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Yr 3 - Core Conditions > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Give some red flags for a respiratory history/examination

A
  • Haemoptysis/brown sputum
  • Weight loss
  • Cough >3 weeks
  • Chest pain
  • Drenching night sweats
  • Foreign travel
  • Smoking history
  • Sudden onset SOB
  • Risk factors for PE
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2
Q

What is the most common lung disease in the UK?

A

Asthma

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3
Q

Give the 3 mechanisms behind airway narrowing in asthma

A
  1. Bronchial muscle contraction
  2. Inflammation caused by mast cell degranulation
  3. Increased mucus production
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4
Q

Asthma often shows a diurnal variation. What does that mean?

A

symptoms often worse in morning

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5
Q

Describe the percussion in asthma

A

Hyperresonance (due to presence of air)

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6
Q

Describe the inflation of the lungs in acute asthma

A

Hyperinflation

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7
Q

Describe the auscultation of the lungs in asthma

A

Bilateral decreased air entry

Wheeze

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8
Q

Are the symptoms/signs in asthma bilateral or unilateral?

A

Bilateral

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9
Q

What is a ‘silent chest’ in asthma a sign of?

A

Severe illness - life-threatening

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10
Q

What is the diagnostic investigation in asthma?

A

Spirometry

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11
Q

How does spirometry and PEFR differ?

A

Both tests measure the speed and efficiency with which air moves in and out of the lungs.

Spirometry - offers a larger set of parametric values regarding lung health than a peak flow meter does and requires a patient to perform specific breathing manoeuvres using a spirometer.

PEFR - can be performed at bedside/patient home

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12
Q

What spirometry result indicates asthma?

A

FEV1/FVC <0.7 (70%) indicates obstructive airway disease

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13
Q

What is the FEV1/FVC ratio?

A

The FEV1/FVC ratio is the ratio of the forced expiratory volume in the first one second to the forced vital capacity of the lungs (i.e. indicates how much air you can forcefully exhale)

Measured by spirometry

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14
Q

Give some other investigations that can be used in chronic asthma?

A
  • Fractional exhaled nitric oxide (FeNO)
  • Bronchodilator reversibility tests
  • Skin prick test - confirm atopy
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15
Q

What bronchodilator reversibility test result indicates asthma?

A

Improvement of FEV1 >12% after bronchodilator therapy is diagnostic

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16
Q

What is the stepwise pharmacological long-term management of asthma

A
  1. Short-acting b2 agonist (SABA) e.g. salbutamol
  2. Add inhaled low dose inhaled corticosteroid (ICS) e.g. beclomethasone
  3. Add long-acting b2 agonist e.g. salmeterol
  4. Two options:
    1. Increase ICS dose
    2. Add leukotriene receptor antagonist e.g. montelukast
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17
Q

What are the aims of pharmacological management of asthma?

A
  • No daytime symptoms
  • No night-time waking due to asthma
  • No asthma attacks
  • No limitations on activity including exercise
  • Minimal side effects from medication
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18
Q

Pathophysiology behind an asthma attack?

A

IgE type 1 hypersensitivity reaction leading to smooth muscle contraction, bronchial oedema and mucus plugging.

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19
Q

What medications can exacerbate asthma?

A
  1. Beta blockers e.g. bisoprolol → contraindication
  2. NSAIDs (some but not all) → caution
  3. AChEIs –> due to increased bronchial secretions
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20
Q

Give some triggers for an asthma attack

A
  • Exposure to allergens e.g. dust, pollution, animal hair or smoke
  • URT or LRTIs
  • Cessation or reduction of asthma medications
  • Concomitant medications e.g. beta blockers, NSAIDs
  • Triggers e.g. exercise, cold air
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21
Q

Give some signs of an acute asthma attack

A
  • Use of accessory muscles of respiration
  • Hyperinflation of the chest
  • Tachypnoea
  • Tachycardia
  • Diaphoresis (sweating)
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22
Q

Give some signs of a severe asthma attack

A
  • Inability to speak in full sentences
  • RR >25
  • Peak flow 33-50% predicted
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23
Q

Give some signs of a life-threatening asthma attack

A
  • PEFR <33% predicted
  • O2 sats <92%
  • Silent chest on auscultation
  • Confusion
  • Bradycardia
  • Hypotension
  • Cyanosis
  • Exhaustion – weak or no respiratory effort
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24
Q

What may bradycardia in a life-threatening asthma attack indicate?

A

Impending respiratory arrest

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25
Q

What does an FeNO test indicate?

A

Measures level of NO in breath which is a sign of inflammation in your lungs

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26
Q

Which bloods are important in acute asthma?

