Respiratory Flashcards

(193 cards)

1
Q

What is acute bronchitis?

A

lower respiratory tract infection where there is inflammation of the large airways but not of the lung parenchyma (i.e. not a pneumonia). Cough is the predominant clinical feature, and the majority of cases are mild and self limiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Epidemiology of acute bronchitis?

A

5% of adults affected per year
Higher in autumn and winter months
Smoking is major risk factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Aetiology of acute bronchitis?

A

Viral;
Rhinovirus
Coronavirus
Adenovirus
Respiratory syncytial virus (RSV)
Influenza A and B
Parainfluenza

Bacterial;
Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Mycoplasma pneumoniae
Bordetella pertussis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Presentation of acute bronchitis?

A

Cough
Headache
Coryza
Sore throat
Mild dyspnoea
Chest wall pain with coughing
Fatigue
Malaise

Signs;
Low-grade fever
Wheeze, especially on forced expiration
Rhonchi that clear with coughing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Differentials for acute bronchitis?

A

Pneumonia
COPD
Acute asthma exacerbation
PE
Post nasal drip
ACE inhibitor induced cough
Lung cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Investigations to diagnose acute bronchitis?

A

Respiratory viral swab
Sputum culture
CRP, LDH
CXR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Management of acute bronchitis?

A

Supportive, fluids and hot teas
Smoking cessation
Safety net to seek advice if this does not resolve in 3-4 weeks

Paracetamol and antibiotics

Consider delayed antibiotics of doxycycline, a 5 day course

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Complications of acute bronchitis?

A

Pneumonia
Persistent cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Prognosis of acute bronchitis?

A

Most recover in 2-3 weeks
Recurrence is common, especially in smokers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Common allergens?

A

Dust mites
Foods (especially nuts, shellfish, eggs, milk and certain fruits)
Grass and tree pollens
Animal dander
Medications (e.g. penicillins, aspirin, ibuprofen)
Insect bites and stings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Epidemiology of allergies?

A

44% of UK population have atleast 1 allergy
Hygiene hypothesis; people who are less exposed to pathogens are more likely to develop allergies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Presentation of allergic reaction?

A

Itchy skin or eyes
Rashes (classically urticarial in IgE mediated hypersensitivity)
Gastrointestinal upset (diarrhoea, abdominal pain or nausea and vomiting)
Swelling of the eyes, lips, mouth or throat
Rhinorrhoea
Sneezing
Shortness of breath or wheeze
Deterioration in asthma or eczema symptoms
Conjunctivitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Differentials for allergic reaction?

A

Chronic urticaria
Hereditary/ drug related angio-oedema
Food intolerance
Food poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Management of allergies?

A

Exclude allergens
Oral antihistamines
Assess nutritional status
Re-introduce allergens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Complications of allergies?

A

Malnutrition
Anaphylaxis
Reduced quality of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is asbestosis?

A

Lung disorders caused by asbestos exposure, including pleural plaques, diffuse pleural thickening, pleural effusions, lung cancer and mesothelioma

Asbestosis is one of these manifestations and is a chronic fibrotic lung disease that typically manifests 10-20 years following exposure to asbestos fibres (often through occupational risks).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Presentation of asbestosis?

A

Symptoms;
Progressive dyspnoea
Dry cough
Weight loss
Fatigue

Signs;
Bilateral fine end expiratory crepitations (predominantly basal)
Finger clubbing
Cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Differentials for asbestosis?

A

Idiopathic pulmonary fibrosis
Pulmonary fibrosis related to rheumatological conditions
Drug induced
COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Investigations to diagnose asbestosis?

A

FVC, TLC, FEV1-FVC
CXR, high resolution CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Management of asbestosis?

A

Smoking cessation
Pulmonary rehabilitation
Oxygen therapy
Vaccination against influenza and pneumococcal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Occupational exposure to asbestos?

A

Construction workers between 1950 and 1990
Those who currently work in old buildings as heating and ventillation engineers, demolition and construction workers, plumbers electricians

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is aspiration pneumonia?

A

inflammation of the lungs after an irritating substance is inhaled (commonly gastric contents or oropharyngeal secretions). This causes a pneumonitis, and may lead to infection caused by the normal flora found in the oropharynx entering the lower respiratory tract.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Epidemiology of aspiration pneumonia?

A

Common in frail elderly population
10% of CAP is secondary to aspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Aetiology of aspiration pneumonia?

