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YEAR 3 & 5 CORE CONDITIONS > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What characterises the presentation of asthma?

A

Cough (worse at night)
Shortness of breath
Wheeze

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2
Q

What 3 factors contribute to airway narrowing in asthma?

A
  1. Bronchial muscle contraction
  2. Mucosal swelling/inflammation due to mast cell and basophil degranulation
  3. Increased mucous production
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3
Q

What kind of reaction is atopic asthma?

A

Asthma is a type 1 hypersensitivity reaction - IgE mediated release of histamine

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4
Q

Name some risk factors for developing asthma

A
  • Atopy/family history of atopy
  • Pollution i.e. living in an inner-city environment
  • Prematurity and low birth weight
  • Viral infections in childhood e.g. bronchiolitis
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5
Q

What often precipitates asthma?

A
  • Cold air - drying of airways causes cell shrinkage which triggers an inflammatory response
  • Exercise
  • Emotion
  • Allergens
  • Smoking
  • Infection
  • Pollution
  • NSAIDs
  • Beta blockers
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6
Q

How can asthma present?

A
  • Dyspnoea
  • Wheeze + chest tightness
  • Nocturnal cough
  • Acid reflux (40-60%)
  • Atopic disease
  • Diurnal variation in symptoms - marked morning dipping of the peak flow
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7
Q

What signs would you see on examination of asthma?

A
  • Tachypnoea
  • Bilateral widespread polyphonic wheeze
  • Reduced air entry
  • Hyperinflated chest -> hyper-resonant percussion
  • Accessory muscle use
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8
Q

What characterises a severe asthma attack?

A

PEFR = 33-50% predicted

Unable to complete full sentences

Pulse > 110 bpm

RR > 25/min

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9
Q

What characterises a life-threatening asthma attack? How do you differentiate between this and near-fatal asthma attack?

A

Life-threatening = PEFR < 33% predicted

  • Silent chest
  • Confusion
  • Exhaustion
  • Cyanosis (sats < 92%)
  • Bradycardia
  • PaO2 < 8kPa
  • Normal CO2 (would expect it to be low in asthma attack due to hyperventilation so if it is normal it indicates failing respiratory effort)

Near-fatal = raised CO2

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10
Q

What would you see on spirometry in asthma?

A

Reduced FEV1/FVC ratio < 0.7 suggesting obstructive patter

Increased residual volume

15% improvement after beta2 agonists/steroids

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11
Q

What is cardiac asthma?

A

Pulmonary oedema (due to heart failure)

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12
Q

What diseases are associated with asthma?

A
  • Atopic diseases
  • GORD
  • Churg-Strauss aka eosinophilic granulomatosis - first presents with asthma
  • Allergic bronchopulmonary aspergillosis
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13
Q

What is the acute management of asthma?

A

O SHIT ME

Oxygen 15L/min via NRBM
Salbutamol 5mg neb back to back
Hydrocortisone 100mg IV or prednisolone 40mg PO for 5 days 
Ipratropium bromide 5mcg neb
Theophylline
Magnesium 1.2-2g IV over 20 min
Escalate
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14
Q

Step 1 of asthma management in adults

A

Step 1: mild intermittent asthma - 100% PEFR

  • Inhaled SABA PRN
  • If used more than 3 times a week go to step 2
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15
Q

Step 2 of asthma management in adults

A

Step 2: daily symptoms - <80% PEFR

- SABA + inhaled corticosteroid e.g. beclometasone (max 2 puffs twice a day)

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16
Q

Step 3 of asthma management in adults

A

Step 3

- SABA + ICS + LABA

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17
Q

Step 4 of asthma management in adults

A

Step 4

  • Increase ICS to medium dose
  • If LABA helped, keep it, if not bin it and replace with LTRA
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18
Q

What is the biggest cause of COPD?

A

Smoking - 10-20% of heavy smokers

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19
Q

What else can cause COPD?

A

Alpha-1-antitrypsin deficiency - alpha-1-antitrypsin inhibits the destruction of the alveolar wall

Pollution

Recurrent infections

Comorbidities

  • CVD
  • Lung cancer
  • Osteoporosis
  • Muscle weakness
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20
Q

What is COPD?

A

A progressive disorder characterised by irreversible obstruction of the airways

Chronic bronchitis = productive cough most days of 3 months per year for 2 years

AND

Emphysema = enlarged air spaces with destruction of alveolar walls

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21
Q

Distinguish between pink puffers and blue bloaters

A

Pink puffers = emphysema

  • increased ventilation to compensate for lack of surface area for gas exchange (decreased perfusion)
  • breathless but not cyanosed

Blue bloaters = chronic bronchitis

  • obstruction leads to increased residual lung volume
  • so there is decreased ventilation but normal perfusion
  • retain carbon dioxide so they rely on hypoxic drive to breathe = type 2 respiratory failure
  • cyanosed but not breathless
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22
Q

What signs would you see on examination of COPD?

