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1
Q

What is the differential diagnosis for an intrapulmonary mass on a CXR?

A

1) lung cancer
2) TB
3) abscess

4) foreign body
5) pulmonary hamartoma

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2
Q

Chronic bronchitis definition

A

defined clinically

cough with sputum production on most days for 3 months over 2 successive years.

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3
Q

Emphysema definition

A

defined histologically as enlarged air spaces distal to terminal bronchioles, with destruction of alveolar walls.

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4
Q

Obstructive Sleep Apnoea

A

Recurrent episodes of partial or complete upper airway obstruction during sleep, causing intermittent hypoxia and sleep fragmentation

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5
Q

Obstructive Sleep Apnoea Syndrome

A

apnoea with daytime somnolence (sleepiness)

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6
Q

Mechanism of Obstructive Sleep Apnoea Syndrome

A

pharynx narrows, creating negative airway pressure due to the airway closure

this causes cessation of air flow, which leads to sleep disruption and arousal

Results in:
o	Fragmented sleep
o	Daytime sleepiness
o	BP surge - increased risk of stroke/heart attack
o	Reduced QOL
o	RTA if untreated
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7
Q

Obstructive Sleep Apnoea investigations

A 
Limited Polysomnography (Limited Sleep Study)
o	home study. Looks at:
	Oxygen Saturations
	Heart Rate
	Flow (through nose and mouth)
	Thoracic and Abdominal effort
	Position

FULL POLYSOMNOGRAPHY
• Inpatient investigation

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8
Q

Apnoea

A

the (near) complete cessation of airflow

4% oxygen desaturation, lasting ≥ 10 secs

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9
Q

Hypopnoea

A

a reduction of airflow to a degree insufficient to meet the criteria for an apnoea

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10
Q

Apnoea-Hypopnoea Index (AHI)

A

Determines how many events patients are having per hour

• AHI ≥15 is diagnostic of OSA

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11
Q

Factors predisposing to OSA

A

High BMI

underlying conditions - tonsils, hypothyroidism, nasal obstruction

triggering factors - alcohol

age

male gender

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12
Q

OSAS treatment

A
  • Explain OSAS
  • Weight loss
  • Avoid triggering factors - alcohol
  • Treat underlying conditions - tonsils, hypothyroidism, nasal obstruction

CPAP

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13
Q

Untreated OSAS

A

Most common presentation – hypertension that is refractory to anti-hypertensives
 Cardiovascular disease
 Increased risk of CVA

o Increased accidents at work/poor concentration
o 4 times more likely to have a RTA (must inform DVLA)

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14
Q

Why does pneumothorax cause lung collapse?

A

Any breach of the pleural space leads to collapse of the elastic lung because there is loss of the negative pressure required for inspiration

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15
Q

pneumothorax

A

Air within the pleural cavity

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16
Q

types of pneumothorax

A

1) Traumatic - penetrating/blunt injury
o Stabbing
o Fractured rib

2) Iatrogenic
o lung biopsy
o pleural aspiration

3) Spontaneous - no preceding trauma/event
o Primary
 Classically happens in tall, thin young men with apical surface blebs. No underlying lung disease

o Secondary
 underlying lung disease (e.g. COPD, cystic fibrosis)
 bullae may rupture

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17
Q

Tension pneumothorax

A

‘One way valve’ leads to increased intrapleural pressure (exceeds atmospheric pressure)

Venous return impaired, cardiac output and blood pressure fall

Patients become hypoxic and hypotensive

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18
Q

Where would you insert a chest drain to relieve the pressure of a tension pneumothorax?

A

2nd intercostal space midclavicular line

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19
Q

Pneumothorax risk factors

A

Smoking
male gender
height

• Underlying lung disease (secondary)

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20
Q

primary pneumothorax pathophysiology

A

Spontaneous rupture of subpleural blebs leads to tear in visceral pleura

Air flows from airways to pleural space (down the pressure gradient)

Elastic lung then collapses

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21
Q

signs and symptoms of pneumothorax

A

 Pleuritic chest pain
 Breathlessness (can be minimal if primary)
 Respiratory distress (especially if secondary)

 Reduced air entry on affected side
 Hyper-resonance to percussion
 barrel chest
 Reduced vocal resonance

 Tracheal deviation if tension (+/- circulatory collapse)

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22
Q

Differential diagnosis: pneumothorax

A

PTE, musculoskeletal pain, pleurisy/ pneumonia

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23
Q

Pneumothorax management

A

Primary spontaneous pneumothorax may be treated conservatively if symptoms are minimal
- Observation (serial CXR) - can be as outpatient

Secondary pneumothorax more frequently requires treatment by aspiration or intercostal chest drain (ICD)

Tension pneumothorax ALWAYS requires ICD insertion

If not resolved by a chest drain within 5-7 days, consider surgical intervention

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24
Q

After a spontaneous pneumothorax has resolved on CXR, how long should the patient wait before flying?
A. ≥ 7 days
B. ≥ 14 days
C. ≥ 28 days

A

≥ 7 days

If there is residual air in the pleural space, as they ascend and descend the air can expand and contract –> increased risk of recurrence

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25
Q

After a spontaneous pneumothorax has resolved on CXR, how long should the patient wait before diving?
A. ≥ 2 weeks
B. ≥ 6 weeks
C. should not dive again

A

should not dive again

With a spontaneous pneumothorax, there is at least a 30% risk of recurrence because there is probably an ongoing pathological process that can predispose to further pneumothoraxes

The pressures on scuba diving are far greater than those on flying

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26
Q

Spirometry

A

Forced expiratory manoeuvre from total lung capacity to residual volume, followed by a full inspiration

Most common pulmonary function test

method of differentiating between obstructive airways disorders and restrictive diseases

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27
Q

What is the most effective way of determining the severity of COPD?

