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Phase 3 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is the survival and mortality from lung cancer?

A
  • 10% 10 year survival for lung cancer - lowest survival outcome of any cancer
    • Low survival usually due to late diagnosis or comorbidities
  • Age that lung cancer survival is highest: 15-39 years
  • Commonest cause of death from malignant disease - 21% of cancer deaths
  • 50% of deaths occur in over 75s
  • More common in people living in deprived aras
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2
Q

Describe the aetiology of lung cancer

A

Smoking is the main cause of lung cancer

Other risk factors
> Environmental tobacco soke
> Ionising radiation: radon, uranium
> Air pollution
> Asbestos
> others: fibrosing conditions of the lung, human papilloma virus, hereditary (polymorphisms in cytochrome p450)

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3
Q

What are the signs and symptoms of lung cancer?

A
  • Cough
  • Haemoptysis
  • Shortness of breath
  • Anorexia / weight loss
  • General malaise

Central: usually squamous or small cell carcinoma
> Haemoptysis
> Bronchial obstruction: obstruction pneumonia
> Cough

Peripheral: usually adenocarcinomas
> Few symptoms
> Chest pain if pleura or chest wall involved

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4
Q

How does lung cancer spread locally?

A
  • Pleura: haemorrhagic effusion
  • Hilar lymph nodes
  • Adjacent lung tissue (may involve large vessels leading to haemoptysis)
  • Pericardium: pericardial effusion with subsequent involvement of pericardium
  • Mediastinum:
    > Superior vena caval obstruction
    » Headache, oedema of face & arms, raised JVP

> Recurrent laryngeal nerve: hoarseness if invaded

> Phrenic nerve paralysis e.g. paralysis of right hemidiaphragm, can compromise lung volume

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5
Q

What is a pancoast tumour?

A
  • Tumour that invades apical structures of the lung
  • Involvement of the brachial plexus gives sensory & motor symptoms
  • Severe pain in the shoulder, scapula, arm
  • Weakness in the hands
  • Horner’s syndrome aka oculosympathetic play
    > Invasion of cervical sympathetic chain
    > Symptoms: pupillary constriction, ptosis, enophthalmos, hemifacial anhydrosis (same side of tumour)
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6
Q

How does lung cancer spread distantly?

A
  • Haematogenous: common due to invasion of pulmonary veins
    > Liver, bone, brain, adrenal
  • Lymphatic: cervical lymph nodes
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7
Q

List the non-metastatic effects of lung cancer

A
  • ACTH secretion
    > Leads to adrenal hyperplasia
    > Raised blood cortisol leads to Cushing’s syndrome
  • ADH secretion
    > Retention of water
    > Dilutional hyponatraemia - SIADH
  • Parathyroid hormone related peptide (PTHrP) secretion
    > Osteoclastic activity leads to hypercalcaemia
  • Other non-metastatic effects
    > Encephalopathy
    > Cerebellar degeneration
    > Neuropathy
    > Myopathy
    > Eaton Lambert myasthenia-like syndrome
    > Cancer-associated retinopathy
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8
Q

List the different pathological types of lung cancer

A
  • Non-small cell lung cancer (NSCLC)
    > Adenocarcinoma
    > Squamous cell carcinoma
    > Large cell carcinoma
  • Small cell lung cancer (SCLC)
  • Other
    > Inflammatory myofibroblastic tumour - mesenchymal tissue
    > Adenoid cystic carcinoma - salivary gland-type tumours
    > Tumours of ectopic origin: germ cell tumours
    > Carcinoid
    > Lymphoma
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9
Q

Describe the appearance and main characteristics of adenocarcinoma

A
  • Common in females; also seen in non-smokers (but still associated with smoking)
    > 2/3 arise in the periphery
  • Appearance:
    > Glandular, solid, papillary or lepidic (lines up along alveolar walls)
    > Mucin production
  • Screened for EGFR mutations: ALK, PD-L1, ROS-1
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10
Q

Describe the appearance and main characteristics of squamous cell carcinoma

A
  • Arises centrally from major bronchi
    > Often within dysplastic epithelium following squamous metaplasia
  • Slow growing and metastasise late (good for surgery)
  • May undergo cavitation
  • May block bronchi leading to retention pneumonia or collapse

Appearance: malignant epithelial tumour showing keratinization and intercellular bridges
In situ squamous cell carcinoma may be seen in adjacent airway mucosa

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11
Q

Describe the appearance and main characteristics of large cell carcinoma

A
  • Diagnosis of exclusion
  • Usually arises centrally
  • Undifferentiated malignant epithelial tumour that lacks the cytological features of SCLC & glandular or squamous differentiation
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12
Q

Describe the appearance and main characteristics of small cell lung cancer

A

Usually advanced at diagnosis - most aggressive form of lung cancer
> Metastasises early and widely

Responds to chemotherapy but most patients relapse

Appearance
> Oval to spindle shaped cells
> Inconspicuous nucleoli
> Scant cytoplasm
> Nuclear moulding