A
  • Tachypnoea
  • Flapping tremor
  • Sitting in tripod position
  • Pursed lip breathing for prolonged expiration
  • Use of accessory muscles
  • Hyperinflated barrel chest - decreased cricosternal distance
  • Decreased lung expansion
  • Hyper-resonant percussion
  • Cyanosis
  • Quiet breath sounds over bullae
  • Signs of right heart failure e.g. ankle oedema
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23
Q

What are some complications of COPD?

A
  • Acute infective exacerbations
  • Cor pulmonale
  • Hypertension
  • Polycythaemia
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24
Q

What would an X-ray look like in COPD?

A
  • Hyperinflated chest = more than 6 anterior ribs seen
  • Flat hemidiaphragms
  • Narrow heart
  • Large pulmonary arteries
  • Reduced vascular markings
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25
Q

What is the only intervention shown to improve life-expectancy with COPD?

A

Stopping smoking

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26
Q

What index assesses the severity of COPD?

A

BODE index

  • BMI
  • Obstruction to airflow - FEV1 < 80%
  • Dyspnoea
  • Exercise tolerance
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27
Q

In order to start a COPD patient on long-term oxygen therapy, what criteria must they fulfil?

A

One of:

PaO2 <7.3kPa on two readings more than 3 weeks apart (hypoxaemia whilst breathing room air and are clinically stable), and are non-smokers

PaO2 of 7.3-8kPa + one of evidence of end-organ damage due to hypoxia:

  • Nocturnal hypoxia
  • Polycythemia
  • Peripheral oedema
  • Pulmonary hypertension

Terminal illness

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28
Q

Go through the step-wise management of chronic COPD

A

Step 1…
• SABA (salbutamol) + SAMA (ipratropium)
• Continue SABA as patient goes up the steps but stop SAMA if LAMA is added

Step 2…
• For patients with FEV1 > 50%
add LABA (salmeterol) + LAMA (tiotropium)
• For patients with FEV1 < 50% add LABA + ICS (fluticasone) = seretide

Step 3…
• 3 month trial of LAMA + LABA + ICS (e.g. trimbo)
• If this does not work, revert to LABA + LAMA

Step 4…
• Long Term Oxygen Therapy (LTOT)

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29
Q

What is the 2nd most common cancer worldwide?

A

Lung carcinoma

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30
Q

What are the 2 histological divisions of bronchial carcinoma? What is the most common bronchial carcinoma?

A

Small cell (oat cell) lung carcinoma

Non-small cell lung carcinoma

  • Squamous
  • Adenocarcinoma
  • Large cell
  • Adenocarcinoma in situ

Adenocarcinoma is now the most common lung cancer (40%) - it used to be squamous cell lung carcinoma until the 80s

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31
Q

What does small cell lung cancer arise from?

A

Endocrine cells (Kulchitsky cells)

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32
Q

What type of lung cancer is more aggressive?

A

Small cell lung cancer
Grows rapidly and is highly malignant
70% are disseminated at presentation
Metastasise earlier in their course so often cannot be treated by surgery

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33
Q

What are the main symptoms of bronchial carcinoma (in order of most common) ? Also give some other examples of symptoms.

A

Cough - 80%
Haemoptysis - 70%
Dyspnoea - 60%
Chest pain - 40%

Weight loss, anorexia, lethargy
Recurrent pneumonia

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34
Q

How does an apical Pancoast tumour present?

A

Hoarseness of voice
Horner’s syndrome = ptosis, miosis and anhidrosis
Severe localised pain in the apex and shoulder

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35
Q

On auscultation of the chest, what sounds would be heard in lung cancer?

A

Monophonic wheeze due to partial airway obstruction

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36
Q

What is a potential life threatening complication of lung cancer? How does it present?

A

SVC obstruction due to mediastinal tumour

  • Oedematous neck
  • Stridor
  • Dilated veins in the chest
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37
Q

What are some paraneoplastic syndromes that can be caused by small cell lung carcinomas?

A

Excess ACTH - Cushing’s

Excess ADH - SIADH (causes low sodium)

Lambert-Eaton syndrome

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38
Q

What might you see on a chest Xray of someone with lung cancer?

A
  • Nodule - central = small cell, squamous cell; peripheral = adenocarcinoma, large cell
  • Hilar enlargement
  • Consolidation due to post-obstructive pneumonia
  • Pleural effusion - particularly unilateral
  • Atelectasis
  • Bony metastases
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39
Q

If there is suspicion of lung cancer, what investigations should be carried out?

