Respiratory Flashcards

1
Q
  • A raised NT-proBNP blood test result indicates right ventricular failure
  • Echo can be used to estimate pulmonary artery pressure

What organisms cause hospital acquired pneumonia?

A

Pseudomonas aeruginosa
Staphylococcal aureus
Enterobacteria

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2
Q

Risk factors for aspiration pneumonia?

A

This occurs in patients with an unsafe swallow. Risk factors include stroke, myasthenia gravis, bulbar palsy, alcoholism, and achalasia.

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3
Q

Features of STAPHylococcal pneumonia

A

A bilateral cavitating bronchopneumonia.

Found in: IV drug users, elderly patients, or patients who already have an influenza infection.

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4
Q

Features of a klebsiella pneumonia?

A

Primarily affects the upper lobes resulting in a cavitating pneumonia, presenting with “red-currant” sputum.

Furthermore, there is an increased risk of developing complications including empyema, lung abscesses and pleural adhesions.

Patients at risk of Klebsiella pneumonia are those with weakened immune systems such as elderly, alcoholics, and diabetics.

Additional at-risk groups include patients with malignancy, chronic obstructive pulmonary disease, long term steroid use and renal failure.

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5
Q

Features of legionella pneumonia:

A

Fever, myalgia and malaise followed by a dyspnoea and a dry cough. It is associated with Legionnaire’s disease, usually in patients who have been exposed to poor hotel air conditioning.

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6
Q

Investigations for legionella pneumonia:

A

Look for hyponatraemia and deranged LFTs on blood tests. Legionella antigen may be present in the urine.

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7
Q

Summary of pneumocystis jiroveci.

A

This is associated with patients who are immunosuppressed (malignancy or chemotherapy) or HIV positive.
The causative organism is known as pneumocystis jiroveci and is a fungus. In patients who are HIV-positive the risk of PCP increases when the CD4+ <200 cells/uL.
Symptoms include exertional dyspnoea, dry cough, and fever.

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8
Q

What is curb 65?

A

Used to classify the severity of pneumonia:

C – confusion: An abbreviated mental test of ≤8

U – urea: >7mmol/L

R - Respiratory rate: ≥30/ min

B - blood pressure <90 systolic and/ or <60mmHg diastolic

65 - age: >65year old

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8
Q

What is curb 65?

A

Used to classify the severity of pneumonia:

C – confusion: An abbreviated mental test of ≤8

U – urea: >7mmol/L

R - Respiratory rate: ≥30/ min

B - blood pressure <90 systolic and/ or <60mmHg diastolic

65 - age: >65year old

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9
Q

Signs of pleural effusion on examination:

A

The trachea is central or deviated away from the affected side (if large).
Chest expansion is reduced on the affected side.
The percussion note is stony dull on the affected side.
On auscultation there are reduced/absent breath sounds over the effusion. There may be bronchial breathing at the upper border of the pleural effusion.
Vocal resonance/tactile vocal fremitus is reduced over the effusion.

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10
Q

How are the causes of pleural effusion subdivided?

A

Causes of pleural effusions are mainly divided into exudative (protein content >35 g/L) and transudative (protein content <35 g/L)

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11
Q

Causes of an exudative pleural effusion:

A

Infections such as pneumonia or TB.

Malignancy such as bronchial carcinoma, mesothelioma, or lung metastases.

Inflammatory conditions such as rheumatoid arthritis, lupus, or acute pancreatitis.

Pulmonary infarct (for example secondary to a pulmonary embolism) and trauma.

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12
Q

Causes of an exudative pleural effusion:

A

Infections such as pneumonia or TB.

Malignancy such as bronchial carcinoma, mesothelioma, or lung metastases.

Inflammatory conditions such as rheumatoid arthritis, lupus, or acute pancreatitis.

Pulmonary infarct (for example secondary to a pulmonary embolism) and trauma.

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13
Q

Causes of an transudative pleural effusion:

A

Transudative pleural effusions are caused by imbalances in the Starling forces that govern the formation of interstitial fluid.

Conditions that increase the capillary hydrostatic pressure (forcing fluid out of the pulmonary capillaries into the pleural space) include congestive cardiac failure.
Conditions that reduce the capillary oncotic pressure (impairing the reabsorption of fluid from the pleural space into the pulmonary capillaries) include cirrhosis, nephrotic syndrome/chronic kidney disease, and gastrointestinal malabsorption/malnutrition (eg. Coeliac disease).
Less common causes of transudative pleural effusions include hypothyroidism and Meig’s syndrome (described by the triad of ascites, pleural effusion, and benign ovarian tumour).

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14
Q

Read aloud:

A

Glucose: low in rheumatoid arthritis, TB, or malignancy

pH: <7.2 in empyema

Amylase: raised in pancreatitis

Immunology: rheumatoid factor is useful if rheumatoid arthritis is suspected; anti-nuclear antibody (ANA) is useful if systemic lupus erythematosus (SLE) is suspected; complement is typically low in pleural effusions caused by rheumatoid arthritis or SLE.

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15
Q

What is Lights criteria?

A

Used to determine transudative vs exudative pleural effusion:

If the protein content is equivocal (25-35 g/L), Light’s criteria can be applied:

This states that an effusion is an exudate if: the pleural fluid to serum protein ratio is >0.5, the pleural fluid to serum LDH ratio is >0.6, or the pleural fluid LDH is >2/3 the upper reference limit for serum LDH.

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16
Q

Non-small cell lung cancer encompassess what main cancers?

A

Non-small cell lung cancer makes up around 80% of lung cancer and includes:

  • Adenocarcinoma (around 40%)
  • Squamous cell carcinoma (around 20%)
  • Large-cell carcinoma (around 10%)
  • Other types (around 10%)
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17
Q

Describe what is characteristic about small cell lung cancer:

A

Small cell lung cancer cells contain neurosecretory granulesthat can releaseneuroendocrine hormones. This makes SCLC responsible for multiple paraneoplastic syndromes.

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18
Q

A patient with lung cancer presents with facial swelling, difficulty breathing and distended veins in the neck and upper chest and Pemberton’s sign. What is the underlying issue?

A

Superior vena cava obstructionis a complication of lung cancer. It is caused by direct compression of the tumour on the superior vena cava. It presents with facial swelling, difficulty breathing and distended veins in the neck and upper chest.

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19
Q

What is Pemberton’s sign?

A

“Pemberton’s sign” is where raising the hands over the head causes facial congestion and cyanosis. This is a medical emergency.

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20
Q

What is the triad seen in Horner’s syndrome?