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13
Q

Describe the appearance and main characteristics of carcinoid tumours

A
  • Neuroendocrine tumour, classified as typical or atypical
  • Can be central or peripheral & can metastasise but much better prognosis than other lung cancers
  • Histology
    > Polypoid nodule in bronchus
    > Well-circumscribed outline
    > Lymphoma (purple)
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14
Q

Describe the pathogenesis of lung cancer

A

Lung cancer is a multi-step process which involves the chronic irritation of cells by carcinogens

> There is increased cell turnover and progressive accumulation of genetic abnormalities in molecules involved in cell cycle, signalling & angiogenesis pathways

Phenotypic changes are potentially reversible but genotypic alterations persist
> Normal tissue > hyperplasia > metaplasia > dysplasia > carcinoma in situ > invasive cancer > metastasis

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15
Q

Describe the targeted therapies used in non-small cell lung cancers

A

Non-squamous non-small cell lung cancer:

EGFR receptor mutations: tyrosine kinase inhibitors

EML4-ALK gene fusions: ALK inhibitors

ROS-1 oncogenic fusion

KRAS mutations: sotorasib

BRAF mutations: BRAF inhibitors

All NSCLC:
PD-L1: PD-L1 inhibitors

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16
Q

List cancers that frequently metastasise to the lung

A

Breast
Colon
Head & neck
Kidney - cannonball metastases
Testicular carcinoma
Sarcoma

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17
Q

Name the stain used in TB to identify AAFB (acid alcohol fast bacilli)

A

Ziehl-Neelsen stain

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18
Q

Describe the cause, characteristics and histology of mesothelioma

A

Mesothelioma is a primary pleural tumour (also occurs in peritoneum, pericardium & tunica vaginalis)

Cause: asbestos exposure
> Asbestos bodies can be found in the lung (bronchial washings) - macrophages try to eat refractile fibre and release free radicals

Very long lag period before disease develops

Histology: either epithelioid or sarcomatoid appearance or both (biphasic)

Malignant mesothelioma: compression of the lung causes respiratory compromise
> Characteristic feature: invasion of horizontal fissure

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19
Q

List signs and symptoms of pleural effusion

A

Symptoms
- Dyspnoea
- Fever
- Sputum
- Cachexia
- Fatigue
- Haemoptysis
- Chest pain
- Cough

Signs
- Fingernail clubbing
- Ascites
- Lymphadenopathy
- Chest: coarse crackles, stony dullness on percussion, reduced breath sounds
- decreased vocal resonance and decreased vocal fremitus

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20
Q

How do you differentiate between a transudate and an exudate?

A

Light’s criteria

Any 1 of 3: exudate

Protein level > 30g/l
Fluid protein:serum protein ratio > 0.5
Fluid LDH:serum LDH ratio >0.6 or Fluid LDH > 2/3 maximum serum normal

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21
Q

List the causes of pleural effusion

A

Transudate
> Heart failure
> Cirrhosis
> Renal failure - nephrotic syndrome
> Hypothyroidism
> Hypoalbuminaemia
> Peritoneal dialysis
> Protein losing enteropathy

Exudate
> Malignancy
> Infection
> Empyema
> TB
> Haemothorax
> PE
> Pancreatitis
> Drug induced
> Post-CABG

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22
Q

Which investigations are used to diagnose a pleural effusion?

A

CXR - meniscus sign

CT scan

Ultrasound

Bloods: CRP, WCC

Sampling: never drain undiagnosed effusion, limits diagnosis
> Local anaesthetic thoracoscopy: direct visual examination of pleural with a thoracoscope (used in undiagnosed cytology negative pleral effusion)

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23
Q

How are pleural effusions managed?

A

Management is symptom-driven (i.e. only treat if symptomatic, like dyspnoea)

> Chest drain +/- talc pleurodesis
> Talc pleurodesis sticks lung to chest wall, removing space between lung & chest wall so fluid does not build up between layers

Indwelling pleural catheter is an option if talc fails or lung is trapped

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24
Q

Describe the different types of pleural infection and their management

A

50% of pneumonias have an associated effusion

> Complex parapneumonic effusion
> pH < 7.2
> LDH > 1000
> Glucose <2.2
> Loculated on ultrasound
> Drain

> Empyema
> Presence of pus or bacteria: quickly drain, severe condition

Management
> Drainage 12-16F
> IV antibiotics
> Fibrinolytics
> Surgery

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25
Q

Describe the pathophysiology of allergy

A

Immediate:
Recognition of antigen by APC & T cells

IgE & mast cell mediated
> production of IL-4 & IL-13

Delayed:
Mediated by reactive T cells
Production of IL-12 & interferon gamma

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26
Q

Define asthma

A

Allergic inflammation of the airway characterised by reversible obstruction and diurnal variation