A

Breech in mechanisms which prevent aspiration

Swallowing difficulties (stroke, bulbar palsy, oesophageal strictures, neuromuscular disorders such as multiple sclerosis, achalasia)
Impaired consciousness (seizures, general anaesthesia, alcohol or drug intoxication)
Tracheo-oesophageal fistulae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Presentation of aspiration pneumonia?
Cough (which may be productive of purulent sputum) Shortness of breath Chest pain Fevers Malaise
26
Differentials for aspiration pneumonia?
COPD PE Bronchitis
27
Investigations to diagnose aspiration pneumonia?
Sputum culture Blood tests; WCC, CRP CXR; consolidation
28
Management of aspiration pneumonia?
Initial antibiotic; co-amoxiclav Consider complications such as empyema if failure to resolve
29
What is asthma?
Hyper-reactive airway disease characterised by intermittent recurrent symptoms of wheeze, cough, SOB and chest tightness caused by reversible bronchoconstriction, hyperreactivity and chronic inflammation
30
Triggers for asthma?
Cold air and exercise Pollution and cigarette smoke Allergens such as animal dander, dust mites and pollen Irritants such as perfumes, paints or air fresheners Medications such as NSAIDs or beta-blockers
31
Risk factors for asthma?
Family history of asthma or atopy Personal history of atopy (eczema, allergic rhinitis, allergic conjunctivitis) Exposure to smoke, including maternal smoking in pregnancy Respiratory infections in infancy Prematurity and low birth weight Obesity Social deprivation Occupational exposures (e.g. flour dust, isocyanates from paint)
32
Presentation of asthma?
Wheeze Dyspnoea Cough Chest tightness Diurnal variation; symptoms worse at night/ early morning Signs; Tachypnoea Increased work of breathing Hyperinflated chest Expiratory polyphonic wheeze throughout the lung fields Decreased air entry (if severe)
33
Differentials for asthma?
Bronchiectasis Vocal cord dysfunction COPD GORD Eosinophillic granulomatosis with polyangiitis
34
Investigations to diagnose asthma?
FeNO; >50ppb FBC, eosinophil count Bronchodilator reversibility Spirometry Direct bronchial challenge test
35
Management of asthma?
Non pharmacological; Teach good inhaler technique and review this regularly Spacer devices can be used to optimise medication delivery Regular peak flow monitoring Smoking cessation Advice on avoiding triggers where possible (e.g., certain medications) Ensure vaccinations are up to date, including annual influenza vaccination Assess for occupational asthma by asking if symptoms are better when the patient is away from work and arrange specialist referral if this is suspected Pharamcological; LABA+ ICS combination inhaler MART; maintenance and reliver therapy inhaler LTRA LAMA
36
When to refer to secondary care for asthma?
Uncertainty regarding diagnosis Suspected occupational asthma Severe or life-threatening asthma requiring admission to hospital Multiple exacerbations requiring oral steroid treatment per year
37
Types of pneumococcal vaccine?
pneumococcal polysaccharide vaccine (PPV) protecting against 23 serotypes of pneumococcus pneumococcal polysaccharide conjugate vaccine (PCV) protecting against 13. (given in childhood imms)
38
Who should recieve PPV vaccine?
Over 65 year olds Splenic dysfunction or asplenia (e.g. coeliac disease, sickle cell disease) Chronic respiratory disease (e.g. COPD) Chronic heart disease (e.g. heart failure) Chronic kidney disease (e.g. CKD stage 4 or 5) Chronic liver disease (e.g. cirrhosis) Patients with diabetes requiring anti-diabetic medication Immunosuppression (e.g. HIV, chemotherapy, long-term steroid usage) Cochlear implant Those at risk of cerebrospinal fluid leakage (e.g. skull fracture) Those exposed to metal fumes at work (e.g. welders)
39
What is bihilar lymphadenopathy?
Bilateral hilar lymphadenopathy refers to the enlargement of lymph nodes around both hila of the lungs due to inflammation, infection or malignancy.
40
Aetiology of bilateral hilar lymphadenopathy?
Inflammatory: sarcoidosis Infective: tuberculosis, mycoplasma, histoplasmosis Malignancy: lymphoma (Hodgkin more common than non-Hodgkin), carcinoma Pneumoconioses (diseases due to inhalation of dusts/fibres): silicosis, berylliosis
41
What is bronchiectasis?
Chronic lung disease where inflammation and obstruction causes damage to the bronchial walls leading to their permanent dilation May affect whole lobe or one lung
42
Aetiology of bronchiectasis?
40% of patients have no identifiable cause Most common cause is severe LRTI (pneumonia, TB, influenza) Immunodeficiency (HIV, common variable immunodeficiency) Defective mucociliary clearance (cystic fibrosis, primary ciliary dyskinesia e.g. Kartagener syndrome) Allergic Bronchopulmonary Aspergillosis (ABPA) Autoimmune disease (rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease) Airway obstruction (inhaled foreign bodies, bronchial carcinoma, severe obstructive lung disease e.g. COPD/asthma) Chronic aspiration Congenital defects of the large airways (Marfan’s, tracheobronchomegaly)
43
Presentation of bronchiectasis?
Symptoms include: Productive cough lasting at least 8 weeks Copious production of purulent sputum Dyspnoea Haemoptysis Chest pain Fatigue Weight loss Examination; Coarse crackles on auscultation Wheeze Rhonchi (snoring sounds caused by secretions in the larger airways) Finger clubbing
44
Investigations to diagnose bronchiectasis?
Sputum culture Spirometry Bloods; WCC, CRP CXR High resolution CT Rheumatological serology Serum immunoglobulins HIV serology Test for cystic fibrosis Bronchoscopy
45
Management of bronchiectasis?
Conservative; Sputum clearance exercises Smoking cessation Pulmonary rehabilitation Influenza and pneumococcal vaccination Medical management; Treat with antibiotics Treat comorbidities Surgical; Lung resection Treat haemoptysis Consider lung transplantation
46
What is COPD?
Chronic obstructive pulmonary disease (COPD) involves airway obstruction that is usually progressive. It encompasses both emphysema (where alveolar wall destruction leads to enlargement of the distal airspaces) and chronic bronchitis (persistent or recurrent productive cough usually due to mucus hypersecretion).
47
Risk factors for COPD?
Tobacco smoking and passive smoke exposure Marijuana smoking Occupational exposure to dusts and fumes Household air pollution from wood or coal burning Alpha-1 antitrypsin deficiency
48
Factors associated with poor prognosis of COPD?
Poor exercise tolerance Smoking Low body mass index Multi-morbidity and frailty Exacerbations requiring admission to hospital or frequent exacerbations Severe obstruction on spirometry (as measured by a lower FEV1) Chronic hypoxia Cor pulmonale
49
Pathophysiology of chronic bronchitis?
As a protective reaction to smoke or other pollutants, goblet cells hypersecrete mucus in the bronchi and bronchioles of the lungs. Cilia are not able to remove the excess mucus and so it obstructs the small airways. Ongoing inflammation causes remodelling and thickening of the airway walls that also contributes to obstruction.
50
Pathophysiology of emphysema?