A

Partial ptosis
Anhidrosis
Miosis

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21
Q

How does a recurrent laryngeal nerve palsy present in lung cancer?

A

Recurrent laryngeal nerve palsy presents with a hoarse voice. It is caused by cancer pressing on or affecting the recurrent laryngeal nerve as it passes through the mediastinum.

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22
Q

What is Limbic encephalitis?

A

Limbic encephalitis. This is a paraneoplastic syndrome where small cell lung cancer causes the immune system to make antibodies to tissues in the brain, specifically the limbic system, causing inflammation in these areas. This causes symptoms such as short term memory impairment, hallucinations, confusion and seizures. It is associated with anti-Hu antibodies.

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23
Q

What is Lambert eaton syndrome?

A

Lambert-Eaton myasthenic syndrome is a result of antibodies produced by the immune system against small cell lung cancer cells. These antibodies also target and damage voltage-gated calcium channels sited on the presynaptic terminals in motor neurones. This leads to weakness, particularly in the proximal muscles but can also affect intraocular muscles.

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24
Q

Symptoms of Lambert-Eaton syndrome:

A

Weakness, particularly in the proximal muscles but can also affect intraocular muscles causing:
Diplopia
Ptosis
Affect pharyngeal muscles causing slurred speech and dysphagia.

Patients may also experience dry mouth, blurred vision, impotence and dizziness due to autonomic dysfunction.

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25
Q

In older smokers with symptoms of Lambert-Eaton syndrome consider what?

A

Small cell lung cancer

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26
Q

Mesothelioma is strongly linked to what?

A

Asbestos inhalation

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27
Q

Treatment for mesothelioma?

A

The prognosis is very poor. Chemotherapy can improve survival but it is essentially palliative.

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28
Q

In patients with pneumonia NICE advises anyone with a score greater than what to be admitted to hospital?

A

1 or 2 consider admitting
3 urgent admission

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29
Q

Common pathogens that cause pneumonia:

A
  • Streptococcus pneumoniae (50%)
  • Haemophilus influenzae(20%)
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30
Q

What pathogen is commonly seen causing pneumonia in CF patients?

A
  • Pseudomonas aeruginosa in patients with cystic fibrosis or bronchiectasis
  • Staphylococcus aureus in patients with cystic fibrosis
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31
Q

Moraxella catarrhalis causes pneumonia in what patients?

A

In immunocompromised patients or those with chronic pulmonary disease

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32
Q

Which electrolyte needs to be monitored in Legionella pneumophila and why?

A

Hyponatraemia(low sodium) due to causing an SIADH.

SIADH = Syndrome of inappropriate antidiuretic hormone secretion (excess ADH).

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33
Q

What patients typically get legionella pneumophila?

A

Patients that have had cheap hotel holidays.

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33
Q

Which pneumonia causes erythema multiforme and neurological symptoms in young patients?

A

Mycoplasma pneumoniae.

This causes milder pneumonia and can cause a rash - erythema multiforme.

It can also cause neurological symptoms in young patients in exams.

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34
Q

Coxiella burnetii AKA “Q fever”.

A

This is linked to exposure to animals and their bodily fluids. Patient is a farmer with a flu like illness?

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35
Q

Remember the 5 causes of atypical pneumonia with the mnemonic:

A

“Legions of psittaci MCQs”

M – mycoplasma pneumoniae
C – chlamydydophila pneumoniae
Qs – Q fever (coxiella burnetii)

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36
Q

Summary of fungal pneumonia:

Read aloud if don’t know!

A

Pneumocystis jiroveci (PCP) pneumonia occurs in patients that are immunocompromised. It is particularly important in patients with poorly controlled or new HIV with a low CD4 count. It usually presents subtly with a dry cough without sputum, shortness of breath on exertion and night sweats.

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37
Q

Treatment for PCP pneumonia:

A

Treatment is with co-trimoxazole (trimethoprim/sulfamethoxazole) known by the brand name “Septrin”. Patients with low CD4 counts are prescribed prophylactic oral co-trimoxazole to protect against PCP.

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38
Q

How do LAMA’s work?
+ name one

A

Long-acting muscarinic antagonists (LAMA), for example tiotropium. These block the acetylcholine receptors. Acetylcholine receptors are stimulated by the parasympathetic nervous system and cause contraction of the bronchial smooth muscles. Blocking these receptors leads to bronchodilation.

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39
Q

Name of a commonly used ICS for chronic asthma:

A

Beclometasone

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40
Q

How does montelukast work in chronic asthma?

A

Leukotriene receptor antagonists, for example, montelukast. Leukotrienes are produced by the immune system and cause inflammation, bronchoconstriction and mucus secretion in the airways. Leukotriene receptor antagonists work by blocking the effects of leukotrienes.

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41
Q

Summary of theophylline use in asthma:

A

Theophylline. This works by relaxing the bronchial smooth muscle and reducing inflammation. Unfortunately, it has a narrow therapeutic window and can be toxic in excess so monitoring plasma theophylline levels in the blood is required. This is done 5 days after starting treatment and 3 days after each dose changes.

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42
Q

If you see a patient with a thoracotomy scar in your OSCEs, they are likely to have had one of what three procedures?

A

A lobectomy, pneumonectomy or lung volume reduction surgery for COPD.

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43
Q

What are the two different types of thoracotomy scar?

A

Anterolateral
Posterolateral

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44
Q

How to interpret the cause of a thoracotomy scar clinically:

A

If you see a patient with a thoracotomy scar in your OSCEs, they are likely to have had a lobectomy, pneumonectomy or lung volume reduction surgery for COPD. If they have no breath sound on that side, this indicates a pneumonectomy rather than lobectomy. If they have absent breath sound in a specific area on the affected side (e.g., the upper zone), but breath sounds are present in other areas, this indicates a lobectomy. Lobectomies and pneumonectomies are usually used to treat lung cancer. In the past, they were often used to treat tuberculosis, so keep this in mind in older patients. If it is a cardiology examination and they have a right-sided mini-thoracotomy incision, this is more likely to indicate previous minimally invasive mitral valve surgery.

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45
Q

When would you be likely to use Bipap as non-invasive ventilation?

A

The criteria for initiating Bipap: Respiratory acidosis (pH < 7.35, PaCO2 >6) despite adequate medical treatment.

You would be likely to use Bipap in type 2 respiratory failure typically due to COPD>

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46
Q

What is required prior to starting non-invasive ventilation and why?

A

Chest x-ray to rule out a pneumothorax.