A
  1. Chest X-Ray - is it central or peripheral?
  2. CT scan - signs of malignancy
  3. PET scan
  4. Bronchoscopy and biopsy = confirmatory test
    ○ Bronchoscopy with transbronchial biopsy for central nodes
    ○ CT-guided transthoracic biopsy for peripheral nodes
  5. CT scan of chest-abdo-pelvis for staging
  6. Lung function tests to check suitability for lobectomy
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40
Q

Who is most at risk of a primary spontaneous pneumothorax?

A

Tall, skinny, young males - rupture of subpleural bullae

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41
Q

What are the main causes of secondary pneumothorax

A

Connective tissue disease

  • Marfan’s syndrome
  • Ehlers-Danlos syndrome

Obstructive lung disease

  • Asthma
  • COPD

Infective lung disease

  • TB
  • Pneumonia

Fibrotic lung disease

  • Cystic fibrosis
  • Idiopathic pulmonary fibrosis

Neoplastic disease
- Bronchial carcinoma

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42
Q

What are the two groups of traumatic causes of pneumothorax? Give examples of each

A

Iatrogenic

  • Insertion of a central line
  • Positive pressure ventilation

Non-iatrogenic

  • Penetrating trauma
  • Blunt trauma with rib fracture
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43
Q

In women what is a risk factor for pneumothorax?

A

Endometriosis - occur during menstruation

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44
Q

How does it classically present?

A

Sudden onset of unilateral pleuritic pain with progressively worsening breathlessness

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45
Q

What signs would you find on examination of a pneumothorax?

A
  • Reduced chest expantion expansion
  • Hyper-resonant percussion note
  • Reduced/absent breath sounds, with no added sounds
  • Reduced vocal resonance
  • Pulsus paradoxicus - pulse slows on inspiration
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46
Q

What additional signs would be seen in a tension pneumothorax?

A
  • Tracheal deviation away from affected side
  • Raised JVP
  • Haemodynamic instability - low BP, high HR
  • Distended neck veins (mediastinum is pushed over and compressing the great veins)
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47
Q

What is the most important investigation in a suspected pneumothorax?

A

Chest X-Ray - will show areas devoid of lung markings

don’t do a CXR in tension pneumothorax as it delays management

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48
Q

How do you treat a primary pneumothorax depending on the size?

A

Size < 2cm and/or patient is not breathless - consider discharge and review in 2-4 weeks

Size > 2cm - aspirate with 16/18G cannula in 2nd intercostal space mid-clavicular line under local anaesthetic

  • If resolves and breathing improves, consider discharge and review in 2-4 weeks
  • If doesn’t resolve, insert chest drain in 5th intercostal space mid-axillary line and admit patient
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49
Q

How do you treat secondary pneumothorax depending on the size?

A

Size < 1cm - admit and give high flow oxygen and observe for 24 hours

Size 1-2cm - aspirate with 16-18G cannula

  • If successful and size now <1cm, admit for 24 hours and give high flow oxygen
  • If unsuccessful, chest drain required

Size > 2cm - Chest drain in 5th intercostal space mid-axillary line

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50
Q

What are the different divisions of a pleural effusion?

A

Transudates - protein < 25g/L
Exudates - protein > 35g/L
Haemothorax = blood in pleural space
Chylothorax = lymph with fat in pleural space
Empyema = pus in the pleural space
Haemopneumothorax = both blood and air in pleural space

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51
Q

What causes a transudative pleural effusion?

A

Increase in venous pressure causing increased hydrostatic pressure

  • Cardiac failure
  • Constrictive pericarditis

Hypoproteinaemia causing reduced oncotic pressure

  • Liver cirrhosis
  • Nephrotic syndrome
  • Malabsorption
  • CKD

Others

  • Hypothyroidism
  • Meig’s syndrome - ascites, pleural effusion, benign ovarian tumour
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52
Q

What causes an exudative pleural effusion?

A

Increased leakiness of the pleural capillaries secondary to infection, inflammation and malignancy

Infection

  • Pneumonia
  • TB

Malignancy

  • Bronchial carcinoma
  • Lymphoma
  • Mesothelioma

PE - Pulmonary infarction

Autoimmune

  • Rheumatoid arthritis
  • SLE
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53
Q

How does a pleural effusion present?

A

Small pleural effusions (<300ml) are often asymptomatic

OR

Dyspnoea
Pleuritic chest pain
Dry, non-productive cough

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54
Q

What signs might you see on examination of pleural effusion?

A

Palpation

  • Decreased expansion
  • Decreased tactile vocal fremitus
  • Tracheal deviation away from effusion (mediastinal shift = effusion > 1L)

Percussion
- Stony dull percussion note

Auscultation

  • Diminished breath sounds
  • Decreased vocal resonance
  • Bronchial breathing above the effusion where lung is compressed
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55
Q

What can be seen on a chest x-ray in pleural effusion?