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27
Q

Describe the pathophysiology of asthma

A

Characterised by invasion of macrophages & T lymphocytes

Scabby epithelium and thickened basement membrane

Thickened smooth muscle with mast cells within
> Contain granules with histamine and leukotrienes which trigger smooth muscle constriction

Mucociliary impairment leads to sputum production

Turbulent airflow caused by expiratory phase narrowing leads to wheeze and breathlessness

Bronchial hyperreactivity and hypersensitivity

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28
Q

List asthma triggers

A
  • Exercise
  • Cold
  • Allergen exposure (dust mites, cats)
  • Chemical exposure: salicylates/aspirin, spicy food, perfume, NSAIDs, beta blockers
  • Viral infections
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29
Q

Describe the tests used in the diagnosis of asthma

A
  • Peak flow measurements: diurnal variation
  • Methacholine or histamine challenge: bronchial hyperresponsiveness
    » Drop of >20% FEV1 by <8 mg/ml methacholine (may also use histamine or mannitol)
  • Spirometry: reversible airflow obstruction - improvement >15% in FEV1 after 5mg nebulised salbutamol
  • Skin scratch test: allergens
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30
Q

Describe the management of asthma

A
  • Short acting beta agonist: salbutamol
  • Corticosteroids: beclomethasone, budesonide
  • Long acting beta agonist: salmeterol
  • Leukotriene receptor antagonists: montelukast
  • Long acting muscarinic antagonist: ipratropium
  • Biological therapy
    > Anti-IgE: omalizumab
    > Anti-TNF: infliximab
    > IL-5: mepolizumab
    > IL-13:
  • Interventional: bronchial thermoplasty, vagus nerve ablation
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31
Q

List the features of acute severe and life-threatening asthma

A

Severe asthma
> Peak expiratory flow: 33-50% of normal
> Can’t complete sentences in one breath
> Respiratory rate > 25 breaths per minute
> Pulse >110 bpm

Life-threatening
> PEFR <33% predicted
> SpO2 <92%
> Silent chest, cyanosis, feeble respiratory effort
> Arrhythmia or hypotension
> Exhaustion, altered consciousness
> ABG: severe hypoxia, lowered pH

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32
Q

Describe the management of an acute severe asthma attack

A

Oxygen to maintain SpO2 94-98%

Salbutamol 5mg or terbutaline 10mg via an oxygen-driven nebuliser

Prednisolone (oral) 40-50mg
> Or hydrocortisone IV 100mg if unable to take oral

If life-threatening features are present

> IV magnesium sulphate 1.2-2g infusion over 20 minutes

> Nebulised beta 2 agonist more frequently e.g. salbutamol 5mg up to every 15-30 minutes

> If patient is still not improving senior clinical may consider use of IV salbutamol or aminophylline or progression to mechanical ventilation

After discharge: treatment with oral prednisolone (40-50mg until recovery, minimum 5 days) & ICS

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33
Q

Describe extrinsic allergic alveolitis (EAA) and its triggers

A

aka hypersensitivity pneumonitis

Acute illness due to type III reaction - serum sickness or immune complex sickness

Subacute: days to weeks
> Type IV: T-cell mediated reaction

Triggers
> Each one has an antibody that can be measured in serum e.g. avian precipitans

  • Bird dander
  • Mushroom worker’s lung
  • Farmer’s lung: fungal spores (Micropolyspora faeni) - secondary to exposure to mouldy hay in stables
  • Aspergillus lung
  • Cheese workers or mollusc shell workers
  • Malt worker’s lung or humidifier lung
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34
Q

Describe the clinical presentation of EEA

A

4-6h after exposure

  • Wheeze
  • Cough
  • Fever
  • Chills
  • Headache
  • Myalgia
  • Malaise
  • Fatigue
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35
Q

Describe the pathophysiology of EEA

A

Immune complex disease: acute inflammation, neutrophils, consolidation

Impairment of lung function
> Thickening of septae, filling alveoli with fluid

> Passive movement of gas by diffusion is reduced: type 1 respiratory failure
> Measured by carbon monoxide gas transfer during full PFTs

> Airspace shadowing on CXR

> Biopsy shows a granuloma with giant cells

> CT scan: bilateral ground glass changes

Chronic exposure
> Pulmonary fibrosis: interstitial scarring from chronic tissue remodelling / repair pathways

> Emphysema: interstitial destruction from neutrophilic enzyme release

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36
Q

Describe the management of EEA

A
  • Allergy: avoid trigger
  • Inflammation
    > Corticosteroids
  • Oxygen supplementation
37
Q

Describe how interstitial lung disease presents on pulmonary function tests

A
  • Restrictive effects
    > Reduced RV & TLC

> Reduced FEV1 & FVC but normal or even increased FEV1/FVC ratio on spirometry

Gas exchange
> Decreased PaO2 and increased A-a O2 gradient: decreased DLCO and V/Q mismatch
> PaCO2 is normal: eucapnia maintained by increased VE until late