Non-invasive ventilation is contraindicated for pneumothorax).

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47
Q

How is Bipap for a respiratory acidosis monitored?

A

Repeat an ABG 1 hour after every change and 4 hours after that until stable. The IPAP is increased by 2-5 cm increments until the acidosis resolves.

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48
Q

Indications for CPAP:

A

Obstructive sleep apnoea
Congestive cardiac failure
Acute pulmonary oedema

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49
Q

Explain how CPAP works:

A

CPAP stands for continuous positive airway pressure. It provides continuous air being blown into the lungs that keeps the airways expanded so that air can more easily travel in and out. It is used to maintain the patient’s airway in conditions where it is prone to collapse.

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50
Q

What are the two medications that slow the progression of IPF?

A

Pirfenidone is an antifibrotic and anti-inflammatory

Nintedanib is a monoclonal antibody targeting tyrosine kinase

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51
Q

How is interstitial lung disease diagnosed?

A

Diagnosis of interstitial lung disease requires a combination of clinical features and high resolution CT scan of the thorax. HRCT shows a “ground glass” appearance with interstitial lung disease. When diagnosis is unclear lung biopsy can be used to take samples of the lung tissue and confirm the diagnosis on histology.

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52
Q

What drugs can induce pulmonary fibrosis?

A
  • Amiodarone
  • Cyclophosphamide
  • Methotrexate
  • Nitrofurantoin
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53
Q

Pulmonary fibrosis can occur secondary to what conditions?

A
  • Alpha-1 antitripsin deficiency
  • Rheumatoid arthritis
  • Systemic lupus erythematosus (SLE)
  • Systemic sclerosis
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54
Q

What is hypersensitivity pneumonitis?

A

Hypersensitivity pneumonitis is a type III hypersensitivity reaction to an environmental allergen that causes parenchymal inflammation and destruction in people that are sensitive to that allergen.

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55
Q

How is hypersensitivity pneumonitis diagnosed?

A

Bronchoalveolar lavage involves collecting cells from the airways during bronchoscopyby washing the airways with fluid then collecting that fluid for testing. This shows raised lymphocytes and mast cells in hypersensitivity pneumonitis.

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56
Q

How is hypersensitivity pneumonitis managed?

A

Management is by removing the allergen, giving oxygen where necessary and steroids.

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57
Q

Example of causes of hypersensitivity pneumonitis:

A

Examples of specific causes:

Bird-fanciers lung is a reaction to bird droppings

Farmers lung is a reaction to mouldy spores in hay

Mushroom workers’ lung is a reaction to specific mushroom antigens

Malt workers lung is a reaction to mould on barley

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58
Q

Practice: Defining, presentation, diagnosis and management of cryptogenic organising pneumonia:

Read aloud summary after:

A

Cryptogenic organising pneumonia was previously known as bronchiolitis obliterans organising pneumonia. It involves a focal area of inflammation of the lung tissue. This can be idiopathic or triggered by infection, inflammatory disorders, medications, radiation or environmental toxins or allergens.

Presentation is very similar to infectious pneumonia with shortness of breath, cough, fever and lethargy. It also presents on similarly to pneumonia on a chest xray with a focal consolidation.

Diagnosis is often delayed due to the similarities to infective pneumonia. Lung biopsy is the definitive investigation. Treatment is with systemic corticosteroids.

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59
Q

What are the four main complications of asbestosis?

A

Lung fibrosis
Pleural thickening and pleural plaques
Adenocarcinoma
Mesothelioma

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60
Q

How are pleural effusions grouped?

A

Exudative = High protein
Transudative = Low protein

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61
Q

Causes of exudative pleural effusion:

A

Lung cancer
Pneumonia
Rheumatoid arthritis
Tuberculosis

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62
Q

Causes of transudative pleural effusion:

A

Congestive cardiac failure
Hypoalbuminaemia
Hypothroidism
Meig’s syndrome

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63
Q

Understanding exudative vs transudative pleural effusion:

A

Exudative causes are related to inflammation. The inflammation results in protein leaking out of the tissues in to the pleural space (ex- meaning moving out of). Think of the causes of inflammation.

Transudative causes relate to fluid moving across into the pleural space (trans- meaning moving across). Think of the causes of fluid shifting.

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64
Q

What is Meig’s syndrome?

A

Right sided pleural effusion with ovarian malignancy

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65
Q

Why is the pleural effusion commonly on the right side in Meig’s syndrome?

A

Pleural effusion is usually bilateral, but in patients with Meigs syndrome, it is usually unilateral with a predominance on the right side due to the larger diameter of transdiaphragmatic lymphatic channels on the right side.

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66
Q

Presentation of pleural effusion:

A
  • Shortness of breath
  • Dullness to percussion over the effusion
  • Reduced breath sounds
  • Tracheal deviation away from the effusion if it is massive.
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67
Q

Investigations for a patient with suspected pleural effusion:

A

Chest xray shows:

Blunting of the costophrenic angle
Fluid in the lung fissures
Larger effusions will have a meniscus. This is a curving upwards where it meets the chest wall and mediastinum.
Tracheal and mediastinal deviation if it is a massive effusion.

Taking a sample of the pleural fluid by aspiration or chest drain is required to analyse it for protein count, cell count, pH, glucose, LDH and microbiology testing.

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68
Q

Treatment for pleural effusion:

A

Conservative management may be appropriate as small effusions will resolve with treatment of the underlying cause. Larger effusions often need aspiration or drainage.

Pleural aspiration involves sticking a needle in and aspirating the fluid. This can temporarily relieve the pressure but the effusion may recur and repeated aspiration may be required.

Chest drain can be used to drain the effusion and prevent it recurring.

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69
Q

Define empyema and it’s management:

A

Empyema is where there is an infected pleural effusion. Suspect an empyema in a patient who has an improving pneumonia but new or ongoing fever. Pleural aspiration shows pus, acidic pH (pH < 7.2), low glucose and high LDH. Empyema is treated by chest drain to remove the pus and antibiotics.

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70
Q

When to aspirate a pneumothorax?

A

If SOB and/or there is a > 2cm rim of air on the chest x-ray then it will require aspiration and reassessment.

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71
Q

When to put a chest drain in for a pneumothorax:

A

If aspiration fails twice it will require a chest drain.

Unstable patients or bilateral or secondary pneumothoraces generally require a chest drain.

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72
Q

Management of a tension pneumothorax:

WORD FOR WORD

A

“Insert a large bore cannula into the second intercostal space in the midclavicular line.”

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73
Q

Where are chest drains inserted?

