resp Flashcards
1
Q
what is Idiopathic pulmonary fibrosis
A
Idiopathic pulmonary fibrosis (IPF, previously termed cryptogenic fibrosing alveolitis) is a chronic lung condition characterised by progressive fibrosis of the interstitium of the lungs. Whilst there are many causes of lung fibrosis (e.g. medications, connective tissue disease, asbestos) the term IPF is reserved when no underlying cause exists.
2
Q
who is Idiopathic pulmonary fibrosis most common in
A
IPF is typically seen in patients aged 50-70 years and is twice as common in men.
3
Q
features of Idiopathic pulmonary fibrosis
A
Features
progressive exertional dyspnoea bibasal crackles on auscultation dry cough clubbing
4
Q
diagnosis of Idiopathic pulmonary fibrosis
A
Diagnosis
spirometry: classically a restrictive picture (FEV1 normal/decreased, FVC decreased, FEV1/FVC increased) impaired gas exchange: reduced transfer factor (TLCO) imaging: bilateral interstitial shadowing (typically small, irregular, peripheral opacities - 'ground-glass' - later progressing to 'honeycombing') may be seen on a chest x-ray but high-resolution CT scanning is the investigation of choice and required to make a diagnosis of IPF ANA positive in 30%, rheumatoid factor positive in 10% but this does not necessarily mean that the fibrosis is secondary to a connective tissue disease. Titres are usually low
CT scan showing advanced pulmonary fibrosis including ‘honeycombing’
5
Q
management and prognosis of Idiopathic pulmonary fibrosis
A
Management
pulmonary rehabilitation very few medications have been shown to give any benefit in IPF. There is some evidence that pirfenidone (an antifibrotic agent) may be useful in selected patients (see NICE guidelines) many patients will require supplementary oxygen and eventually a lung transplant
Prognosis
poor, average life expectancy is around 3-4 years
6
Q
Asthma: stepwise management in adults
A
The management of stable asthma is now well established with a step-wise approach:
Step Management
Step 1 Inhaled short-acting B2 agonist as required
Step 2 Add inhaled steroid at 200-800 mcg/day* 400 mcg is an appropriate starting dose for many patients. Start at dose of inhaled steroid appropriate to severity of disease
Step 3 1. Add inhaled long-acting B2 agonist (LABA)
- Assess control of asthma:
- good response to LABA - continue LABA
- benefit from LABA but control still inadequate: continue LABA and increase inhaled steroid dose to 800 mcg/day* (if not already on this dose)
- no response to LABA: stop LABA and increase inhaled steroid to 800 mcg/ day.* If control still inadequate, institute trial of other therapies, leukotriene receptor antagonist or SR theophylline
Step 4 Consider trials of:
- increasing inhaled steroid up to 2000 mcg/day*
- addition of a fourth drug e.g. Leukotriene receptor antagonist, SR theophylline, B2 agonist tablet
- the BTS say there is little evidence to separate the different options available. They do however suggest that leukotriene receptor antagonists are least likely to cause side-effects. Monitoring of serum concentrations may also be required for theophyllines
Step 5 Use daily steroid tablet in lowest dose providing adequate control. Consider other treatments to minimise the use of steroid tablets
Maintain high dose inhaled steroid at 2000 mcg/day* (*beclometasone dipropionate or equivalent)
Refer patient for specialist care
7
Q
use of Leukotriene receptor antagonists in asthma
A
Leukotriene receptor antagonists
e.g. Montelukast, zafirlukast have both anti-inflammatory and bronchodilatory properties should be used when patients are poorly controlled on high-dose inhaled corticosteroids and a long-acting b2-agonist particularly useful in aspirin-induced asthma associated with the development of Churg-Strauss syndrome
8
Q
MOA of long acting beta agonists in asthma
A
Long acting B2-agonists acts as bronchodilators but also inhibit mediator release from mast cells. Recent meta-analysis showed adding salmeterol improved symptoms compared to doubling the inhaled steroid dose
9
Q
the most important intervention in COPD
A
Whilst long-term oxygen therapy may increase survival in hypoxic patients, smoking cessation is the single most important intervention in patients with COPD
10
Q
General management of COPD
A
General management
smoking cessation advice annual influenza vaccination one-off pneumococcal vaccination
11
Q
COPD first line meds
A
Bronchodilator therapy
a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment
for patients who remain breathless or have exacerbations despite using short-acting bronchodilators the next step is determined by the FEV1
12
Q
second line therapy for COPD
A
for patients who remain breathless or have exacerbations despite using short-acting bronchodilators the next step is determined by the FEV1
FEV1 > 50%
long-acting beta2-agonist (LABA), for example salmeterol, or: long-acting muscarinic antagonist (LAMA), for example tiotropium
FEV1 < 50%
LABA + inhaled corticosteroid (ICS) in a combination inhaler, or: LAMA
For patients with persistent exacerbations or breathlessness
if taking a LABA then switch to a LABA + ICS combination inhaler otherwise give a LAMA and a LABA + ICS combination inhaler
13
Q
when should theophylines be considered in COPD
A
Oral theophylline
NICE only recommends theophylline after trials of short and long-acting bronchodilators or to people who cannot used inhaled therapy the dose should be reduced if macrolide or fluoroquinolone antibiotics are co-prescribed
14
Q
when should mucolytics be considered in COPD
A
Mucolytics
should be 'considered' in patients with a chronic productive cough and continued if symptoms improve
15
Q
how do you aspirate a pleural effusion
A
Pleural aspiration
as above, ultrasound is recommended to reduce the complication rate a 21G needle and 50ml syringe should be used fluid should be sent for pH, protein, lactate dehydrogenase (LDH), cytology and microbiology
16
Q
how do you distinguish between an exudate and a transudate
A
Light’s criteria was developed in 1972 to help distinguish between a transudate and an exudate. The BTS recommend using the criteria for borderline cases:
exudates have a protein level of >30 g/L, transudates have a protein level of 0.5 pleural fluid LDH divided by serum LDH >0.6 pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
17
Q
after a pleural effusion tap when should a chest drain be placed in situ
A
Pleural infection
all patients with a pleural effusion in association with sepsis or a pneumonic illness require diagnostic pleural fluid sampling if the fluid is purulent or turbid/cloudy a chest tube should be placed to allow drainage if the fluid is clear but the pH is less than 7.2 in patients with suspected pleural infection a test tube should be placed
18
Q
low glucose in pleural fluid tap is characteristic of what
A
low glucose: rheumatoid arthritis, tuberculosis
19
Q
raised amylase in pleural fluid is characteristic of what
A
raised amylase: pancreatitis, oesophageal perforation
20
Q
heavy blood staining in pleural fluid is characteristic of what
A
heavy blood staining: mesothelioma, pulmonary embolism, tuberculosis
21
Q
main subtypes of non small cell lung cancer
A
There are three main subtypes of non-small cell lung cancer:
Squamous cell cancer
typically central associated with parathyroid hormone-related protein (PTHrP) secretion → hypercalcaemia strongly associated with finger clubbing hypertrophic pulmonary osteoarthropathy (HPOA)
Adenocarcinoma
most common type of lung cancer in non-smokers, although the majority of patients who develop lung adenocarcinoma are smokers typically located on the lung periphery
Large cell lung carcinoma
22
Q
most common lung cancer in non smokers
A
Lung adenocarcinoma
most common type in non-smokers peripheral lesion
whilst it is the most common lung cancer in non smokers, the majority of people diagnosed with it are smokers.
23
Q
30-year-old woman who presented with a productive cough. This patient has x-ray findings consistent with dextrocardia and bronchiectasis (tram-track opacities). Hyperinflation is also seen in this film.
what disease might you suspect?
A
Kartagener’s syndrome (also known as primary ciliary dyskinesia) was first described in 1933 and most frequently occurs in examinations due to its association with dextrocardia (e.g. ‘quiet heart sounds’, ‘small volume complexes in lateral leads’)
Features
dextrocardia or complete situs inversus bronchiectasis recurrent sinusitis subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
24
Q
4 most common signs found in a patient with a PE other than chest pain and SOB
A
The PIOPED study1 in 2007 looked at the frequency of different symptoms and signs in patients who were diagnosed with pulmonary embolism.
The relative frequency of common clinical signs is shown below:
Tachypnea (respiratory rate >16/min) - 96% Crackles - 58% Tachycardia (heart rate >100/min) - 44% Fever (temperature >37.8°C) - 43%
25
whats the textbook triad of presenting features for a PE and how common does these ACTUALLY occur in PE
We know from experience that few patients (around 10%) present with the medical student textbook triad of pleuritic chest pain, dyspnoea and haemoptysis. Pulmonary embolism can be difficult to diagnose as it can present with virtually any cardiorespiratory symptom/sign depending on it's location and size.