A

Blunting of costophrenic angles - 200ml of fluid required to be seen
Meniscus-shaped margin

Large effusion (>1L)

  • Complete opacification of the lung
  • Mediastinal shift
  • Tracheal deviation away from the effusion
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56
Q

What is used for diagnosis of the pleural effusion?

A

Diagnotic thoracentesis

- Percuss upper border of pleural effusion and choose a site 1 or 2 intercostal spaces below it

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57
Q

What cytology results would indicate what in pleural fluid analysis?

A

Neutrophils ++

  • Pneumonia
  • PE

Lymphocytes ++

  • Malignancy
  • TB
  • RA, SLE, sarcoidosis

Mesothelial cells ++
- Pulmonary infarction

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58
Q

What clinical chemistry results would indicate what in pleural fluid analysis?

A

Protein

  • <25g/L = transudate
  • > 35g/L = exudate

Low glucose, low pH, high LDH

  • Empyema
  • Malignancy
  • TB
  • RA, SLE

Raised amylase
- Pancreatitis

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59
Q

What is calculated if the protein content of the effusion is equivocal (25-35g/L)? What levels are indicative of which type of pleural effusion?

A

Calculate Light’s Criteria

Transudative…
• Pleural fluid protein: serum protein ration < 0.5
• Pleural fluid LDH: serum LDH ratio < 0.6
• Pleural fluid LDH < 2/3 the upper limit of normal serum LDH

Exudative…
• Pleural fluid protein: serum protein ration > 0.5
• Pleural fluid LDH: serum LDH ratio > 0.6
• Pleural fluid LDH > 2/3 the upper limit of normal serum LDH

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60
Q

What are the most common organisms to cause a CAP?

A
  1. Streptococcus pneumoniae
  2. Haemophilus influenzae
  3. Moraxella catarrhalis
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61
Q

Name some atypical causes of CAP

A

Mycoplasma pneumoniae
Legionella
Chlamydia pneumoniae

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62
Q

What is HAP defined as?

A

Pneumonia 48 hours after admission (or 5+ days depending on trust) or has been in hospital in past month

63
Q

What most commonly causes a hospital acquired pneumonia?

A
  1. Gram negative enterobacteria
  2. Staphylococcus aureus
  3. Pseudomonas
  4. Klebsiella pneumoniae
64
Q

What are the main symptoms of pneumonia?

A
  • Shortness of breath
  • Cough
  • Productive in adults - purulent sputum
  • Often dry in infants/elderly or atypical pneumonia
  • Sometimes haemoptysis

• Pleuritic chest pain - most painful on inspiration

  • Fever, rigors
  • Vomiting
65
Q

What microbiological studies may be done in pneumonia?

A

Blood cultures
Sputum culture and gram stain
Legionella/Pneumococcal urinary antigens

66
Q

What investigation is diagnostic of pneumonia?

A

Chest X-ray

67
Q

What would loss of right heart border show?

A

Right middle lobe pneumonia

68
Q

What severity score is used in pneumonia? Interpret each score

A

CURB-65

Confusion - AMTS < 8
Urea > 7mmol/L
Respiratory rate > 30/min
BP < 90/60 mmHg
Age > 65
0-1 = PO antibiotics as an outpatient
2 = consider hospital admission
3 = definite hospital admission/consider ITU
69
Q

What is the main cause of a PE?

A

Venous thrombosis from a deep vein of the leg/pelvis

Clots break off, pass through veins to the right side of the heart before lodging in a pulmonary artery

70
Q

What types of emboli exist?

A 
Septic emboli from endocarditis - IVDU
Fat - long-bone fractures
Air - surgery, trauma
Neoplastic cells - prostate/breast cancers most commonly
Parasites
Amniotic fluid embolism
Foreign bodies - IVDU, iatrogenic
71
Q

List the main risk factors for PE

A 
Recent surgery (abdo/pelvic/hip/knee)
Pregnancy, COCP, HRT 
Leg fracture
Thrombophilia e.g. antiphospholipid syndrome 
Reduced mobility
Maligancy
Previous PE
Nephrotic syndrome
72
Q

How does a PE present?

A

Sudden onset SOB
Pleuritic chest pain, worse on inspiration
Haemoptysis
Syncope

73
Q

What signs might you find on examination of a PE?

A
  • Pyrexia
  • Cyanosis
  • Tachypnoea
  • Tachycardia
  • Hypotension
  • Raised JVP
  • Pleural rub
  • Pleural effusion
  • signs of DVT
74
Q

What investigation is both diagnostic and prognostic of a PE?

A

CTPA

75
Q

What bloods must you do in suspected PE?

A

Bloods

  • FBC
  • Coagulation screen
  • D-dimer
76
Q

How might an ECG look in PE?