A

Chest drains are inserted into the “triangle of safety”. This triangle is formed by:

The 5th intercostal space (or the inferior nipple line)
The mid axillary line (or the lateral edge of the latissimus dorsi)
The anterior axillary line (or the lateral edge of the pectoris major)

The needle is inserted just above the rib to avoid the neurovascular bundle that runs just below the rib. Once the chest drain is inserted obtain a chest xray to check the positioning.

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74
Q

The triangle of safety is made up by what?

A

The 5th intercostal space (or the inferior nipple line)

The mid axillary line (or the lateral edge of the latissimus dorsi)

The anterior axillary line (or the lateral edge of the pectoris major)

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75
Q

What prophylaxis should be given for people at risk of VTE?

A

Low molecular weight heparin such as enoxaparin

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76
Q

What scoring system is used for PE’s?

A

Wells Score

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77
Q

Patients with a PE will likely show up as what on an ABG?

A

Patients with a pulmonary embolism often have a respiratory alkalosis when an ABG is performed. This is because the high respiratory rate causes them to “blow off” extra CO2. As a result of the low CO2, the blood becomes alkalotic. It is one of the few causes of a respiratory alkalosis, the other main cause being hyperventilation syndrome.

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78
Q

Initial treatment for a PE:

A

The initial recommended treatment is apixaban or rivaroxaban.

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79
Q

What is used in place of apixaban/rivaroxaban to treat a PE and why?

A

Low molecular weight heparin (LMWH) is an alternative where these are not suitable, or in antiphospholipid syndrome.

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80
Q

Long-term anticoag options post VTE:

A

The options for long term anticoagulation in VTE are warfarin, a NOAC or LMWH.

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81
Q

3 most common direct-acting oral anticoagulants

A

Apixaban
Dabigatran
Rivaroxaban

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82
Q

What is first line VTE prophylaxis in patients that are pregnant or have cancer?

A

LMWH

83
Q

When to thrombolyse a PE?

A

Where there is a massive PEwith haemodynamic compromise there is a treatment option called thrombolysis.Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous. It is only used in patients with a massive PE where the benefits outweigh the risks.

84
Q

How does pulmonary hypertension anatomically change the heart?

A

Right ventricular hypertrophy
Dilated pulmonary arteries

85
Q

Read aloud the 5 groups that can cause pulmonary hypertension:

A

Group 1 – Primary pulmonary hypertension or connective tissue disease such as systemic lupus erythematous (SLE)
Group 2 – Left heart failure usually due to myocardial infarction or systemic hypertension
Group 3 – Chronic lung disease such as COPD
Group 4 – Pulmonary vascular disease such as pulmonary embolism
Group 5 – Miscellaneous causes such as sarcoidosis, glycogen storage disease and haematological disorders

86
Q

Signs and symptoms of pulmonary hypertension:

A

Shortness of breath is the main presenting symptom.

Other signs and symptoms are:

Syncope
Tachycardia
Raised JVP
Hepatomegaly
Peripheral oedema.

87
Q

Investigations for pulmonary hypertension:

A

ECG Changes

The right sided heart strain causes ECG changes such as:

Right ventricular hypertrophy seen as larger R waves on the right sided chest leads (V1-3) and S waves on the left sided chest leads (V4-6)
Right axis deviation
Right bundle branch block

Chest Xray Changes

Dilated pulmonary arteries
Right ventricular hypertrophy

Other investigations

A raised NT-proBNP blood test result indicates right ventricular failure
Echo can be used to estimate pulmonary artery pressure

88
Q

Management for pulmonary hypertension:

A

Primary pulmonary hypertension can be treated with:

IV prostanoids (e.g. epoprostenol)
Endothelin receptor antagonists (e.g. macitentan)
Phosphodiesterase-5 inhibitors (e.g. sildenafil)

Secondary pulmonary hypertension is managed by treating the underlying cause such as pulmonary embolism or SLE.

Supportive treatment for complications such as respiratory failure, arrhythmias and heart failure.

89
Q

Describe the classical sarcoidosis exam patient:

A

The typical MCQ exam patient is a 20-40 year old black woman presenting with a dry cough and shortness of breath. They may have nodules on their shins suggesting erythema nodosum.

90
Q

What organ system is most commonly affected in sarcoidosis? How?

A

Lungs (affecting over 90%)

Mediastinal lymphadenopathy
Pulmonary fibrosis
Pulmonary nodules

Note: Fever, fatigue and weight loss are other systemic symptoms.

91
Q

How may the liver be affected in sarcoidosis?

A
  • Liver nodules
  • Cirrhosis
  • Cholestasis
92
Q

How may the eyes be affected in sarcoidosis?

A
  • Uveitis
  • Conjunctivitis
  • Optic neuritis
93
Q

How may the skin be affected in sarcoidosis?

A
  • Erythema nodosum (tender, red nodules on the shins caused by inflammation of the subcutaneous fat)
  • Lupus pernio (raised, purple skin lesions commonly on cheeks and nose)
  • Granulomas develop in scar tissue
94
Q

How may the heart be affected in sarcoidosis?

A
  • Bundle branch block
  • Heart block
  • Myocardial muscle involvement
95
Q

How may the kidneys be affected in sarcoidosis?

A
  • Kidney stones (due to hypercalcaemia)
  • Nephrocalcinosis
  • Interstitial nephritis
96
Q

Read aloud the rarer manifestations of sarcoidosis:

A

Central nervous system (affecting around 5%)

Nodules
Pituitary involvement (diabetes insipidus)
Encephalopathy

Peripheral Nervous System (affecting around 5%)

Facial nerve palsy
Mononeuritis multiplex

Bones (affecting around 2%)

Arthralgia
Arthritis
Myopathy

97
Q

Lofgren’s syndrome a specific presentation of sarcoidosis, is characterised by what triad?

A

Erythema nodosum
Bilateral hilar lymphadenopathy
Polyarthralgia (joint pain in multiple joints)

98
Q

What blood tests are done for sarcoidosis?

A

Raised serum ACE. This is often used as a screening test.
Hypercalcaemia (rasied calcium) is a key finding.

Raised serum soluble interleukin-2 receptor
Raised CRP
Raised immunoglobulins

99
Q

What imaging is done for sarcoidosis and what does it show?

A

Chest xray shows hilar lymphadenopathy.

High-resolution CT thorax shows hilar lymphadenopathy and pulmonary nodules.

MRI can show CNS involvement.

PET scan can show active inflammation in affected areas.

100
Q

What is the gold standard for diagnosing sarcoidosis?