A

spirometry

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28
Q

which limb of the Flow/ Volume Loop is effort dependent?

A

Inspiratory limb

Expiratory limb is effort independent - Relies on the elastic recoil of the lung

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29
Q

why does air trapping occur?

A

Expiration is effort independent.

If you increased the pressure outside the lungs, it leads to dynamic airway collapse

no matter how hard you squeeze, you can’t get more air out

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30
Q

What is considered to be a “normal” FEV1?

A

FEV1 of 85% predicted may be considered “normal”

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31
Q

Obstructive lung disease on pulmonary function tests

A

FEV1/FVC ratio <70% (0.7)

FVC is relatively well preserved, but they only manage to get it out very slowly – i.e. there is obstruction to air flow, i.e. decreased FEV1

“church and steeple pattern” on flow/volume loop

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32
Q

How do you determine COPD severity?

A

The severity of COPD is stratified by percentage predicted FEV1

– mild > 80%
– moderate 50-80%
– severe 30-50%
– very severe <30%

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33
Q

Reversibility testing

A

Nebulised or inhaled salbutamol is given

Spirometry is measured before and 15 minutes after salbutamol

15% change AND 400ml reversibility in FEV1 are suggestive of asthma

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34
Q

restrictive lung disease on pulmonary function tests

A
  • Both FEV1 AND FVC are reduced
  • FEV1/ FVC ratio >70% (normal)
  • Flow/volume and volume/time loops appear normal but smaller (absolute volume reduction)
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35
Q

Causes of restrictive lung disease

A

– Interstitial lung disease
– Kyphoscoliosis/ chest wall abnormality

  • Neuromuscular disease – GBS, polymyositis
  • Obesity – one of the more common causes
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36
Q

Transfer factor

A

measure of gas exchange in the lungs

Anything that impacts gas exchange will cause a low transfer factor

Give px single breath of very low [carbon monoxide]

CO has very high affinity to Hb
Measure concentration in expired gas to derive uptake in the lungs

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37
Q

Name 4 things that will caused a reduction in transfer factor

A

– Emphysema
– Interstitial lung disease
– Pulmonary vascular disease
– Anaemia (increased in polychthaemia)

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38
Q

Oximetry

A

Non-invasive measurement of saturation of haemoglobin by oxygen

NB: Depends on adequate perfusion
– Not accurate in shock or cardiac failure

Does NOT measure carbon dioxide, so therefore no measurement of ventilation

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39
Q

Main causes of Hypoxaemia

A

Ventilation/ perfusion mismatch (eg COPD, pneumonia)

Hypoventilation (eg drugs, neuromuscular disease)

Shunt (eg congenital heart disease)

Low inspired oxygen (altitude, flight)

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40
Q

Ventilation & perfusion

A

Ventilation refers to the movement of gas into and out of alveoli.

Perfusion refers to the flow of blood through the pulmonary capillaries.

must be matched for efficient gas exchange.

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41
Q

Alveolar oxygen equation

A

The difference between the calculated alveolar pO2 and the arterial pO2 is the alveolar arterial (A-a) oxygen gradient

Difference between alveolar and arterial oxygen partial pressures should be <2-4 kPa

more than this suggests V/Q mismatch

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42
Q

Hypoxemic respiratory failure (type I)

A
  • failure of oxygen exchange (perfusion problem)
  • generally caused by V/Q mismatch
  • characterized by PaO2 < 60 mmHg
  • normal PaCO2

e.g.
o pulmonary oedema
o pneumonia

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43
Q

Hypercapnic respiratory failure (type II)

A
  • failure to remove CO2
  • generally caused by problems with ventilation
  • characterized by a PaCO2 > 50 mmHg.
  • Hypoxemia is common

Common causes include:
o drug overdose
o neuromuscular disease
o chest wall abnormalities

Remember: type 2 has 2 problems: low O2 AND high CO2 = HYPOXIA + HYPERCAPNIA

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44
Q

acute respiratory failure

A

characterized by life-threatening derangements in arterial blood gases and acid-base status

o develops over minutes to hours
o pH is less than 7.3

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45
Q

chronic respiratory failure

A

manifestations are less dramatic

develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration.

Therefore, the pH usually is only slightly decreased.

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46
Q

Blood gas analysis (respiratory perspective)

A

Always look at the pO2 first
– Is the patient in respiratory failure requiring additional oxygen?

Then look at the PCO2 (type 1 vs type 2 respiratory failure)
– High in type 2 respiratory failure

Then consider acid base balance

Acute respiratory acidosis
– elevated pCO2
– normal bicarbonate
– acidosis

Compensated respiratory acidosis
– elevated pCO2
– elevated bicarbonate (renal compensation)
– not acidotic

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47
Q

What type of respiratory failure does cardiac failure cause?

