Respiratory Flashcards
1
Q
COPD
A
A chronic lung condition characterised by breathlessness due to poorly reversible and progressive airflow obstruction.
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.
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
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).
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
6
Q
Traditional division of COPD patients
A
Pink puffers and blue bloaters
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
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.
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.
10
Q
gold standard investigation for COPD
A
Clinical presentation + spirometry (FEV1/FVC <0.7 = obstruction. Bronchodilator irreversible = COPD. Bronchodilator reversible = asthma)
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
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).
13
Q
What is centriacinar emphysema
A
respiratory bronchioles only, smokers.
14
Q
what is panacinar emphysema
A
A1AT deficiency.
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
16
Q
general management of COPD
A
stop smoking!! Pneumococcal vaccine, annual flu vaccine
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)
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)
19
Q
3rd line management for COPD
A
LTOT long term oxygen therapy
20
Q
Asthma
A
A chronic inflammatory disorder of large airways characterised by recurrent episodes of reversible airway narrowing.
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)
22
Q
risk factors for asthma
A
Allergens, atopy, smoking, previous respiratory tract infection
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
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).
25
history for asthma
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).
26
gold standard investigations for asthma
Spirometry with reversibility testing. Obstructive pattern: FEV1 <80% of predicted normal, FEV1/FVC ratio <0.7. Bronchodilator reversible (>12% FEV1 improved).
27
Differential diagnoses for asthma
Cystic fibrosis, COPD, bronchiectasis, alpha-1-antitrypsin deficiency
28
general management of asthma
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
29
Exacerbations of asthma management
OSHITME: oxygen, SABA salbutamol, Hydrocortisone (ICS), Ipratropium bromide, Theophylline, MgSO4, escalate (ventilation – BiPAP bilevel positive airway pressure)
30
Respiratory failure
Defined as arterial PO2 <8kPa.
31
2 subtypes of respitatory failure
Type 1 is associated with a normal or low pCO2
Type 2 is associated with a raised pCO2
32
aetiology of type 1 resp failure
Severe pneumonia
Pulmonary embolism
Acute asthma
Pulmonary fibrosis
Acute LVF
33
aetiology of type 2 resp failure
COPD
Neuromuscular disorders impairing ventilation e.g. myasthenia gravis
Reduced respiratory drive e.g. sedative drugs
34
pathology of type 1 resp failure
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
35
pathology of type 2 resp failure
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
36
presentations of resp failure caused by hypercapnia
headache, change of behaviour, coma, warm extremities
37
presentations of resp failure caused by hypoxaemia
dyspnoea, confusion, tachypnoea, tachycardia, cyanosis, arrhythmia
38
1st line investigation of resp failure
Pulse oximetry (SpO2 <80%), chest x-ray, blood gas analysis, end-tidal carbon dioxide monitoring (capnometry)
39
gold standard investigations of resp failure
ABG (type 1: hypoxaemia without hypercapnia. Type 2: hypoxaemia with hypercapnia. pH <7.38)
40
Management of type 2 resp failure
Treat underlying cause
Give oxygen facemask
Assisted ventilation if PaO2 <8kPa despite 60% O2.
41
management of type 2 resp failure
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.
42
What is hypersensitivity pneumonitis
An interstitial lung disease caused by an immunologic reaction to inhaled antigens.
43
aetiology of hypersensitivity pneumonitis
Thermophilic bacteria (mouldy hay, compost, air conditioner ducts)
Fungi (mouldy maple bark, barley or wood dust)
Avian proteins (bird droppings and feathers)
44
clinical manifestations of acute hypersensitivity pneumonitis
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
45
Clinical manifestations of chronic hypersensitivity pneumonitis
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
46
1st line investigations for hypersensitivity pneumonitis
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
47
Gold standard investigations for hypersensitivity pneumonitis
Exposure to allergen + high resolution chest CT: ground glass shadowing
48
management of hypersensitivity pneumonitis
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.
49
Coal workers pneumoconiosis (CWP)
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.
50
clinical features of CWP
Asymptomatic but coexisting chronic bronchitis is common
CXR: many round opacities especially in upper zone
51
management of CWP
Avoid exposure to coal dust
Treat co-existing chronic bronchitis
Claim compensation
52
Progressive massive fibrosis (PMF)
Due to progression of CWP, which causes progressive dyspnoea, fibrosis and eventually cor pulmonale
53
CXR presentation of PMF
usually bilateral, upper-mid zone fibrotic masses develop from periphery towards hilum
54
management of PMF
Avoid exposure to coal dust
Claim compensation
55
caplans syndrome
The association between rheumatoid arthritis, pneumoconiosis, and pulmonary rheumatoid nodules.