A
  • FBC – infection
  • CRP – infection
  • Eosinophil count
  • Total IgE
  • IgE to aspergillus
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27
Q

Which imaging is 1st line in acute asthma?

A

CXR - but doesn’t delay management

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28
Q

What may a CXR in acute asthma show?

A

usually normal (may show hyperinflation or bronchial wall thickening)

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29
Q

Give the stepwise pharkmacological management in an acute asthma attack (ABCDE)

A
  1. Oxygen
  2. Nebulised salbutamol (high dose)
  3. Nebulised ipratropium bromide if needed
  4. Steroid therapy - oral prednisolone or IV hydrocortisone
  5. IV Magnesium sulphate
  6. IV aminophylline
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30
Q

When would ipratropium bromide be given in acute asthma? What is the effect of this?

A

Add for patients with acute severe or life-threatening asthma or to those with a poor initial response to b2 agonist therapy.

Combining nebulised ipratropium bromide with a nebulised b-2 agonist produces significant bronchodilation than a b-2 agonist alone.

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31
Q

Who should steroid therapy be administered to in patients presenting with an acute asthma attack?

A

ALL patients with acute asthma

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32
Q

What steroids should be used in acute asthma?

A

Oral prednisolone 40-50mg

If oral route unavailable (likely) → IV hydrocortisone

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33
Q

How long should oral prednisolone be continued for following an acute asthma attack?

A

5 days or until full recovery

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34
Q

When would you consider giving IV magnesium sulphate in acute asthma?

A
  • Acute severe asthma who have not had a good response to inhaled therapy
  • Life-threatening or near-fatal asthma
  • Only use after consultation with senior medical staff
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35
Q

What would reduced air entry in acute asthma indicate?

A

significant airway compromise

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36
Q

What would absent air entry on auscultation in acute asthma indicate?

A

Underlying pneumothorax

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37
Q

What would dullness on percussion in acute asthma indicate?

A

Pleural effusion

Lobar collapse

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38
Q

Typical ABG results in acute asthma?

A

Low PaO2, low PaCO2

If PaCO2 normal or raised → major concern

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39
Q

What is COPD?

A

A triad of chronic bronchitis, emphysema and small airway fibrosis causing irreversible obstruction of air flow; bronchitis or emphysema can be the predominant condition.

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40
Q

Most common cause of COPD?

A

Smoking (95%)

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41
Q

Other causes of COPD?

A
  • Dust, silica, pollutants
  • Alpha 1 antitrypsin deficiency (a-1 is a protease inhibitor)
    • Autosomal dominant
    • Raises risk for lung and liver disease
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42
Q

COPD is usually a combination of chronic bronchitis and emphysema. What are these 2 conditions?

A

‘Chronic bronchitis’ - chronic inflammation of the bronchi (usually defined as a productive cough on most days for 3 months a year over 2 successive years)

‘Emphysema’ - enlargement of air spaces in the terminal bronchioles leading to inefficient gas exchange ratios and poor air outflow

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43
Q

What is the pathogenesis behind COPD?

A

Chemicals and heat trigger inflammation in bronchi and lung parenchyma

  • Bronchi → persistent inflammation leads to scarring and mucus hyperplasia (bronchitis)
  • Parenchyma → inflammation leads to alveolar wall loss (emphysema)
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44
Q

Give some triggers for COPD exacerbations

A
  • Viral or bacterial lung infection (acute bronchitis or pneumonia)
  • Smoking
  • Exposed to smoke or air pollution
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45
Q

Give some symptoms of COPD

A
  • Dyspnoea (may only happen at first when exercising)
  • Chronic productive cough (sputum usually colourless, may become green in LRTIs)
  • Recurrent LRTIs
  • Fatigue
  • Headache (due to CO2 retention)
  • Trouble taking a deep breath
  • Chest tightness
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46
Q

Give some symptoms of an exacerbation of COPD

A
  • More coughing, wheezing, or SOB than usual
  • Changes in colour, thickness or amount of mucus
  • Feeling tired for more than 1 day
  • Swelling of legs or ankles
  • O2 levels lower than normal
  • Severe → cyanosis, severe SOB, chest pain, confusion
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47
Q

What signs are seen in a COPD exacerbation?

A
  • Accessory muscle use & pursed lips
  • Tachypnoea
  • Hyperinflation
  • Reduction of cricosternal distance
  • Reduced chest expansion
  • Hyper resonant percussion
  • Decreased/quiet breath sounds
  • Wheeze on auscultation (due to inflammatory airway oedema and mucous obstruction)
  • Cyanosis
  • Cor pulmonale (signs of RHF)
  • CO2 retention flap
  • Reduced conscious level
  • Severe → tachycardia, tachypnoea, hypoxia, cyanosis, reduced consciousness
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48
Q

What is the typical spirometry finding in COPD?