38
Q

Define and list the risk factors for idiopathic pulmonary fibrosis (IPF)

A

IPF is a form of chronic fibrosing interstitial lung disease of unknown aetiology; it is limited to the lung and worsens over time

Risk factors

> Smoking: current or ex-smokers 1.6x more likely

> Male sex

> Heartburn (acid reflux): treat with PPI

> Age: age of onset >50 years

> Genetics: 2-5% of IPF cases are familial

39
Q

List the signs and symptoms of IPF

A
  • Progressive dyspnoea: gradual onset
  • Fingernail clubbing (2/3)
  • Productive cough
  • Cyanosis
  • Crackles
    > Fine bilateral, bibasal
    > End-inspiratory crackles
  • Progression over months-years
40
Q

Describe the pathophysiology of IPF

A
  • Repeated cycles of injury and repair - an unidentified agent causes epithelial injury
    > Dysregulated repair process leads to fibrosis
  • Reduced compliance, lung capacity & gas exchange
  • Harder breathing is required to take up oxygen & oxygen levels fall with time
41
Q

List the investigations used in IPF

A
  • Spirometry: restrictive
  • CXR: reticular pattern
    > Tends to affect periphery & lower zones
    > Bibasal + posterior
    > Honeycomb change reflects true fibrotic process
  • Surgical lung biopsy
    > Usual interstitial pneumonia (UIP) is the histopathological appearance
    > Fibroblast foci & honeycomb cysts
  • High resolution lung CT
42
Q

What is the prognosis for IPF?

A

Gradual deterioration, median survival 3-5 years, 10 year survival <15%

Acute exacerbation
> Clear increase in symptoms over 30 days or less
> New X-ray changes in both lungs (absence of infection or other causes)
> High risk
» In-hospital mortality >50%
» 1 Year survival is 22%
» No difference between subtypes of ILD (IPF v non-IPF)

43
Q

Describe the treatment for IPF

A

Anti-fibrotic drugs
> Pirfenidone and nintadenib: slow deterioration of IPF

Oxygen
> Home and portable oxygen if in respiratory failure

Pulmonary rehabilitation
> Improvement in dyspnoea but must be continued to sustain benefits

Lung transplant
> <65 years

Immunosuppressive treatment is not beneficial

44
Q

Define and list the signs and symptoms of sarcoidosis

A

Sarcoidosis is a multi-system granulomatous disorder of unknown cause characterised by the classic triad of bilateral hilar lymphadenopathy, erythema nodosum (shin rash) and arthritis

Other signs
- fatigue
- fever
- weight loss
- dry cough
- dyspnoea
- chest discomfort
- sweats
- lungs involved in 90% of cases
- female > male, peak age 20-39 years

45
Q

Which investigations are used in sarcoidosis?

A

CXR
Bilateral hilar lymphadenopathy progresses to bilateral hilar lymphadenopathy + parenchymal changes and eventually pulmonary fibrosis

Bronchoscopy
> Cytology or biopsy to confirm diagnosis
> exclude lymphoma, TB or lung cancer

Bronchoalveolar lavage (BAL)
> Lymphocytic alveolitis

Transbronchial lung biopsy (TBLB)
> Non-necrotising granuloma

Transbronchial needle aspirate (TBNA)
> Needle aspirate of mediastinal lymph node
> Giant cells present in non-necrotising granuloma

Lung function
> Restrictive usually (but obstructive also possible)

Blood tests
> Hb mildly reduced
> ESR elevated
> Calcium is elevated (altered vitamin D metabolism)
> Increased gamma globulins
> ACE increased in 60%

46
Q

Describe the treatment of sarcoidosis, its prognosis and associated causes of death

A

Most cases need no treatment - steroids if declining lung function

Prognosis
> mainly good, >50% resolve by 3 years
> progressive fibrosis in 25%
> <5% die

Causes of death: fibrotic lung disease or complications of cardiac or neurological sarcoid

47
Q

Define COPD and list causes

A
  • Characterised by progressive airflow obstruction
  • Not fully reversible - does not change markedly over several months
  • Causes
    • Smoking
    • Burning biomass fuels (wood-burning stoves)
    • Coal mining
      Air pollution
48
Q

Explore the pathogenesis of COPD, focusing on the effects of cigarette smoking

A
  • Reduced cilial motility, airway inflammation, mucus hypertrophy and hypertrophy of goblet cells: increased sputum production leads to chronic cough
  • Increased protease activity, anti-proteases inhibited
  • Oxidative stress - increased free oxygen radicals (hydrogen peroxide)
  • Squamous metaplasia - higher risk of lung cancer
    > Also increases epithelial permeability, facilitating carcinogen diffusion from alveoli into bloodstream
    > Increases risk of other cancers e.g. bladder, oesophageal cancer & cardiovascular risk
49
Q

How do host genetics impact on the development of COPD?

