea
Lower exercise tolerance

186
Q

non-pulmonary signs of sarcoidosis

A

Lymphadenopathy
Hepatomegaly
Glaucoma

187
Q

investigations for sarcoidosis

A

Blood: raised ESR, lymphopenia
24h urine: raised calcium
CXR is abnormal
Lung function tests: may be normal or show reduced lung volumes
Tissue biopsy: diagnostic and shows non-caseating granulomata

188
Q

management for sarcoidosis

A

Acute sarcoidosis: bed rest, NSAIDs
Indications for corticosteroids
Parenchymal lung disease
Uveitis
Hypercalcaemia
Neurological or cardiac involvement
Other therapy: in severe illness give IV methylprednisolone

189
Q

Goodpasture’s syndrome

A

(Anti-glomerular basement membrane (Anti-GBM) disease)
Rare. Auto-antibodies to type IV collagen which is present in glomerular and alveolar basement membranes. A pulmonary-renal syndrome.

190
Q

pathology of Goodpastures

A

Caused by anti-glomerular basement membrane antibodies – bind kidney basement membrane and alveolar membrane

191
Q

clinical manifestations of goodpastures

A

Renal disease – oliguria/anuria, haematuria, AKI, renal failure
Lung disease – pulmonary haemorrhage, SOB, haemoptysis

192
Q

investugations for goodpastures

A

Diagnosis: anti-GBM in circulation/ kidney
CXR: infiltrates due to pulmonary haemorrhage, often in lower zones
Kidney biopsy: crescent glomerulonephritis

193
Q

management of Goodpastures

A

Plasma exchange
Corticosteroids
Cyclophosphamide
Treat shock

194
Q

Wegeners granulomatosis

A

(granulomatosis with polyangiitis [GPA])
A systemic ANCA-associated vasculitis characterised by dominant upper respiratory tract, lung and renal involvement and cANCA positivity.
A multisystem disorder of unknown cause characterised by necrotising granulomatous inflammation and vasculitis of small and medium vessels.

195
Q

clinical manifestations of GPA

A

Nasal symptoms – nasal obstruction, ulcers, or destruction of nasal septum
Acute renal failure
Pulmonary symptoms – cough, haemoptysis or pleuritis
Skin purpura or nodules
Peripheral neuropathy
Mononeuritis multiplex

196
Q

1st line investigations for GPA

A

FBC: raised eosinophils, raised CRP/ESR, tissue biopsy shows granulomas, CT chest shows lung nodules, urinalysis (haematuria), ANCA positive

197
Q

gold standard investigations for GPA

A

cANCA positive + symptoms

198
Q

gold standard investigations for GPA

A

cANCA positive + symptoms

Phase 2a Medicine (10 decks)

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