A

The gold standard for confirming the diagnosis of sarcoidosis is by histology from a biopsy. This is usually done by doing bronchoscopy with ultrasound guided biopsy of mediastinal lymph nodes.

101
Q

What does histology show in sarcoidosis?

A

The histology shows characteristic non-caseating granulomas with epithelioid cells.

102
Q

Tests for other organ involvement:

  • read aloud
A

Tests for other organ involvement

U&Es for kidney involvement
Urine dipstick or urine albumin-creatinine ratio to look for proteinuria indicating nephritis
LFTs for liver involvement
Ophthalmology review for eye involvement
ECG and echocardiogram for heart involvement
Ultrasound abdomen for liver and kidney involvement

103
Q

First line treatment for sarcoidosis:

A

No treatment is considered as first line in patients with no or mild symptoms as the condition often resolves spontaneously.

Oral steroids are usually first line where treatment is required and are given for between 6 and 24 months. Patients should be given bisphosphonates to protect against osteoporosis whilst on such long term steroids.

104
Q

Second line treatment for sarcoidosis:

A

Second line options are methotrexate or azathioprine
Lung transplant is rarely required in severe pulmonary disease.

105
Q

Prognosis for sarcoidosis:

A

Sarcoidosis spontaneously resolves within 6 months in around 60% of patients. In a small number of patients it progresses with pulmonary fibrosis and pulmonary hypertension, potentially requiring a lung transplant. Death in sarcoidosis is usually when it affects the heart (causing arrhythmias) or the central nervous system.

106
Q

Explain obstructive sleep apnoea:

Practice aloud for OSCE’s!

A

Obstructive sleep apnoeais caused by the collapse of the pharyngeal airway during sleep. It is characterised by apnoea episodes during sleep where the person will stop breathing periodically for up to a few minutes. The partner usually reports this as the patient is unaware of these episodes.

107
Q

Features of OSA:

Practice aloud for OSCE’s!

A

Apnoea episodes during sleep (reported by partner)
Snoring
Morning headache
Waking up unrefreshed from sleep
Daytime sleepiness
Concentration problems
Reduced oxygen saturation during sleep

Severe cases can cause hypertension, heart failure and can increase the risk of myocardial infarction and stroke.

108
Q

Approach to investigating OSA in a GP:

Practice aloud for OSCE’s!

A

The Epworth Sleepiness Scale is used to assess symptoms of sleepiness associated with obstructive sleep apnoea.

TOM TIP: If interviewing someone that you suspect has obstructive sleep apnoea ask about their daytime sleepiness and their occupation. Daytime sleepiness is a key feature that should make you suspect obstructive sleep apnoea. Patients that need to be fully alert for work, for example heavy goods vehicle operators, require urgent referral and may need amended work duties whilst awaiting assessment and treatment.

109
Q

Management of OSA:

Practice aloud for OSCE’s!

A

Referral to an ENT specialist or a specialist sleep clinic where they can perform sleep studies. This involves the patient sleeping in a laboratory whilst staff monitor their oxygen saturations, heart rate, respiratory rate and breathing to establish any apnoea episodes and the extent of their snoring.

The first step in management is to correct reversible risk factors by advising them to stop drinking alcohol, stop smoking and lose weight.

The next step is to use a continuous positive airway pressure (CPAP) machine that provides continuous pressure to maintain the patency of the airway.

Surgery is another option. This involves quite significant surgical restructuring of the soft palate and jaw. The most common procedure is called uvulopalatopharyngoplasty (UPPP).

110
Q

Limbic encephalitis is associated with what antibodies?

A

Anti-hu antibodies

111
Q

What is SIADH and what resp condition is it seen in?

A

Syndrome of inappropriate antidiuretic hormone secretion (excess ADH).

Legionella pneumonia.

112
Q

Explain the pathophysiology of asthma:

A

The pathophysiology of the condition is due to a type 1 hypersensitivity reaction, whereby an allergen causes cross-linking of IgE on mast cells, releasing histamine and leukotrienes. These produce the symptoms of bronchoconstriction and inflammation.

113
Q

What indicates obstructive lung disease in lung function tests:

A

Obstructive lung diseasecan be diagnosed whenFEV1is less than 75% ofFVC(FEV1:FVC ratio < 75%). This suggests that there is some obstruction slowing the passage of air getting out of the lungs. The person may have a relatively good lung volume but the air is only able to move in and out of the lungs slowly due to obstruction.

114
Q

What indicates restrictive lung disease in lung function tests:

A

IfFEV1andFVCareequally reducedandFEV1:FVC ratio > 75%this suggestsrestrictive lung disease. Restrictive lung disease is where there is a restriction to the ability of the lungs to expand and take air in.

115
Q

Common causes of restrictive lung disease:

A
  • Interstitial lung disease
  • Neurological (i.e. motor neurone disease)
  • Scoliosis or chest deformity
  • Obesity
116
Q

Features of Chlamydophila psittaci pneumonia

A

Chlamydophila psittaci is an intracellular bacteria that results in psittacosis. It is acquired from contact with infected birds such as parrots, cattle, horse and sheep.
Features include lethargy, arthralgia, headache, anorexia, dry cough and fever.
Additional features include: hepatitis; splenomegaly; nephritis; infective endocarditis; meningoencephalitis and a rash.

117
Q

Pneumonia management:

A

Management of patients with pneumonia consists of:

Oxygen to keep O2 saturations above 94%

Fluid management

Analgesia if patients have pleuritic chest pain. Paracetamol 1g/6 hours (Max. 4g 24hours)

Antibiotics can be given orally for patients who are not nil by mouth and are managed in the community. However, for severe pneumonia Intravenous route is required.

Follow up appointments are organized for 6 weeks and CXR could be repeated at this time if there are complications or symptoms have not resolved.

Please note that specific pneumonias have specific antibiotic requirements.

118
Q

Summary of prevention of pneumonia:

A

The pneumococcal vaccine protects against Streptococcus pneumoniae. There are two types of this vaccine either the conjugate or the polysaccharide vaccine. The polysaccharide vaccine covers a greater number of serotypes and is more commonly used in comparison the conjugate vaccine.

Pneumococcal vaccine is routinely offered as three injections at the age of 2 months, 4 months and 12-13 months.

People aged 65 years and older and those in at-risk groups should be offered the pneumococcal vaccine.

