Respiratory Flashcards

(75 cards)

1
Q
A

Coal worker’s Pneumoconiosis

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2
Q

What is pneumoconiosis?

A

Coal worker’s pneumoconiosis*, sometimes referred to as ‘black lung disease’, is an occupational lung disease caused by long term exposure to coal dust particles.

It is most commonly experienced by those who have been involved in the coal mining industry and severity is linked to the extent of exposure. Often there is a long lead time between the first exposure and the development of the disease.

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3
Q

What is the pathophysiology of pneumoconiosis?

A
  1. Coal dust (2-5 μm in size) is inhaled and enters the lungs.
  2. The dust reaches the terminal bronchioles and there it is engulfed by alveolar and interstitial macrophages.
  3. The dust particles are then moved by the macrophages via the mucociliary elevator and removed from the body as mucus.
  4. In coal miners who are exposed over many years, the system is overwhelmed and the macrophages begin to accumulate in the alveoli, which starts an immune response, causing damage to the lung tissue.
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4
Q

What are the 2 types of pneumoconiosis?

A
  • Simple pneumoconiosis
  • Progressive Massive Fibrosis
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5
Q

How does simple pneumoconiosis present? What can it lead to?

A
  • Is the commonest type of pneumoconiosis.
  • Patients are often asymptomatic.
  • Its presence increases the risk of lung diseases such as COPD.
  • Simple pneumoconiosis may lead to Progressive Massive Fibrosis (PMF), occurring in around 30% of those with stage 3 grading.
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6
Q

How do we stage Pneumoconiosis?

A

International Labour Office:
Category 1: some opacities but normal lung markings visible
Category 2: large number of opacities but normal lung markings visible
Category 3: large number of opacities with normal lung not visible

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7
Q

How does Progressive Massive Fibrosis present? What happens to the lung function?

A
  • Dust exposure causes patients to develop round fibrotic masses which can be several centimetres in diameter.
  • These are most commonly in the upper lobes.
  • The exact pathogenesis is not known.
  • Patients are often symptomatic and have both breathlessness on exertion and cough, some may have black sputum.
  • Lung function testing shows a mixed obstructive/restrictive picture.
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8
Q

What are the ix for pneumoconiosis?

A
  • Chest x-ray: upper zone fibrosis
  • Spirometry: restrictive lung function tests - a normal or slightly reduced FEV1 and a reduced FVC
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9
Q

What is the most common type of pneumonia?

A

bacterial pneumonia is by far the most common type of pneumonia seen in clinical practice. Other infective causes include:
* viral
* fungal (e.g. Pneumocystis jiroveci)

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10
Q

What organisms cause pneumonia? What are the main features?

A
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11
Q

What are HAPs?

A

Patients who develop pneumonia within hospitals (occuring 48 hours or more after admission) are said to have hospital-acquired pneumonia.

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12
Q

What investigations would you do for pneumonia?

A
  • Chest x-ray - the classical x-ray finding in pneumonia is consolidation
  • Bloods - full blood count (would usually show a neutrophilia in bacterial infections), urea and electrolytes - check for dehydration (remember the ‘U’ for urea in CURB-65),
    also other changes seen with some atypical pneumonias - CRP
    raised in response to infection
  • Arterial blood gases - indicated if the oxygen saturations or low or the patient has pre-existing respiratory disease, for example, COPD
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13
Q

How do we manage pneumonia?

A

Patients with pneumonia require the following:
antibiotics: to treat the underlying infection
* supportive care, for example:
* oxygen therapy if the patient is hypoxaemic
* intravenous fluids if the patient is hypotensive or shows signs of dehydration

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14
Q

What score do we use to risk stratify?

A

serum urea result > 7 (urea is the ‘U’ in CURB-65).

Patients are stratified for risk of death as follows:
* 0: low risk (less than 1% mortality risk) - NICE recommend that treatment at home should be considered (alongside clinical judgement)
* 1 or 2: intermediate risk (1-10% mortality risk) - NICE recommend that ‘ hospital assessment should be considered (particularly for people with a score of 2)’
* 3 or 4: high risk (more than 10% mortality risk) - NICE recommend urgent admission to hospital

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15
Q

What other marker does NICE recomment to use in a primary care setting?

A

NICE also mention point-of-care CRP test. This is currently not widely available but they make the following recommendation with reference to the use of antibiotic therapy:
* CRP < 20 mg/L - do not routinely offer antibiotic therapy
* CRP 20 - 100 mg/L - consider a delayed antibiotic prescription
* CRP > 100 mg/L - offer antibiotic therapy

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16
Q

What antibiotics are used for pneumonia?