A

FEV1/FVC <0.7

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49
Q

What SpO2 should you aim for in COPD patients?

A

88-92%

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50
Q

How can COPD affect the heart?

A

COPD can cause low oxygen levels in the blood, thereby placing additional stress on the heart.

This can lead to right ventricle hypertrophy and potentially cor pulmonale

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51
Q

What is cor pulmonale?

A

Cor pulmonale is a condition that causes the right side of the heart to fail.

Long-term high blood pressure in the arteries of the lung and right ventricle of the heart can lead to cor pulmonale

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52
Q

What may an FBC show in COPD?

A

Raised MCV - polycythaemia

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53
Q

What may an ABG show in COPD?

A

Low PaO2

Raised PaCO2 (type 2 respiratory failure)

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54
Q

What is the purpose of a sputum sample in COPD exacerbation?

A

Enables targeted antibiotic therapy

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55
Q

What may a CXR show in COPD

A
  • Hyperinflated chest (>6 anterior ribs)
  • Bullae
  • Decreased peripheral vascular markings
  • Flattened hemidiaphragms
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56
Q

How should oxygen be delivered to COPD patients during acute exacerbations?

A

Use a venturi mask and titrate oxygen appropriately.

If the patient is conscious, sit them upright as this can also help with oxygenation.

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57
Q

Give the pharmacological management of an acute COPD exacerbation

A
  1. Oxygen
  2. Nenuclised salbutamol
  3. Nebulised ipratropium bromide
  4. Steroids
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58
Q

What steroids should be used in the management of a COPD exacerbation?

A

Oral prednisolone (IV hydrocortisone if needed)

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59
Q

Give the stepwise pharmacological management of chronic COPD

A

Step 1 – Short acting B2-agonist (SABA) OR short acting muscarinic antagonist (SAMA)

Step 2 – Add LABA AND LAMA

Step 3 – LAMA + LABA + ICS

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60
Q

What can lung cancers be divided into?

A

Small cell & non small cell tumours

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61
Q

Are small cell or non small cell lung cancers more common?

A

Non-small cell (80%)

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62
Q

What is the most common type of NSCLC?

A

Adenocarcinoma (40%)

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63
Q

What is the 2nd most common type of NSCLC?

A

Squamous cell carcinoma (20%)

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64
Q

Give some red flag symptoms for lung cancer

A
  • Cough
  • Haemoptysis
  • Dyspnoea
  • Chest pain
  • Weight loss
  • N&V
  • Anorexia
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65
Q

Lung cancer can present with Horner’s syndrome. Give the location of the tumour in this instance

A

Apical → interrupted sympathetic supply to face

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66
Q

Lung cancer can lead to many complications.

What chest signs could be seen during an examination?

A
  • Consolidation – pneumonia
  • Collapse – absent breath sounds, ipsilateral tracheal deviation
  • Pleural effusion – stony dull percussion, decreased vocal resonance and breath sounds
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67
Q

Are SCLCs or NSCLCs more likely to cause paraneoplastic syndromes?

A

SCLCs

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68
Q

Give some paraneoplastic syndromes that can be caused by lung cancer

A
  • Cushing’s syndrome → ectopic ACTH secretion
  • SIADH → ectopic SIADH syndrome
  • Lambert-Eaton syndrome
  • Hyperparathyroidism
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69
Q

How does parathyroid hormone affect calcium?

A

parathyroid hormone stimulates the release of calcium from large calcium stores in the bones into the bloodstream (hyperparathyroidism → hypercalcaemia)

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70
Q

Give the pathology behind lung cancer manifesting as SOB

A

If cancer invades major airways

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71
Q

Give the pathology behind lung cancer manifesting as haemoptysis

A

Invasion of cancer into airways (friable tissue) may lead to bleeding

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72
Q

Give the pathology behind lung cancer manifesting as pain

A

Local invasion affecting the lining of the pleural cavity or bone, causing pain

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73
Q

Give the pathology behind lung cancer manifesting as a pleural effusion

A

Can cause inflammatory reactions which can leads to the accumulation of fluid in the pleural space

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74
Q

Give the pathology behind lung cancer manifesting as a superior vena cava obstruction

A

Cancer may invade into surrounding lung tissues, leading to compression of the draining of the SVC leading to dyspnoea and facial plethora due to venous congestion

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75
Q

Give the pathology behind lung cancer manifesting as a pneumothorax

A

Invasion of the tumour may lead to a communication between the lung parenchyma and the pleural cavity, resulting in the collapse of the lung

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76
Q

Give the pathology behind lung cancer manifesting as atelectasis

A

Invasion may lead to total obstruction of the airway leading to collapse of that lobe

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77
Q

What is the 1st line investigation in suspected lung cancer?