26
All patients with symptoms or signs suggestive of a PE should have a history taken, examination performed and a chest x-ray to exclude other pathology. if you still suspect a PE after this what should you do
If a PE is still suspected a two-level PE Wells score should be performed:
27
contents of a two-level PE Wells score
Clinical feature Points
Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
An alternative diagnosis is less likely than PE 3
Heart rate > 100 beats per minute 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1
Malignancy (on treatment, treated in the last 6 months, or palliative) 1
Clinical probability simplified scores
PE likely - more than 4 points
PE unlikely - 4 points or less
28
if a two level PE wells score suggests a PE is likely, what do you do?
If a PE is 'likely' (more than 4 points) arrange an immediate computed tomography pulmonary angiogram (CTPA). If there is a delay in getting the CTPA then give low-molecular weight heparin until the scan is performed.
If a PE is 'unlikely' (4 points or less) arranged a D-dimer test. If this is positive arrange an immediate computed tomography pulmonary angiogram (CTPA). If there is a delay in getting the CTPA then give low-molecular weight heparin until the scan is performed.
If the patient has an allergy to contrast media or renal impairment a V/Q scan should be used instead of a CTPA.
29
The consensus view from the British Thoracic Society and NICE guidelines on CTPA vs V/Q scan in suspected PE
-- computed tomographic pulmonary angiography (CTPA) is now the recommended initial lung-imaging modality for non-massive PE. Advantages compared to V/Q scans include speed, easier to perform out-of-hours, a reduced need for further imaging and the possibility of providing an alternative diagnosis if PE is excluded
- - if the CTPA is negative then patients do not need further investigations or treatment for PE
- - ventilation-perfusion scanning may be used initially if appropriate facilities exist, the chest x-ray is normal, and there is no significant symptomatic concurrent cardiopulmonary disease
30
on a CTPA, whats the name given for an embolus that is stuck at the bifurcation of the pulmonary tree into the left and right pulmonary arteries?
a saddle embolus
31
ECG changes seen in PE
ECG
-- the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - 'S1Q3T3'. However this change is seen in no more than 20% of patients
-- right bundle branch block and right axis deviation are also associated with PE
-- sinus tachycardia may also be seen
32
management of Primary pneumothorax
Recommendations include:
if the rim of air is < 2cm and the patient is not short of breath then discharge should be considered
otherwise aspiration should be attempted
if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted
patients should be advised to avoid smoking to reduce the risk of further episodes - the lifetime risk of developing a pneumothorax in healthy smoking men is around 10% compared with around 0.1% in non-smoking men
33
management of Secondary pneumothorax
Recommendations include:
if the patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.
otherwise aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater then 1cm) a chest drain should be inserted. All patients should be admitted for at least 24 hours
if the pneumothorax is less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours
regarding scuba diving, the BTS guidelines state: 'Diving should be permanently avoided unless the patient has undergone bilateral surgical pleurectomy and has normal lung function and chest CT scan postoperatively.'
34
DD for Chest x-ray: cavitating lung lesion
Differential
abscess (Staph aureus, Klebsiella and Pseudomonas)
squamous cell lung cancer
tuberculosis
Wegener's granulomatosis
pulmonary embolism
rheumatoid arthritis
aspergillosis, histoplasmosis, coccidioidomycosis
35
what is Wegener's granulomatosis
Granulomatosis with polyangiitis (GPA), formerly known as Wegener's granulomatosis (WG), is a systemic disorder that involves both granulomatosis and polyangiitis. It is a form of vasculitis (inflammation of blood vessels) that affects small- and medium-size vessels in many organs. Damage to the lungs and kidneys can be fatal. It requires long-term immunosuppression.[1] When referred to as Wegener's granulomatosis, it is named after Friedrich Wegener, who described the disease in 1936.[2] Because of Wegener's association with the German Nazi party, professional bodies and journals have replaced his name with a descriptive name.[3]
Granulomatosis with polyangiitis is part of a larger group of vasculitic syndromes called systemic vasculitides or necrotizing vasculopathies, all of which feature an autoimmune attack by an abnormal type of circulating antibody termed ANCAs (antineutrophil cytoplasmic antibodies) against small and medium-size blood vessels.
- polyangiitis = inflammation of multiple blood vessels or lymph vessels
- Granuloma[a] (plural granulomas or granulomata) is an inflammation found in many diseases. It is a collection of immune cells known as macrophages.[1] Granulomas form when the immune system attempts to wall off substances that it perceives as foreign but is unable to eliminate.
36
what is histoplasmosis
infection by a fungus found in the droppings of birds and bats in humid areas. It is not serious if confined to the lungs but can be fatal if spread throughout the body.
37
what is coccidioidomycosis
a serious fungal disease of the lungs and other tissues, endemic in the warmer, arid regions of America.
38
The 2010 NICE guidelines on COPD clearly define which patients should be assessed for and offered long-term oxygen therapy (LTOT). Patients who receive LTOT should breathe supplementary oxygen for at least 15 hours a day. Oxygen concentrators are used to provide a fixed supply for LTOT.
Assess patients if any of the following:
Assess patients if any of the following:
very severe airflow obstruction (FEV1
39
Lung cancer: risk factors
Smoking
increases risk of lung ca by a factor of 10
Other factors
```
asbestos - increases risk of lung ca by a factor of 5
arsenic
radon
nickel
chromate
aromatic hydrocarbon
cryptogenic fibrosing alveolitis
```
Factors that are NOT related
coal dust
Smoking and asbestos are synergistic, i.e. a smoker with asbestos exposure has a 10 * 5 = 50 times increased risk
40
5 things asbestos exposure can cause in your lungs
Pleural plaques
Pleural plaques are benign and do not undergo malignant change. They are the most common form of asbestos related lung disease and generally occur after a latent period of 20-40 years.
Pleural thickening
Asbestos exposure may cause diffuse pleural thickening in a similar pattern to that seen following an empyema or haemothorax. The underlying pathophysiology is not fully understood.
Asbestosis
The severity of asbestosis is related to the length of exposure. This is in contrast to mesothelioma where even very limited exposure can cause disease. The latent period is typically 15-30 years. Asbestosis typically causes lower lobe fibrosis. As with other forms of lung fibrosis the most common symptoms are shortness-of-breath and reduced exercise tolerance.
Mesothelioma
Mesothelioma is a malignant disease of the pleura. Crocidolite (blue) asbestos is the most dangerous form.
Possible features
progressive shortness-of-breath
chest pain
pleural effusion
Patients are usually offered palliative chemotherapy and there is also a limited role for surgery and radiotherapy. Unfortunately the prognosis is very poor, with a median survival from diagnosis of 8-14 months.
Lung cancer
Asbestos exposure is a risk factor for lung cancer and also has a synergistic effect with cigarette smoke.
41
what are pleural plaques
Pleural plaques are benign and do not undergo malignant change. They are the most common form of asbestos related lung disease and generally occur after a latent period of 20-40 years.
Characterized by areas of fibrous thickening on the lining of the lungs (pleura) or diaphragm, the condition typically arises 20 to 30 years after asbestos exposure. The plaques can calcify over time, but they do not cause long-term health problems.
Pleural plaques are benign, which means they are not cancerous. Furthermore, they cannot become cancerous over time. In nearly every case, there are no symptoms, but some patients describe pain or an uncomfortable grating sensation as they breathe
Pleural plaques are almost exclusively caused by exposure to asbestos, but having the condition does not necessarily mean that you will develop a more serious asbestos-related disease like asbestosis or mesothelioma. However, because the presence of plaques suggests a significant past exposure to asbestos, mesothelioma or lung cancer may arise later in life.
42
normal blood urea range
Results of the blood urea nitrogen test are measured in milligrams per deciliter (mg/dL) in the United States and in millimoles per liter (mmol/L) internationally. In general, 7 to 20 mg/dL (2.5 to 7.1 mmol/L) is considered normal.
43
curb 65 criteria of severe pneumonia
CURB-65 criteria of severe pneumonia
Confusion (abbreviated mental test score of 8 or less)
urea over 7 mmol/L
Respiratory rate >= 30 / min
BP: systolic under 90 diastolic under 60.
age at least 65 years
0 or 1 = 1.5% mortality = outpatient care
2 = 9.2% mortality =inpatient vs observation admission
≥ 3 = 22% mortality = inpatient admission with consideration for ICU admission with score of 4 or 5
Patients with 3 or more (out of 5) of the above criteria are regarded as having a severe pneumonia
Other factors associated with a poor prognosis include:
presence of coexisting disease
hypoxaemia (pO2
44
6 common causes of Respiratory alkalosis
Common causes
```
anxiety leading to hyperventilation
pulmonary embolism
salicylate poisoning*
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
altitude
pregnancy
```
*salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis
45
what does a PE normally look like on a CXR
The vast majority of patients with a pulmonary embolism have a normal chest x-ray.
46
what is caplan's syndrome
Caplan's syndrome (or Caplan disease or Rheumatoid pneumoconiosis[1]) is a combination of rheumatoid arthritis (RA) and pneumoconiosis that manifests as intrapulmonary nodules, which appear homogenous and well-defined on chest X-ray.[2]
Caplan syndrome occurs only in patients with both RA and pneumoconiosis related to mining dust (coal, asbestos, silica)
Caplan syndrome presents with cough and shortness of breath in conjunction with features of rheumatoid arthritis such painful joints and morning stiffness. Examination should reveal tender, swollen MCP joints and rheumatoid nodules; auscultation of the chest may reveal diffuse râles that do not disappear on coughing or taking a deep breath.