A

Management of low-severity community acquired pneumonia
* amoxicillin is first-line
* if penicillin allergic then use a macrolide or tetracycline
* NICE now recommend a 5 day course of antibiotics for patients with low severity community acquired pneumonia

Management of moderate and high-severity community acquired pneumonia
* dual antibiotic therapy is recommended with amoxicillin and a macrolide
* a 7-10 day course is recommended
* NICE recommend considering a beta-lactamase stable penicillin such as co-amoxiclav, ceftriaxone or piperacillin with tazobactam and a macrolide in high-severity community acquired pneumonia

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17
Q

What is the discharge criteria for pneumonia?

A

NICE recommend that patients are not routinely discharged if in the past 24 hours they have had 2 or more of the following findings:
* temperature higher than 37.5°C
* respiratory rate 24 breaths per minute or more
* heart rate over 100 beats per minute
* systolic blood pressure 90 mmHg or less
* oxygen saturation under 90% on room air
* abnormal mental status
* inability to eat without assistance.

They also recommend delaying discharge if the temperature is higher than 37.5°C.

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18
Q

How soon should patients with pnemonia recover? What follow up is required?

A

All cases of pneumonia should have a repeat chest X-ray at 6 weeks after clinical resolution to ensure that the consolidation has resolved and there is no underlying secondary abnormalities (e.g. a lung tumour).

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19
Q

What are the RFs for aspiration pneumonias?

A

Risk factors for the development of aspiration pneumonia include:
* Poor dental hygiene
* Swallowing difficulties
* Prolonged hospitalization or surgical procedures
* Impaired consciousness
* Impaired mucociliary clearance

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20
Q

What zones are commonly affected in aspiration pneumonias?

A

The right middle and lower lung lobes are the most common sites affected, due to the larger calibre and more vertical orientation of the right main bronchus.

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21
Q

What organisms tend to cause aspiration pneumonias?

A

The bacteria implicated in aspiration pneumonia may be aerobic or anaerobic

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22
Q

Who does mycoplasma infections (causing pneumonia) commonly affect?

A

Often affects younger patients
Epidemics of Mycoplasma pneumoniae classically occur every 4 years

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23
Q

What are the features of mycoplasma infections?

A
  • the disease typically has a prolonged and gradual onset
  • flu-like symptoms classically precede a dry cough
  • bilateral consolidation on x-ray
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24
Q

What are the complications of mycoplasma pneumoniae?