A

ECG

  • Tachycardia
  • Right bundle branch block
  • Right axis deviation
  • S1 Q3 T3 pattern - deep S wave in lead 1, Q wave inverted in lead 3, inverted T wave in lead 3
77
Q

What other test is useful in PE?

A

V/Q scan to see if there is a ventilation-perfusion mismatch

78
Q

What score assesses the clinical probability of a PE? What do the scores indicate and how do they affect your subsequent investigations?

A

Well’s score (if score is greater than 4, immediate CTPA or treat with LMWH)

  • Clinical signs of DVT
  • Pulse > 100 bpm
  • Recent surgery
  • Previous DVT
  • Haemoptysis
  • Cancer
  • Alternative diagnosis is less likely than PE

Score < 4 = low-risk -> do D-Dimer, if positive do CTPA, if negative discharge

Score >4 = high-risk -> do CTPA

79
Q

What is the treatment for PE?

A

If haemodynamically unstable, thrombolyse with alteplase

LMWH for 5 days
Unfractioned heparin if renal impairment

Then start DOAC or warfarin for 3 months

If unprovoked PE, continue anticoagulation for longer than 3 months.
If caused by malignancy, continue for 6 months

80
Q

What pathological features are there in pulmonary fibrosis?

A
  • Fibrosis and remodelling of the interstitium
  • Chronic inflammation
  • Hyperplasia of type II epithelial cells (the ones that secrete pulmonary surfactant to decrease surface tension within alveoli)
81
Q

What are some risk factors for developing pulmonary fibrosis?

A

Smoking
Occupation - silica, asbestos, heavy metals, mouldy foliage
Chronic viral infections - hepatitis C, EBV
GORD with micro-aspiration
Drugs e.g. methotrexate, nitrofurantoin, amiodarone, bleomycin
Rheumatological conditions e.g. sarcoidosis, ankylosing spondylitis, RA, scleroderma

82
Q

How does pulmonary fibrosis present?

A 
Dry cough
Exertional dyspnoea
Malaise
Weight loss
Arthralgia
83
Q

What signs would you see on examination of pulmonary fibrosis?

A

Clubbing in 50%
Bilateral fine end-inspiratory crepitations
Decreased chest expansion

84
Q

What are the main complications of pulmonary fibrosis?

A

Respiratory failure

Increased risk of lung cancer

85
Q

What are the diagnostic tests for pulmonary fibrosis?

A

Bronchoscopy

Lung biopsy

86
Q

What would you see on CT scan of pulmonary fibrosis?

A

Honeycombing
Loss of architecture
Reticular abnormality
Interlobular septal thickening

87
Q

What would spirometry show in pulmonary fibrosis?

A

Restrictive pattern i.e. FEV1/FVC > 0.7

88
Q

How do you manage a patient with pulmonary fibrosis?

A
  • Supportive oxygen therapy
  • Flu vaccination
  • High dose prednisolone
  • Opiates for excessive cough in end stage disease
  • Smoking cessation
  • Palliative care
89
Q

Why does hyperventilation lead to peripheral paraesthesia?

A
  • Hydrogen ions and calcium are bound to serum albumin
  • When blood becomes alkalotic, the bound hydrogen ions dissociate from albumin
  • The albumin can bind with more calcium so there is less freely ionised calcium, leading to hypocalcaemia
90
Q

What causes a type 1 respiratory failure?

A

V/Q mismatch

  1. Reduced ventilation but normal perfusion e.g. pulmonary oedema, bronchoconstriction
  2. Reduced perfusion but normal ventilation e.g. PE
91
Q

Name 4 categories of causes of type 2 respiratory failure

A
  1. Increased resistance due to airway obstruction e.g. COPD
  2. Reduced compliance of lung tissue/chest wall e.g. rib fractures, obesity
  3. Reduced strength of respiratory muscles e.g. MND, Guillan-Barré
  4. Drugs acting on respiratory centre e.g. opiates
92
Q

What is fluoroscopy used for in respiratory?

A

It is used to view the function and movement of lungs, diaphragm and chest movements
Used to check for masses in chest, obstruction, pleural effusions and loss of elasticity

93
Q

What are the normal ranges on an ABG?

A 
pH : 7.35-7.45
PaCO2: 4.7-6.0
PaO2: 11-13
HCO3-: 22-26
Base excess: -2 to +2
94
Q

List some causes of a chronic cough (8+ weeks)

A 
· Cigarette smoke
· Use of ACE inhibitor
· Asthma
· Gastro-oesophageal reflux disease
· COPD
· Eosinophilic bronchitis
· Post-nasal drip 
· Tumour – bronchial carcinoma, lymphoma, metastatic carcinoma
95
Q

What is a MART?

A

Maintenance and reliever therapy (MART) = a form of combined ICS and fast-acting LABA treatment in a single inhaler

96
Q

What are the side effects of beta-2 agonists?