47
Rheumatoid arthritis: respiratory manifestations
A variety of respiratory problems may be seen in patients with rheumatoid arthritis:
pulmonary fibrosis
pleural effusion
pulmonary nodules
bronchiolitis obliterans
complications of drug therapy e.g. methotrexate pneumonitis
pleurisy
Caplan's syndrome - massive fibrotic nodules with occupational coal dust exposure
infection (possibly atypical) secondary to immunosuppression
48
normal body temp range
36-37 degrees C
hypothermia is 35 and below
heat stroke at 41-42
death at 43 and above.
49
NICE issued guidance in 2008 on the management of respiratory tract infection, focusing on the prescribing of antibiotics for self-limiting respiratory tract infections in adults and children in primary care. what are the guidelines:
A no antibiotic prescribing or delayed antibiotic prescribing approach is generally recommended for patients with acute otitis media, acute sore throat/acute pharyngitis/acute tonsillitis, common cold, acute rhinosinusitis or acute cough/acute bronchitis.
However, an immediate antibiotic prescribing approach may be considered for:
children younger than 2 years with bilateral acute otitis media
children with otorrhoea who have acute otitis media
patients with acute sore throat/acute pharyngitis/acute tonsillitis when 3 or more Centor criteria are present
The Centor criteria* are as follows:
presence of tonsillar exudate
tender anterior cervical lymphadenopathy or lymphadenitis
history of fever
absence of cough
If the patient is deemed at risk of developing complications, an immediate antibiotic prescribing policy is recommended
are systemically very unwell
have symptoms and signs suggestive of serious illness and/or complications (particularly pneumonia, mastoiditis, peritonsillar abscess, peritonsillar cellulitis, intraorbital or intracranial complications)
are at high risk of serious complications because of pre-existing comorbidity. This includes patients with significant heart, lung, renal, liver or neuromuscular disease, immunosuppression, cystic fibrosis, and young children who were born prematurely
are older than 65 years with acute cough and two or more of the following, or older than 80 years with acute cough and one or more of the following:
- hospitalisation in previous year
- type 1 or type 2 diabetes
- history of congestive heart failure
- current use of oral glucocorticoids
The guidelines also suggest that patients should be advised how long respiratory tract infections may last:
acute otitis media: 4 days
acute sore throat/acute pharyngitis/acute tonsillitis: 1 week
common cold: 1 1/2 weeks
acute rhinosinusitis: 2 1/2 weeks
acute cough/acute bronchitis: 3 weeks
*if 3 or more of the criteria are present there is a 40-60% chance the sore throat is caused by Group A beta-haemolytic Streptococcus
50
when should a person not be prescribed antibiotics for a respiratory tract infection
A no antibiotic prescribing or delayed antibiotic prescribing approach is generally recommended for patients with acute otitis media, acute sore throat/acute pharyngitis/acute tonsillitis, common cold, acute rhinosinusitis or acute cough/acute bronchitis.
51
COPD: management of acute exacerbations, NICE guidelines
NICE guidelines from 2010 recommend the following:
increase frequency of bronchodilator use and consider giving via a nebuliser
give prednisolone 30 mg daily for 7-14 days
it is common practice for all patients with an exacerbation of COPD to receive antibiotics. NICE do not support this approach. They recommend giving oral antibiotics 'if sputum is purulent or there are clinical signs of pneumonia'
52
common causes of acute exacerbation of COPD
The most common bacterial organisms that cause infective exacerbations of COPD are:
Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis
Respiratory viruses account for around 30% of exacerbations, with the human rhinovirus being the most important pathogen.
53
4 types of Obstructive lung disease
Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans
54
spirometry in obstructive lung disease
FEV1 - significantly reduced
FVC - reduced or normal
FEV1% (FEV1/FVC) - reduced
55
7 types of restrictive lung disease
```
Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis
Neuromuscular disorders
```
56
spiromtery in restirctive lung disease
FEV1 - reduced
FVC - significantly reduced
FEV1% (FEV1/FVC) - normal or increased
57
if a patient has a history that sounds like asthma but is currently asymptomatic, what would be first line?
The new British Thoracic Society guidelines take a more practical approach to diagnosing asthma. If a patient has typical symptoms of asthma a trial of treatment is recommended. Normal spirometry when the patient is well does not exclude a diagnosis of asthma. The smoking history is unlikely to be relevant at her age.
58
how do you initially diagnose asthma
Whilst the diagnosis of asthma remains largely clinical, the British Thoracic Society (BTS) guidelines do offer some guidance on how we should approach this problem, for both adults and children. They recommend we classify patients as having either a high, intermediate or low probability of asthma based on the presence or absence of certain symptoms:
For adults it is recommend that they have a clinical assessment including spirometry (or Peak Expiratory Flow measurement if spirometry is not available):
When assessing patients we should therefore look for symptoms which may support a diagnosis of asthma, and those which may point to an alternative diagnosis. The BTS produced a list of features which are helpful when deciding this:
If a patient has many symptoms which make a diagnosis of asthma more likely (i.e. a high probability) then the BTS recommend that we start a trial of treatment. A good response is considered a positive 'test of reversibility'. If a patient has a poor response to treatment then further investigations should be considered.
For patients with a low probability of asthma then an alternative diagnosis should be sought. Further investigations and referral to a respiratory specialist should be considered.
If a patient has an intermediate probability of asthma the BTS recommend 'to carry out further investigations, including an explicit trial of treatments for a specified period, before confirming a diagnosis and establishing maintenance treatment. '. The accompanying algorithm suggests this decision should be partly guided by the FEV1/FVC ratio - a ratio of 400 ml improvement in FEV1 is considered significant
before and after 400 mcg inhaled salbutamol in patients with diagnostic uncertainty and airflow obstruction present at the time of assessment
if there is an incomplete response to inhaled salbutamol, after either inhaled corticosteroids (200 mcg twice daily beclometasone equivalent for 6-8 weeks) or oral prednisolone (30 mg once daily for 14 days)
It is now advised to interpret peak flow variability with caution due to the poor sensitivity of the test
diurnal variation % = [(Highest - Lowest PEFR) / Highest PEFR] x 100
assessment should be made over 2 weeks
greater than 20% diurnal variation is considered significant
59
clinical Features which make a diagnosis of asthma more likely
More than one of the following symptoms: wheeze, breathlessness, chest tightness and cough, particularly if:
symptoms worse at night and in the early morning
symptoms in response to exercise, allergen exposure and cold air
symptoms after taking aspirin or beta blockers
History of atopic disorder
Family history of asthma and/or atopic disorder
Widespread wheeze heard on auscultation of the chest
Otherwise unexplained low FEV1 or PEF (historical or serial readings)
Otherwise unexplained peripheral blood eosinophilia
60
clinical Features which make a diagnosis of asthma less likely
Prominent dizziness, light-headedness, peripheral tingling
Chronic productive cough in the absence of wheeze or breathlessness
Repeatedly normal physical examination of chest when symptomatic
Voice disturbance
Symptoms with colds only
Significant smoking history (ie > 20 pack-years)
Cardiac disease
Normal PEF or spirometry when symptomatic
61
What is the most appropriate initial treatment for suspected asthma?
The BTS state the following: Patients should start treatment at the step most appropriate to the initial severity of their asthma
This means that for some patients prescribing a corticosteroid inhaler in addition to a salbutamol inhaler is appropriate. The BTS suggest the following patients would benefit from a corticosteroid inhaler:
Inhaled steroids should be considered for patients with any of the following asthma-related features:
exacerbations of asthma in the last two years
using inhaled β2 agonists three times a week or more
symptomatic three times a week or more
waking one night a week
62
The British Thoracic Society (BTS) published guidelines in 2002 on the use of non-invasive ventilation in acute respiratory failure. Following these the Royal College of Physicians published guidelines in 2008: key indications and starting settings for NIV
Non-invasive ventilation - key indications
COPD with respiratory acidosis pH 7.25-7.35
type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
cardiogenic pulmonary oedema unresponsive to CPAP
weaning from tracheal intubation
Recommended initial settings for bi-level pressure support in COPD
Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O
Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O
back up rate: 15 breaths/min
back up inspiration:expiration ratio: 1:3
63
what is young's syndrome
Young's syndrome, also known as azoospermia sinopulmonary infections, sinusitis-infertility syndrome and Barry-Perkins-Young syndrome, is a rare condition that encompasses a combination of syndromes such as bronchiectasis, rhinosinusitis and reduced fertility.[1][2][3] In individuals with this syndrome, the functioning of the lungs is usually normal but the mucus is abnormally viscous. The reduced fertility (azoospermia) is due to functional obstruction of sperm transport down the genital tract at the epididymis where the sperms are found in viscous, lipid-rich fluid
64
what is bronchiectasis
Bronchiectasis describes a permanent dilatation of the airways secondary to chronic infection or inflammation.