A

Alpha 1 antitrypsin deficiency
> Serine proteinase inhibitor
> M alleles: normal variant

> SS and ZZ homozygotes: clinical disease
> Unable to counterbalance destructive enzymes in lung
> Non-smokers get emphysema, smokers get emphysema much earlier

50
Q

Describe emphysema and the different types

A

Emphysema is the destruction of lung parenchyma
> Abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles
> Patients may present with weight loss - too breathless to eat & make meals
» Leads to hypoxaemia and pulmonary hypertension in end-stage disease

Types
- Centri-acinar: damage around respiratory bronchioles, more in upper lobes

  • Pan-acinar: uniformly enlarged from the level of the terminal bronchioles distally; can get large bullae
  • Paraseptal: does not cause airflow obstruction, subpleural - individuals are prone to pneumothorax as bullae can rupture
51
Q

Describe the pathophysiology of chronic bronchitis

A

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

> Small airway disease
> Bronchiolitis in airways of 2-3mmm (early feature of COPD)
> Narrowing of bronchioles due to mucus plugging, inflammation and fibrosis

Infiltration of airways with neutrophils, CD4+ & CD8+ lymphocytes, macrophages
> Release inflammatory mediators
» TNF, IL-8
» Neutrophil elastase, proteinase 3, cathepsin G (from activated neutrophils)
> Elastase & MMPs (from macrophages)
> Reactive oxygen species

  • Squamous metaplasia
  • Mucus gland hyperplasia - mucus plugging
52
Q

Describe the mechanisms of airflow obstruction in COPD

A
  • Loss of elasticity and alveolar attachments due to emphysema

> Airway collapse on expiration
> Causes airtrapping & hyperinflation > increased work of breathing > breathlessness
> Dynamic hyperinflation: worsening with exercise due to shorter respiratory cycles

> Goblet cell metaplasia with mucus plugging of lumen

> Thickening of the bronchiolar wall: smooth muscle hypertrophy and peribronchial fibrosis

53
Q

Describe the investigations used in COPD

A

CXR
> Black lung fields due to decreased vascular markings
> Hyperinflation
> blackened hemidiaphragms
> Heart appears long & thin
> Increased number of anterior rib ends above diaphragm

Spirometry
> Obstructive pattern: FEV1/FVC ratio < 70% (both reduced)
> Flow volume loop shows classical church and steeple pattern: severe airflow obstruction

Stage 1: mild, 80% predicted FEV1
Stage 2: moderate, 50-79% predicted FEV1
Stage 3: severe, 30-49% predicted FEV1
Stage 4: very severe, <30% predicted FEV1

54
Q

Describe the management of COPD

A
  • Smoking cessation: only intervention which slows progression
  • Inhaled bronchodilators
    > Short-acting beta agonists: salbutamol (SABA)
    > Long-acting beta agonists: salmeterol (LABA)
    > Long-acting muscarinic antagonists: tiotropium (LAMA)
  • Inhaled corticosteroids
    > Budesonide and fluticasone - combination inhalers
  • Oxygen therapy (severe patients)
    > If respiratory failure at rest
  • Oral theophyllines
    > Controversial
  • Mucolytics - carbocysteine
    > Thin sputum
    > Ease cough
  • Nebulised therapy
    Usually reserved for exacerbations
55
Q

Describe the “blue bloater” COPD patient

A
  • Low respiratory drive
  • Type 2 respiratory failure: low oxygen, high CO2
  • Cyanosis
  • Warm peripheries
  • Bounding pulse
  • Flapping tremor
  • Confusion, drowsiness
    Right heart failure - oedema, raised JVP
56
Q

Describe the “pink puffer” COPD patient

A
  • High respiratory drive - pulmonary stretch receptors
  • Type 1 respiratory failure: low oxygen, low CO2
  • Desaturates on exercise
  • Pursed lip breathing
  • Use accessory muscles
  • Wheeze
  • Indrawing of intercostals
  • Tachypnoea
57
Q

Compare COPD & asthma

A

COPD
- Cells: CD8 T lyphocytes, macrophages, neutrophils
- Caused by noxious agent
- Progressive & irreversible

Asthma
- Cells: CD4 T lymphocytes, eosinophils
- Caused by a sensitising agent
- Completely reversible
- Spirometry: >400ml responsibility on spirometry following inhaler

58
Q

Describe the presentation, assessment and DDX of an acute exacerbation of COPD

A
  • Presentation
    • Increased dyspnoea
    • Worsening cough
    • Increasing sputum volume / purulence
  • Asessment / monitoring
    • CXR
    • ECG
    • FBC, U&Es, LFTs & CRP
    • Sputum miscroscopy & culture
    • Oxygen saturations
    • ABG
  • DDX
    • Pneumonia
    • Pneumothorax
    • PE
    • Left ventricular failure
      Lung cancer
59
Q