A

Fine tremor
Headache
Muscle cramps
Palpitations

97
Q

What is the MRC Dyspnoea Scale?

A
  1. Not troubled by breathlessness except on strenuous exercise
  2. Short of breath when hurrying or walking up a slight incline
  3. Walks slower than contemporaries on level ground because of breathlessness
    or has to stop for breath when walking at own pace
  4. Stops for breath after walk about 100m or after a few minutes on level ground
  5. Too breathless to leave the house or breathless on dressing/undressing
98
Q

What are the different stages of COPD on spirometry?

A

Stage 1 = Mild - FEV1 ≥ 80%

Stage 2 = Moderate - FEV1 50-79%

Stage 3 = Severe - FEV1 30-49%

Stage 4 Very Severe FEV1 <30%

99
Q

What are some contraindications to spirometry?

A

Recent MI
Current ACS
Recent thorax surgery
Haemoptysis

100
Q

How would you treat a mild asthma attack?

A

Up to 10 puffs salbutamol inhaler

101
Q

What is the management of a tension pneumothorax?

A
  • Sit patient up
  • Oxygen - high flow 15L/min NRBM
  • Aspirate - 16/18G cannula in 2nd intercostal space mid-clavicular line
  • Then insert chest drain in 5th intercostal space mid-axillary line
102
Q

What is an open pneumothorax?

A 
Large defect (>60% size of trachea) in chest wall
When chest expands, air goes in through defect rather than down trachea
No gas exchange in pleural space
No tension
103
Q

Give examples of what can cause hyperventilation

A 
CNS infection
Subarachnoid haemorrhage
Panic attack
Pulmonary emboli (through reflex hyperventilation)
Aspirin overdose
Any cause of hypoxia (through hyperventilation driven by peripheral chemoreceptors)
Anaemia
DKA initially
104
Q

What medication can be given for COPD patients who struggle with thick phlegm?

A

Carbocisteine = mucolytic

105
Q

What features are characteristic of aspiration pneumonia?

A
  • Occurs in patients with unsafe swallow e.g. stroke, myasthenia gravis, achalasia
  • R lung more commonly affected because right bronchus is wider and more vertical which facilitates passage of aspirate
106
Q

What features are characteristic of klebsiella pneumonia?

A
  • More common in immunocompromised, elderly, diabetics, alcoholics, malignancy
  • Red-currant sputum
  • Primarily affects upper lobes - causes cavitating pneumonia
  • Gram-negative anaerobic rod
  • Increased risk of empyema, lung abscess, pleural adhesions
107
Q

What features are characteristic of staphylococcal pneumonia?

A
  • Bilateral cavitating bronchopneumonia

* More common in IVDU, elderly patients or those who already have influenza infection

108
Q

What features are characteristic of mycoplasma pneumonia?

A
  • Presents with flu-like symptoms - arthralgia, myalgia, dry cough, headache
  • Usually affects younger patients
  • Can have auto-immune manifestation due to cold agglutinins causing autoimmune haemolytic anaemia
109
Q

What are some potential complications of mycoplasma pneumonia?

A

Erythema multiforme

Stevens-Johnson syndrome

Guillain-Barre

Meningoencephalitis

110
Q

What features are characteristic of chlamydophila psittaci pneumonia?

A
  • Acquired from contact with infected birds, cattle, horse, sheep
  • Can cause hepatitis, splenomegaly, nephritis, infective endocarditis, meningoencephalitis, rash
111
Q

What is the empirical therapy for CAP in outpatients?

A

Antibiotics given for 5 days

Previously healthy pts -monotherapy with amoxicillin/doxycycline/macrolide

Patients with comorbidities
- Combination therapy: co-amoxiclav/cefuroxime + macrolide/doxycycline

112
Q

What antibiotic is given for chlamydia pneumoniae?

A

Tetracyclines e.g. doxycycline

113
Q

What antibiotic is given for legionella and pseudomonas?

A

Quinolone e.g. ciprofloxacin/levofloxacin

114
Q

What are some potential complications of pneumonia?

A

Within days
• Pleural effusion
• Empyema - patient has partially recovered but then develops spike in temperature
• Lobar collapse - result of sputum retention
• VTE
• Pneumothorax - particularly with Staphylococcus aureus

Days to weeks
• Lung abscess
• Sepsis
• Respiratory failure, ARDS

115
Q

Summarise the pathophysiology of sarcoidosis

A

Formation of non-caseating granulomas within the lungs and lymphatic system

A granuloma is a collection of WBCs (mononuclear cells and macrophages) , surrounded by lymphocytes, plasma cells, mast cells, fibroblasts, and collagen

116
Q

What are the stages of chronic sarcoidosis based on CXR findings?