65
7 broad causes of bronchiectasis
Causes
post-infective: tuberculosis, measles, pertussis, pneumonia
cystic fibrosis
bronchial obstruction e.g. lung cancer/foreign body
immune deficiency: selective IgA, hypogammaglobulinaemia
allergic bronchopulmonary aspergillosis (ABPA)
ciliary dyskinetic syndromes: Kartagener's syndrome, Young's syndrome
yellow nail syndrome
66
archetypal COPD patient
NICE recommend considering a diagnosis of COPD in patients over 35 years of age who are smokers or ex-smokers and have symptoms such as exertional breathlessness, chronic cough or regular sputum production.
67
4 investigations recommended to diagnose COPD
he following investigations are recommended in patients with suspected COPD:
post-bronchodilator spirometry to demonstrate airflow obstruction: FEV1/FVC ratio less than 70%
chest x-ray: hyperinflation, bullae, flat hemidiaphragm. Also important to exclude lung cancer
full blood count: exclude secondary polycythaemia
body mass index (BMI) calculation
68
severity grading of COPD
The severity of COPD is categorised using the FEV1*:
```
Post-bronchodilator FEV1/FVC, FEV1 (of predicted), Severity
< 0.7 > 80% Stage 1 - Mild**
< 0.7 50-79% Stage 2 - Moderate
< 0.7 30-49% Stage 3 - Severe
< 0.7 < 30% Stage 4 - Very severe
```
If a patient falls into the mild category they must have symptoms present to give a diagnosis of COPD.
69
classical signs of right upper lobe consolidation on CXR
abnormal opacity within the right upper lobe abutting the horizontal fissure.
70
6 broad causes of white shadowing on a CXR
There are numerous causes of white shadowing in the lungs including:
```
consolidation
pleural effusion
collapse
pneumonectomy
specific lesions e.g. tumours
fluid e.g. pulmonary oedema
```
71
6 common causes of a respiratory alkalosis
Common causes
```
anxiety leading to hyperventilation
pulmonary embolism
salicylate poisoning*
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
altitude
pregnancy
```
*salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis
72
10 common causes of haemoptysis
```
1 - lung cancer
2 - PE
3 - TB
4 - pulmonary oedema
5 - LRTI
6 - bronchiectasis
7 - mitral stenosis
8 - aspergilloma
9 - wegener's granulomatosis
10 - goodpasture's syndrome
```
73
main symptoms of goodpasture's
Haemoptysis
Systemically unwell: fever, nausea
Glomerulonephritis
haemoptysis
74
main symptoms of wegener's granulomatosis
Upper respiratory tract: epistaxis, sinusitis, nasal crusting
Lower respiratory tract: dyspnoea, haemoptysis
Glomerulonephritis
Saddle-shape nose deformity
haemoptysis
75
main symptoms of aspergilloma
Often past history of tuberculosis.
Haemoptysis may be severe
Chest x-ray shows rounded opacity
haemoptysis
76
main symptoms of mitral stenosis
```
Dyspnoea
Atrial fibrillation
Malar flush on cheeks
Mid-diastolic murmur
haemoptysis
```
77
main symptoms of bronchiectasis
Usually long history of cough and daily purulent sputum production
haemoptysis
78
main symptoms of LRTI
Usually acute history of purulent cough
| haemoptysis
79
main symptoms of PE
Pleuritic chest pain
Tachycardia, tachypnoea
haemoptysis
80
main symptoms of TB
Fever, night sweats, anorexia, weight loss
| haemoptysis
81
main symptoms of pulmonary oedema
Dyspnoea
Bibasal crackles and S3 are the most reliable signs
haemoptysis
82
main symptoms of lung cancer
History of smoking
Symptoms of malignancy: weight loss, anorexia
haemoptysis
83
stratification of acute severe asthma
Patients with acute severe asthma are stratified into moderate, severe or life-threatening
```
Moderate:
PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm
```
```
Severe:
PEFR 33 - 50% best or predicted
Can't complete sentences
RR > 25/min
Pulse > 110 bpm
```
```
Life-threatening:
PEFR < 33% best or predicted
Oxygen sats < 92%
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma
```
Note that a patient having any one of the life-threatening features should be treated as having a life-threatening attack.
84
treatment of acute severe asthma
Treatment is initiated with 100% oxygen, nebulised salbutamol and ipratropium bromide nebulisers and IV hydrocortisone
British Thoracic Society guidelines
magnesium sulphate recommended as next step for patients who are not responding (e.g. 1.2 - 2g IV over 20 mins)
little evidence to support use of IV aminophylline (although still mentioned in management plans)
if no response consider IV salbutamol
The SIGN guidelines give clear instructions on how to escalate care.
1. Oxygen
2. Salbutamol nebulisers
3. Ipratropium bromide nebulisers
4. Hydrocortisone IV OR Oral Prednisolone
5. Magnesium Sulfate IV
6. Aminophylline/ IV salbutamol
85
The most common bacterial organisms that cause infective exacerbations of COPD are:
Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis
Respiratory viruses account for around 30% of exacerbations, with the human rhinovirus being the most important pathogen.
86
NICE guidelines on treating infective exacerbation of COPD
NICE guidelines from 2010 recommend the following:
increase frequency of bronchodilator use and consider giving via a nebuliser
give prednisolone 30 mg daily for 7-14 days
it is common practice for all patients with an exacerbation of COPD to receive antibiotics. NICE do not support this approach. They recommend giving oral antibiotics 'if sputum is purulent or there are clinical signs of pneumonia'
87
what is cystic fibrosis
Cystic fibrosis (CF) is an autosomal recessive disorder causing increased viscosity of secretions (e.g. lungs and pancreas). It is due to a defect in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which codes a cAMP-regulated chloride channel
In the UK 80% of CF cases are due to delta F508 on the long arm of chromosome 7. Cystic fibrosis affects 1 per 2500 births, and the carrier rate is c. 1 in 25
88
Organisms which may colonise cyctic fibrosis patients
Staphylococcus aureus
Pseudomonas aeruginosa
Burkholderia cepacia*
Aspergillus
89
Community acquired pneumonia (CAP) may be caused by the following infectious agents:
```
Streptococcus pneumoniae (accounts for around 80% of cases)
Haemophilus influenzae
```
Staphylococcus aureus: commonly after the 'flu
atypical pneumonias (e.g. Due to Mycoplasma pneumoniae)
viruses
Klebsiella pneumoniae is classically in alcoholics
90
the most common cause of community acquired pneumonia and characteristic features
Streptococcus pneumoniae (pneumococcus) is the most common cause of community-acquired pneumonia
Characteristic features of pneumococcal pneumonia
rapid onset
high fever
pleuritic chest pain
herpes labialis
91
treatment of community acquired pneumonia
The British Thoracic Society published guidelines in 2009:
low or moderate severity CAP: oral amoxicillin. A macrolide should be added for patients admitted to hospital
high severity CAP: intravenous co-amoxiclav + clarithromycin OR cefuroxime + clarithromycin OR cefotaxime + clarithromycin
the current BNF has slightly different recommendations for high severity CAP: intravenous benzylpenicillin + clarithromycin OR benzylpenicillin + doxycycline. For 'life-threatening' infections the BNF recommends the same as the BTS guidelines for high-severity CAP
92
what is Kartagener's syndrome
Kartagener's syndrome (also known as primary ciliary dyskinesia) was first described in 1933 and most frequently occurs in examinations due to its association with dextrocardia (e.g. 'quiet heart sounds', 'small volume complexes in lateral leads')
Features
dextrocardia or complete situs inversus
bronchiectasis
recurrent sinusitis
subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
93
what is legionnaire's disease
Legionnaire's disease is caused by the intracellular bacterium Legionella pneumophilia. It is typically colonizes water tanks and hence questions may hint at air-conditioning systems or foreign holidays. Person-to-person transmission is not seen
94
features of legionnaire's
Features
```
flu-like symptoms including fever (present in > 95% of patients)
dry cough
relative bradycardia
confusion
lymphopaenia
hyponatraemia
deranged liver function tests
pleural effusion: seen in around 30% of ptients
```
95
diagnosis and management of legionaire's
Diagnosis
urinary antigen
Management
treat with erythromycin
96
Factors which may improve survival in patients with stable COPD
Factors which may improve survival in patients with stable COPD
smoking cessation - the single most important intervention in patients who are still smoking
long term oxygen therapy in patients who fit criteria
lung volume reduction surgery in selected patients
97
Cor pulmonale features and management
Cor pulmonale
features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2
use a loop diuretic for oedema, consider long-term oxygen therapy
ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICE
98
bronchiectasis - After assessing for treatable causes (e.g. immune deficiency) management is as follows
Bronchiectasis describes a permanent dilatation of the airways secondary to chronic infection or inflammation. After assessing for treatable causes (e.g. immune deficiency) management is as follows:
physical training (e.g. inspiratory muscle training) - has a good evidence base for patients with non-cystic fibrosis bronchiectasis
postural drainage
antibiotics for exacerbations + long-term rotating antibiotics in severe cases
bronchodilators in selected cases
immunisations
surgery in selected cases (e.g. Localised disease)
99
Most common organisms isolated from patients with bronchiectasis:
Most common organisms isolated from patients with bronchiectasis:
Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae
100
Sarcoidosis: management
Sarcoidosis is a multisystem disorder of unknown aetiology characterised by non-caseating granulomas. It is more common in young adults and in people of African descent
Indications for steroids:
patients with chest x-ray stage 2 or 3 disease who have moderate to severe or progressive symptoms. Patients with asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatment
hypercalcaemia
eye, heart or neuro involvement
101
what is sarcoidosis
Sarcoidosis is a multisystem disorder of unknown aetiology characterised by non-caseating granulomas. It is more common in young adults and in people of African descent
102
what is myasthenia gravis
Myasthenia gravis (from Greek μύς "muscle", ἀσθένεια "weakness", and Latin: gravis "serious"; abbreviated MG) is an either autoimmune or congenital neuromuscular disease that leads to fluctuating muscle weakness and fatigue. In the most common cases, muscle weakness is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction,[1] inhibiting the excitatory effects of the neurotransmitter acetylcholine on nicotinic receptors at neuromuscular junctions. Alternatively, in a much rarer form, muscle weakness is caused by a genetic defect in some portion of the neuromuscular junction, that is inherited at birth as opposed to developing it through autoimmunity later in life or through passive transmission by the mother's immune system at birth.[2]
Myasthenia is treated medically with acetylcholinesterase inhibitors or immunosuppressants, and, in selected cases, thymectomy. The disease incidence is 3–30 cases per million per year and rising as a result of increased awareness
103
what is erythema multiforme
Erythema multiforme is a skin condition of unknown cause, possibly mediated by deposition of immune complex (mostly IgM) in the superficial microvasculature of the skin and oral mucous membrane that usually follows an infection or drug exposure. It is an uncommon disorder, with peak incidence in the second and third decades of life.