Describe the treatment of an acute exacerbation of COPD

A

Oxygen 28% via venturi mask at 4L/min or 1.2L/min via nasal cannula if SpO2 <88%

Corticosteroids
> Prednisolone oral 25g-40mg each morning for 5 days

○ If patient unable to take oral treatment
> Hydrocortisone IV 100mg immediately
> Then 50mg 6 hourly if need to continue

Bronchodilators
> Nebulisation should be with air
> Supplementary oxygen via nasal cannula during nebulisation
> 1-6L/min to maintain oxygen saturation 88-92%

Salbutamol 2.5-5mg nebules 4x daily

Ipratropium 0.5mg nebules 4x daily (add if poor response to salbutamol)

IV bronchodilators
> Aminophylline infusion may be considered if no response to nebulised therapy

Non-invasive mechanical ventilation (NIMV)
> If worsening repiratory acidosis or hypercapnia despite achieving target oxygen & adequate immediate therapy

Antibiotics
> Indicated in the presence of increased sputum purulence, raised inflammatory markers or focal radiological changes

Mucolytic therapy
Aid sputum clearance: acetylcysteine oral 600mg once daily

60
Q

If one mass is identified on CXR, what is the DDX?

A
  • Tumour
    > Malignant most likely: lung cancer, carcinoid / lymphoma

> Benign: pulmonary hamartoma

  • Infection
    > Abscess or TB
    » Fever, cough, spit, night sweats
  • Inflammation
    > Sarcoid or rheumatoid nodules
61
Q

If more than one mass is identified on CXR, what is the DDX?

A

Metastases - weight loss

Infection - fever, cough

62
Q

Describe the appearance of large abscesses on CXR

A

Cavity results in appearance of an air-fluid level as lung parenchyma has liquefied

63
Q

Describe the appearance of different stages of TB on CXR

A

Primary
- Asymptomatic
- Fever, cough, blood stained spit
- Non-specific infection appearance on CXR
- Right hilar nodes

Post primary
- Reactivation - years later, reduced immunity
- Cavities mainly in upper segments

Miliary
- Haematogenous spread
- Immune compromised
- Poor prognosis

Chronic changes
- Calcification of lungs and nodes
- Scarring of upper zones

64
Q

List the causes of consolidation and signs of consolidation on CXR

A

Consolidation consists of replacing air with a collection of substances
> Pus: pneumonia
> Fluid: pulmonary oedema
> Blood: haemorrhage
> Cells: tumour

Air bronchogram: hallmark of consolidation - appearance of solid background instead of air allows contrast & visualisation of airways

  • Silhouette sign: loss of normal structures & their silhouettes
  • Lingular consolidation: loss of left heart border
  • Right lower lobe collapse: loss of silhouette of right diaphragm
  • Right middle lobe: loss of right heart border
  • Left upper lobe: veil-like opacity, loss of left heart border
  • Left lower lobe: loss of left hemidiaphragm border, sail sign (triangular shape seen behind heart)
65
Q

Define a pneumothorax and describe its causes

A

A breach of the pleural space leads to free air in the pleural cavity and collapse of the elastic lung

Causes

  • Spontaneous

> Primary: no underlying lung disease; risk factors include male, smoker, tall - rupture of subpleural blebs/bullae

> Secondary: underlying disease, emphysema, asthma, pulmonary fibrosis

  • Iatrogenic: CT-guided lung biopsy, transbronchial lung biopsy, pleural aspirate
  • Traumatic: rib fracture, penetrating chest wall injury/stab wound
66
Q

Describe the signs and symptoms of pneumothorax

A
  • Symptoms
    • Pleuritic chest pain
    • Breathlessness
    • Respiratory distress
  • Signs
    • Hyperresonant percussion
    • Reduced breath sounds
    • Reduced vocal resonance
67
Q

Describe the diagnosis and treatment of a pneumothorax

A
  • Diagnosis
    CXR
    ○ Tracheal deviation + mediastinal shift to the opposite side
    ○ Depressed hemidiaphragm
  • Treatment
    Pneumothorax
    ○ Observation or aspiration or intercostal chest drain (with underwater seal)
    ○ Depends on size of pneumothorax, symptoms, presence of coexisting lung disease

Tension pneumothorax
○ Immediate needle decompression by inserting a large bore needle (venflon) into the 2nd intercostal space in the midclavicular line
○ Then needs formal intercostal chest drain inserted
○ Don’t wait for CXR to treat

68
Q

Describe the risks of a tension pneumothorax

A

One way valve: increased intrapleural pressure

○ Decreased venous return
○ Decreased cardiac output
○ Decreased blood pressure
○ Decreased oxygen saturation
○ PEA arrest without intervention

Pushes other structures: tracheal deviation, compression of great vessels & heart

69
Q

Which score determines the likelihood of a PE? Include its criteria and management steps

A
  • Wells score
  • Pre-test probability score

○ Criteria: haemoptysis, pulse rate, previous VT events

○ > 4 points: PE likely
» Perform CT pulmonary angiogram (CTPA)