At-risk groups include chronic heart, liver or renal conditions. These include liver cirrhosis, nephrotic syndrome, post-transplant and renal failure. Additionally, patients who are immuno-suppressed due to AIDS or chemotherapy; or have decreased spleen function due to splenectomy, asplenia or sickle cell disease qualify for this group. Furthermore, patients with chronic lung conditions such as COPD or bronchiectasis would be applicable.

Some patients within the at-risk group require a vaccination every 5 years. These include patients with decreased splenic function and nephrotic syndrome.

119
Q

(ABG) which shows a pH 7.32, pO2 7 kPa, pCO2 7.5 kPa, bicarbonate 45 mmol/l.

Interpret and explain this ABG:

A

The pH is <7.35, confirming that this is an acidosis, and the raised pCO2 suggests that this is of a respiratory origin. The raised bicarbonate (HCO3) shows that there is metabolic compensation. However, such high levels, which takes time to develop, indicate long-term compensation for chronic respiratory acidosis due to his underlying COPD

120
Q

Why does COPD with empysema present with reduced Diffusing Capacity of the lungs for Carbon Monoxide (DLCO)

A

The patient has a history of chronic obstructive pulmonary disease. The histology finding of destruction to the alveolar walls is indicative of emphysema. In this condition the DLCO is reduced due to the destruction of the alveolar wall, the surface available for diffusion is reduced.

121
Q

Pathophysiology of TB:

A

Tuberculosis (TB) is a chronic granulomatous disease caused byMycobacterium tuberculosis.

122
Q

Explain the finding on x-ray for TB:

A

Some patients are not able to contain the primary infection, and it disseminates widely via the bloodstream. This is known as miliary TB (due to the characteristic pattern on chest X-rays like ‘millet-seeds’ when re-infection of lungs occurs after passing through circulation).

123
Q

General presentation of TB:

A

Subacute to chronic in onset
Symptoms depend on the main site of infection, but are usually accompanied by;
night sweats
fever
weight loss

Chronic cough productive of purulent sputum +/- haemoptysis.
Can get bronchiectasis, pneumonia and pleural effusions.

124
Q

Genitourinary presentation in TB:

A

Second most affected organ system outside of the lungs.
Causes ‘sterile’ pyuria, kidney pathology, abscesses, salpingitis and infertility, epididymo-orchitis.

125
Q

Summary of the investigations done for a patient with TB:

A

Chest X-ray
Sputum samples for culture and sensitivity testing (at least three needed - may need to consider lavage or sputum induction if cannot produce)
Samples from non-pulmonary sites: may need biopsy and needle aspiration
Samples are stained with Ziehl-Neelsen or Auramine staining for direct microscopy
For culture, Lowenstein-Jensen (LJ) media is needed.
PCR - GeneXpert, rapid results with additional drug sensitivity tested as well.
Interferon-Gamma Release Assays (IGRAs) - cannot tell difference between latent or active TB, and not useful in very young or immunosuppressed patients. Results are obtained rapidly, however, and are not affected by prior BCG.
Mantoux test - usually offered to contacts of infected patients. Positive in those who have had the BCG vaccine.

126
Q

Summary of the management of TB:

A
  • Isoniazid, rifampicin, ethambutol, and pyrazinamide for 2 months, then Isoniazid and rifampicin for a further 6 months.
  • Extended duration in TB meningitis, pericarditis, and spinal TB.
127
Q

Side effects of rifampicin:

A

Liver toxicity
Hepatic enzyme (p450) inducer
Turns bodily fluids red/orange colour.

128
Q

Caseating granulomas (with a ‘cheese-like’ necrotic core) are typical of what resp condition?

A

TB

129
Q

Indication for long term oxygen therapy for COPD patients:

A

Long-term oxygen is considered in patients with COPD if the PaO2 <7.3 or 7.3-8 PLUS peripheral oedema, pulmonary hypertension, nocturnal hypoxaemia, or secondary polycythaemia. This patient has a PaO2 between 7.3-8 kPa and polycythaemia. Note that current smoking is no longer a contraindication for home oxygen therapy (though it is highly inadvisable).

130
Q

A 68-year-old woman presents to the two-week wait clinic with a three-month history of a dry cough, shortness of breath, weight loss, fatigue, and painful wrist swelling. There is no past medical history or family history of note and she has never smoked.

On examination, she is cachexic and has finger clubbing. Her chest X-ray reveals a peripherally located nodule with minimal pleural involvement.

Which of the following is the most likely diagnosis and why?

A

This is the most likely diagnosis as adenocarcinomas are the most common form of lung cancer in non-smokers and on imaging they are peripherally located. This lady also has clubbing and hypertrophic pulmonary osteoarthropathy, as indicated by the painful wrist swelling, which is seen with adenocarcinomas

131
Q

Acute asthma in children management:

A

Oxygen saturations should be maintained between 94-98% with high flow oxygen if necessary.

Inhaled salbutamol

Nebulised salbutamol

Add nebulised ipratropium bromide
If O2 saturations remain <92% add magnesium sulphate

Add intravenous salbutamol if no response to inhaled therapy

If severe or life-threatening acute asthma not responsive to inhaled therapy, add aminophylline

All patients should receive steroids. They should only be given IV if the patient is unable take the dose orally
You should contact a senior if the patient is not responding to salbutamol or ipratropium.

132
Q

What is bronchiectasis?

A

Bronchiectasis is permanent dilation of the bronchi and bronchioles due to chronic infection.

133
Q

What are the common symptoms of bronchiectasis?

A
  • Productive Cough
  • Large amounts of purulent sputum
  • Haemoptysis

Signs included:
- Finger clubbing
- Coarse inspiratory crepitations
- Dyspneoa
- Wheeze

134
Q

Summary of the investigations for bronchiectasis:

A
  • Spirometry: bronchiectasis has an obstructive pattern of disease. Additionally, it allows clinicians to assess the reversibility of the disease and severity
  • Sputum culture: to identify pathogens and guide management with antibiotics.
    Chest X-ray: thickened bronchial walls, and cystic appearance, otherwise known as tramline and ring shadows
  • High-resolution CT: This is the best diagnostic investigation of bronchiectasis. It is monitoring the severity of the condition and can guide management.
  • Bronchoscopy: This allows clinicians to locate areas of obstruction, haemoptysis or sample tissue for culture.
135
Q

Conservative managment of bronchiectasis includes what?