The condition varies from a mild, self-limited rash (E. multiforme minor)[1] to a severe, life-threatening form known as erythema multiforme major (or erythema multiforme majus) that also involves mucous membranes.
104
what is Mycoplasma pneumoniae
Mycoplasma pneumoniae is a cause of atypical pneumonia which often affects younger patients. It is associated with a number of characteristic complications such as erythema multiforme and cold autoimmune haemolytic anaemia. Epidemics of Mycoplasma pneumoniae classically occur every 4 years. It is important to recognise atypical pneumonias as they may not respond to penicillins or cephalosporins due to it lacking a peptidoglycan cell wall.
105
features of Mycoplasma pneumoniae infection
Features
the disease typically has a prolonged and gradual onset
flu-like symptoms classically precede a dry cough
bilateral consolidation on x-ray
complications may occur as below
106
complications of Mycoplasma pneumoniae infection
Complications
cold agglutins (IgM) may cause an haemolytic anaemia, thrombocytopenia
erythema multiforme, erythema nodosum
meningoencephalitis, Guillain-Barre syndrome
bullous myringitis: painful vesicles on the tympanic membrane
pericarditis/myocarditis
gastrointestinal: hepatitis, pancreatitis
renal: acute glomerulonephritis
107
investigations and management of suspected mycoplasma pneumoniae infection
Investigations
diagnosis is generally by Mycoplasma serology
positive cold agglutination test
Management
erythromycin/clarithromycin
tetracyclines such as doxycycline are an alternative
108
Pulmonary embolism: management
The NICE guidelines of 2012 provided some clarity on how long patients should be anticoagulated for after a pulmonary embolism (PE). Selected points are listed below.
Low molecular weight heparin (LMWH) or fondaparinux should be given initially after a PE is diagnosed. An exception to this is for patients with a massive PE where thrombolysis is being considered. In such a situation unfractionated heparin should be used.
a vitamin K antagonist (i.e. warfarin) should be given within 24 hours of the diagnosis
the LMWH or fondaparinux should be continued for at least 5 days or until the international normalised ratio (INR) is 2.0 or above for at least 24 hours, whichever is longer, i.e. LMWH or fondaparinux is given at the same time as warfarin until the INR is in the therapeutic range
warfarin should be continued for at least 3 months. At 3 months, NICE advise that clinicians should 'assess the risks and benefits of extending treatment'
NICE advise extending warfarin beyond 3 months for patients with unprovoked PE. This essentially means that if there was no obvious cause or provoking factor (surgery, trauma, significant immobility) it may imply the patient has a tendency to thrombosis and should be given treatment longer than the norm of 3 months
for patients with active cancer NICE recommend using LMWH for 6 months
Thrombolysis
thrombolysis is now recommended as the first-line treatment for massive PE where there is circulatory failure (e.g. hypotension). Other invasive approaches should be considered where appropriate facilities exist
109
Asthma: occupational. what is it? what causes it? what do you do?
Patients may either present with concerns that chemicals at work are worsening their asthma or you may notice in the history that symptoms seem better at weekends / when away from work.
Exposure to the following chemicals is associated with occupational asthma:
```
isocyanates - the most common cause. Example occupations include spray painting and foam moulding using adhesives
platinum salts
soldering flux resin
glutaraldehyde
flour
epoxy resins
proteolytic enzymes
```
Serial measurements of peak expiratory flow are recommended at work and away from work.
Referral should be made to a respiratory specialist for patients with suspected occupational asthma.
110
what is COPD (in lay terms)
In the United States, the term "COPD" includes two main conditions—emphysema (em-fih-SE-ma) and chronic bronchitis (bron-KI-tis). (Note: The Health Topics article about bronchitis discusses both acute and chronic bronchitis.)
In emphysema, the walls between many of the air sacs are damaged. As a result, the air sacs lose their shape and become floppy. This damage also can destroy the walls of the air sacs, leading to fewer and larger air sacs instead of many tiny ones. If this happens, the amount of gas exchange in the lungs is reduced.
In chronic bronchitis, the lining of the airways is constantly irritated and inflamed. This causes the lining to thicken. Lots of thick mucus forms in the airways, making it hard to breathe.
Most people who have COPD have both emphysema and chronic bronchitis. Thus, the general term "COPD" is more accurate.
111
what is bronchiectasis
Bronchiectasis describes a permanent dilatation of the airways secondary to chronic infection or inflammation.