A

type 1

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48
Q

What type of respiratory failure does pneumonia cause?

A

type 1

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49
Q

What type of respiratory failure does severe fatigue cause?

A

type 2

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50
Q

What type of respiratory failure does pulmonary embolism cause?

A

type 1

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51
Q

What is the appearance of emphysematous lungs on CXR?

A

emphysema causes hyperinflation – lungs appear bigger on CXR

CXR features:
•	>9 posterior ribs above the diaphragm
•	>6 anterior ribs above the diaphragm
•	Heart looks long and thin because the lung volume has increased
•	Hemidiaphragms are flat

• lungs are blacker due to loss of lung tissue

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52
Q

What level of oxygen therapy is recommended for patients with hypercapnic tendency?

A

24-28% oxygen is usually recommended

patients with hypercapnic tendency will become more hypercapnic and drowsy if you give them too much oxygen

aim for SpO2 88–92 % (targeted oxygen therapy)

Over 92% - higher risk for developing hypercapnia

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53
Q

How do you treat COPD exacerbation?

A

Remember: ONAP

  • Oxygen
  • Nebulised bronchodilators
  • Antibiotics
  • Prednisolone
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54
Q

pCO2 high and the HCO3 low

A

respiratory acidosis and metabolic acidosis

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55
Q

pCO2 low and the HCO3 high

A

respiratory alkalosis and metabolic alkalosis

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56
Q

NON-INVASIVE VENTILATION IN COPD

A

Provides positive pressure to the airways to support breathing

  • Reduces respiratory rate
  • Improves dyspnoea and gas exchange
  • Lowers mortality
  • Reduces need for ventilation in ITU
  • Reduces length of hospital stay
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57
Q

COR PULMONALE

A

Clinical syndrome of:
• Right heart failure secondary to lung disease
• Salt and water retention leading to peripheral oedema

treat with diuretics and oxygen therapy

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58
Q

signs of cor pulmonale

A
  • Peripheral oedema
  • Raised jugular venous pressure
  • A systolic parasternal heave
  • Loud pulmonary second heart sound
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59
Q

Chronic Obstructive Pulmonary Disease (COPD) Definition

A

• COPD is characterised by airflow obstruction.

The airflow obstruction is:
• usually progressive
• not fully reversible
• does not change markedly over several months.

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60
Q

Chronic Bronchitis

A

defined clinically

production of sputum on most days for at least 3 months in at least 2 years

affects the larger airways > 4mm

inflammation leads to scarring and thickening of airways

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61
Q

Emphysema

A

abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles

defined histologically

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62
Q

Bronchiolitis

A

small airways disease

narrowing of the bronchioles due to:
• mucus plugging
• inflammation
• fibrosis

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63
Q

Effects of Cigarette Smoking on the lungs

A

damages cilia, causing decreased motility and decreased mucous clearance. This predisposes to infections and neutrophilic infiltration -> decreased lung function

goblet cell hyperplasia -> chronic cough

Activation of proteases and inactivation of antiproteinases -> tissue destruction

Free radicals

Squamous metaplasia

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64
Q

Mechanisms of Airflow Obstruction in COPD

A

smoking & inflammatory response destroy interstitial tissue -> loss of elasticity

airways collapse on expiration -> causes air trapping and hyperinflation

Goblet cell metaplasia with mucus plugging of lumen

Thickening of the bronchiolar wall due to inflammation

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65
Q

Diagnosis of COPD

A

Consider the diagnosis of COPD for people who are:
◦ over 35
◦ smokers or ex-smokers

with any of:
	exertional breathlessness
	chronic cough
	regular sputum production
	frequent winter ‘bronchitis’
	wheeze
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66
Q

Treatment of COPD

A

Remember: ABCS + oxygen

A - anticholinergics (muscarinic agonists: tiotropium)
B - bronchodilators (SABA: salbutamol; LABA: salmeterol)
C - Inhaled Corticosteroids (Budesonide and fluticasone – combination inhalers)

S = smoking cessation

Oxygen therapy for patients with very severe lung disease

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67
Q

phenotypes of end-stage COPD

A

Blue Bloater

Pink Puffer

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68
Q

Blue bloater

A

 chronic bronchitics

 cyanosis
 warm peripheries
 bounding pulse due to hypercapnia
 flapping tremor
 confusion, drowsiness – due to raised CO2
 right heart failure - due to chronic pulmonary HTN
 Oedema, raised JVP

 low respiratory drive, loss of sensitivity to CO2
 Type 2 respiratory failure - ↓PaO2, ↑PaCO2,
 Become more hypercapnic with oxygen therapy

cyanosed but not breathless

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69
Q

Pink Puffer

A

 Emphasematous patients

 high respiratory drive
 Type 1 respiratory failure - ↓PaO2

 pursed lips – improve efficiency of breathing
 use accessory muscles – stabilise the chest wall to make breathing more efficient
 wheeze
 indrawing of intercostals
 tachypnoea

Breathless but not cyanosed

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70
Q

inflammatory processes in COPD vs asthma

A

asthma

  • mainly eosinophilic
  • CD4+ T lymphocytes

COPD

  • neutrophilic
  • increased numbers of macrophages and CD8+ T lymphocytes.
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71
Q

SARCOIDOSIS

A

multisystem inflammatory disease of unknown aetiology

predominantly affects the lungs and intrathoracic lymph nodes

characterised by non-necrotising granulomatous inflammation

diagnosis of exclusion

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72
Q

What kind of inflammation is typically seen in sarcoidosis?