A

Conservative management:

  • Patient Education
  • Support Group
  • Chest Physiotherapy - Postural drainage at least twice daily to aid mucous drainage
  • Smoking Cessation
136
Q

Medical managment of bronchiectasis:

A
  • Antibiotics - according to local guidelines, and bacterial sensitivities. Patient with recurrent exacerbations may require long term antibiotic treatment.
  • Bronchodilators - Including salbutamol can be given to patients with symptoms of dyspneoa and wheeze such as COPD, ABPA, asthma
  • Corticosteroid - Prednisolone is used in ABPA treatment
  • Carbocysteine - Mucolytic which reduces the viscosity of sputum.
137
Q

Surgical management of bronchiectasis:

A
  • Surgical excision of localized area of disease or cessation of haemoptysis.
  • Lung transplant may be indicated in certain patients.
138
Q

What are the 5 groups of causes that lead to pulmonary hypertension?

A

Group 1 – Primary pulmonary hypertension or connective tissue disease such as systemic lupus erythematous (SLE)
Group 2 – Left heart failure usually due to myocardial infarction or systemic hypertension
Group 3 – Chronic lung disease such as COPD
Group 4 – Pulmonary vascular disease such as pulmonary embolism
Group 5 – Miscellaneous causes such as sarcoidosis, glycogen storage disease and haematological disorders.

139
Q

Signs and symptoms of pulmonary hypertension:

A

Shortness of breath is the main symptom.

Syncope
Tachycardia
Raised JVP
Hepatomegaly
Peripheral oedema.

140
Q

What ECG changes are seen in pulmonary hypertension as a result of right heart strain?

A

Right ventricular hypertrophy seen as larger R waves on the right sided chest leads (V1-3) and S waves on the left sided chest leads (V4-6).

Right axis deviation.

Right bundle branch block.

141
Q

Investigations for pulmonary hypertension:

A
  • A raised NT-proBNP blood test result indicates right ventricular failure
  • Echo can be used to estimate pulmonary artery pressure.
142
Q

How is primary pulmonary hypertension treated?

A

Primary pulmonary hypertension can be treated with:

IV prostanoids (e.g. epoprostenol)
Endothelin receptor antagonists (e.g. macitentan)
Phosphodiesterase-5 inhibitors (e.g. sildenafil)

Supportive treatmentfor complications such as respiratory failure, arrhythmias and heart.

143
Q

What is sarcoidosis?

A

Sarcoidosis is a granulomatous inflammatory condition. Granulomas are nodules of inflammation full of macrophages.

It is usually associated with chest symptoms but also has multiple extra-pulmonary manifestations such as erythema nodosum and lymphadenopathy. Symptoms can vary dramatically from asymptomatic (in up to 50%) to severe and life-threatening.

144
Q

Epidemiology of sarcoidosis?

A

There are two spikes in incidence, in young adulthood and again around age 60. Women are affected more often and` it occurs more frequently in black people compared with other ethnic groups.

145
Q

How does sarcoidosis affect the lungs?

A

Mediastinal lymphadenopathy
Pulmonary fibrosis
Pulmonary nodules

146
Q

Systemic symptoms of sarcoidosis?

A

Fever
Weightloss
Fatigue

147
Q

What key blood tests are done for sarcoidosis?

A

Raised serum ACE. This is often used as a screening test.
Hypercalcaemia (rasied calcium) is a key finding.

Raised serum soluble interleukin-2 receptor
Raised CRP
Raised immunoglobulins

148
Q

What is the treatment for NSCLC?

A

First-line: lobectomy
Curative radiotherapy can also be offered to patients with stage I, II and III NSCLC.
Chemotherapy should be offered to patients with stage III and IV NSCLC to control the disease and improve quality of life.

149
Q

What is the treatment for SCLC.

A

Generally palliative chemotherapy, as tumours are disseminated on presentation.

150
Q

What type of lung cancer is most common?

A

Adenocarcinoma

151
Q

What is Kussmaul breathing and what is it seen in?

A

Kussmaul breathing is a deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also kidney failure. It is a form of hyperventilation, which is any breathing pattern that reduces carbon dioxide in the blood due to increased rate or depth of respiration.

152
Q

What is Cheyne-Stokes respiration?

A

Cheyne-Stokes respiration is a specific form of periodic breathing (waxing and waning amplitude of flow or tidal volume) characterized by a crescendo-decrescendo pattern of respiration between central apneas or central hypopneas.

Slow - fast - stop, repeat.

  • seen in heart failure, and sleep apnoea.
153
Q

Most common type of lung cancer?

A

Adenocarcinoma (especially in non-smokers).

154
Q

Which lung cancer cavitates?

A

Squamous cell carcinoma

155
Q

Read the summary of small cell carcinoma:

A
  • Arise from endocrine cells (Kulchitsky cells). These are APUD cells, and as a result, these tumours will secrete many poly-peptides mainly ACTH.
  • They can also cause various presentations such as Addison’s and Cushing’s disease.
  • Small cell carcinoma spreads very early and is almost always inoperable at presentation.
  • These tumours do respond to chemotherapy, but the prognosis is generally poor.
156
Q

Which cancer commonly causes hypercalcemia?

A

SCC - often causes hypercalcaemia – by bone destruction or production of PTH analogues (PTHrp).

157
Q

Treatment of non-small cell lung cancer:

A
  • First-line: lobectomy
  • Curative radiotherapy can also be offered to patients with stage I, II and III NSCLC.
  • Chemotherapy should be offered to patients with stage III and IV NSCLC to control the disease and improve quality of life.
158
Q

Treatment of small cell lung cancer:

A

Generally palliative chemotherapy, as tumours are disseminated on presentation.

159
Q

Antibiotic for legionella pneumonia?

A

Clarithromycin

160
Q

HIV patient with a pneumonia.

  • What’s the organism?
A

Pneumocystis jiroveci

  • treat with co-trimoxazole.
161
Q

SVC obstruction management

A

SVC Obstruction management is S S S
Sit them up
Stat dose of Steroids
Stenting

162
Q

Samter’s triad?
- hint what medication needs to be avoided in asthmatics?

A

In patients with asthma, aspirin and other NSAIDs should be avoided as these may precipitate an asthma exacerbation.

The combination of asthma, aspirin sensitivity and nasal polyps is known as Samter’s triad.

163
Q

Chest x-ray for TB shows what?

A

Upper zone opacities.
Bilateral hilar lymphadenopathy.

164
Q

How to differentiate sarcoidosis from TB?

A

Sarcoidosis - a common cause for bilateral hilar lymphadenopathy. Presenting features can mimic TB and is common in the same age group as well.

However, there is commonly multi-system involvement at presentation including polyarthralgia, erythema nodosum, lupus pernio. There is usually no haemoptysis and the cough tends to be non-productive.

165
Q

What is first line for COPD patients?