Inflammation in the lungs is usually countered by antiproteases such as alpha-1 antitrypsin, however the activity of these is reduced by smoke and other pollutants. Without sufficient antiprotease activity, proteolytic enzymes produced by inflammatory cells break down the walls of the alveoli. This causes enlargement of the terminal airspaces and reduces the surface area available for gas exchange.
51
GOLD classification of COPD?
Grade 1; mild, post bronchodilator FEV1 >80% Grade 2; moderate, post bronchodilator FEV1 50-79% Grade 3; severe, post bronchodilator FEV1 30-49% Grade 4; very severe, post bronchodilator FEV1 <30%
52
MRC dyspnoea scale?
Grade 0; I only get breathless with strenuous exercise. Grade 1; I get short of breath when hurrying on level ground or walking up a slight hill. Grade 2; On level ground, I walk slower than people of the same age because of breathlessness, or I have to stop for breath when walking at my own pace. Grade 3; I stop for breath after walking about 100 yards or after a few minutes on level ground. Grade 4; I am too breathless to leave the house, or I am breathless when dressing or undressing.
53
Signs and symptoms of COPD?
Symptoms; Shortness of breath that worsens with exertion Reduced exercise tolerance Chronic productive cough Recurrent lower respiratory tract infections Wheeze In more advanced cases, systemic symptoms such as weight loss and fatigue may be present Examination; Wheeze or crackles on auscultation Accessory muscle usage Pursed lip breathing (this creates a small amount of positive end expiratory pressure to prevent the alveoli from collapsing) Cyanosis Hyperinflation of the chest Cachexia Raised JVP and peripheral oedema (indicating cor pulmonale has developed)
54
Investigations to diagnose COPD?
Spirometry Bloods; polycythaemia/ anaemia, BNP, alpha-1 antitrypsin ECG CXR Sputum culture
55
Differentials for COPD?
Asthma Bronchiectasis Heart failure Interstitial lung disease Lung cancer TB
56
Management of COPD?
Patient education, smoking cessation Nutritional support Annual influenza, one off pneumococcal vaccination SABA/ SAMA ICS LABA LAMA Thyophyline Long term oxygen therapy if; Oxygen saturations <92% in air or cyanosis FEV1 <30% predicted (consider referring if <49%) Polycythaemia Peripheral oedema or raised jugular venous pressure (suggesting cor pulmonale)
57
What is cystic fibrosis?
Multisystem autosomal recessive condition that leads to bronchiectasis, pancreatic insufficiency and fertility problems
58
Epidemiology of cystic fibrosis
Most common genetic disease in white populations 1 in 25 people with European ancestry carrying a causative gene 1 in 2500 babies born in the UK have the condition
59
Aetiology of cystic fibrosis?
Mutations in the cystic fibrosis transmembrane conductance regulator gene on chromosome 7 Most common of these is called F508del which is a type of deletion mutation and results in the CTFR protein not being transported to the surface of cells CFTR protein is responsible for regulating chloride ion transport across the cell membrane. If this is defective, there is an increase in the viscosity of mucus produced and so secretions are thickened throughout the body. In the sweat glands however, chloride is transported the opposite way and so mutations cause excess chloride to be transported onto the skin, explaining why sweat testing in CF reveals raised sweat chloride
60
Presentation of cystic fibrosis?
Respiratory features; Bronchiectasis (chronic productive cough, dyspnoea) Frequent lower respiratory tract infections Chronic sinusitis Nasal polyps Increased incidence of pneumothoraces GI features; Meconium ileus Distal intestinal obstruction syndrome Rectal prolapse Pancreatic insufficiency cirrhosis and portal hypertension Gall stones Failure to thrive in infancy Prolonged neonatal jaundice Reproductive features; Congenital absence of vas deferens Thickened cervical mucus MSK features; Finger clubbing Osteopenia or osteoporosis secondary to malnourishment Short stature Non-specific joint and muscular pains
61
Differentials for cystic fibrosis?
Bronchiectasis Coeliac disease Primary ciliary dyskinesia
62
Investigations to diagnose cystic fibrosis?
Neonates are screened by heel prick test Chloride sweat test; >60nmol/ L is diagnostic Genetic testing Other tests; Faecal elastase - to test for pancreatic insufficiency Glucose testing - to assess for diabetes secondary to pancreatic insufficiency Sputum microbiology Bloods CXR CT chest DEXA scan Liver USS
63
Management of cystic fibrosis?
Review every 3-6 months Peer, social and psychological support Physiotherapy Dietician Dornase alpha; mucoactive agent Hypertonic saline nebuliser Antibiotic prophylaxis - flucloxacillin to prevent Staphylococcus aureus should be given from diagnosis until 3-6 years old. Lumacaftor-ivacaftor (Orkambi) is a treatment licensed for patients with two copies of the F508del mutation Creon Insulin Nasal steroids
64
Prognosis of cystic fibrosis?
Median survival is 46 for men and 41 for women
65
Differentials for haemoptysis?
Lung cancer Carcinoid tumour Bronchitis Bronchiectasis Airway trauma Pneumonia Tuberculosis Lung abscess Granulomatosis with polyangiitis Goodpastures syndrome PE AV malformation Mitral stenosis Iatrogenic
66
Investigations to find cause of haemoptysis?
Urinalysis Sputum culture of acid fast bacilli ECG Bloods; FBC, U+E, coagulation CXR CT chest Bronchoscopy
67
Risk factors for influenza infection?
Hyposplenism Chronic diseases of the respiratory, cardiovascular, renal, liver, neurological systems Diabetes mellitus Immunosuppression Morbid obesity Pregnancy
68
Types of influenza virus?
Influenza A - capable of causing pandemics and epidemics; found in humans, birds and pigs; multiple different sub-types; most common cause of seasonal flu infections Influenza B -capable of epidemics only; only found in humans; only one subtype Influenza C - mainly occurs in humans, but also found in dogs and pigs Influenza D - only found in cattle; not known to cause illness in humans
69
Presentation of influenza?
The incubation period is typically 1-4 days and patients can remain infectious for 7-21 days. Fever > 37.8°C Nonproductive cough Myalgia Headache Malaise Sore throat Rhinitis
70
Differentials for influenza?
Sepsis Meningitis Common cold Streptococcal pharyngitis LRTI Infectious mononucleosis
71
Complications of influenza?
Pulmonary - viral pneumonia, secondary bacterial pneumonia (particularly S. aureus) , worsening of chronic conditions (eg. COPD and asthma) Cardiovascular - myocarditis, heart failure Neurological - encephalopathy Gastrointestinal - anorexia and vomiting are common
72
What is interstitial lung disease?
Large group of diseases that cause inflammation and ultimately fibrosis of the interstitium of the lung
73
Aetiology of interstitial lung disease?
Idiopathic pulmonary fibrosis; commonest cause Hypersensitivity pneumonitis Sarcoidosis Asbestosis Lung damage; pneumonia or TB Irritants; dust/ silica Connective tissue disease; RA, SLE, systemic sclerosis, sjogren's syndrome Medications; Amiodarone, Nitrofurantoin and Bleomycin Radiation
74
Classification of interstitial lung disease?