A

non-necrotising granulomatous inflammation

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73
Q

What are Asteroid bodies?

A

filaments of cytokeratin

only ever see asteroid bodies in relation to sarcoidosis

74
Q

causes of Pulmonary Fibrosis

A
  • Smoking
  • Radiation
  • RA
  • Idiopathic
  • Drug Induced – Amiodarone, Nitrofurantoin, Methotrexate, Cocaine
75
Q

Usual Interstitial Pneumonia (UIP)

A

used interchangeably with idiopathic pulmonary fibrosis (IPF)

form of interstitial lung disease characterized by progressive fibrosis (scarring) of both lungs.

76
Q

Radiological features of idiopathic pulmonary fibrosis

A
  • PERIPHERAL Interstitial pattern of fibrosis

* Subpleural honeycombing

77
Q

symptoms of idiopathic pulmonary fibrosis

A
  • Breathlessness (worse with exercise)
  • Hacking dry cough
  • Fatigue and weakness
  • Appetite and weight loss
  • Clubbing
78
Q

diagnosis of idiopathic pulmonary fibrosis

A

High-resolution CT (HRCT) - honeycombing

If classical signs are not seen on HRCT, then the patient will have Video-Assisted Thoracoscopic Surgery (VATS)
• Used to biopsy the lung

79
Q

pathophysiology of idiopathic pulmonary fibrosis

A

Unknown

Theory that free radicals perpetuate damage and fibrosis

progression of fibroblast proliferation leads to scar tissue formation = fibroblast focus

collagen gets laid down (irreversible damage) –> progressive breathlessness

80
Q

Extrinsic Allergic Alveolitis (EEA)

A

= Hypersensitive Pneumonitis (HSP)

Delayed allergic response (type III & IV hypersensitivity)

lungs develop immune response (hypersensitivity) to something inhaled -> inflammation of the lung (pneumonitis)

Body generates antibodies (sensitisation) against trigger

Repeat exposure causes immune complexe formation
-> deposit in kidneys and small capillaries of the lungs

Immune complexes activate complement -> destruction of the lungs; sets up a process of remodelling/repair -> fibrosis and emphysema

Non-necrotizing granulomatous inflammation can occur

81
Q

Differentiation between sarcoidosis and EEA

A

Both have non-necrotising granulomatous inflammation in the lung

The difference is that in sarcoidosis the inflammation (and thereby the granulomas) is in the interstitium alone

In hypersensitive pneumonitis, the inflammation is in the alveolar air spaces
• This is because the allergen is being inhaled, and it stays in the air spaces, therefore this is where the inflammatory reaction occurs

82
Q

Which form(s) of lung cancer are most closely linked to smoking?

A

squamous and small cell lung cancer

83
Q

Risk factors for lung cancer

A
  • smoking
  • Environmental tobacco smoke
  • Ionising radiation
  • Air pollution
  • Asbestos
84
Q

Signs and Symptoms of Lung Cancer

A
  • Cough
  • Haemoptysis
  • Shortness of Breath
  • Chest pain
  • Weight loss/Anorexia
  • General malaise

NB: There will be different symptoms depending on where the tumour is

85
Q

symptoms of central lung tumours

A

Central tumours arise in and around hilus of the lung (carina and main airways) and are usually squamous or small cell carcinomas

Haemoptysis – more likely to invade into blood vessels if central

Bronchial obstruction

SOB

retention pneumonia – secretions will be retained behind site of obstruction, and this can be superimposed by infection

Cough

86
Q

symptoms of peripheral lung tumours

A

predominantly adenocarcinomas

probably few symptoms as the main airways and blood vessels are unaffected

Pain if pleura or chest wall involved

may be picked up on routine CXR

87
Q

symptoms of SVC obstruction by a tumour

A

o Oedema of face and arms
o Raised JVP
o Dilated veins on chest wall
o Plethoric face – headache worse on stooping

88
Q

What are 3 possible effects of local spread of a lung tumour?

A

1) SVC obstruction
2) phrenic nerve paralysis – hemidiaphragm paralysis
3) recurrent laryngeal nerve paralysis - causes hoarse voice

89
Q

Common sites of lung tumour metastasis

A

Haematogenous spread –> liver, bone, brain, adrenal

Lymphatic spread –> Cervical lymph nodes

90
Q

What are possible non-metastatic effects of a lung tumour?

A

ACTH secretion -> Cushing’s syndrome

ADH secretion -> hyponatraemia due to water retention

PTHrP secretion -> hypercalcaemia

91
Q

What is the most aggressive form of lung cancer?

A

small cell carcinoma

  • Metastasizes early and widely
  • Often initial good response to chemotherapy – but most patients relapse
92
Q

Which form of lung cancer is associated with keratinzation and/or intercellular bridges?