□ CTPA positive: anticoagulate
	> Risk stratification
				
□ CTPA negative
			
> PE suspected: proximal leg vein ultrasound scan
				
> PE not suspected

○ < 4 points: PE unlikely
> Quantitative D dimer test
□ Positive: perform CTPA
□ Negative: unlikely PE

70
Q

Describe the risk stratification process for PE

A

High risk - haemodynamic instability
> Systolic BP < 90mmHg or drop >40mmHg for more than 15 mins in absence of other cause
> Cardiac arrest

Intermediate
> Intermediate-high: haemodynamically stable but PESI III-V, RV dysfunction and elevated troponin
> Intermediate-low: haemodynamically stable but PESI III-V, of RV dysfunction and elevated troponin one or none positive

Low: no risk factors

71
Q

Describe the treatment algorithm for a patient with suspected PE and haemodynamic instability

A

Assess RV with TTE

> No RV dysfunction: search for other causes of instability

> RV dysfunction: perform CTPA

> > Positive CTPA: treat high risk PE
> Haemodynamic support
> Reperfusion therapy

> > Negative CTPA: search for other causes of instability

72
Q

What haemodynamic support would be provided to a patient with PE?

A

Volume optimisation: 500ml saline bolus

Vasopressors and inotropes
Norepinephrine: increased RV inotropy and systemic BP
Dobutamine: increased RV inotropy

Mechanical circulatory support– ECMO: rapid short-term support combined with oxygenator

73
Q

Discuss the options for reperfusion therapy for PE patients

A
  • Systemic thrombolysis:
    > Agents: rtPA (alteplase, tenecteplase), streptokinase, urokinase

> Indication: high risk (massive) PE

  • Catheter-directed thrombolysis
    > EKOS system, safer in terms of bleeds, lower doses used & allows for direct clot retrieval; however, not readily available and takes time to set up
  • Surgical embolectomy: rarely performed, high risk
74
Q

Describe the management of an intermediate and low risk PE

A

Intermediate risk
- RV dyfunction
- PESI class III-V
- Cardiac troponin
> Elevated: intermediate-high

> > No clear strategy
Monitor closely
Rescue reperfusion is available
Routine use of thrombolysis is not recommended

> Normal: intermediate-low
> Hospitalisation
> Anticoagulation
>Observation to ensure stabilisation
>Routine use of thrombolysis is not recommended

Low risk
> Routine use of thrombolysis is not recommended

75
Q

Describe the severity score used in pulmonary embolism

A

PESI score - Pulmonary Embolism Severity Index

> Risk factors for mortality risk
> Age
> Cardiorespiratory disease
> Cancer
> Pulse rate
> Blood pressure
> Oxygen saturation

76
Q

List complications following a PE

A
  • RV dysfunction
  • Right ventricle cannot cope with increased afterload
  • Post-thrombotic syndrome

Chronic Thromboembolic Pulmonary Hypertension (CTEPH)

77
Q

How is residual lung volume measured?

A
  • Unable to measure residual volume in spirometry
  • 2 methods
  • Helium dilution - inspire known quantity of inert gas
  • Body plethysmography
    ○ Respiratory manoeuvres in a sealed box leads to changes in air pressure
    ○ Can derive lung volumes
    ○ Archimedes principles
  • Lung volumes reduced in restrictive lung diseases
  • Increased RV and RV/TLC in obstructive lung disease
78
Q

List the causes of type 1 and type 2 respiratory failure

A
  • Type 1: low oxygen, normal/low PaCO2
    • Aim SpO2 94 - 98%
    • Causes
      ○ Pneumonia
      ○ Pulmonary embolism
      ○ Pulmonary oedema
      ○ Pulmonary fibrosis
  • Type 2: low oxygen, high PaCO2
  • Aim SpO2 88 - 92%
  • Causes
    > COPD
    > Neuromuscular disease / severe kyphoscoliosis
    > Obesity hypoventilation
    > Opiate overdose
79
Q

Describe the formula used to calculate an anion gap and its interpretation

A
  • Calculate for metabolic acidosis differential diagnosis
  • Anion gap = [Na+] - ([Cl-] + [HCO3-])
  • Normal anion gap 8 - 16 mmol/L
  • Acidaemia = high [H+] or low HCO3
  • Raised anion gap: making too much H+ or can’t get rid of it
    • Renal failure
    • Diabetic or other ketoacidosis
    • Lactic acidosis
    • Toxins e.g. salicylate
  • Normal anion gap: losing too much HCO3
    • Renal tubular acidosis
    • Diarrhoea
    • Carbonic anhydrase inhibitors
      Ureteric diversion
80
Q

Define obstructive sleep apnoea

A
  • Recurrent episodes of partial or complete upper (pharyngeal) airway obstruction during sleep, intermittent hypoxia & sleep fragmentation
  • Obstructive sleep apnea syndrome (OSAS) manifests as excessive daytime sleepiness
81
Q