Upper zones predominant: Hypersensitivity pneumonitis Ankylosing spondylitis Radiotherapy Tuberculosis Sarcoidosis Lower zones predominant: Rheumatoid arthritis Asbestosis Idiopathic Drugs
75
Presentation of interstital lung disease?
Insidious and progressive onset of; Dry cough Shortness of breath Reduced exercise tolerance Fatigue Anorexia Weight loss Signs; Cyanosis Clubbing Cachexia Fine end-inspiratory crackles location depends on where in the lung is affected do not clear on coughing
76
Differentials for interstitial lung disease?
Pulmonary oedema Lymphangitis carcinomatosis COPD Lung cancer
77
Investigations to diagnose interstitial lung disease?
Bloods; FBC, U+E, LFT, bone profile, CRP, Autoimmune screen, serum ACE CXR High resolution CT Spirometry Bronchoscopy Lung biopsy
78
Management of interstitial lung disease?
IPF; Pirfenidone- reduces fibroblast proliferation Nintedanib- tyrosine kinase inhibitor Smoking cessation Hypersensitivity pneumonitis; Potential for reversal if causative agent is removed Steroids Immunosuppression; cyclophosphamide, azathioprine
79
Risk factors for lung cancer?
Tobacco smoking (e.g. cigarettes, pipes, cigars) Passive smoke exposure Occupational exposures (e.g. beryllium, cadmium, arsenic, asbestos, silica) Radon exposure Family history of lung cancer Radiation to the chest (e.g. in lymphoma treatment) Air pollution Immunosuppression (e.g. HIV, medications) Increasing age
80
Classification of lung cancer?
Small cell lung cancer; neuroendocrine cells of lung Non small cell lung cancer has 2 types; Adenocarcinoma; arising from type 2 alveolar epithelial cells Large cell carcinoma
81
What staging is used to stage lung cancer?
TNM
82
Presentation of lung cancer?
Symptoms; Persistent cough Haemoptysis Dyspnoea especially on exertion Chest pain Weight loss Recurrent chest infections, or infections resistant to treatment Anorexia Signs; Cachexia Finger clubbing Lung collapse from tumour Pleural effusion Paraneoplastic syndrome; small cell cancer Cushings syndrome SIADH Lambert- Eaton myasthenic syndrome Humoural hyperglycaemia
83
Differentials for lung cancer?
Lung metastases Mesothelioma Tuberculosis Bronchiectasis
84
Investigations to diagnose lung cancer?
In primary care, patients should be referred on a 2 week wait pathway in the following situations: Aged 40+ with unexplained haemoptysis Chest X-ray findings suspicious for lung cancer Urgent chest X-ray in patients who have smoked and are over 40 years with one of the following; Cough Fatigue Shortness of breath Chest pain Weight loss Anorexia Sputum cytology Diagnostic thoracocentesis Bloods; FBC, U+E, LFT, CRP CT chest with contrast Biopsy Spirometry CT TAP PET CT/ MRI
85
Management of lung cancer?
Smoking cessation Advanced care planning Chemotherapy Immunotherapy Radiotherapy Lobectomy Wedge resection Pneumonectomy Hilar node sample
86
Complications of lung cancer?
Spread to lymph nodes, liver, brain, bones, adrenal glands, contralateral lung Horners syndrome SVC obstruction Malignant pleural effusion Hoarse voice Persistent LRTI Raised hemidiaphragm Brachial plexus injury
87
Prognosis of lung cancer?
Average 5 year survival rate of 17% Small cell lung cancers are aggressive and are usually metastatic at the time of presentation, hence curative treatment is not possible
88
What is a lung nodule?
Rounded opacity in the lung that measures under 3cm in diameter (if over 3cm would be referred to as a mass). They are a common incidental finding on chest X-rays and CT scans and there are a wide variety of causes, as well as agreed criteria for follow up
89
Aetiology of lung nodules?
Inflammatory causes; Granuloma Rheumatoid nodule Infective causes; Lung abscess Small focus of pneumonia Tuberculosis Fungal - e.g. aspergillosis, histoplasmosis Neoplastic; Primary lung cancer Metastasis Carcinoid tumour Lymphoma Benign neoplasia Congenital; Lung cyst AV malformation Pulmonary sequestration Bronchial atresia with mucous plugging
90
Differentials for lung nodules?
Artefact Nipple shadow Skin lesion Bone lesion Summation of markings
91
Investigations to diagnose lung nodules?
If the nodule is detected on X-ray, a CT chest may be done to better delineate it. Nodules considered to have a 10% or more risk of being malignant should be considered for biopsy, either excisional or image-guided.
92
Management of lung nodules?
If a nodule is under 5mm diameter or 80mm3 volume, or looks clearly benign (e.g. a hamartoma), or if the patient is unfit for any treatment it does not need any follow up. 5-6mm nodules should be followed up with a CT in 1 year. 6-8mm nodules should be followed up with a CT in 3 months. For nodules over 8mm, the Brock model is used to estimate the risk of lung cancer. Under 10% risk of lung cancer is classed as low risk and patients can continue surveillance. Patients with a risk of 10% or over should have a PET-CT to further risk assess, with higher risk nodules recommended to undergo biopsy or excision
93
What is a lung abscess?
Collection of pus in the lung parenchyma that causes a cavity to form. An air-fluid level is often seen on imaging due to necrotic debris within the cavity
94
Risk factors for lung abscess?
Chronic aspiration Poor oral hygiene Immunosuppression Thoracic trauma Recent trauma
95
Aetiology of lung abscess?
Aspiration Necrotising pneumonia Tuberculosis Bronchial obstruction Infective endocarditis Contagious spreaf
96
Presentation of lung abscess?
Fevers Productive cough Shortness of breath Lethargy Night sweats Weight loss Can cause haemoptysis Abscesses near the pleura can cause pleuritic chest pain Signs; Finger clubbing Localised dullness to percussion Reduced air entry over the abscess
97
Differentials for lung abscess?
Bronchiectasis Tuberculosis Lung cancer
98
Investigations to diagnose lung abscess?
Sputum MC&S Blood test; CRP, WCC, LFT, U+E CXR; round lesion with an air-fluid level; the right lower lobe is the most commonly affected area due to aspiration CT chest with contrast Bronchoscopy Pus MC&S
99
Management of lung abscess?
Antibiotic treatment: broad spectrum antibiotics (e.g. co-amoxiclav) should be initiated, via the intravenous route for the first 2-3 weeks then continue oral treatment for 4-8 weeks as guided by microbiology and local guidelines as well as clinical progress Supportive management Chest physio Surgical drainage
100
Complications of lung abscess?
Empyema Bronchopleural fistula Pneumothorax Sepsis Abscesses elsewhere in the body due to haematogenous spread
101
What is OSA?
Upper airway becomes completely or partially obstructed during sleep, causing apnoeas (where breathing temporarily stops) or hypopnoeic episodes (decreased airflow during breathing). These episodes cause oxygen desaturations which cause brief arousals from sleep which can be hundreds of times per night
102
Epidemiology of OSA?
85% remain undiagnosed Around half are overweight OSA is strongly linked with cardiovascular disease and the metabolic syndrome, and is a significant risk factor for coronary artery disease, type 2 diabetes and stroke
103
Risk factors for OSA?