A

CXR

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78
Q

Is pleural effusion typically unilateral or bilateral in lung cancer?

A

Unilateral

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79
Q

Give some potential CXR features in lung cancer

A
  • Nodules
  • Hilar enlargement
  • Lung collapse
  • Pleural effusion – usually unilateral in cancer
  • Consolidation
  • Peripheral opacity – a visible lesion in the lung field
  • Bony metastases
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80
Q

What staging system is used to stage lung cancer?

A

TNM

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81
Q

What investigation can be used in the staging of lung cancer?

A

CT scan of chest, abdomen and pelvis

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82
Q

What is the most common type of lung cancer in the UK?

A

Adenocarcinoma

83
Q

Which lung cancer is the least likely to be related to smoking?

A

Adenocarcinoma

84
Q

What cells do adenocarcinomas arise from?

A

Arises from mucous cells in bronchial epithelium

85
Q

Which type of lung cancer is most likely to cause a pleural effusion?

A

Adenocarcinoma (and mesotheliomas)

86
Q

Which type of lung cancer is most commonly related to hypercalcaemia?

A

Squamous cell carcinoma

87
Q

Lung cancer can cause hypercalaemia via which 2 mechanisms?

A
  1. bone destruction
  2. production of PTH analogues
88
Q

What cells do small cell lung cancers arise from?

A

From endocrine cells (Kulchitsky cells) – these are APUD cells

89
Q

Which 2 hormones with SCLCs most typically secrete? Why?

A

Due to high grade neuroendocrine nature → adrenocorticotropic hormone (ACTH) and anti-diuretic hormone (ADH)

90
Q

SCLC is also associated with Addison’s disease. What is the pathophysiology behind this?

A

Tissue destruction of the adrenal glands → low cortisol (and aldosterone)

91
Q

What is Lambert-Eaton syndrome?

A

The result of antibodies produced by the immune system against small cell lung cancer cells

92
Q

Why are SCLCs responsible for multiple paraneoplastic syndromes?

A

SCLCs contain neurosecretory granules that can release neuroendocrine hormones

93
Q

Pathophysiology behind Lambert-Eaton syndrome?

A

Antibodies target and damage voltage-gated calcium channels in motor neurons

94
Q

Symptoms of Lambert-Eaton?

A
  • Proximal weakness
  • Intraocular muscle weakness – diplopia (double vision)
  • Levator muscles in eyelid weakness – ptosis
  • Pharyngeal muscle weakness – slurred speech, dysphagia
  • Reduced tendon flexes
95
Q

What cells does mesothelioma affect?

A

A lung malignancy affecting the mesothelial cells of the pleura.

96
Q

What is mesothelioma strongly linked to?

A

Asbestos exposure

97
Q

What is the latent period between asbestos exposure and development of mesothelioma?

A

Up to 45 years

98
Q

What is a pneumothorax

A

Air within the pleural space.

99
Q

What are the 2 major classifications of a pneumothorax?

A

Spontaneous & traumatic

100
Q

Spontaneous pnuemothorax’s can be 1ary or 2ary. What is the difference?

A

1ary → No underlying lung pathology

2ary → Underlying lung pathology

101
Q

What type of patient does a 1ary spontaneous pneumothorax present in?

A

Tall thin young men

Typical Presentation in Exams – Young, tall, thin man presenting with sudden breathlessness and pleuritic chest pain, possibly whilst playing sports.

102
Q

Give some underlying pathologies that can lead to 2ary spontaneous pneumothorax’s

A
  • Connective tissue disease e.g. Marfan’s syndrome, Ehlers-Danlos syndrome
  • Obstructive lung disease e.g. asthma, COPD
  • Infective lung disease e.g. TB, pneumonia
  • Fibrotic lung disease e.g. cystic fibrosis, idiopathic pulmonary fibrosis
  • Neoplastic disease e.g. bronchial carcinoma
103
Q

Traumatic pneumothorax’s can be classified into iatrogenic and non-iatrogenic causes.