A

Stage 0 - normal findings (but positive bronchoalveolar lavage)

Stage I - bilateral hilar lymphadenopathy

Stage II - bilateral hilar lymphadenopathy with reticular or ground-glass opacities (peripheral infiltrates)

Stage III - bilateral reticular or ground-glass opacities without hilar lymphadenopathy

Stage IV - pulmonary fibrosis

117
Q

How does acute sarcoidosis present? Also, what syndrome is a subtype of sarcoidosis with an acute presentation and what are the main features?

A
  • General non-specific symptoms e.g. fever, malaise, anorexia, weight loss
  • Breathlessness, cough and chest pain

Lofgren syndrome
• Highly acute presentation with FEVER and following triad:
1. Migratory polyarthritis - symmetrical arthritis that primarily affects the ankles
2. Erythema nodosum - primarily affects extensor surfaces of lower legs
3. Bilateral hilar lymphadenopathy

118
Q

What are some extra-pulmonary manifestations of chronic sarcoidosis?

A
  • Constitutional: fatigue, weight loss, arthralgia, and low-grade fever. Peripheral lymphadenopathy is most frequent extra-pulmonary manifestation
  • Neurological: meningitis, peripheral neuropathy, bilateral Bell’s palsy
  • Ocular: uveitis, keratoconjunctivitis sicca, blurred vision
  • Cardiac: arrhythmias, restrictive cardiomyopathy.
  • Abdominal: hepatomegaly, splenomegaly, renal stones.
  • Dermatological: erythema nodosum, lupus pernio (purple skin lesions on nose, cheeks, chin, ears)
119
Q

What is the gold standard test for diagnosis of sarcoidosis?

A

Bronchoscopy + biopsy - shows evidence of a non-caseating granuloma

120
Q

What is the prognosis of the different stages of sarcoidosis?

A

Stage 0 and 1 – usually resolve spontaneously

Stage 2+ and acute disease – may improve with NSAIDs and bed rest

121
Q

If a patient with sarcoidosis has extrapulmonary manifestations, what is the treatment?

A

Steroids (prednisolone 40mg for 4-6 weeks then taper dose over 1 year) - first line

Methotrexate - second line

Hydroxychloroquine - third line

122
Q

Name some diseases that also feature non-caseating granulomas and are possible DDx for sarcoidosis

A
  • Hodgkin lymphoma - alcohol-induced pain, pruritis, hx of EBV, Reed-Sternberg cells
  • Non-Hodgkin lymphoma - lymphadenopathy, splenomegaly, bone marrow suppresion
  • Pneumoconiosis - exposure to mineral dust, chronic cough, progressive exertional dyspnoea
  • Granulomatosis with polyangiitis (Wegener’s) - chronic sinusitus with thick purulent discharge, treatment-resistant pneumonia, glomerulonephritis
123
Q

What is the pathophysiology behind dormant TB?

A

Mycobacteria enter the alveoli where they are engulfed by alveolar macrophages and replicated within them - in most cases, the initial infection is contained in the lungs (hilar lymph nodes) by the immune system and does not spread so does not cause an acute illness

124
Q

What area of the lung does TB usually affect?

A

Upper lobe

125
Q

What are the main pulmonary symptoms of TB?

A
  • Chronic productive cough +/- haemoptysis

* Shortness of breath

126
Q

What is miliary TB?

A

Some patients’ immune systems are not able to contain the primary infection, and so it disseminates widely via the bloodstream

It is known as miliary TB due to the characteristic pattern on CXR like ‘millet-seeds’ when re-infection of lungs occurs after passing through circulation.

127
Q

What is the second most affected organ system (after the lungs) in TB? How does it present?

A

Genito-urinary system

Sterile pyuria
Kidney pathologies
Abscesses
Salpingitis and infertiltiy
Epididymo-orchitis
128
Q

What investigations are done in active TB?

A
  1. CXR
  2. 3 separate sputum samples including one early morning sample
    - Samples are Ziehl-Neelsen stained - rapid direct microscopy for acid-fast bacilli
    - For culture, Lowenstein- Jensen media is needed (takes 4-8 weeks due to slow bacterial growth and sensitivities take 3-4 weeks more)
129
Q

What test screen people at high risk for TB? What causes false positives and false negatives?

A

Mantoux tuberculin skin test

  • Tuberculin protein is injected into the dermis
  • After 48-72 hours, level of inflammation is assessed by measuring diameter

False positives in previously immunised
False negatives in sarcoidosis, Hodgkin’s lymphoma

130
Q

What test for latent TB is not affected by previous vaccination?

A

Interferon-Gamma Release Assays

Positive test indicates immune system has prior recognition of TB antigens = previous, latent or active TB

131
Q

What is the treatment of TB?