A
  • cold agglutins (IgM): may cause an haemolytic anaemia, thrombocytopenia
  • erythema multiforme, erythema nodosum
  • meningoencephalitis, Guillain-Barre syndrome and other immune-mediated neurological diseases
  • bullous myringitis: painful vesicles on the tympanic membrane
  • pericarditis/myocarditis
  • gastrointestinal: hepatitis, pancreatitis
  • renal: acute glomerulonephritis
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25
What are the investigations for mycoplasma pneumoniae?
diagnosis is generally by Mycoplasma serology positive cold agglutination test
26
How do we manage mycoplasma pneumoniae?
doxycycline or a macrolide (e.g. erythromycin/clarithromycin)
27
How do legionella and mycoplasma compare?
28
CT scan showing a large pneumothorax developing in a patient with Pneumocystis jiroveci pneumonia
29
What is PCP/Pneumocystis jiroveci?
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
30
Who should be given PCP prophylaxis?
all patients with a CD4 count < 200/mm³
31
How does PCP present?
dyspnoea dry cough fever very few chest signs Extrapulmonary manifestations are rare (1-2% of cases), may cause * hepatosplenomegaly * lymphadenopathy * choroid lesions
32
What is a complication of PCP?
Pneumothorax is a common complication of PCP
33
What are the ix for PCP?
* CXR: typically shows bilateral interstitial pulmonary infiltrates but can present with other x-ray findings e.g. lobar consolidation. May be normal * exercise-induced desaturation * sputum often fails to show PCP, bronchoalveolar lavage (BAL) often needed to demonstrate PCP (silver stain shows characteristic cysts)
34
How is PCP managed?
* co-trimoxazole * IV pentamidine in severe cases * aerosolized pentamidine is an alternative treatment for Pneumocystis jiroveci pneumonia but is less effective with a risk of pneumothorax * steroids if hypoxic (if pO2 < 9.3kPa then steroids reduce risk of respiratory failure by 50% and death by a third)
35
What are the features of a PE?
* chest pain * typically pleuritic * dyspnoea * haemoptysis * tachycardia * tachypnoea * respiratory examination -classically the chest will be clear + however, in real-world clinical practice findings are often found TRIAD 1. Pleuritic pain 2. Dyspnoea 3. Haemoptysis
36
What is the pulmonary embolism rule-out criteria (PERC)?
* all the criteria must be absent to have negative PERC result, i.e. rule-out PE * this should be done when you think there is a low pre-test probability of PE, but want more reassurance that it isn't the diagnosis * this low probability is defined as < 15%, although it is clearly difficult to quantify such judgements * a negative PERC reduces the probability of PE to < 2%
37
What score is used to measure the likeliness of a PE? How is it interpreted?
38
What should be done if a PE is likely (>4 points)?
* arrange an immediate computed tomography pulmonary angiogram (CTPA) * If there is a delay in getting the CTPA then interim therapeutic anticoagulation should be given until the scan is performed. -> direct oral anticoagulant (DOAC) such as apixaban or rivaroxaban * If the CTPA is +ve then a PE is diagnosed * If the CTPA is -ve then consider a proximal leg vein US scan if DVT is suspected
39
What should be done if a PE is unlikely (4 points or less)?
arranged a D-dimer test * if positive arrange an immediate computed tomography pulmonary angiogram (CTPA). If there is a delay in getting the CTPA then give interim therapeutic anticoagulation until the scan is performed * if negative then PE is unlikely - stop anticoagulation and consider an alternative diagnosis
40
When would a V/Q scan be used?
V/Q scanning may be used initially if appropriate facilities exist, the chest x-ray is normal, and there is no significant symptomatic concurrent cardiopulmonary disease. V/Q scanning is also the investigation of choice if there is renal impairment (doesn't require the use of contrast unlike CTPA)
41
What are the ECG findings commonly seen in PE?
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'
42
Who are low-risk PE patients eligible for outpatient tx?
* Pulmonary Embolism Severity Index (PESI) score used to risk stratify * key requirements would clearly be haemodynamic stability, lack of comorbidities and support at home
43
What is the mainstay of treatment for PEs? What if there is renal impairment? or antiphospholipid syndrome?
Anticoagulants * DOACs - apixaban or rivaroxaban (both DOACs) should be offered first-line following the diagnosis of a PE * if neither apixaban or rivaroxaban are suitable then either LMWH followed by dabigatran or edoxaban OR LMWH followed by a vitamin K antagonist (VKA, i.e. warfarin) * if renal impairment is severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA * if the patient has antiphospholipid syndrome (specifically 'triple positive' in the guidance) then LMWH followed by a VKA should be used
44
How long should anticoagulation be given for?
* At least 3 months * continuing anticoagulation after this period is partly determined by whether the VTE was provoked or unprovoked: if provoked pt no longer at risk. If unprovoked, patient may still be at risk. * Provoked - stopped after initial 3 months (3-6 in cancer) * Unprovoked - continued for 3 further months (6 months) --> NICE recommend that whether a patient has a total of 3-6 months anticoagulant is based upon balancing a person's risk of VTE recurrence and their risk of bleeding
45
How should a patient with PE and haemodynamic instability be managed?
Thrombolysis * thrombolysis is now recommended as the first-line treatment for massive PE where there is circulatory failure (e.g. hypotension)
46
What should patients with repeat PEs be given?
inferior vena cava (IVC) filters - stopping clots formed in the deep veins of the leg from moving to the pulmonary arteries.
47
Right-sided pneumothorax
48
What are the RFs for a pneumothorax?
* pre-existing lung disease: COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia * connective tissue disease: Marfan's syndrome, rheumatoid arthritis * ventilation, including non-invasive ventilation * catamenial pneumothorax is the cause of 3-6% of spontaneous pneumothoraces occurring in menstruating women. It is thought to be caused by endometriosis within the thorax