Give some examples for both

A

Iatrogenic → central line insertion, positive pressure ventilation, lung biopsy

Non-iatrogenic → penetrating trauma, blunt trauma with rib fracture

104
Q

Give some symptoms of a pneumothorax

A
  • Sudden onset SOB
  • Pleuritic chest pain
105
Q

How is each factor affected in a pneumothorax:

  • Chest expansion
  • Percussion
  • Breath sounds
  • Vocal resonance
A
  • Chest expansion → reduced on affected side
  • Percussion → hyper resonance on affected side
  • Breath sounds → reduced/absent on affected side with no added sounds
  • Vocal resonance → reduced on affected side
106
Q

What is the 1st line investigation in a pneumothorax?

107
Q

What type of cannula is used to aspirate a pneumothorax?

A

A 16-18G cannula under local anaesthetic

108
Q

What is a tension pneumothorax?

A

Caused by trauma to the chest wall that creates a one-way valve that lets air in but not out of the pleural space.

109
Q

Pathology behind a tension pneumothorax?

A
  1. One-way valve means that during inspiration, air is drawn into the pleural space and during expiration, the air is trapped in the pleural space.
  2. More air keeps getting drawn into the pleural space with each breath and cannot escape.
  3. This creates pressure inside the thorax that will push the mediastinum across, kink the big vessels in the mediastinum and cause cardiorespiratory arrest.
110
Q

Signs of a tension pneumothorax?

A
  • Tracheal deviation away from the side of the pneumothorax
  • Reduced air entry to affected side
  • Increased resonant to percussion on affected side
  • Tachycardia
  • Hypotension
111
Q

Management of tension pneumothorax?

A

ABCDE approach

Immediate needle decompression using a 16-gauge cannula (large bore cannula) inserted at the second intercostal space in the mid-clavicular line on the affected side.

Chest drain insertion (then obtain CXR for positioning)

112
Q

Where must the needle be inserted in a tension pneumothorax?

A

Needle must be inserted just above the 3rd rib to avoid damaging the neurovascular bundle

113
Q

What is a pleural effusion?

A

The abnormal buildup of fluid in the pleural cavity.

114
Q

What protein count defines an exudative fluid?

A

High (>35 g/L)

115
Q

What protein count defines a transudative fluid?

A

Low (<25g/L)

116
Q

What is the pathophysiology behind an exudative pleural effusion?

A

Increased pleural and capillary permeability due to inflammation, resulting in protein leaking out of tissues into pleural space

117
Q

What are the most common causes of exudative pleural effusions?

A
  • Infection – pneumonia, tuberculosis
  • Malignancy – bronchial carcinoma, mesothelioma, lung metastases
118
Q

What is the pathophysiology behind transudative pleural effusions?

A

Disruption in hydrostatic pressure → increase in pulmonary hydrostatic pressure forces fluid out of pulmonary capillaries into pleural space

Disruption in oncotic pressure → impaired reabsorption of fluid from pleural space into pulmonary capillaries

119
Q

What are the 2 most common causes of transudative pleural effusions?

A
  • Heart failure
  • Liver failure (cirrhosis)
120
Q

Would nephrotic syndrome cause a transudative or exudative pleural effusion?

A

Transudative

121
Q

Would hypoalbuminaemia cause a transudative or exudative pleural effusion?

A

Transudative

122
Q

Define an empyema

A

pus in pleural space

123
Q

Disruption of which structure leads to a chylothorax?

A

Chyle in pleural space due to disruption of thoracic duct (neoplasm, trauma, infection/inflammation)

124
Q

Are transudative or exudative pleural effusions more likely to be bilateral?

A

Transudative pleural effusions are more likely to be bilateral whilst exudative pleural effusions are more likely to be unilateral.

125
Q

Symptoms of a pleural effusion?

A
  • Dyspnoea (SOB)
  • Reduced exercise tolerance
  • Pleuritic chest pain
  • Other areas to cover in history:
    • Symptoms suggestive of lung cancer → haemoptysis, weight loss
    • Symptoms suggestive of heart failure → orthopnoea, paroxysmal nocturnal dyspnoea, leg swelling
    • Symptoms suggestive of lung infection → productive cough, fever
    • Social history → smoking history (lung cancer risk), asbestos exposure (mesothelioma)
126
Q

Chest signs possibly seen in pleural effusion:

  • trachea
  • chest expansion
  • percussion
  • auscultation
  • vocal resonance/tactile vocal fremitus
A
  • trachea → central/deviated away from affected side (if large)
  • chest expansion → reduced on affected side
  • percussion → stony dull on affected side
  • auscultation: reduced/absent breath sounds over effusion & bronchial breathing at upper border of effusion
  • vocal resonance/tactile vocal fremitus → reduced over effusion
127
Q

Why would an ECG be indicated in a pleural effusion?