112
chronic SOB DD
```
Chronic obstructive pulmonary disease
Heart failure
Asthma
Aortic stenosis
Recurrent pulmonary emboli
Lung cancer
Pulmonary fibrosis
Bronchiectasis
Anaemia
Obesity
```
113
charachteristic features of heart failure
A history of ischaemic heart disease or hypertension may be present
Orthopnoea and paroxysmal nocturnal dyspnoea are characteristic
Bibasal crackles and a third heart sound (S3) are the most reliable features of left-sided failure
Right heart failure causes peripheral oedema and a raised JVP
SOB
114
features of Aortic stenosis
Chest pain, SOB and syncope seen in symptomatic patients
An ejection systolic murmur radiating to the neck and narrow pulse pressure are found on examination
SOB
115
features of Recurrent pulmonary emboli
There may be a history of predisposing factors e.g. Malignancy
Pleuritic chest pain and haemoptysis may be seen but symptoms are often vague
Tachycardia and tachypnoea are common in the acute situation
Symptoms of right heart failure may develop in severe cases
SOB
116
features of Lung cancer
Normally seen in smokers
Haemoptysis, chronic cough or unresolving infection are common presentations
Systemic symptoms e.g. Weight loss and anorexia
SOB
117
features of Pulmonary fibrosis
Progressive shortness of breath may be the only symptom
Fine bibasal crackles are typical
Spirometry shows a restrictive pattern
SOB
118
features of Bronchiectasis
Affected patients may produce large amounts of purulent sputum
Patients may have a history of previous infections (e.g. Tuberculosis, measles), bronchial obstruction or ciliary dyskinetic syndromes e.g. Kartagener's syndrome
SOB
119
features of Anaemia
There may be a history of gastrointestinal symptoms
Pallor may be seen on examination
SOB
120
what is this scoring system? - CHA2DS2-VASc
Used to determine the need to anticoagulate a patient in atrial fibrillation
121
what is this scoring system? - ABCD2
Prognostic score for risk stratifying patients who've had a suspected TIA
122
what is this scoring system? - NYHA
Heart failure severity scale
123
what is this scoring system? - DAS28
Measure of disease activity in rheumatoid arthritis
124
what is this scoring system? - Child-Pugh classification
A scoring system used to assess the severity of liver cirrhosis
125
what is this scoring system? - Wells score
Helps estimate the risk of a patient having a deep vein thrombosis
126
what is this scoring system? - MMSE
Mini-mental state examination - used to assess cognitive impairment
127
what is this scoring system? - HAD
Hospital Anxiety and Depression (HAD) scale - assesses severity of anxiety and depression symptoms
128
what is this scoring system? - PHQ-9
Patient Health Questionnaire - assesses severity of depression symptoms
129
what is this scoring system? - SCOFF
Questionnaire used to detect eating disorders and aid treatment
130
what is this scoring system? - CURB-65
Used to assess the prognosis of a patient with pneumonia
131
what is this scoring system? -
AUDIT
CAGE
FAST*
Alcohol screening tool
*FAST is also mnemonic to help patients/relatives identify the symptoms of a stroke
132
what is this scoring system? - Epworth Sleepiness Scale
Used in the assessment of suspected obstructive sleep apnoea
133
what is this scoring system? - IPSS
International prostate symptom score
134
what is this scoring system? Gleason score
Indicates prognosis in prostate cancer
135
what is this scoring system? Waterlow score
Assesses the risk of a patient developing a pressure sore
136
what is this scoring system? FRAX
Risk assessment tool developed by WHO which calculates a patients 10-year risk of developing an osteoporosis related fracture
137
what is this scoring system?Ranson criteria
Acute pancreatitis
138
what is this scoring system?MUST
Malnutrition
139
Carbon monoxide poisoning
Carbon monoxide has high affinity for haemoglobin and myoglobin resulting in a left-shift of the oxygen dissociation curve and tissue hypoxia. There are approximately 50 per year deaths from accidental carbon monoxide poisoning in the UK
Questions may hint at badly maintained housing e.g. student houses
```
Features of carbon monoxide toxicity
headache: 90% of cases
nausea and vomiting: 50%
vertigo: 50%
confusion: 30%
subjective weakness: 20%
severe toxicity: 'pink' skin and mucosae, hyperpyrexia, arrhythmias, extrapyramidal features, coma, death
```
Typical carboxyhaemoglobin levels
30% severe toxicity
Management
100% oxygen
hyperbaric oxygen
```
Indications for hyperbaric oxygen*
loss of consciousness at any point
neurological signs other than headache
myocardial ischaemia or arrhythmia
pregnancy
```
*as stated in the 2008 Department of Health publication 'Recognising Carbon Monoxide Poisoning'
140
management of Paracetamol overdose
Management
| activated charcoal if ingested
141
management of Salicylate overdose
Management
urinary alkalinization is now rarely used - it is contraindicated in cerebral and pulmonary oedema with most units now proceeding straight to haemodialysis in cases of severe poisoning
haemodialysis
142
management of Opioid/opiates overdose
Naloxone
143
management of Benzodiazepines overdose
Flumazenil
144
management of Tricyclic antidepressants overdose
Management
IV bicarbonate may reduce the risk of seizures and arrhythmias in severe toxicity
arrhythmias: class 1a (e.g. Quinidine) and class Ic antiarrhythmics (e.g. Flecainide) are contraindicated as they prolong depolarisation. Class III drugs such as amiodarone should also be avoided as they prolong the QT interval. Response to lignocaine is variable and it should be emphasized that correction of acidosis is the first line in management of tricyclic induced arrhythmias
dialysis is ineffective in removing tricyclics
145
management of Lithium overdose
Management
mild-moderate toxicity may respond to volume resuscitation with normal saline
haemodialysis may be needed in severe toxicity
sodium bicarbonate is sometimes used but there is limited evidence to support this. By increasing the alkalinity of the urine it promotes lithium excretion
146
management of Warfarin overdose
Vitamin K, prothrombin complex
147
management of Heparin overdose
Protamine sulphate
148
management of Beta-blockers overdose
Management
if bradycardic then atropine
in resistant cases glucagon may be used
149
management of Ethylene glycol overdose
Management has changed in recent times
ethanol has been used for many years
works by competing with ethylene glycol for the enzyme alcohol dehydrogenase
this limits the formation of toxic metabolites (e.g. Glycoaldehyde and glycolic acid) which are responsible for the haemodynamic/metabolic features of poisoning
fomepizole, an inhibitor of alcohol dehydrogenase, is now used first-line in preference to ethanol
haemodialysis also has a role in refractory cases
150
management of Methanol poisoning
Management
fomepizole or ethanol
haemodialysis
151
Organophosphate insecticides overdose management
Management
atropine
the role of pralidoxime is still unclear - meta-analyses to date have failed to show any clear benefit
152
management of Digoxin overdose
Digoxin-specific antibody fragments
153
management of Iron overdose
Desferrioxamine, a chelating agent
154
management of Lead overdose
Dimercaprol, calcium edetate
155
management of Carbon monoxide overdose
Management
100% oxygen
hyperbaric oxygen
156
management of Cyanide toxicity
Hydroxocobalamin; also combination of amyl nitrite, sodium nitrite, and sodium thiosulfate
157
the causes of clubbing
The causes of clubbing may be divided into cardiac, respiratory and other
Cardiac causes
cyanotic congenital heart disease (Fallot's, TGA)
bacterial endocarditis
atrial myxoma
```
Respiratory causes
lung cancer
pyogenic conditions: cystic fibrosis, bronchiectasis, abscess, empyema
tuberculosis
asbestosis, mesothelioma
fibrosing alveolitis
```
```
Other causes
Crohn's, to a lesser extent UC
cirrhosis, primary biliary cirrhosis
Graves' disease (thyroid acropachy)
rare: Whipple's disease
```
158
Chest x-ray: pulmonary oedema
Features of pulmonary oedema on a chest x-ray may include:
interstitial oedema
bat's wing appearance
upper lobe diversion (increased blood flow to the superior parts of the lung)
Kerley B lines
pleural effusion
cardiomegaly may be seen if there is cardiogenic cause
159
what is Bronchial breathing
This occurs in both inspiration and expiration with a gap in between. Difficult to describe how it
sounds, but pattern different to vesicular breathing (although many people with airways obstruction
have normal breath sounds that go on into middle or late expiration). You can mimic the sound by
putting your tongue on the roof of your mouth and breathing through open mouth.
Bronchial breathing heard when sound generated in the central airways is transmitted unchanged
through lung substance – ie. When the lung itself is solid as in consolidation but the air passages
remain open. Sound is conducted normally to the small airways and then modified by air in alveoli, but
solid lug conducts the sounds better straight to the lung surface and stethoscope.
If the central airways are obstructed by say a tumour, no transmission of sound will take place and no
bronchial breathing will be heard despite the presence of solid lung. An exception is seen in the upper
lobes, where it can be heard even if there is blockage.
Causes: pneumonia (almost always), lung abscess near the chest wall, dense fibrosis, effusion (can
hear above the effusion because it may compress lung), over a collapsed lung if the airway is patent
(rare, but can hear in upper lobes).
160
what are Wheezes (rhonchi)
Wheezes (rhonchi)
These are prolonged musical sounds, largely occurring on expiration (can be inspiratory though) –
due to localised narrowing of the bronchial tree. Caused by vibration of the walls of a bronchus near
to its point of closure.
Most patients with wheeze have many (=polyphonic wheeze), each coming from a single, narrowed
area. As the lung gets smaller on expiration, the airways also get smaller, and each narrowed airways
reaches a critical phase when it produces a wheeze and then stops doing so. So during expiration
you usually get lots of wheezes in sequence and together. A single wheeze indicates a single
narrowing – carcinoma or foreign body (=monophonic wheeze).
Wheezes are typical of airways narrowing of any cause – asthma and bronchitis are the most
common (smooth muscle contraction, inflammatory changes and increased bronchial secretions
cause narrowing). Sometimes patient with these conditions have no wheezes, in which case you can
ask them to take a deep breath in and blow out hard. Occasionally, wheezing can also be heard in
pulmonary oedema.
Don’t say “bronchospasm” – this is narrowing caused only by smooth muscle contraction, whereas
wheeze is usually multifactorial.
Wheeze-like breath sounds can disappear in severe asthma and emphysema because of low rates of
airflow – amount of wheeze does not correlate with severity of disease – PEFR is a better
measurement.
Causes: chronic bronchitis, asthma, emphysema, pulmonary oedema
161
what are Crackles (crepitations, rales)
There are two main types of crackles:
(1) “Coarse” crackles occur when there is fluid in the larger bronchi and a bubbling sound can be
heard that clears or alters as the secretions causing the sound are cleared on coughing or deep
breathing.
(2) “Fine” crackles sound like velcro – they occur on inspiration and are high-pitched, explosive
sounds. The mechanism for them is though to be: where you have premature closure of the small
airways at the end of expiration, you need to overcome the surface tension keeping them closed on
the next inspiration to open them. When they eventually “pop open”, crackles are produced. During
inspiration, larger bronchi open before smaller ones, so crackles from chronic bronchitis and
bronchiectasis occur early. Conditions largely involving the alveoli (LVF, fibrosis, pneumonia) tend to
produce crackles later on inspiration.
Note whether crackles are localised – this would be expected in pneumonia and mild bronchiectasis.
Pulmonary oedema and fibrosing alveolitis typically affect both lung bases equally.
Normal people, especially smokers, may have a few basal crackles – these usually clear with a few
deep breaths.