A

squamous cell carcinoma

93
Q

Which form of lung cancer is most commonly seen in females and non-smokers?

A

adenocarcinoma

94
Q

Which Molecular Target has been Identified in non-small cell lung cancer?

A

Epidermal Growth Factor Receptor (EGFR) with ALK fusion gene

Chromosomal translocation

Puts the ALK gene right next to EML4 -> leads to a constitutive activation of a tyrosine kinase leading to increased cell proliferation

• Inhibit with Crizotinib

Others:
• Cetuximab
• Erlotinib

95
Q

Which drug can be used to treat PDL1 positive lung tumours?

A

Nivolumab

PDL1 stops T cells killing tumour cells

Blocking PDL1 stops tumour cells evading the immune system

96
Q

Common sources of metastases to the lung

A 
Almost any cancer can spread to the lung but common sites of origin are:
•	Breast
•	Colorectal
•	Kidney
•	Head and neck
•	Testicular
•	Bone (osteosarcoma) – Sarcomas
•	Melanoma
•	Thyroid
97
Q

differential diagnosis for a lung mass on CXR

A 
cancer
TB granuloma
abscess
cyst
pulmonary hamartoma
98
Q

Mesothelioma

A

Primary pleural tumour

also occurs in peritoneum, pericardium and tunica vaginalis testis

  • Almost always due to asbestos exposure
  • Very long lag period before disease develops

Tumour has either an epithelial or sarcomatoid appearance, or a mixture of both (biphasic)

99
Q

atelectasis

A

lung collapse

100
Q

4 causes of Bilateral Hilar adenopathy (=enlargement of mediastinal lymph nodes)

A

1) Sarcoidosis
2) Lymphoma
3) TB
4) Malignancy

101
Q

Causes of whiteout of hemithorax

A
  • Pneumonectomy
  • Effusion ->Fluid pushes mediastinum away
  • Collapse -> creates a space, mediastinal structures move towards it

i.e. in a white lung:

if the mediastinum is pushed to the opposite side it’s a PLEURAL EFFUSION

If the mediastinum is towards the affected side, it’s a PNEUMONECTOMY or a LUNG COLLAPSE

102
Q

What kinds of lung pathology cause a shift of mediastinal structures towards the affected side?

A
  • Collapse
  • Post pneumonectomy
  • Pulmonary agenesis & hypoplasia
103
Q

What kinds of lung pathology cause a shift of mediastinal structures away from the affected side?

A
  • Pleural effusion

- Diaphragmatic hernia

104
Q

What kinds of lung pathology cause the mediastinal structures to remain central?

A
  • Consolidation
  • Mesothelioma

remember: Consolidation is Central

105
Q

What should you be concerned about with a CXR showing a dark lung with mediastinal shift?

A

Dark lung with mediastinal shift = pneumothorax until proven otherwise

106
Q

How can a minor change in calibre of the airway lead to airway collapse?

A

Tiny changes in calibre/radius of the airway leads to massive changes in resistance to air flow

This means that much more pressure needs to be generated to expire air

this pressure causes airway collapse

107
Q

What is allergy?

A

an immune system mediated intolerance of an external factor

Requires exposure to a specific trigger

108
Q

What is the effect of chronic allergy?

A

Chronic exposure to allergens leads to changes in structure due to activation of healing and repair pathways (tissue remodelling)

This leads to changes in cells, and scarring/fibrosis in airways

results in a thickened, chronically narrowed airway
that becomes less sensitive to asthma treatments over time

109
Q

hyperreactivity

A

a normal process that is heightened in some people

the more of the stimulus there is, the bigger the reaction will be

110
Q

effect of allergy on the airways

A

Increases resistance

Causes wheeze/stridor – turbulence
 Due to changes in airway calibre and air flow
 Turbulence happens at junctions
 Turbulence occurs where the flow is disrupted by asymmetrical narrowing

111
Q

Extrathoracic airway disease

A

airways held open by cartilage rings e.g. larynx

Disease in this area affects the flow of air in

Not affected by expiration because they are held open by cartilage rings
i.e. not susceptible to changes in intra-thoracic pressure because of the cartilage rings

Disease in these airways affects the flow of air into the lungs
o Disease here causes STRIDOR (inspiratory)

112
Q

Intrathoracic airway disease

A

Airways are soft and flaccid. Susceptible to intra-thoracic pressure because there are no supportive cartilage rings

o Collapse very easily upon deep expiration
o Disease in this region causes WHEEZE (expiratory)
o These are the airways affected by asthma
o Sputum due to decreased mucous clearance

113
Q

Stepwise management of asthma

A

Step 1: occasional relief bronchodilator: SABA as required

Step 2: regular inhaled preventer therapy - ICS

Step 3: ICS + LABA. If LABA not working, add one of:
o Leukotriene receptor antagonist
o oral theophylline

Step 4: high-dose ICS + regular bronchodilators - e.g. nebulised therapy, anti-muscarinics

Step 5: regular corticosteroid tablets

114
Q

Clinical Definition of asthma

A

chronic inflammatory condition of the airways that causes recurrent episodes of:
o Wheezing
o Breathlessness
o chest tightness
o cough
o particularly at night and/or early morning

symptoms are usually associated with widespread but variable bronchoconstriction and airflow limitation that is at least partly reversible