A
  • Look for cardiac cause of chest pain and breathlessness
  • Look for signs of right heart strain (PE)
128
Q

Why would a urine dip be indicated in pleural effusion?

A
  • assess for proteinuria which may indicate nephrotic syndrome
129
Q

Potential blood tests in a pleural effusion:

A
  • FBC → may show raised WCC (infection)
  • U&Es → may show raised creatinine (renal impairment)
  • LFTs & coagulation profile → may show low albumin and raised ALT/AST (cirrhosis)
  • CRP → infection
  • Blood cultures → infection
  • ABG → if oxygenation affected
  • D-dimer → if PE suspected
  • Amylase → if pancreatitis suspected
  • TFTs → if hyperthyroidism suspected
130
Q

1st line imaging in pleural effusion?

131
Q

Give some potential CXR findings in a pleural effusion

A
  • Unilateral → typically exudative
  • Bilateral → typically transudative
  • Blunting of costophrenic angles (>200ml fluid needed to be visible on PA film)
  • Fluid in lung fissures
  • Meniscus (curving upwards where effusion meets chest wall and mediastinum) if large
  • White out of one hemifield if large
  • Tracheal and mediastinal deviation if massive
132
Q

Thoracentesis is indicated in all patients except who?

A

Required in all patients except those with clear evidence of HF (raised JVP, pitting ankle oedema, signs on CXR)

133
Q

What would purulent pleural fluid upon aspiration indicate?

134
Q

What would bloody fluid upon aspiration indicate?

A

malignancy, PE or trauma

135
Q

Pleural effusion CXR findings:

136
Q

Management of large pleural effusions?

A
  • ABCDE approach if required
  • Pharmacological:
    • Diuretics in HF
    • Antibiotics in infection
  • Larger effusions:
    • Pleural aspiration with needle (temporary symptomatic relief but may recur)
    • Drainage via chest drain (can prevent it recurring)
137
Q

Give some complications of a pleural effusion

A
  • Empyema → infected pleural effusion
  • Lung damage
  • Pneumothorax
  • Pleural thickening
138
Q

Pathophysiology of pneumonia?

A
  1. Inflammation leads to fluid and blood cells leaking into the alveoli.
  2. The infection spreads across the alveoli and eventually the lung tissue becomes consolidated, impairing the gas exchange due to reduced ventilation.
139
Q

What are the 3 most common causative organism in community acquired pneumonia (CAP)?

A
  • Streptococcus pneumoniae → most common
  • Haemophilus influenzae
  • Mycoplasma pneumoniae
140
Q

Give some symptoms of a pneumonia

A
  • Fever
  • Malaise
  • Rigors
  • Cough
  • Purulent sputum
  • Pleuritic chest pain
  • Haemoptysis
141
Q

Chest examination findings in pneumonia?

A
  • Percussion → dull (due to lung tissue collapse and/or consolidation)
  • Vocal resonance/tactile fremitus → increased
  • Bronchial breath sounds
  • Focal coarse crackles
  • Pleural rub
142
Q

What are bronchial breath sounds?

A
  • Harsh sounds equally loud on inspiration & expiration are equal
  • Audible pause between inspiration & expiration
143
Q

What are focal coarse crackles in pneumonia?

A

these are air passing through sputum in airways

144
Q

what is a pleural rub? cause?

A

An audible sound heard in patients with pleurisy

Caused by layers of pleura rubbing against each other

145
Q

Why is a urine sample for antigen testing required in pneumonia?

A

To distinguish between legionella and pneumococcal urinary antigens

146
Q

After how many days of starting Abx should inflammatory markers be repeated in pneumonia?

147
Q

Typical Abx management of moderate-severe CAP?

A

IV antibiotics 7-10 day course of dual Abx (amoxicillin + macrolide e.g. co-amoxiclav + clarithromycin)

148
Q

Typical Abx management of mild CAP?

A

5-day course of oral Abx (amoxicillin or macrolide)

149
Q

Define hospital acquired pneumonia

A

A LRTI that develops >48 hours after hospital admission

150
Q

Top 3 causative organisms of hospital acquired pneumonia?

A
  • Pseudomonas aeruginosa
  • Staph. aureus
  • Enterobacteria
151
Q

Who does aspiration pneumonia occur in?

A

Occurs in patients with an unsafe swallow

152
Q

Risk factors for aspiration pneumonia?

A
  • Myasthenia gravis
  • Bulbar palsy
  • Alcoholism
  • Achalasia
153
Q

Which lung is more affected in aspiration pneumonia? Why?

A

R lung more affected due to R bronchus being more vertical and wider

154
Q

What are the criteria of the CURB 65 score?