56
Silicosis
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
57
58
management of silicosis
Avoid exposure to silica
Claim compensation
59
asbestosis
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
60
clinical features of asbestosis
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
61
management of asbestosis
Symptomatic
Patients are often eligible for compensation
62
features of byssinosis
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
63
Bronchiectasis
An abnormal permanent dilation of bronchi accompanied by inflammation in their walls and in adjacent lung parenchyma.
64
post infection causes of bronchiectasis
TB, pneumonia, H. influenzae, S. pneumoniae
65
non-post infection causes of bronchiectasis
cystic fibrosis, asthma, HIV, ABPA (allergic bronchopulmonary aspergillosis)
66
pathology of bronchiectasis
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.
67
symptoms of bronchiectasis
Persistent cough
Copious purulent sputum
Intermittent haemoptysis
68
signs of bronchectasis
Finger clubbing
Coarse inspiratory crepitations
Wheeze
69
complications of bronchiectasis
Pulmonary hypertension and RVF
Pneumothorax
Deposition of serum amyloid A protein in β-pleated sheets in multiple organs (AA amyloidosis)
70
1st line investigations for bronchiectasis
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
71
gold standard investigations for bronchiectasis
High resolution chest CT (thickened, dilated bronchi – signet ring sign - and cysts at the end of bronchioles. Big broncho:arterial ratio)
72
management of bronchiectasis
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
73
Cystic fibrosis
An inherited disorder caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene.
74
genetics of CF
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
75
pathology of CF
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.
76
CF manifestations in Neonates
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
77
CF manifestations in children and young adults
Respiratory; cough, wheeze, recurrent infections
GI; pancreatic insufficiency (DM), gallstones, cirrhosis
Other; male infertility, osteoporosis, arthritis, vasculitis, nasal polyps
Liver disease develops late
78
first line investigations for CF
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
79
Gold standard investigations for CF
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
80
management of CF
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
treatment of advanced lung disease of CF
oxygen, diuretics, non-invasive ventilation, lung transplant
82
pleural effusion
An accumulation of excess fluid within the pleural space.
83
haemothorax
Blood in the pleural space
84
empyema
Pus in the pleural space
85
chylothorax
Chyle (lymph with fat) in the pleural space
86
hemopneumothorax.
Both blood and air in the pleural space
87
aetiology of transudate pleural effusion
due to increased hydrostatic pressure or low oncotic pressure. E.g., congestive heart failure, liver cirrhosis, nephrotic syndrome, hypalbuminaemia
88
aetiology of exudate pleural effusion
due to inflammation causing increased vascular permeability. E.g., cancer, TB, pneumonia, rheumatoid arthritis
89
division of pleural effusions
Exudate (protein >35g/L)
Transudate (protein <25g/L)
90
pathology of pleural effusion
Increased pulmonary venous congestion (LVF), inflammation of the pleura (pneumonia, pulmonary embolism, autoimmune disease), infiltration of the pleura (malignancy)
91
clinical manifestations of pleural effusions
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
1st line investigations for pleural effusion
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
Gold standard investigation for pleural effusion
Chest x-ray (decreased costophrenic angles – blunting. Excess fluid appears white. Fluid in lung fissures. Tracheal and mediastinal deviation)
94
management of pleural effusion
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
pneumothorax
The presence of air within the pleural space.
96
aetiology of pneumothorax
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
pathology of pneumothorax
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
clinical manifestations of pneumothorax
Sudden onset of unilateral pleuritic chest pain
Breathlessness (depends on size of pneumothorax)
Patients with asthma or COPD may present with sudden deterioration
99
1st line investigations for pneumothorax
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
gold standard investigation for pneumothorax
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
management of Small primary spontaneous pneumothorax (visible rim <2cm) and not SOB
self-healing, consider discharge and follow-up chest x-ray.