Key Features:
 increased airway hyper-responsiveness resulting in episodic bronchoconstriction
 inflammation of the bronchial walls
 increased mucus secretion

115
Q

Airway pathology in acute severe asthma

A

Lumen of airways filled with mucous/eosinophils

Thick basement membrane

smooth muscle hypertrophy – infiltrated by MAST CELLS

airway oedema

Destruction of epithelium

116
Q

Diagnosis of asthma

A

Appropriate clinical history + Supportive physiological tests

  • variable peak flow
  • Bronchial Hypersensitivity when tested with methacholine
  • Reversible Airflow Obstruction: ≥ 15% improvement in FEV1 after 5mg nebulised salbutamol
117
Q

Pleural Effusion

A

accumulation of abnormal volume of fluid in the pleural space

Normal volume of pleural fluid < 15ml
difficult to detect < 500ml clinically

118
Q

Symptoms of Pleural Effusion

A

may be asymptomatic

SOB
cough
pleuritic chest pain

119
Q

clinical signs of Pleural Effusion

A 
	Reduced chest expansion
	Reduced tactile vocal fremitus
	Stony dull percussion note
	Quiet breath sounds
	Bronchial breathing above fluid level
	Rub with pleural inflammation
120
Q

causes of Pleural Effusion

A

Increased hydrostatic pressure (congestive cardiac failure)

Decreased osmotic pressure (hypoalbuminaemia, e.g. in liver disease/nephrotic syndrome)

Increased vascular permeability (pneumonia) may cause damage to the underlying blood vessels

Decreased lymphatic drainage (mediastinal carcinoma)

121
Q

bilateral pleural effusion

A

cause is usually obvious

– Usually transudate
– No need to sample initially
– Treat underlying cause (e.g. increase diuretics for heart failure) and repeat imaging

do not drain these patients because fluid will keep on accumulating

122
Q

Unilateral pleural effusion

A

• Should be investigated

Many causes, main causes to think about:
–	Infection
–	Malignancy
–	PTE 
–	Inflammatory causes
–	TB
123
Q

Transudate vs Exudate

A

requires paired serum sample - apply Light’s criteria

Transudate:

  • protein <30g/L
  • LDH <2/3 of upper limit of normal
  • often bilateral
  • usually clear

Exudate:

  • protein >30g/L
  • LDH >2/3 of upper limit of normal
  • often unilateral
  • clear, cloudy or blood stained
124
Q

Common causes of transudate

A

cardiac failure
nephrotic syndrome
liver cirrhosis
hypoalbuminaemia

125
Q

Common causes of exudate

A

bacterial pneumonia
TB
malignancy
mesothelioma

126
Q

Investigation procedure for pleural effusion

A

1) history/exam/CXR
2) aspirate if exudate suspected
3) CT if no diagnosis from aspirate
4) VATS/biopsy if still no diagnosis

127
Q

MANAGEMENT OF LIFE THREATENING ACUTE EXACERBATION OF ASTHMA

A

High flow oxygen

Nebulised bronchodilators (salbutamol + ipatropium bromide)

Oral prednisolone

Oral doxycycline

IV magnesium

Consider IV aminophylline infusion

128
Q

Anti-muscarinics: Mechanism of Action

A

Inhibition of cholinergic M1 and M3 receptors in lung

This causes a reduction in cGMP

Result is an inhibition of parasympathetic-mediated bronchoconstriction

129
Q

Side Effects of Anti-muscarinics

A

Blurred vision, dry mouth, urinary retention

cant see, cant pee, cant spit

130
Q

Mechanism of Action: theophylline

A

Non-selective inhibition of phosphodiesterase

causes increased intracellular cAMP -> bronchial smooth muscle relaxation

Immunomodulatory action - improved mucociliary clearance and anti-inflammatory effect

NB: Narrow therapeutic window

131
Q

List two factors that affect theophylline dosing

A

Metabolised in the liver

  • caution in liver disease
  • caution with concomitant use of enzyme inducers (rifampicin) and inhibitors (clarithromycin, ciprofloxacin)

Smoking increases theophylline clearance – dose may need adjusted following smoking cessation

132
Q

Most common cause of pneumonia (typical)

A

streptococcus pneumoniae

Also:
Haemophilus influenzae
Moraxella cattharalis
Staphylococcus aureus

133
Q

Typical presentation of pneumonia

A

e.g. streptococcus pneumoniae infection

often presents with signs of sepsis and chest symptoms:
o cough
o purulent sputum
o pleuritic chest pain
o dyspnoea
134
Q

Atypical organisms causing pneumonia

A

 Legionella pneumophila
 Mycoplasma pneumonia
 Coxiella burnetti (Q fever).

135
Q

How would you assess pneumonia severity?

A

CURB65 scoring system

C - Confusion (new disorientation to place, person & time)

U -Blood urea >7mmol/L

R - Respiratory rate >30 breaths per minute

B - Diastolic BP <60mmHg

65 - Age ≥ 65 years

outpatient treatment can be considered in patients with a CURB65 score of 0 to 1

136
Q

What trumps CURB 65? (i.e. you have severe pneumonia regardless of CURB score)

A

o Sepsis
o Multi-lobar consolidation
o Hypoxia

137
Q

Complications in CAP

A

depend on the infecting pathogen and the patient’s baseline health.