A
  • C – Confusion (AMTS = 8)
  • U – Urea >7mmol/l
  • R – Respiratory rate >/= 30
  • B – Blood pressure <90 systolic and/or <60mmHg diastolic
  • 65 – Age >/= 65 y/o
155
Q

Define atypical pneumonia

A

Pneumonia caused by an organism that cannot be cultured in the normal way or detected using a gram stain

156
Q

How does the antibiotic management for atypical pneumonia change?

A

Do not respond to penicillins

Treated with:

  • Macrolides e.g. clarithromycin
  • Fluroquinolones e.g. levofloxacin
  • Tetracyclines e.g. doxycycline
157
Q

What are the 3 most common causative organisms of atypical pneumonia?

A
  1. Legionella pneumophila (Legionnaire’s disease)
  2. Mycoplasma pneumoniae
  3. Chlamydophila pneumoniae
158
Q

Cause of Legionella pneumonia?

A

Infected water supplies or air conditioning units

Typical patient → Cheap hotel holiday and presents with hyponatraemia

159
Q

What electrolyte disturbance does Legionella pneumonia present with?

A

Hyponatraemia by causing an SIADH (excess secretion of ADH causes excess absorption of water → dilution of sodium)

160
Q

how does mycoplasma pneumonia typically present?

A
  • Milder pneumonia
  • Rash → erythema multiforme characterised by varying sized ‘target lesions’ formed by pink rings with pale centres
  • Can cause neurological symptoms in young patients
161
Q

What rash is characteristic of mycoplasma pneumoniae?

A

erythema multiforme → characterised by varying sized ‘target lesions’ formed by pink rings with pale centres

162
Q

What patient is chlamydophila pnuemoniae typically seen in?

A

School aged child with mild to moderate chronic pneumonia and wheeze

163
Q

Why can COPD lead to 2ary polycythaemia?

A

COPD (and sleep apnoea) can cause an increase in erythropoietin, due to not enough oxygen reaching the body’s tissues.

164
Q

Give 3 endocrine manifestations of paraneoplastic syndromes in lung cancer

A
  1. Hypercalcaemia
  2. SIADH
  3. Ectopic Cushing’s syndrome
165
Q

What 4 cancers are most commonly associated with hypercalcaemia?

A
  1. Lung
  2. Breast
  3. Renal
  4. Myeloma
166
Q

What type of lung cancer is most commonly associated with hypercalcaemia?

A

Squamous cell carcinoma

167
Q

Describe symptoms seen in hypercalaemia of malignancy

A

Stones → renal stones, flank pain, frequent urination

Bones → bone pain

Moans → confusion, depression, dementia, memory loss

Groans → N&V, diarrhoea, abdominal pain

168
Q

Cause of symptoms seen in ectopic Cushing’s syndrome?

A

caused by production of ACTH by non-pituitary tissue leading to hypercortisolism.

169
Q

Signs & symptoms typical of Cushing’s syndrome?

A
  • Truncal obesity
  • Facial plethora
  • Pathologic striae
  • Dorsocervical fat pad enlargement
  • Proximal muscle weakness
  • Hyperpigmentation
  • Psychosis, and confusion

Note - ECS caused by small cell lung cancer (SCLC), or other aggressive tumours, may have an atypical presentation with muscle wasting and weight loss instead of classical sings of hypercortisolism such as moon facies and weight gain.

170
Q

What electrolyte abnormalities are seen in Ectopic Cushing’s syndrome? (Na, K+)

A

Hypokalaemia & hypernatraemia

171
Q

What type of lung cancer is ectopic Cushing’s syndrome typically associated with?

A

Small cell lung cancer

172
Q

What is the most common neurological manifestation of small cell lung cancer

A

Lambert-Eaton myasthenic syndrome (LEMS)

173
Q

What is LEMS?

A

LEMS is a rare autoimmune disorder of the neuromuscular junction and may precede the diagnosis of lung cancer.

174
Q

What is typically the initial symptom of LEMS?

A

Progressive proximal, lower greater than upper extremity weakness is nearly always the initial symptom.

175
Q

LEMS vs myasthenia gravis?

A

Myasthenia gravis → the acetylcholine receptor on the nerve is affected,

LEMS → the voltage gated calcium channel on the nerve is affected

176
Q

Why is thoracentesis not indicated in a pleural effusion in heart failure patients?

A

Patients who present with clearcut evidence of conditions known to cause pleural effusions, such as congestive heart failure, do not require thoracentesis.

177
Q

What type of pneumonia is associated with erythema multiforme?