Causes: LVF, fibrosing alveolitis, extrinsic allergic alveolitis, pneumonia, bronchiectasis, chronic
bronchitis, asbestosis.
162
what is a Pleural rub
Caused by the inflamed surfaces of the pleura rubbing together – it sounds like a creaking noise. You
can try to imitate it by placing one hand over the ear and rubbing the back of that hand with the
fingers of the other.
Pleural rub is usually heard on both inspiration and expiration. Make sure you’re not just moving the
stethoscope on the chest if you think you hear it. Coarse crackles can also sound like rubs – a cough
will shift the former.
If there is any pain, ask the patient to show you where it is – this will often localise the rub.
Causes: pleural inflammation (pneumonia, pulmonary embolism), effusion.
163
ARDS: diagnostic criteria
```
ARDS:
Acute onset
Ratio (PaO2/FiO2) less than 200
Diffuse infiltration
Swan-Ganz Wedge pressure less than 19 mmHg
```
Pulmonary capillary wedge pressure (PCWP) provides an indirect estimate of left atrial pressure (LAP). PCWP is measured by inserting balloon-tipped, multi-lumen catheter (Swan-Ganz catheter) into a peripheral vein, then advancing the catheter into the right atrium, right ventricle, pulmonary artery, and then into a branch of the pulmonary artery
Acute respiratory distress syndrome (ARDS)
164
Marfan syndrome features
```
MARFAN'S:
Mitral valve prolapse
Aortic Aneurysm
Retinal detachment
Fibrillin
Arachnodactyly
Negative Nitroprusside test (differentiates from homocystinuria)
Subluxated lens
```
165
Metabolic acidosis: causes
```
KUSSMAL:
Ketoacidosis
Uraemia
Sepsis
Salicylates
Methanol
Alcohol
Lactic acidosis
```
Metabolic acidosis is commonly classified according to the anion gap.
Normal anion gap ( = hyperchloraemic metabolic acidosis)
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison's disease
```
Raised anion gap
lactate: shock, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol
```
166
Hemoptysis: causes
```
HEMOPTYSIS:
Haemorrhagic diathesis
Edema [LVF due to mitral stenosis]
Malignancy
Others [eg: vasculitis]
Pulmonary vascular abnormalities
Trauma
Your treatment [anticoagulants]
SLE
Infarction in lungs
Septic
```
167
Pulmonary fibrosis: causes
```
SCAR:
Upper lobe:
Silicosis/ Sarcoidosis
Coal worker pneumonconiosis
Ankylosing spondylitis
Radiation
Lower lobe:
Systemic sclerosis
Cyptogenic fibrosing alveolitis
Asbetosis
Rheumatoid arthritis
```
168
Wheezing: causes
```
ASTHMA:
Asthma
Small airways disease
Tracheal obstruction
Heart failure
Mastocytosis or carcinoid
Anaphylaxis or allergy
```
169
Chest X-ray: cavitating lesions differential
```
"If you see HOLES on chest X-ray, they are WEIRD":
Wegener's syndrome
Embolic (pulmonary, septic)
Infection (anaerobes, pneumocystis, TB)
Rheumatoid (necrobiotic nodules)
Developmental cysts (sequestration)
Histiocytosis
Oncological
Lymphangioleiomyomatosis
Environmental, occupational
Sarcoid
Alternatively: L=Left atrial myxoma
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170
Lung cancer: notorious consequences
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SPEECH:
Superior vena cava syndrome
Paralysis of diaphragm (Phrenic nerve)
Ectopic hormones
Eaton-Lambert syndrome
Clubbing
Horner syndrome/ Hoarseness
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171
skin Mole: signs of trouble
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ABCDE:
Asymmetry
Border irregular
Colour irregular
Diameter usually > 0.5cm
Elevation irregular
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172
Post-operative fever causes
Six W's:
Wind: pulmonary system is primary source of fever first 48 hours, may have pneumonia
Wound: infection at surgical site
Water: check IV for phlebitis
Walk: deep venous thrombosis, due to pelvic pooling or restricted mobility related to pain and fatigue
Whiz: urinary tract infection if urinary catheterization
Wonder drugs: drug-induced fever
173
if you treat someone with ABX for a pneumonia and it fails to clear, what is the most important thing to dp? why might this happen?
need to re-image the chest. especially if the fever has not settled, if there is a swinging pyrexia (fluctuating) this is usually suggestive of a collection of pus somewhere. this can be a para-pneumonic effusion or an empyema in the pleural space or a cavity of pus in the parenchyma that needs a longer course of abs, 4-6 weeks, and maybe postural drainage.
174
what X-ray findings might you get in bronchiectasis
tramlines and ring shadows, these are affected bronchi seen end on, perhaps quite tough to spot. (these are different to the signet ring shadows seen on a chest CT)
175
if a PT with a chronic lung condition has just been hospitalised for the first time in a long while what should you always do
BTS says - take the opportunity to review the PTs self management skills. best way is via a personalised action plan., no PT should leave hospital without one. need to check what therapies they are taking, when and how.
with asthma it should also be noted that any admission should be followed up by an appt with an asthma specialist within 30 days.
176
who gets IV magnesium sulphate
asthmatics who fail to show a good initial response to bronchodilators, or those in life threatening or near fatal asthma.
magnesium sulphate recommended as next step for patients who are not responding (e.g. 1.2 - 2g IV over 20 mins)
177
objective signs that a patient is losing control of their asthma
waking at night with wheeze, cough or chest pain.
increased use of bronchodilators.
decreased effectiveness of bronchodilators
work days missed through asthma
any change in exercise tolerance.
178
a patient who is hospitalised with an acute asthma attack. when can they be discharged home
once stable on their regular therapy for 24 hours. their peak flows must be at least 75% OF best or predicted. this is a good time to check inhaler technique and that they have a plan to prevent future readmission.
179
what is in seretide
salmeterol 50 micrograms and fluticasone (variable odse - 100, 250 500 micrograms, but the higher doses are used more in COPD.
180
advice to give someone about what to do in an asthma atttack
1 - take the reliever immediately
2 - sit down and loosen tight clothing. do not lie down
3 - if no improvement take one puff every minute for 5 minutes or until symptoms improve.
4 - if symptoms don't improve in 5 minutes call 999
5 - continue to take 1 puff every minute until help arrives.
181
important principles of an outpatient prescriiption
can be computer generated inc the date. PT name, address and form of medication. signature must be handwritten. total quantity to be supplied must be in words and figures. date of birth, except for a child under 12, and GMC number are not required.
182
how do CPAP and NIV work
CPAP is delivered throughout the respiratory cycle, not changing on inspiration or expiration.
NIV, also known as BiPAP, aids the inspiration by delivering higher pressures during inspiration and dropping to a CPAP during expiration. this allows retained CO2 to be expired as a result of the positive end-expiratory pressure 'stunting' the airways open.
183
classic signs of a pneumothorax
decreased air entry, reduced expansion, hyper resonant percussion.
184
how does chostochondritis present
presents insidiously until it causes severe sharp pain originating from the anterior chest wall and often radiating around the back. rule out more serious causes first.
185
depression and abdo pain and general aches in a smoker?
hypercalcaemia due to skeletal met of a cancer or PTH secretion by a squamous cell tumour.
stones - renal stones
bones - pain and sometimes pathological fractures.
groans - abdo pain from ulcers, nausea, indigestion, or constipation
psychic moans - lethargy, fatigue, depression.
186
what neuro areas can a pancoast tumour affect
sympathetic nexus causing horners
brachial plexus
recurrent laryngeal nerve
187
hyponatraemia in someone with possible lung cancer?
suggests SIADH due to ectopic hormone secretion by a small cell tumour. these make up about 20% of lung cancers.
188
Lung cancer: small cell
| overview
Features
usually central
arise from APUD* cells
associated with ectopic ADH, ACTH secretion
ADH → hyponatraemia
ACTH → Cushing's syndrome
ACTH secretion can cause bilateral adrenal hyperplasia, the high levels of cortisol can lead to hypokalaemic alkalosis
Lambert-Eaton syndrome: antibodies to voltage gated calcium channels causing myasthenic like syndrome
Management
usually metastatic disease by time of diagnosis
patients with very early stage disease (T1-2a, N0, M0) are now considered for surgery. NICE support this approach in their 2011 guidelines
however, most patients with limited disease receive a combination of chemotherapy and radiotherapy
patients with more extensive disease are offered palliative chemotherapy
189
Metastatic bone pain - management
Metastatic bone pain may respond to NSAIDs, bisphosphonates or radiotherapy
Bone pain often responds well to NSAIDs. Both radiotherapy and bisphosphonates have a role in managing bony pain but these are not first-line treatments.
The SIGN guidelines do not explicitly state which treatments are first-line for bone pain (NSAID, bisphosphonate or radiotherapy). However, applying the principles of the WHO analgesic ladder and also the results of Cochrane reviews (see link) the most appropriate first-line treatment would be an NSAID.