Pleural effusions in pneumococcal pneumonia are relatively common

Can develop into empyema if infected

Patients with CAP who have impaired splenic function may develop overwhelming pneumococcal
sepsis, potentially leading to death

138
Q

How can you induce a sputum sample?

A

nebulise with isotonic saline to induce coughing.

139
Q

Presentation of advanced HIV

A

manifests as recurrent, severe infections and/or opportunistic malignancies.

signs and symptoms are those of the presenting illness, meaning

HIV infection should be suspected as an underlying illness when unusual infections present in apparently healthy individuals.

140
Q

What increases the risk of sexual transmission of HIV?

A 
o high HIV viral load
o trauma (including sexual assault)
o co-existing STIs
o ulcerative conditions - HSV/syphilitic chancre
o if the index male is uncircumcised
141
Q

High risk groups for HIV

A

 MSM who have had unprotected sex

 Individuals from high prevalence countries with sexual or vertical transmission risk

 IVDU, especially those from high prevalence area

 Individuals exposed to blood via injection, tattoo, piercing or transfusion in high-risk countries or nonprofessional settings

 Sexual contacts of the above

 Anyone diagnosed with a STI

142
Q

Barriers to HIV testing

A 
Patient barriers:
 May not think they are at risk
 Worried regarding confidentiality, stigma, immigration issues
 Employment issues
 Criminalisation issues
 Insurance

Doctor barriers:
 May not think of testing
 May assume patient is not at risk
 Fear of embarrassing/offending patient
 Lack of time
 Perceived lack of counselling skills
 Logistic issues to get result back to patient

143
Q

What pre-test discussion is required prior to a HIV test?

A

 Why testing is indicated i.e. due to clinical presentation or symptoms

 Benefits to testing i.e. if positive the success of HIV therapy, if negative the ability to concentrate on other investigations/diagnoses

 How/when result will be available

144
Q

Name 4 opportunistic infections

A

o CMV
o Candida
o PCP
o Toxoplasma

145
Q

How does HIV affect the immune system?

A

HIV gains entry to Th by binding to CD4 and other glycoproteins and co-receptors (i.e. CXCR4/CCR5).

Th are depleted as HIV progresses, causing:
o Impaired B cell activation
o Impaired antibody production
o impaired cytotoxic T cell immunity.

At CD4 <350 individuals begin to become symptomatic

<200 - increased risk of opportunistic infections- PCP.

<100 risk of serious infections - mycoplasma and CMV

146
Q

Name 4 AIDS defining illnesses

A

PCP
CMV
Mycoplasma infections (TB)
Candidiasis

147
Q

Definition of an exacerbation of COPD

A

a sustained worsening of the patient’s symptoms from their usual stable state which is beyond normal day-to-day variations, and is acute in onset.

Common symptoms:
 worsening breathlessness
 cough
 increased sputum production
 change in sputum colour
148
Q

Management of an Exacerbation of COPD

A

Assess severity: Symptoms, ABG, CXR

Controlled oxygen therapy

Bronchodilators: Air-driven nebulised salbutamol
and ipratropium bromide

Corticosteroids oral prednisolone

Antibiotics: if signs of bacterial infection (purulent sputum, increased sputum volume, ++ WCC, ++CRP)

149
Q

Describe the clinical signs and CXR changes of a pleural effusion.

A

A pleural effusion is fluid in the pleural space

Clinical signs:
 decreased breath sounds
 stony dull to percussion
 decreased tactile or vocal fremitus

CXR:
 need >300 ml of fluid to be present to see on CXR
 uniformly white appearance
 blunting of costophrenic angles.
 A meniscus at the upper edge
150
Q

Which patients are candidates for long term oxygen therapy?

A

In (COPD) patients who have:

 PaO2 <7.3 kPa when stable
 OR PaO2 7.3 – 8 kPa

AND any of:
 secondary polycythaemia
 nocturnal hypoxaemia
 peripheral oedema
 pulmonary hypertension

Must be NON-SMOKERS FOR >3 MONTHS

151
Q

Name three cell types and three inflammatory mediators involved in airway inflammation in asthma.

A

Eosinophils - degranulate releasing leukotrienes -> damage the epithelium -> cell loss causes bronchial hyper-responsiveness

Mast cells - degranulate releasing histamine → bronchoconstriction

Dendritic cells - present allergens to T lymphocytes

IL-4 stimulates IgE production by plasma cells

IL-5 - activates eosinophils

IL-13 stimulates mucus secretion

152
Q

Pathological Features in the Asthmatic Airways

A 
 Plasma exudation
 Oedema
 Smooth Muscle hypertrophy
 Mucus plugging
 Shedding of epithelium
 thickened basement membrane
 Inflammatory cell infiltration
153
Q

Symptoms Suspicious of Lung Cancer

A
  • Cough - that doesn’t go away, or a long-standing cough gets worse
  • Recurrent infections
  • Breathlessness – lobar/lung collapse (co-existing COPD)
  • Haemoptysis
  • Unexplained weight loss
  • Night sweats
  • Chest and/or shoulder pains
  • Hoarse voice -> invasion of RLN
154
Q

Signs Suspicious of Lung Cancer

A
  • Finger clubbing
  • Dull percussion/Reduced air entry
  • Cachexia

From metastases
o Hepatomegaly
o Cervical lymphadenopathy (supraclavicular)
o bony tenderness

  • Horner’s syndrome (Pancoast tumour)
  • Evidence of superior vena cava obstruction (SVCO)
  • Evidence of spinal cord compression (SCC)
  • Cushingoid
155
Q

What are the main risk factors for the development of lung cancer?