Obesity Male sex Older age Decreased muscle tone - e.g. alcohol excess, sedative medications, muscular dystrophy or other neuromuscular disorders Anatomical defects - e.g. retrognathia, macroglossia Large neck circumference Adenotonsillar hypertrophy (particularly in children) Sleeping supine Down’s syndrome
104
Pathophysiology of OSA?
During sleep there is a normal loss of muscle tone in the oropharynx. In most people, there is still sufficient airway patency during sleep so that it does not become obstructed. Patients with OSA, however, require the muscle tone when awake to counteract additional pressures on their airway and so are unable to maintain patency when asleep.
105
Presentation of OSA?
Unrefreshing sleep, or frequent waking at night Daytime sleepiness Others may witness snoring, apnoeas, gasping or choking during sleep Nocturia Difficulty concentrating Morning headaches Behavioural problems and hyperactivity in children Signs; Obesity Large neck circumference Jaw abnormalities (retrognathia or micrognathia) Mouth breathing or nasal speech (due to nasopharyngeal obstruction, e.g. due to adenotonsillar enlargement)
106
Differentials for OSA?
Insomnia Sleep disturbance Restless leg syndrome Narcolepsy Hypothyroidism Depression Medications; SSRI, benzodiazepines GORD
107
Investigations to diagnose OSA?
STOP-Bang asks about snoring, sleepiness, apnoeas, hypertension, obesity, neck circumference, age and sex and gives a low, medium or high risk of OSA. The Epworth sleepiness scale focuses on daytime sleepiness and asks how likely the patient would be to fall asleep in a variety of situations (e.g. when watching TV). This gives a result of either normal daytime sleepiness or mild, moderate or severe excessive daytime sleepiness. Sleep study; apnoea hypoxia index Mild OSA: AHI 5-14 per hour Moderate OSA: AHI 15-30 per hour Severe OSA: AHI over 30 per hour
108
Management of OSA?
Patient education Sleep on side rather than supine Weight loss Reduction in alcohol intake Smoking cessation CPAP Tonsillectomy
109
OSA and driving?
If OSA is suspected or mild, advise patients not to drive until symptoms are controlled. If this is not achieved within 3 months, they should inform the DVLA. If OSA is moderate or severe, patients should inform the DVLA immediately and not drive; this will be reviewed by the DVLA and they may be allowed to drive once symptoms are controlled.
110
Complications of OSA?
Road traffic collisions Accidents at work or home Deterioration in mental health, including irritability and depression CVD and metabolic complications; Stroke Coronary artery disease Hypertension that may be treatment resistant Congestive heart failure Type 2 diabetes
111
What is pleural effusion?
Collection of fluid in the pleural cavity
112
Aetiology of pleural effusion?
Examples of transudative causes include: Heart failure Nephrotic syndrome Cirrhosis Hypoalbuminaemia Examples of exudative causes include: Pneumonia (a “parapneumonic effusion”) Malignancy Tuberculosis Pulmonary embolism Rheumatoid arthritis Systemic lupus erythematosus Pancreatitis Trauma
113
Classification of pleural effusion?
Transudates are classified as pleural fluid with a protein level less than 25g/L (assuming a normal serum protein). Exudates are classified as pleural fluid with a protein level more than 35g/L. For intermediate effusions, Light’s criteria are used - if any of the following are true then the effusion is an exudate: The ratio of pleural to serum protein is greater than 0.5 The ratio of pleural to serum LDH is greater than 0.6 The pleural fluid LDH is greater than ⅔ of the upper limit of normal serum value
114
Presentation of pleural effusion?
Symptoms; Shortness of breath Reduced exercise tolerance Dry cough Pleuritic chest pain Signs; Reduced chest expansion on the affected side Dullness to percussion over the effusion Reduced or absent breath sounds over the effusion Loss of vocal resonance over the effusion Large pleural effusions may cause tracheal deviation away from the effusion Respiratory distress (e.g. accessory muscle usage)
115
Differentials for pleural effusion?
Haemothorax Chylothorax Empyema Mesothelioma
116
Investigations to diagnose pleural effusion?
Pleural tap FBC, CRP, U+E, LFT, clotting, ANA, amylase CXR Pleural biopsy Echo Fibroscan
117
Management of pleural effusion?
Supportive management, O2 Antibiotics if infectious cause Diuretics USS guided aspiration Pleural drain Pleurodesis can be chemical (where an irritant is injected into the pleural space, sealing it shut via a fibrotic reaction) or surgical via thoracotomy or thoracoscopy
118
What is pneumocystis pneumonia (PCP)?
Infection caused by the fungus Pneumocystis Jirovecii. Usually affects patients who are immunocompromised, for example patients with late-stage HIV or those on immunosuppressant medications after an organ transplant
119
Epidemiology of PCP?
Reducing due to improvement in HIV ARVT
120
Aetiology of PCP?
PCP is caused by Pneumocystis Jirovecii, a fungus that causes pulmonary infections. Patients at risk of PCP are those who are immunocompromised (it is classed as an opportunistic infection, and an AIDS-defining illness in those with HIV).
121
Risk factors for PCP?
HIV with a CD4 count below 200 Steroids or other immunosuppressive medications Previous organ transplant Congenital immunodeficiencies (e.g. hypogammaglobulinaemia) Severe malnutrition Comorbid lung disease Haematological malignancies
122
Presentation of PCP?
Fever Dry cough Exertional breathlessness Chest pain
123
Differentials for PCP?
Bacterial/ viral pneumonia TB PE
124
Investigations to diagnose PCP?
Oxygen saturations ABG Sputum sample FBC, CRP, HIV test and CD 4 count CXR CT Bronchoscopy with bronchoalveolar lavage
125
Management of PCP?
Supportive treatment with analgesia, oxygen if hypoxic, consider holding immunosuppressant treatment High dose co-trimoxazole Steroid in moderate/ severe disease with PaO2 < 11kPa, either oral prednisolone or IV hydrocortisone
126
What is pneumonia?
inflammatory condition of the lung parenchyma caused by infection. Alveoli become filled with inflammatory cells and microorganisms, leading to consolidation of the lung tissue. This impairs gas exchange and can lead to hypoxia.
127
Epidemiology of pneumonia?
Community-acquired pneumonia has an incidence of 5-10 per 1000 adults in the UK per year. Approximately 22-42% of these cases require admission to hospital. Mortality estimates range from 5 to 14%, with half of these being in people aged over 84 years
128
Aetiology of pneumonia?
Most common; streptococcus pneumonia Haemophilus influenzae Moraxella catarrhalis Atypicals; Mycoplasma pneumoniae, Legionella pneumophila and Chylmydophila psittaci HAP; >48 hours after hospital admission pseudomonas aeruginosa, staphylococcus aureus
129
Classification of CAP?
Using CURB-65; Confusion Urea > 7mmol/L Respiratory rate > 30 breaths/min Blood pressure < 90 systolic and/or < 60mmHg diastolic 65 years or older 30 day mortality; CURB-65 0 - 0.7% CURB-65 1 - 3.2% CURB-65 2 - 13% CURB-65 3 - 17% CURB-65 4 - 41.5% CURB-65 5 - 57% A CURB-65 score of 0-1 requires home treatment, 2 should consider hospital admission, 3-5 admit to hospital and consider ITU referral.
130
Presentation of pneumonia?