A

Isoniazid, rifampicin, ethambutol and pyrazinamide for 2 months

Then isoniazid and rifampicin for a further 4 months

132
Q

What are the side effects of isoniazid?

A
  • Constipation
  • Peripheral neuropathy - give pyridoxine to prevent this
  • SLE-like symptoms
  • Hepatitis
133
Q

What are the side effects of rifampicin?

A
  • Anorexia
  • Pseudomembranous colitis
  • Orange colouration of excreted bodily fluids
  • Drug interactions (CYP450 inducer)
  • Liver toxicity
134
Q

What is the main side effect to be aware of of ethambutol?

A

Optic neuritis - red/green colourblindness

135
Q

What are the side effects of pyrazinamide?

A
  • Sideroblastic anaemia
  • Arthralgia
  • Hepatotoxicity
136
Q

What are some risk factors for sleep apnoea?

A

• Obesity - especially around the neck - most important risk factor
• Alcohol consumption before sleep
• Sedative/beta-blocker use before sleep
• Smoking
• Family history
• Hypothyroidism
• Structural abnormalities that impair respiratory flow
○ Adenotonsillar hyperplasia - in children
○ Nasal septum deviation
○ Enlarged uvula, tongue, soft palate
○ Overbite with small chin
• Neuromuscular disease

137
Q

What is the gold standard test for sleep apnoea?

A

Polysomnography:

  • EEG
  • Electro-oculogram to measure REM sleep
  • Electromyogram to measure muscle movement
138
Q

How many apnoeas per hour is diagnostic of sleep apnoea?

A

At least 5 apnoeas (>10 seconds without breathing) per hour + symptoms = diagnostic

Mild OSA = 1-14/hour
Moderate OSA = 15-30/hour
Severe OSA = >30/hour

139
Q

What is the most effective intervention for sleep apnoea/

A

Weight loss

140
Q

What is the therapy of choice for symptomatic sleep apnoea/

A

CPAP - delivered via a nasal mask or full face mask

Needs to be worn for 8 hours each night

141
Q

What is the most common cause of bronchiectasis in developed countries and what is the most common worldwide?

A

Cystic fibrosis - developed countries

TB - worldwide

142
Q

What is the main symptom of bronchiectasis?

A 
Chronic cough
\+/- Production of large amounts of foul smelling sputum
\+/- Sputum may contain flecks of blood
Worse in the mornings
Can be brought on by changes in posture
143
Q

What are the classic risk factors for carbon monoxide poisoning?

A 
Recent house move
Faulty/old boiler
House fire 
Use of gas fire 
BBQ in tent to warm up
Motor vehicle exhausts 
Poorly ventilated areas
144
Q

By which mechanisms does an increase in carboxyhaemoglobin cause hypoxia?

A

The affinity of haemoglobin for CO is 240x stronger than for O2

Increased COHb causes hypoxia via:

  • Decreased oxygen-carrying capacity of Hb
  • Shift in O2 dissociation curve to the left, increasing affinity for O2 but decreasing release of O2 in tissue
  • Binding of CO to myoglobin leading to cardiac ischaemia and decreased cardiac output
145
Q

How does someone with carbon monoxide poisoning present?

A
  • Headache, dizziness, fatigue, nausea/vomiting
  • Altered mental status, seizures, loss of consciousness/coma
  • Cherry-red lips
146
Q

How do you diagnose carbon monoxide poisoning?

A

Abnormal COHb level on venous/arterial CO oximetry on ABG/VBG
>3-4% in non-smokers
>10-15% in smokers

Pulse oximeters cannot distinguish between COHb and oxyhaemoglobin so sats will appear normal!

147
Q

What is the management for carbon monoxide poisoning?

A

Secure airway if necessary

100% Oxygen immediately via NRBM - continue giving until patient is asymptomatic for at least 6 hours and COHb level normalises

Fluids to improve perfusion

148
Q

Where are mesothelial cells?

A

They line the body’s cavities e.g. pleura, peritoneum, pericardium, testes

149
Q

What causes pleural mesothelioma?

A

Asbestos exposure

150
Q

What are the most common symptoms of pleural mesothelioma?

A 
Shortness of breath
Chest pain (non-pleuritic)
151
Q

What is the diagnostic investigation of pleural mesothelioma?

A

Pleuroscopy with stained biopsy - mesothelioma cells and psammoma bodies

152
Q

How is pleural mesothelioma broadly managed?

A
  • Radiotherapy +/- chemotherapy

* Pleurectomy or pneumonectomy in cases of severely impaired pulmonary function

153
Q

What physio technique is commonly used to remove excess sputum?

A

Postural drainage - relies of effects of gravity to drain secretions from lung segments into the central airways where it can be removed via coughing techniques

YEAR 3 & 5 CORE CONDITIONS (30 decks)

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