102
management of Large primary spontaneous pneumothorax (visible rim >2cm) and/or SOB
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
management of tension PTX
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
non-small cell lung cancer
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
risk factors for non-small cell lung cancer
Cigarette smoking, asbestos, coal, radon exposure, pulmonary fibrosis, COPD, genetics
106
key presentations of non-small cell lung cancer
Persistent cough, shortness of breath, haemoptysis, weight loss, chest pain, wheeze, recurrent infections
107
1st line investigations of non-small cell lung cancer
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
gold standard investigations for non-small call lung cancer
Bronchoscopy and biopsy (endobronchial lesions, histological diagnosis)
109
management of non-small cell lung cancer
1st line - surgical excision (e.g., lobectomy, segmentectomy/wedge resection, pneumonectomy.) Metastasised = chemotherapy and radiotherapy.
Palliative (radiotherapy, SVC stent, tracheal stent, pain relief)
110
small cell lung cancer
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
aeitology of small cell lung cancers
Exclusively cigarette smokers, 15% of bronchial carcinomas
112
pathophysiology of small cell lung cancers
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
key presentations of SCLC
Persistent cough, shortness of breath, haemoptysis, chest pain, wheeze, recurrent infections
114
1st line investigations of SCLC
Chest x-ray (central mass, hilar lymphadenopathy, pleural effusion)
CT chest, abdomen, pelvis (lymphadenopathy, mediastinal invasion, staging)
Sputum culture (malignant cells in sputum)
115
Gold standard investigations for SCLC
Bronchoscopy and biopsy (endobronchial lesions, malignant cells, high nuclear to cytoplasm ratio)
116
management of SCLC
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
mesothelioma
A malignant tumour arising in the pleura from mesothelial cells and showing a diffuse pattern of growth over the pleural surfaces.
118
pathology of mesothelioma
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
clinical manifestations of mesothelioma
Breathlessness, often due to a large pleural effusion
Chest pain
Weight loss and malaise are often profound
120
investigations for mesothelioma
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
management of mesothelioma
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
pulmonary hypertension
A mean pulmonary artery pressure >25mmHg at rest or >30mmHg during exercise.
123
subtypes of pulmonary hypertension
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
aetiology of pulmonary hypertension
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
pathology of pulmonary hypertension
Chronic hypoxia and obliterative pulmonary fibrosis both lead to the development of raised pressure in the pulmonary arterial circulation.
126
clinical manifestations of pulmonary hypertension
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
investigations for pulmonary hypertenstion
CXR: enlarged proximal pulmonary arteries which taper distally
ECG: RVH, and P pulmonale (peaked P waves)
Echo: right ventricular dilation/ hypertrophy
128
management of pulmonary hypertension
Oxygen
Warfarin due to high risk of intrapulmonary thrombosis
Diuretics for oedema
Oral CCBs – pulmonary vasodilators
Treat underlying cause
129
Tuberculosis
Infectious granulomatous caseating disease caused by mycobacterium tuberculosis bacteria
130
4 TB causing mycobacteirae
M. tuberculosis, M. africanum, M. microtis, M. bovis
131
pathophysiology of TB
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
key presentations of TB
Productive cough (sputum), cough > 3 weeks, haemoptysis, breathlessness, chest pain, lymphadenopathy
Weight loss, low grade fever, anorexia, night sweats, malaise, pyrexia
133
signs of TB
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
1st line investigations for TB
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
Gold standard for TB
Sputum culture (positive)
136
management of TB
* 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
pneumonia
An infection of the lung parenchyma caused by bacterial organisms.