Fever Malaise Rigors Cough Purulent sputum Pleuritic chest pain Haemoptysis Signs; Tachypnoea Tachycardia Hypotension Cyanosis Pyrexia Dullness to percussion over the consolidated area Increased vocal resonance/ tactile vocal fremitus over the consolidated area Bronchial breathing over the consolidated area Pleural rub may be heard due to inflammation of the adjacent pleura
131
Differentials of pneumonia?
Bronchiectasis Tuberculosis Lung cancer Bronchitis
132
Investigations to diagnose pneumonia?
Bedside; Sputum MC+S ABG Urinary legionella and pneumococcal antigens Bloods; FBC, CRP, U+E, LFT Mycoplasma serology CXR CT chest
133
Management of pneumonia?
Conservative; Oxygen if low saturations IV fluids if dehydrated Analgesia for myalgia or chest pain Escalate for respiratory support (e.g. continuous positive airway pressure or intubation and ventilation) if patients are severely unwell - consider escalation status and patient wishes Medical; Oral Abx; amoxicillin 500mg TDS for 5 days IV co-amoxiclav and clarithromycin for severe disease Patients with pneumonia should be followed up with a repeat chest X-ray after 6 to 8 weeks to screen for an underlying lung cancer
134
Complications of pneumonia?
Parapneumonic effusion Empyema Lung abscess Sepsis
135
What is pneumothorax?
Collection of air in the pleural cavity which may cause collapse of the underlying lung parenchyma
136
Classification of pneumothorax?
Spontaneous Traumatic Primary; with no underlying lung disease Secondary Tension; defect in the pleura that has led to the pneumothorax creates a one-way valve effect whereby air can enter the pneumothorax but not leave it. - This causes the pneumothorax to progressively expand, putting pressure on the heart and great vessels and causing mediastinal shift
137
Presentation of pneumothorax?
Sudden onset shortness of breath Pleuritic chest pain Dry cough Tachypnoea and increased work of breathing Signs; Unilateral reduced expansion Unilateral hyper-resonance to percussion Reduced or absent breath sounds Reduced vocal resonance or tactile vocal fremitus In tension pneumothorax; Tracheal deviation to the contralateral side Tachycardia Hypotension Distended neck veins
138
Investigations to diagnose pneumothorax?
Erect PA chest Xray CT chest ABG
139
Management of pneumothorax?
Tension pneumothorax; Decompress using large bore cannula in 2nd intercostal space in mid clavicular line If fails then open thoracotomy Chest drain after emergency decompression Pleural vent Review in 2-4 weeks Smoking cessation Advise patients not to fly until 7 days after chest imaging has confirmed resolution of the pneumothorax Advise patients they should not take part in underwater diving for life
140
What is a PE?
One or more blood clots lodge in and obstruct the pulmonary arterial vasculature
141
Presentation of PE?
Triad; Sudden-onset shortness of breath (the commonest symptom, present in around half of patients) Pleuritic chest pain Haemoptysis Cough Syncope Signs; Tachypnoea Crackles on auscultation Tachycardia Hypoxia Low-grade pyrexia in some In massive PE: - Hypotension - Cyanosis - Signs of right heart strain (e.g. a raised JVP, parasternal heave and loud P2)
142
What is pulmonary hypertension?
Normal mean pulmonary arterial pressure is 11-20mmHg. Pulmonary hypertension is characterised by an increase in this to above 25mmHg at rest. There are a variety of causes, all of which involve an increase in pulmonary vascular resistance which ultimately leads to right heart failure due to increased backpressure on the right ventricle.
143
Aetiology of pulmonary hypertension?
Pulmonary arterial hypertension - may be idiopathic, familial, associated with other diseases (e.g. HIV, connective tissue disorders or portal hypertension) or secondary to drugs or toxins (e.g. amphetamines, fenfluramine) Chronic pulmonary disease e.g. COPD, interstitial lung disease, bronchiectasis and obstructive sleep apnoea Chronic thromboembolic disease e.g. persistent or recurrent pulmonary emboli Chronic hypoventilation e.g. kyphosis or scoliosis, neuromuscular disorders Left heart disease e.g. chronic left heart failure or mitral stenosis Unclear or multifactorial mechanisms e.g. sarcoidosis, myelofibrosis, glycogen storage diseases
144
Types of pulmonary hypertension?
Group 1: pulmonary arterial hypertension Group 2: secondary to left heart diseases Group 3: secondary to chronic pulmonary diseases and/or hypoxia Group 4: due to chronic thrombotic or embolic disease Group 5: other causes including metabolic disorders, systemic disorders and haematological disease
145
Presentation of pulmonary hypertension?
Progressive shortness of breath Fatigue Syncope Fluid overload with ascites and peripheral oedema (late sign) Raised JVP Parasternal heave Loud P2 Presence of an S3 sound Pansystolic murmur indicative of tricuspid regurgitation (occurs due to the right ventricle becoming pressure and volume overloaded) End-diastolic murmur indicative of pulmonary regurgitation (due to high pulmonary pressures)
146
Differentials for pulmonary hypertension?
COPD Congestive heart failure Interstitial lung disease Mitral stenosis
147
Investigations to diagnose
ECG LFT, TFT, Autoimmune screen CXR High resolution CT CT/ MRI pulmonary angiography TTE Right heart catheterisation
148
Management of pulmonary hypertension
Conservative; As with any chronic disease, patient counselling and education Early involvement of palliative care especially in deteriorating patients or those with troubling symptoms In women of childbearing age with pulmonary arterial hypertension, counselling regarding the risks of pregnancy and provide contraceptive advice Medical; Diuretics for fluid overload Medications that reduce pulmonary vascular resistance: Calcium channel blockers e.g. nifedipine PDE-5 inhibitors e.g. sildenafil Prostacyclin analogues e.g. iloprost Endothelin receptor antagonists e.g. bosentan, ambrisentan Soluble guanylate cyclase stimulators e.g. riociguat Surgical; Thrombo-arterectomy or pulmonary balloon angioplasty may be considered for chronic thromboembolic disease Atrial septostomy is a palliative treatment where a hole is made between the atria to reduce right sided pressures A heart-lung transplant may be considered in severe cases
149
Complications of pulmonary stenosis?
Right heart failure Exertional syncope Alveolar haemorrhage Pulmonary artery dissection Pericardial effusions High risk of death during pregnancy
150
Prognosis of pulmonary stenosis?
If right heart function is preserved at diagnosis, mean survival is approximately 3 years If right heart failure is present or pulmonary hypertension is severe, this decreases to 1 year The best prognosis is seen with pulmonary hypertension secondary to chronic thromboembolic disease, especially if this is amenable to surgical treatment to reduce clot burden
151
What is respiratory alkalosis
pathophysiological state characterised by a decrease in the partial pressure of carbon dioxide in the arterial blood (PaCO2), leading to a high blood pH. Normal PaCO2 is around 4-6kPa, and normal pH 7.35-7.45.
152
Aetiology of respiratory alkalosis?