A
  • Smoking in 85%
  • Passive smoking
  • occupational asbestos
  • silica and nickel exposure
  • pulmonary fibrosis
156
Q

Common sites for lung cancer metastasis

A
  • Lymph nodes
  • Liver
  • Bone
  • Brain
  • Adrenals
157
Q

Common Non-Metastatic Manifestations of Lung Cancer

A

Metabolic – weight loss, anorexia, lassitude

Endocrine
o ectopic ACTH – Cushingoid appearance
o SIADH – hyponatraemia
o Hypercalcaemia – PTHrP, bony metastases

Neurological – Lambert-Eaton syndrome

Skeletal – finger clubbing, hypertrophic osteoarthropathy

158
Q

Emergencies Associated with Lung Cancer

A

Superior vena cava obstruction
• due to mediastinal nodes compressing SVC

Spinal cord compression

159
Q

signs and symptoms of Superior vena cava obstruction

A 
Symptoms 
o	Breathless
o	Dysphagia
o	Stridor
o	swollen oedematous face and right arm

Signs
o venous congestion in the neck
o dilated veins in the arm

160
Q

TNM Staging

A 
T = tumour size
N = LN involvement
M = metastases
161
Q

small cell carcinoma

A

central tumour

highly malignant and associated with worse prognosis

generally present at advanced stage

treat with chemotherapy only

162
Q

Non small cell carcinoma subtypes

A

adenocarcinoma

large cell carcinoma

squamous cell carcinoma

may be managed surgically in stages I/II. Radiotherapy with palliative/curative intent in later stages. Generally less responsive to chemotherapy.

Adenocarcinoma may have specific mutations in EGFR/PD-L1/ALK

163
Q

Large cell carcinoma

A

peripheral tumour

undifferentiated epithelial tumour
may be resectable

164
Q

adenocarcinoma

A

peripheral tumour

more common in women and non-smokers

mucin production

may have mutations in EGFR/PD-L1/ALK

165
Q

squamous cell carcinoma

A

central tumour

associated with smoking

keratinisation

166
Q

Idiopathic Pulmonary Fibrosis

A

specific form of chronic fibrosing interstitial pneumonia of unknown aetiology

limited to the lung

histopathological appearance of usual interstitial pneumonia (UIP) on surgical lung biopsy

known causes of ILD such as drugs, environmental exposure and connective tissue disease have been excluded

167
Q

Name 2 Drugs that can Induce ILD

A

amiodarone

nitrofurantoin

168
Q

What changes would you expect in Total lung capacity (TLC) in obstructive and restrictive lung disease?

A

obstructed = TLC more or less preserved

Reduced in restrictive

169
Q

Serum angiotensin converting enzyme

A

o Test of sarcoid

o Raised in sarcoid patients

170
Q

Describe the histological and radiological changes seen in idiopathic pulmonary fibrosis (usual interstitial pneumonia)

A

honeycombing

ground glass changes

traction bronchiectasis

171
Q

what does ground glass changes on CXR indicate?

A

partial filling of air spaces in the lungs by exudate or transudate

caused by alveolar wall inflammation or thickening and/or partial air-space filling

172
Q

key histological features of IPF

A

Histological pattern of fibrosis is usual interstitial pneumonia (UIP)

patchy interstitial fibrosis, varies in intensity and age (temporal heterogeneity)

fibroblastic foci in early fibrosis

honeycomb change
• Stiffening around the lung with trapping of air
• Deposition of collagen and inflammatory cells -> produce mucin, which blocks the lumen of the airways

173
Q

Pathogenesis of IPF

A

unknown agent causes repeated epithelial cell injury

this leads to inflammation and cell damage

chronic inflammation causes structural changes and fibrosis

alveolar epithelium becomes dysfunctional

174
Q

Which treatments are available for IPF?

A

pirfenidone = antifibrotic and anti-inflammatory

Nintedanib = intracellular inhibitor of multiple tyrosine kinases

Steroids and immunosuppressants are not routinely recommended. Azithioprine may worsen prognosis

Symptom control:

  • LTOT
  • Diuretics
  • Antibiotics
  • Lung transplantation in younger patients
175
Q

dull percussion note

A

collapse

consolidation

fibrosis

pleural effusion (stony dull)

176
Q

hyperresonant percussion note

A

pneumothorax

hyperinflation (COPD)

177
Q

fine crackles

A

pulmonary oedema

178
Q

coarse crackles

A

bronchiectasis

179
Q

pleural rub

A

pneumonia

180
Q

increased vocal resonance

A

consolidation (sound conducts better through solid)

181
Q

decreased vocal resonance

A

COPD

pleural effusion

pneumothorax

J3 (18 decks)

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