138
classification of pneumonia
Community-acquired
Hospital-acquired
Aspiration
Immunosuppression
139
microbiology of pneumonia
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
clinical manifestations of pneumonia
Productive cough
Breathlessness
Chest pain
Fever
Haemoptysis
141
5 signs of pneumonia
Pyrexia
Cyanosis
Confusion
Tachypnoea, tachycardia
142
1st line investiogations of pneumonia
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
Gold standard investigations for pneumonia
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
CURB-65 score
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
results of CURB-65 score
0-1 (outpatient treatment), 2 (short-stay inpatient treatment OR hospital-supervised outpatient treatment), 3-5 (manage as high-severity pneumonia)
146
CURB-65 guided pneumonia treatment
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
general and atypical pneumonia treatment
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
complications of pneumonia
Respiratory failure
Hypotension
Atrial fibrillation
Pleural effusion
Empyema
Lung abscess
Septicaemia
149
features of common cold
Usually caused by rhinovirus infection
Spread by droplets and close personal contact
Incubation period = 12h to 5d
150
symptoms of common cold
Malaise
Slight pyrexia
Sore throat
Watery nasal discharge – becomes mucopurulent after a few days
151
sinusitis
Infection of paranasal sinuses
Complicates allergic rhinitis or an URTI – caused by mucosal oedema and blockage of ostium
152
causes of sinusitis
Strep pneumoniae or H. influenzae
153
symptoms of sinusitis
Frontal headache
Facial pain and tenderness
Nasal discharge
154
treatment of sinusitis
Broad-spectrum abx e.g. co-amoxiclav
Topical corticosteroids – e.g. fluticasone propionate nasal spray to reduce local mucosal swelling
Steam inhalations
155
features of rhinitis
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
seasonal rhinitis
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
perennial rhinitis
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
diagnosis of rhinitis
Clinical
Skin-prick testing and RAST tests (measuring serum IgE antibody against the antigen) to identify causal agents
159
management of rhinitis
Avoid allergens
Antihistamines e.g. cetirizine or loratadine tablets
Decongestants, topical steroids e.g. beclomethasone spray twice daily
160
features of acute pharyngitis
Usually viral – adenoviruses
Sore throat and fever – self-limiting, rarely require symptomatic treatment
161
what does more persistent and severe pharyngitis indicate
bacterial infection – haemolytic Strep, Haemophilus influenzae, staphylococcus aureus
162
treatment of persisitent acute pharyngitis
penicillin IV four times a day for 10d
Erythromycin if allergic
163
Croup
Acute laryngotracheobronchitis
Infection with a parainfluenza virus or measles virus
Symptoms are most severe when <3yo
164
symptoms of croup
Inflammatory oedema involving larynx = hoarse voice, barking cough (croup) and stridor
Tracheitis = burning retrosternal pain
165
treatment of croup
Oxygen therapy
Oral/ IM corticosteroids
Nebulized adrenaline
166
influenza
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
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features of seasonal influenza
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.
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presentation of influenza
Incubation 1-4d
Fever, dry cough, sore throat, coryzal symptoms, headache, malaise, myalgia, conjunctivitis, eye pain, photophobia.
169
diagnosis of influenza
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
high risk influenza patients
Chronic disease: lung, heart, kidney, liver, DM
Immunosuppression: immunodeficiency
Pregnancy
BMI>40, <6months old, >65yr
171
treatment of uncomplicated influenza
symptomatic treatment e.g paracetamol
Antivirals only if high risk
172
complicated influenza
lower respiratory tract infection, exacerbation of any underlying medical condition, all needing hospital admission.
173
treatment of influenza neuraminidase
Antiviral inhibitors:
Oseltamivir
Zanamivir
174
prevention of flu
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
pulmonary embolism
Occlusion of a pulmonary artery by an embolic thrombus.
176
aetiology of PE
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
pathology of PE
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
Clinical manifestations of PE
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
investigations of PE
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
management of PE
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
prevention of PE
Give heparin to all immobile patients.
Stop HRT and the combined contraceptive pill pre-op
182
Sarcoidosis
A multisystem disease of unknown cause in which tissues are infiltrated by granulomas.
183
pathology of sarcoidosis
Presumably the granulomatous inflammation is a reaction to an as yet unidentified antigen
184
clinical manifestations of sarcoidosis
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
pulmonary manifestations of sarcoidosis
Dry cough
Progressive dyspnoea
Lower exercise tolerance
186
non-pulmonary signs of sarcoidosis
Lymphadenopathy
Hepatomegaly
Glaucoma
187
investigations for sarcoidosis
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
management for sarcoidosis
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
Goodpasture's syndrome
(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
pathology of Goodpastures
Caused by anti-glomerular basement membrane antibodies – bind kidney basement membrane and alveolar membrane
191
clinical manifestations of goodpastures
Renal disease – oliguria/anuria, haematuria, AKI, renal failure
Lung disease – pulmonary haemorrhage, SOB, haemoptysis
192
investugations for goodpastures
Diagnosis: anti-GBM in circulation/ kidney
CXR: infiltrates due to pulmonary haemorrhage, often in lower zones
Kidney biopsy: crescent glomerulonephritis
193
management of Goodpastures
Plasma exchange
Corticosteroids
Cyclophosphamide
Treat shock
194
Wegeners granulomatosis
(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
clinical manifestations of GPA
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
1st line investigations for GPA
FBC: raised eosinophils, raised CRP/ESR, tissue biopsy shows granulomas, CT chest shows lung nodules, urinalysis (haematuria), ANCA positive
197
gold standard investigations for GPA
cANCA positive + symptoms
198
gold standard investigations for GPA
cANCA positive + symptoms