Pulmonary oedema Pneumonia Pulmonary embolism Pneumothorax Acute respiratory distress syndrome Anxiety/ panic attack Salicylate poisoning Meningitis/encephalitis Space occupying lesion Traumatic brain injury Hyperthermia Iatrogenic ventillation
153
Presentation of respiratory alkalosis?
Light-headedness Confusion Loss of consciousness Seizures Signs; Tachypnoea (the driver of the respiratory alkalosis) Hyperreflexia Tetany Decreased level of consciousness or confusion
154
ABG results in respiratory alkalosis?
High pH PaCO2; low HCO3- low/ normal
155
What is type 1 respiratory failure?
Type 1 respiratory failure (T1RF) is defined as hypoxaemia (PaO2<8kPa) with low or normal levels of carbon dioxide in the arterial blood
156
What is type 2 respiratory failure?
Type 2 respiratory failure (T2RF) is defined as hypoxaemia (PaO2<8kPa) with hypercapnia (PaCO2>6.5kPa)
157
Presentation of respiratory failure?
Symptoms include: Dyspnoea Headache Light-headedness Confusion Drowsiness Agitation Symptoms related to underlying cause e.g. productive cough and fever in pneumonia Signs include: Tachypnoea (although respiratory rate may be low in some cases of T2RF e.g. opiate overdose) Cyanosis Accessory muscle usage Nasal flaring Signs of central nervous system dysfunction e.g. reduced GCS, irritability Signs related to underlying cause e.g. wheeze in a COPD exacerbation Signs related to hypercapnia (i.e. T2RF only): Flushed skin Bounding peripheral pulses Asterixis Tachycardia or arrhythmia Drowsiness
158
Complications of respiratory failure?
Important complications include: A decline in lung function after recovery from the acute illness Hypoxic ischaemic injury to other organs (e.g. the brain) Cor pulmonale Polycythaemia Death Other complications are associated with CPAP or NIV: Mask leak Pressure sores from tight-fitting masks Hypotension Aspiration (due to gastric inflation) Pneumothorax Epistaxis Complications of invasive ventilation include: Dental injury during intubation Barotrauma (pressure-induced trauma to the lungs) Ventilator-associated pneumonia Tracheomalacia Complications of immobility (e.g. venous thromboembolism, pressure ulcers)
159
What is sarcoidosis?
Multi-system disease that is characterised by the formation of non-caseating granulomas around the body. This leads to inflammation and scarring in the organs affected, most commonly the lungs and skin. Other organs affected include the nerves, the brain, the heart, the liver and the eyes.
160
Epidemiology of sarcoidosis?
4,500 new diagnoses of sarcoidosis each year prevalence around 1 in 10,000 people highest rates seen in Northern Europe (e.g. Sweden, Finland and Denmark) Peak onset is in adults aged between 30 and 55 years old
161
Presentation of sarcoidosis?
Pulmonary manifestations Dry cough Dyspnoea Reduced exercise tolerance Chest pain Clubbing (rare, only if severe fibrosis) Fine crackles on auscultation Dermatological manifestations Erythema nodosum (inflammation of subcutaneous fat leading to tender nodules especially on the shins) Lupus pernio (red/purple plaques and nodules on the face) Hyper or hypopigmentation of the skin Neurological manifestations Meningitis Peripheral neuropathy Facial nerve palsy (may be bilateral) Headache Seizures/encephalopathy Ocular manifestations Uveitis Keratoconjunctivitis sicca Glaucoma Cardiac manifestations Arrhythmias Restrictive cardiomyopathy Syncope Abdominal manifestations Hepatomegaly Splenomegaly Renal stones Systemic manifestations Fatigue Weight loss Arthralgia Low-grade fevers Lymphadenopathy Enlarged parotid glands Lofgren's syndrome refers to the acute onset of: Fever Polyarthralgia Erythema nodosum Bilateral hilar lymphadenopathy (seen on chest X-ray) Heerfordt's syndrome refers to the combination of: Fever Uveitis Parotid swelling Facial nerve palsy
162
Investigations to diagnose sarcoidosis?
ECG Mantoux test Lung function test Ophthalmological examination FBC, LFT, U+E, bone profile, ESR, serum ACE Chest X-ray can be used to stage sarcoidosis as below: Stage 1 - Bilateral hilar lymphadenopathy (BHL) Stage 2 - BHL with peripheral infiltrates Stage 3 - Peripheral infiltrates alone Stage 4 - Pulmonary fibrosis High resolution CT chest PPET scan Echocardiogram Biopsy Bronchoalveolar lavage
163
Management of sarcoidosis?
Conservative; Patient education and support Smoking cessation No active treatment is needed in many cases of sarcoidosis Medical; Steroids e.g. oral prednisolone with a higher dose at induction which is then reduced to a lower maintenance dose Second line immunosuppressants (e.g. if steroids contraindicated or not effective) include methotrexate, mycophenolate or azathioprine Third line treatment is usually with biologics (e.g. infliximab) Surgical; Rarely in severe cases of pulmonary sarcoidosis a lung transplant may be considered In cases of pulmonary sarcoidosis complicated by aspergilloma, surgical management of haemoptysis is sometimes required
164
Complications of sarcoidosis?
Pulmonary fibrosis (stage IV pulmonary sarcoidosis) Cor pulmonale Pulmonary hypertension Aspergillomas can form in cavities left by granulomatous pulmonary disease Arrhythmias and sudden death in cardiac sarcoidosis Low mood and anxiety Complications of long-term steroid use (e.g. osteoporosis, hyperglycaemia)
165
Conditions associated with smoking?
Cancer - smoking is the commonest cause of lung cancer, and contributes to the development of many other tumour types COPD Cardiovascular disease - including stroke, ischaemic heart disease and peripheral vascular disease Peptic ulcers Pregnancy complications (e.g. stillbirth, birth defects, low birth weight) Infertility Osteoporosis Dementia Dental disease
166
Symptoms of nicotine withdrawal?
Mood changes (irritability, frustration, anger, anxiety, depression) Insomnia Poor concentration Increased appetite and weight gain Restlessness Cravings for cigarettes
167
Mechanism of bupropion?
inhibiting reuptake of dopamine and noradrenaline Tablet taken once a day for 6 days then twice a day for 7-9 weeks Should be started 7-14 days before the quit date
168
Contraindications to bupropion?
Epilepsy (decreases seizure threshold) Eating disorders Bipolar disorder Brain tumours Current benzodiazepine or alcohol withdrawal Pregnancy and breast-feeding
169
Side effects of bupropion?
insomnia, hypersensitivity reactions and rarely seizures
170
Varenicline mechanism of action?
partial nicotinic receptor agonist Start 7-14 days before the quit date, usually continued for 12 weeks
171
Contraindications to varenicline?
pregnancy and end-stage renal disease
172
Restrictive lung disease?
Idiopathic pulmonary fibrosis Sarcoidosis Asbestosis Non-pulmonary causes include: Neuromuscular disorders such as motor neuron disease or myasthenia gravis Obesity Skeletal abnormalities e.g. kyphoscoliosis
173
Obstructive lung diseases?
Asthma COPD Bronchiectasis Cystic Fibrosis Extrathoracic causes include: Tracheal stenosis Malignancy obstructing the upper airways Foreign body
174
What is a restrictive lung disease?
Any condition that reduces the lungs' ability to expand may lead to a restrictive defect on spirometry Both FEV1 and FVC are reduced (<80% of the predicted normal values), but the FEV1/FVC ratio is normal (>0.7)