49
How would a pneumothorax present?
* dyspnoea * chest pain: often pleuritic * sweating * tachypnoea * tachycardia
50
How do we categorise a pneumothorax?
A pneumothorax is termed primary if there is no underlying lung disease and secondary if there is.
51
How should a primary pneumothorax be managed?
* if the rim of air is < 2cm and the patient is not short of breath then discharge should be considered * > 2 cm or still short of breath - aspiration should be attempted * if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted
52
How should a secondary pneumothorax be managed?
* 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
53
How should an iatrogenic pneumothorax be managed?
* 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
54
What discharge advice should be given to patients with pneumothoraxes?
* Avoid smoking to reduce risk of further pneumothorax * CAA suggest patients may travel 2 weeks after successful drainage if there is no residual air. The British Thoracic Society say 1 week post check x-ray * Diving should be permanently avoided unless the patient has undergone bilateral surgical pleurectomy and has normal lung function and chest CT scan postoperatively.
55
How should a tension pneumothorax be managed?
Treatment is with needle decompression and chest tube insertion.
56
What causes upper lobe fibrosis?
CHARTS Coal workers pneumoconiosis Histiocytosis Ankylosing spondylitis/Allergic Bronchopulmonary Aspergillosis Radiation TB Silicosis, sarcoidosis
57
How do we classify pleural effusions?
Pleural effusions may be classified as being either a transudate or exudate according to the protein concentration.
58
What type of pleural effusion would cause a high protein fluid on the lungs? What causes this?
Exudate (> 30g/L protein) * infection: pneumonia (most common exudate cause), TB, subphrenic abscess * connective tissue disease: RA, SLE * neoplasia: lung cancer, mesothelioma, metastases * pancreatitis * pulmonary embolism * Dressler's syndrome * yellow nail syndrome
59
What type of pleural effusion would cause a low protein fluid on the lungs? What causes this?
Transudate (< 30g/L protein) * heart failure (most common transudate cause) * hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption) * hypothyroidism * Meigs' syndrome (benign ovarian tumor presents along with ascites and pleural effusion)
60
How would you investigate a pleural effusion?
* Chest X-ray * US for pleural aspiration - 21G needle and 50ml syringe should be used --> pH, protein, lactate dehydrogenase (LDH), cytology and microbiology * contrast CT
61
What is Light's criteria?
if the protein level is between 25-35 g/L, Light's criteria should be applied. An exudate is likely if at least one of the following criteria are met: * pleural fluid protein divided by serum protein >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
62
How should we manage a pleural effusion?
Options for managing patients with recurrent pleural effusions include: * recurrent aspiration * pleurodesis * indwelling pleural catheter * drug management to alleviate symptoms e.g. opioids to relieve dyspnoea
63
What would a COPD Xray show?
* hyperinflation * bullae: if large, may sometimes mimic a pneumothorax * flat hemidiaphragm * also important to exclude lung cancer
64
What would post-bronchodilator spirometry show in a COPD patient?
FEV1/FVC ratio less than 70%
65
How is the severity of COPD characterised?
66
What are the COPD causes?
Smoking! Alpha-1 antitrypsin deficiency Other causes cadmium (used in smelting) coal cotton cement grain
67
What is the main management of COPD?
68
What general advice should be given to COPD patients?
* >smoking cessation advice: including offering nicotine replacement therapy, varenicline or bupropion * annual influenza vaccination * one-off pneumococcal vaccination * pulmonary rehabilitation to all people who view themselves as functionally disabled by COPD (usually Medical Research Council [MRC] grade 3 and above)
69
What other medication can be prescribed for COPD patients?
* Oral Theophylline - 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 * Oral prophylactic antibiotic therapy - azithromycin prophylaxis is recommended in select patients. Patients should not smoke, have optimised standard treatments and continue to have exacerbations. CT thorax (to exclude bronchiectasis) and sputum culture (to exclude atypical infections and tuberculosis). LFTs and an ECG to exclude QT prolongation should also be done as azithromycin can prolong the QT interval * Mucolytics - should be 'considered' in patients with a chronic productive cough and continued if symptoms improve
70
What are 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
71
Who should be offered Long Term Oxygen Therapy?
Assessment is done by measuring arterial blood gases on 2 occasions at least 3 weeks apart in patients with stable COPD on optimal management. Offer LTOT to patients with a pO2 of < 7.3 kPa or to those with a pO2 of 7.3 - 8 kPa and one of the following: * secondary polycythaemia * peripheral oedema * pulmonary hypertension
72
What should be done before prescribing LTOT?
* the risks of falls from tripping over the equipment * the risks of burns and fires, and the increased risk of these for people who live in homes where someone smokes (including e‑cigarettes)
73
How do acute exacerbations of COPD present?
* increase in dyspnoea, cough, wheeze * there may be an increase in sputum suggestive of an infective cause * patients may be hypoxic and in some cases have acute confusion
74
What organisms cause COPD exacerbations?
* 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.
75
How should COPD exacerbations be managed?
* increase frequency of bronchodilator use and consider giving via a nebuliser * give prednisolone 30 mg daily for 5 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' * the BNF recommends one of the following oral antibiotics first-line: amoxicillin or clarithromycin or doxycycline.