Describe the mechanisms behind OSAS

A

Often patients are obese with large neck circumference
- During periods of low muscle tone such as sleep, there is pharyngeal narrowing resulting in negative thoracic pressure

  • This results in arousal during sleep, including waking & sleep fragmentation
  • If untreated, this leads to

> Blood pressure surge (increased sympathetic activity)
> Increased endothelial damage predisposes patients to cardiovascular & cerebrovascular disease

> > > Heart attacks
Strokes
Right heart strain
Cardiovascular disease

  • Sleep disruption
    ○ Daytime sleepiness
    ○ Reduced quality of life
    ○ Road traffic accidents
82
Q

List risk factors and symptoms of OSAS

A

Risk factors
- Male sex
- Age >40
- Obesity
- Often overlaps with COPD

Symptoms
- Snoring
- Witnessed apnoeas
- Disruptive sleep - nocturia / choking / dry mouth / sweating
- Unrefreshed sleep
- Daytime somnolence
- Fatigue
- Low mood
- Poor concentration

83
Q

Describe the assessment of daytime sleepiness in OSAS

A

Epworth Sleepiness Score
> 0-5 lower normal daytime sleepiness
> 6-10 normal daytime sleepiness
> 11-12 mild excessive daytime symptoms
> 13-15 moderate excessive daytime symptoms
> 16-24 severe excessive daytime symptoms

STOP-BANG questionnaire

Berlin questionnaire

84
Q

Describe the investigations used in OSAS

A

Limited polysomnography - limited sleep study
> 5 channel home study
> Oxygen saturations
> Heart rate
> Flow
> Thoracic and abdominal effort (via 2 bands)
> Position

In-patient full polysomnography
> EEG: sleep staging
> Video + audio
> Thoracic & abdominal bands
> Position
> Flow
> Oxygen saturations
> Limb leads
> Snore

Transcutaneous Oxygen Saturations and Carbon dioxide Assessment (TOSCA)
> Home or inpatient
> Indicated for headaches: possibility of CO2 retention overnight

85
Q

Describe apnoea, hypopnoea, respiratory effort-related arousals and oxygen desaturation (ODI)

A
  • Apnoea
    • Cessation (or near cessation) of airflow
    • 4% oxygen desaturation lasting >10 secs
  • Hypopnoea
    Reduction of airflow to a degree insufficient to meet criteria for apnoea
  • Respiratory effort-related arousals
    Arousals associated with a change in airflow that does not meet the criteria for apnoea or hypopnoea
  • Oxygen desaturation (ODI)
    The number of times per hour of sleep that the SpO2 falls >4% from baseline
86
Q

Describe the Apnoea-Hypopnoea Index (AHI)

A
  • Calculated by adding the number of apnoeas and hypopnoeas and dividing by the total sleep time (in hours)
  • AHI >15 is diagnostic of OSA
    • OR AHI 5-15 with compatible symptoms
  • AHI <5 : normal
  • AHI 5-15 : mild
  • AHI 16-30 : moderate
    AHI >30 : severe
87
Q

Describe the Apnoea-Hypopnoea Index (AHI)

A
  • Calculated by adding the number of apnoeas and hypopnoeas and dividing by the total sleep time (in hours)
  • AHI >15 is diagnostic of OSA
    • OR AHI 5-15 with compatible symptoms
  • AHI <5 : normal
  • AHI 5-15 : mild
  • AHI 16-30 : moderate
    AHI >30 : severe
88
Q

Describe the treatment of OSAS

A
  • Treat the symptomatic OSAS - daytime sleepiness
  • AIM: improve daytime somnolence and quality of life
  • Explain OSAS
  • Weight loss
  • Avoid triggering factors - alcohol
  • Treat underlying conditions
    • Tonsils
    • Hypothyroidism
    • Nasal obstruction
  • Continuous positive airway pressure (CPAP)
    • Splints airway open
    • Stops snoring
    • Stops sleep fragmentation
    • Improves daytime sleepiness + QOL
      > Not necessary if no daytime sleepiness
  • Mandibular advancement device (MAD)
    • Mild-moderate OSAS unable to tolerate CPAP
    • Needs good dentition
  • Maxillary-mandibular surgery
    • Problematic patients
    • Severe retrognathia/micrognathia
  • Sleep position trainers
    • Supine OSA
    • Device vibrates when patient lies on back
    • Weeks to change sleeping position
89
Q

Describe the issues OSAS patients may have with driving

A
  • OSAS (day time sleepiness) - likely impairment of driving, inform DVLA
    • Patient’s responsibility to inform the DVLA if diagnosed
  • OSA without DTS - do not need to stop driving or contact DVLA unless previous history of MVC
  • OSAS can hold a Cat I driving license if compliant with treatment and DTS improved
    • Assessed every 3 years

Cat 2 licence holders should be assessed within 4 weeks, annual monitoring by DVLA

Phase 3 (14 decks)

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