A

Mycoplasma pneumonia

178
Q

Define pneumococcal infection

A

Pneumococcal disease is a name for any infection caused by bacteria called Streptococcus** **pneumoniae.

179
Q

What is a PE?

A

When blood clot in pulmonary arterial vasculature develops, usually from an underlying DVT of the lower limbs.

180
Q

Give some risk factors for a PE

A
  • Immobility
  • Recent surgery
  • Long haul flights
  • Pregnancy
  • Hormone therapy with oestrogen
  • Malignancy
  • Polycythaemia
  • SLE
181
Q

Every patient admitted to hospital should be assessed for their risk of VTE. If they are at increased risk of VTE they should receive prophylaxis with what?

A

low molecular weight heparin (LMWH) such as enoxaparin unless contraindicated

anti-compression stocking also used unless contraindicated

182
Q

Give 2 main contraindications for LMWH

A
  • Active bleeding
  • Existing anticoagulation with warfarin or NOAC
183
Q

What is the major contraindication for compression stockings?

A

Significant peripheral arterial disease

184
Q

What is the typical triad of symptoms of a PE?

A
  • Sudden onset SOB
  • Pleuritic chest pain
  • Haemoptysis

Massive PE → above + syncope/shock

Small PE → may be asymptomatic

185
Q

What is the most common ECG sign of a PE?

A

Sinus tachycardia

186
Q

12-lead ECG signs seen in a PE?

A
  • Can be normal
  • Can show sinus tachycardia
  • Massive PE → evidence of right heart strain; P pulmonale, right axis deviation, RBBB, non-specific ST/T wave changes
187
Q

Give some ECG changes seen in right heart strain

A
  • P pulmonale
  • right axis deviation
  • RBBB
  • non-specific ST/T wave changes
188
Q

What is p pulmonale?

A

P pulmonale are big, tall, peaked P waves on ECG → indicates right atrial enlargement (e.g. PE)

189
Q

Most common cause of right axis deviation?

A

Right ventricular hypertrophy

190
Q

What may an ABG show in a PE?

A
  • May be normal
  • May show type 1 respiratory failure (hypoxia without hypercapnia) and/or respiratory alkalosis (due to hyperventilation 2ary to hypoxia)
191
Q

Why may a PE cause anaemia?

A

due to haemoptysis

192
Q

Describe the negative predictive value of a d-dimer test

A

Highly non-specific but has 95% negative predictive value (i.e. useful in ruling out PE if negative)

193
Q

Describe CXR in PE

A

typically normal in PE

194
Q

What is the diagnostic test of choice in a PE?

A

CT pulmonary angiogram (CTPA) → will show filling defect in pulmonary vasculature

195
Q

What is the 1st line investigation in a PE in pregnancy?

A

Duplex US (instead of CTPA)

196
Q

Why may a bedside echocardiogram be useful in a massive PE?

A

In order to assess suitability for thrombolysis

197
Q

How can the Well’s score be used to guide further investigations for a PE?

A

If the Well’s score is 4 or less → measure d-dimer (this has a high negative predictive value but a low specificity so only useful if the clinical suspicion of a PE is low):

If the Well’s score is >4 → further diagnostic imaging is required

198
Q

If the Well’s score is 4 or below and a d-dimer is performed, what does a low d-dimer mean? What does a raised d-dimer mean?

A
  • A low d-dimer excludes a PE
  • A raised d-dimer is an indication for diagnostic imaging (by CTPA or V/Q scan)
199
Q

Immediate harmacological management of a PE?

A
  • Thrombolysis (IV bolus of Alteplase) → indicated in massive PE
  • Initial pharmacological management – start immediately before confirming diagnosis:
    • 1st line → DOACs apixaban or rivaroxaban
    • LMWH (e.g. enoxaparin, dalteparin) → alternative if DOACs not suitable, or in antiphospholipid syndrome
200
Q

What are the long-term anticoagulation options for a PE?

A
  • DOACs
  • Warfarin:
    • Target INR is 2-3
    • When switching to warfarin, continue LMWH for 5 days
  • LMWH → First line treatment in pregnancy or cancer
201
Q

Describe the length of coagulation in a PE with an obvious reversible cause

202
Q

Describe the length of coagulation in a PE if the cause is unclear, there is recurrent VTE or there is an irreversible underlying cause e.g. thrombophilia

A

3+ months (or lifelong)

203
Q

Describe the length of coagulation in a PE in active cancer

204
Q

Give some causes of drug induced pulmonary fibrosis

A
  • Amiodarone
  • Nitrofurantoin
  • Methotrexate

Yr 3 - Core Conditions (33 decks)

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