190
Lung cancer: non-small cell overview
There are three main subtypes of non-small cell lung cancer:
Squamous cell cancer
typically central
associated with parathyroid hormone-related protein (PTHrP) secretion → hypercalcaemia
strongly associated with finger clubbing
hypertrophic pulmonary osteoarthropathy (HPOA)
Adenocarcinoma
most common type of lung cancer in non-smokers, although the majority of patients who develop lung adenocarcinoma are smokers
typically located on the lung periphery
Large cell lung carcinoma
191
Superior vena cava obstruction
| overview inc management
Superior vena cava (SVC) obstruction is an oncological emergency caused by compression of the SVC. It is most commonly associated with lung cancer.
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Features
dyspnoea is the most common symptom
swelling of the face, neck and arms - conjunctival and periorbital oedema may be seen
headache
visual disturbance
pulseless jugular venous distension
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Causes
common malignancies: small cell lung cancer, lymphoma
other malignancies: metastatic seminoma, Kaposi's sarcoma, breast cancer
aortic aneurysm
mediastinal fibrosis
goitre
SVC thrombosis
Management
general: dexamethasone, balloon venoplasty, stenting
small cell: chemotherapy + radiotherapy
non-small cell: radiotherapy
192
Antibiotic therapy is based upon the CURB-65 score in NICE guidelines:
The patient in this scenario fulfills the criteria for raised respiratory rate, raised blood urea nitrogen, low blood pressure and age of 65 or more. Therefore he has a CURB-65 score of 4, which is classified as high risk.
Antibiotic therapy is based upon the CURB-65 score in NICE guidelines:
For the treatment of low-severity community-acquired pneumonia offer a 5day course of a single antibiotic. Consider amoxicillin in preference to a macrolide or a tetracycline. Consider a macrolide or a tetracycline for patients who are allergic to penicillin.
For the treatment of moderate- and high-severity community-acquired pneumonia consider a 7 to 10day course of antibiotic therapy. Consider dual antibiotic therapy with amoxicillin and a macrolide for patients with moderate-severity community-acquired pneumonia. Consider dual antibiotic therapy with a beta-lactamase stable beta-lactam and a macrolide for patients with high-severity community-acquired pneumonia.
Therefore, according to NICE guidelines, the patient in this scenario with a severe community acquired pneumonia would be best treated with a beta-lactam antibiotic (such as cefotaxime) and a macrolide (such as clarithromycin).
193
Iatrogenic pneumothorax
Recommendations include:
less likelihood of recurrence than spontaneous pneumothorax
majority will resolve with observation, if treatment is required then aspiration should be used
ventilated patients need chest drains, as may some patients with COPD
194
HIV: Pneumocystis jiroveci pneumonia
Pneumocystis jiroveci commonly presents desaturation on exertion and often Chest x-ray appears normal. It almost exclusively happens in immunosuppressed patients. In this case it assumes a background history of HIV. Swaziland has one of the highest prevalences of HIV in the world (source WHO). The patient has had recurrent chest infections which in such a young patient should be suggestive of immunosuppression.
Pulmonary embolism could cause the desaturation but would not explain the recurrent chest infections.
HIV: Pneumocystis jiroveci pneumonia
Whilst the organism Pneumocystis carinii is now referred to as Pneumocystis jiroveci, the term Pneumocystis carinii pneumonia (PCP) is still in common use
Pneumocystis jiroveci is an unicellular eukaryote, generally classified as a fungus but some authorities consider it a protozoa
PCP is the most common opportunistic infection in AIDS
all patients with a CD4 count
195
Bronchiectasis: management
Bronchiectasis: management
Bronchiectasis describes a permanent dilatation of the airways secondary to chronic infection or inflammation. After assessing for treatable causes (e.g. immune deficiency) management is as follows:
physical training (e.g. inspiratory muscle training) - has a good evidence base for patients with non-cystic fibrosis bronchiectasis
postural drainage
antibiotics for exacerbations + long-term rotating antibiotics in severe cases
bronchodilators in selected cases
immunisations
surgery in selected cases (e.g. Localised disease)
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Most common organisms isolated from patients with bronchiectasis:
Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae
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196
Lung cancer: referral
Despite a normal chest x-ray an ex-smoker with shortness of breath, weight loss and hyponatraemia should be investigated on an urgent basis for lung cancer. This approach is supported by current NICE guidelines. Whilst gastrointestinal cancer is a possibility the normal MCV is not entirely consistent with chronic blood loss
Lung cancer: referral
The 2005 NICE cancer referral guidelines gave the following advice:
Consider immediate referral for patients with:
signs of superior vena caval obstruction (swelling of the face/neck with fixed elevation of jugular venous pressure)
stridor
Refer urgently patients with:
persistent haemoptysis (in smokers or ex-smokers aged 40 years and older)
a chest X-ray suggestive of lung cancer (including pleural effusion and slowly resolving consolidation)
a normal chest X-ray where there is a high suspicion of lung cancer
a history of asbestos exposure and recent onset of chest pain, shortness of breath or unexplained systemic symptoms where a chest x-ray indicates pleural effusion, pleural mass or any suspicious lung pathology
Refer urgently for chest x-ray for patients with any of the following:
haemoptysis
unexplained or persistent (longer than 3 weeks): chest and/or shoulder pain, dyspnoea, weight loss, chest signs, hoarseness, finger clubbing, cervical or supraclavicular lymphadenopathy, cough, features suggestive of metastasis from a
lung cancer (for example, secondaries in the brain, bone, liver, skin)
underlying chronic respiratory problems with unexplained changes in existing symptoms
197
Cystic fibrosis: features
Presenting features
neonatal period (around 20%): meconium ileus, less commonly prolonged jaundice
recurrent chest infections (40%)
malabsorption (30%): steatorrhoea, failure to thrive
other features (10%): liver disease
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Other features of cystic fibrosis
short stature
diabetes mellitus
delayed puberty
rectal prolapse (due to bulky stools)
nasal polyps
male infertility, female subfertility
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198
Chest x-ray: lung metastases
The chest x-ray shows cannonball metastases which are most commonly caused by renal cell cancer. A CT abdomen is the most appropriate test to investigate this possibility.
Other tests should of course be considered including a prostate specific antigen.
Chest x-ray: lung metastases
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Lung metastases are seen with a wide variety of cancers including:
breast cancer
colorectal cancer
renal cell cancer
bladder cancer
prostate cancer
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Multiple, round well-defined lung secondaries are often referred to as 'cannonball metastases'. They are most commonly seen with renal cell cancer but may also occur secondary to choriocarcinoma and prostate cancer.
Chest x-ray showing cannonball metastases secondary to renal cell cancer. Multiple well defined nodules are noted distributed in both lung fields
199
Cystic fibrosis: management
Management of cystic fibrosis involves a multidisciplinary approach
Key points
regular (at least twice daily) chest physiotherapy and postural drainage. Parents are usually taught to do this. Deep breathing exercises are also useful
high calorie diet, including high fat intake*
vitamin supplementation
pancreatic enzyme supplements taken with meals
heart and lung transplant
*this is now the standard recommendation - previously high calorie, low-fat diets have been recommended to reduce the amount of steatorrhoea
200
who needs weaning off steroids and who doesnt
patients who have had a course of steroids shorter than 3 weeks and of doses less than 40mg do not need gradual weaning, unless they have a history of repeated steroid use or previous adrenal suppression.
201
abdo pain and postural hypotension in someone with lung cancer?
adbo pain and postural hypotension is suggestive of adrenocortical insufficiency. in a pt with lung cancer this is most likely to be due to mets of the cancer to the adrenal glands, causing secondary addison disease.
202
what causes aminophylline toxicity
cyp450 inhibitors. causes abdo pain, loose stools and vomiting. used in COPD patients
203
who is obliged to fill out the medical certificate of cause of death for a patient who dies
a doctor who attended to the patient in their last illness. they should have seen the patient at least twice.
204
how does chlamydia pneumoniae present
pharyngitis and otitis before progressing to pneumonia. quite different from the other atypical pneumonias.
205
what type of pneumonia does staphylococcus cause
a cavitiating pneumonia in those at either end of the age spectrum or with underlying lung disease.
206
what type of pneumonia does klebsiella cause
its a rare cause of pneumonia. it causes cavitations particularly in the upper lobes in immunocompromised populations such as the elderly and alcoholics.
207
what does pulmonary fibrosis look like on xray
reticulo-nodular shadowing in the lower zones that is criss crossing lines or tiny nodules or both
208
causes of metabolic alkalosis
Metabolic alkalosis may be caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly to problems of the kidney or gastrointestinal tract
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Causes
vomiting / aspiration (e.g. peptic ulcer leading to pyloric stenos, nasogastric suction)
diuretics
liquorice, carbenoxolone
hypokalaemia
primary hyperaldosteronism
Cushing's syndrome
Bartter's syndrome
congenital adrenal hyperplasia
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209
result of vitamin B3 deficiency
B3 Niacin Pellagra
dermatitis
diarrhoea
dementia