175
What is an obstructive lung disease?
Any narrowing or obstruction of the airways can cause an obstructive defect on spirometry FEV1 is reduced (<80% of the predicted normal value) and the FEV1/FVC ratio is also reduced (<0.7) FVC may be normal or reduced to a lesser extent than FEV1
176
What is TB?
Infection with the Mycobacterium tuberculosis bacterium
177
Risk factors for TB?
HIV Immunosuppression Close contact with infected individuals Being from a high-risk country - countries with high rates of TB include India, Pakistan, Romania, Somalia and Eritrea Homelessness Malnutrition Child Elderly
178
Epidemiology of TB?
A quarter of the global population has been infected with TB Around 5-10% of these will develop active TB Worldwide, TB is the second commonest cause of death from infection (after COVID-19) More than 80% of TB deaths occur in low and middle-income countries In the UK there were 4411 cases of TB in 2021 The majority of cases are in people born outside the UK The highest rates are concentrated in urban areas (36% in London in 2021) Significant progress has been made in reducing the incidence of TB in the UK, with cases more than halving between 2011 and 2021
179
Presentation of TB?
Systemic: Night sweats Fevers Weight loss Malaise Lymphadenopathy lymph nodes are typically enlarged and non-tender may form sinus tracts if chronic cervical and supraclavicular nodes are most commonly affected Respiratory: Chronic productive cough Haemoptysis Shortness of breath Collapse or pleural effusion leading to dullness on percussion and reduced breath sounds over the affected area Neurological: Meningitis causing headaches and meningism Focal neurological signs (classically cranial nerve lesions due to involvement of the basal meninges) Decreased consciousness Genitourinary: Renal TB may present with haematuria and flank pain Epididymo-orchitis may present with pain and swelling Salpingitis (TB of the fallopian tube) may cause pain and vaginal bleeding Musculoskeletal: Pott's syndrome (spinal TB) causes back pain, spinal deformities and neurological deficits Arthritis causes joint pain and swelling Osteomyelitis may lead to a painful 'cold abscess' with localised swelling and erythema, sometimes wiht a draining abscess Psoas abscesses may present with a classic triad of fever, limp and back pain Gastrointestinal: Ileocaecal TB can cause bowel obstruction with abdominal pain and constipation Ascites may result from perotineal TB Intestinal TB may mimic IBD with abdominal pain and bloody diarrhoea Pericardial: Pericardial effusions may cause a raised JVP and pulsus parodoxus Constrictive pericarditis also causes a raised JVP and may present with signs of right-sided heart failure such as peripheral oedema and hepatic congestion Cutaneous: Erythema nodosum (tender nodules, usually on the shins) Lupus vulgaris refers to painful nodular skin lesions caused by TB, usually around the face Miliary TB may spread to the skin causing a widespread rash Scrolfuloderma is direct invasion of the skin from a TB-infected lymph node or bone, forming ulcerating and fistulating tracts from subcutaneous nodules usually around the neck area Adrenal: TB is the leading cause of adrenal insufficiency worldwide Symptoms include fatigue, lightheadedness, nausea and abdominal pain Signs include hypotension and skin hyperpigmentation
180
Differentials for TB?
Malignancy Sarcoidosis Lymphoma
181
Investigations to diagnose TB?
Mantoux test Sputum MC+S Ziehl- Neelsen microscopy FBC, CRP, U+E, mycobacterial MCS, HIV testing CXR; Cavitation Pleural effusion Mediastinal or hilar lymphadenopathy Parenchymal infiltrates, especially in the upper lobes Miliary TB (tiny nodules throughout the lung fields) Joint or spinal X-rays if suspected skeletal involvement CT head for suspected CNS TB Ultrasound of lymphadenopathy, the genitourinary system or the abdomen Echocardiogram for suspected pericardial disease Biopsy or needle aspiration
182
Management of TB?
Latent TB; Three months of isoniazid, pyridoxine and rifampicin OR Six months of isoniazid and pyridoxine ACTIVE; Medical treatment includes: The standard regimen for active pulmonary TB, which is 2 months of isoniazid (with pyradoxine), rifampicin, ethambutol and pyrazinamide, followed by isoniazid (with pyradoxine) and rifampicin alone for a further 4 months Longer courses of antibiotics in TB meningitis, pericardial and spinal TB Steroids may be added in the initial weeks of antibiotic treatment for CNS and pericardial TB Multidrug-resistant TB often requires 18-24 months of treatment with at least six drugs These second-line antibiotics include amikacin, macrolides, quinolones and capreomycin Surgical treatment involves: In selected cases of multidrug or extensively drug-resistant TB a lung resection may be considered This is either unilateral or of both lung apices Patients need adequate lung function to be eligible Some types of extra-pulmonary TB may warrant surgical treatment e.g. drainage of renal abscesses
183
Complications of TB?
Bronchiectasis Antibiotic resistance Transmission of TB Psychosocial distress Aspergilloma Pulmonary fibrosis Death
184
Prognosis of TB
With treatment, 90% of patients worldwide with TB are cured Untreated TB has around 70% mortality at 10 years for smear-positive cases, verus 20% for smear-negative cases Poor prognostic factors include older age, HIV co-infection and more extensive disease Multidrug and extensively drug-resistant TB also confer a poorer prognosis, with only 48% of patients cured with treatment
185
Side effects of rifampicin?
Red/orange discolouration of bodily fluids CYP450 induction (i.e. reduces effectiveness of other medications such as the combined oral contraceptive pill) Hepatotoxicity
186
Side effects of isoniazid?
Peripheral neuropathy (prevented by co-administration of pyridoxine) Hepatotoxicity CYP450 inhibition
187
Side effects of pyrazinamide?
Arthralgia Hyperuricaemia (may cause gout) Hepatotoxicity
188
Side effects of ethambutol?
Retrobulbar neuritis
189
Aetiology of URTI?
Coronaviruses Adenoviruses Enteroviruses Respiratory syncytial virus Metapneumovirus Influenza viruses
190
Presentation of URTI?
Coryza (which may manifest as rhinorrhoea, nasal congestion and loss of smell) Sneezing Cough Sore throat (may be erythematous on examination) Low-grade fever Malaise Headache Hoarse voice Conjunctival injection
191
Differentials for URTI?
Allergic rhinitis Influenza Whooping cough Infectious mononucleosis Nasal foreign body
192
Management of URTI?
Adequate fluid intake Rest Vapour rubs (e.g. Vicks) Inhaling steam or using nasal saline drops to help with nasal congestion Lozenges or analgesic sprays for sore throat Simple analgesia (paracetamol/ibuprofen) for fevers or pain Intranasal congestants should be used in the short term only as these can cause rebound symptoms if used chronically Prevent spread with good hand-hygeine, avoid sharing towels etc. Safety net people to seek medical advice if symptoms continue to worsen or are not improving beyond 10 days
193
Complications of URTI?
Acute otitis media Sinusitis COPD exacerbation Pneumonia