A

A SABA or SAMA is the first-line pharmacological treatment of COPD.

Nothing long term initially!

166
Q

Second line for a COPD patient with no asthmatic features?

A

Add a long-acting beta2-agonist (LABA) + long-acting muscarinic antagonist (LAMA).

If already taking a SAMA, discontinue and switch to a SABA

2nd line = SABA + LABA + LAMA

167
Q

Second line for a COPD patient with asthmatic features?

A

LABA + inhaled corticosteroid (ICS)

If patients remain breathless or have exacerbations offer triple therapy i.e. LAMA + LABA + ICS

If already taking a SAMA, discontinue and switch to a SABA.

168
Q

How is severity of COPD classified?

A

The severity of COPD is based upon the FEV1 spirometry reading.

169
Q

What would be classed as very severe COPD?

A

FEV1 of less than 30%

170
Q

TB ix when in GP land:

A

Sputum culture, chest x-ray and HIV test.

A HIV test should be offered to all patients with TB.

171
Q

What is ipatropium?

A

SAMA

172
Q

1st line for COPD

A

SAMA or SABA

173
Q

Management of a secondary pneumothorax?
>2cm
<1cm

A

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.

174
Q

1st line to acutely manage a PE:

A

DOAC - use even in cases of cancer.

175
Q

Legionella pneumonia treatment

A

Erythromycin / Clarithromycin

176
Q

What should be used to treat TB in the initial active phase?

A

Initial phase - first 2 months (RIPE)
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol (the 2006 NICE guidelines now recommend giving a ‘fourth drug’ such as ethambutol routinely - previously this was only added if drug-resistant tuberculosis was suspected)

177
Q

Suspected PE with a Wells PE score ≤4 - ix how?

A

D-dimer

178
Q

Diagnosis of legionella pneumophillia

A

Legionella pneumophilia is best diagnosed by the urinary antigen test

179
Q

Diagnosis of legionella pneumophillia

A

Legionella pneumophilia is best diagnosed by the urinary antigen test

180
Q

Spironolactone = what class?

A

Aldosterone antagonist

181
Q

Diagnostic criteria for adults with asthma:

A

Asthma may be diagnosed if any of the following criteria are met (in adults):
An exhaled FeNO of 40 parts per billion or greater.
A post-bronchodilator improvement in lung volume of 200 ml.
A post-bronchodilator improvement in FEV1 of 12% or more.
A peak expiratory flow rate variability of 20% or more.
An FEV1/FVC ratio <70% (it is an obstructive lung disease).

182
Q

Lung function tests for pulmonary fibrosis:

A

Restrictive spirometry picture (FEV1:FVC >70%, decreased FVC)
Impaired gas exchange (reduced TLCO)

183
Q

The features of a severe asthma attack:

A

The features of acute severe asthma are: PEFR 33-50% best or predicted, inability to complete full sentences, RR >25/min and pulse >110 bpm.

184
Q

Most common organism found in patients with bronchiectasis:

A

H.influenza

185
Q

What type of ventilation is used in COPD?

A

BIPAP

CPAP (Continuous Positive Airway Pressure) is another form of non-invasive ventilation but is not as effective as BIPAP in COPD. It is used in type one respiratory failure and is particularly useful in pulmonary oedema.

186
Q

Avoid erythromycin in long QT

A

Avoid erythromycin in long QT

187
Q

Thoughts and feelings on SAMA + LAMA?

A

COPD: Discontinue SAMA (switch to SABA) if commencing LAMA

188
Q

What lung cancer secretes ACTH and can cause Cushing’s syndrome

A

Small cell

189
Q

Adult with asthma not controlled by a SABA - add what?

A

Low-dose ICS

190
Q

Gynaecomastia is associated with what type of lung cancer?

A

Gynaecomastia - associated with adenocarcinoma of the lung

191
Q

A 30-year-old woman is admitted with pneumonia to hospital. She has a fever and a dry cough. On examination erythema multiforme is noted and bloods show she has a normocytic anaemia.

A

Mycoplasma pneumonia

192
Q

Pt SOB background of COPD. Confirmed to have a 2.5cm pneumothorax, what’s the management?

A

Chest drain because secondary
Chest drain because SOB

If a secondary pneumothorax > 2cm and/or the patient is short of breath then patient should be treated with chest drain (not aspiration) as first-line.

193
Q

Pulmonary oedema management:

A

SODIUM
Sit up
Oxygen
Diuretics
Inotropes
Underlying causes
Monitor and reassess

194
Q

Use of inotropes in pulmonary oedema:

A

Inotropic drugs should only be started when there is hypotension and evidence of reduced organ perfusion. In these cases, dobutamine is usually first-line treatment.

  • late management done in ICU
195
Q

1st line tx for sarcoidosis

A
  • No treatmentis considered as first line in patients with no or mild symptoms as the condition often resolves spontaneously.
  • Oral steroidsare usually first line where treatment is required and are given for between 6 and 24 months. Patients should be givenbisphosphonatesto protect against osteoporosis whilst on such long term steroids.
  • Second line options aremethotrexateorazathioprine
  • Lung transplantis rarely required in severe pulmonary disease
196
Q

Mycoplasma pneumonia
- what rash is seen?
- what is diagnostic?

A

Erythema multiforme / Erythema nodosum
Serology

197
Q

Tx for mycoplasma pneumonia

A

doxycycline or a macrolide(e.g. erythromycin/clarithromycin)

198
Q

How to treat a secondary pneumothorax?

A

Chest drain

199
Q

PE first line normal BP:

A

DOAC

200
Q

treatment of choice for allergic bronchopulmonary aspergillosis?

A

Oral prednisolone

201
Q

Treatment for PCP pneumonia:

A

Co-trimoxazole

202
Q

CAP curb 0-1 give

A

CURB 0-1: amoxicillin 500mg TDS (or doxycycline or clarith or eryth)

203
Q

CAP curb 2 give

A

CURB 2: amoxicillin 500mg TDS and clarithromycin 500mg BD or erythro 500mg QDS

204
Q

CAP curb 3-5 give

A

CURB 3-5: co-amoxiclav 500/125mg TDS and clarith 500mg BD or eryth 500mg QDS

Treat for 5 days

205
Q

Lower UTI

A

Non-pregnant, uncomplicated women:

  • nitrofurantoin (if eGFR>45) 100 m/r BD or 50mg QDS for 3 days
  • trimethoprim 200mg BD for 3 days

Treat men for 7 days

206
Q

3rd trimester UTI give…

A

Amoxicillin