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1MBChB Revision > Respiratory > Flashcards

Respiratory Flashcards

1
Q

what is coryza

A

acute viral infection of the nasal passages; highly infectious due to rhinoviruses, coronaviruses and
adenoviruses. Spread via droplets, facilitated by overcrowding and poor ventilation.

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2
Q

symptoms of coryza

A 
watery nasal discharge 
mild pyrexia
malaise
sneezing 
tiredness
sore nose and throat
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3
Q

complications of coryza

A

sinusitis
acute bronchitis
secondary infection
otitis media

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4
Q

treatments of coryza

A

bed rest
fluids
isolation
herbal extracts

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5
Q

what is sinusitis

A

bacterial/fungal infection of paranasal sinuses, usually preceded by coryza. Can occur with asthma.

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6
Q

symptoms of sinusitis

A

frontal headache, facial pain
purulent rhinorrhoea
fever

can be split into:
Acute: 1 week – 1 month
Subacute: 1-3 months
Chronic: >3 months

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7
Q

investigations for sinusitis

A

CT of paranasal sinuses, MRI to demonstrate bony landmarks

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8
Q

treatment of sinusitis

A

Nasal decongestants (xylometazoline)

Broad-spectrum antibiotics (co-amoxiclav)

Topical corticosteroid
(fluticasone propionate nasal spray)

FESS for ventilation and drainage

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9
Q

what is rhinitis

A

Sneezing attacks, nasal blockage/discharge occurring >1hr on most days.

can be split into seasonal and perennial

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10
Q

what is seasonal rhinitis

A

Limited period of the year; “hay-fever” but not restricted to grass pollen.
Intermittent rhinitis

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11
Q

symptoms of seasonal rhinits

A

Nasal irritation, rhinorrhoea, sneezing
Itchy eyes and ears
Irritated soft palate
Wheeze

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12
Q

what is perennial rhinitis

A

Throughout the whole year
Split into:

Allergic: caused by faeces of dust mites; cats; industrial dust and fumes.

Non-allergic: no identifiable stimulus, but eosinophilic granulocytes are present in secretions.

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13
Q

symptoms of perennial rhinitis

A

Nasal blockage, rhinorrhoea

Loss of smell and taste

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14
Q

treatment of general rhinits

A

Antihistamines (loratidine, cetirizine)

Topical corticosteroids (beclometasone,
fluticasone propionate)

CysLT antagonist (montelukast)

Anti-inflammatory (sodium
cromoglicate)

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15
Q

what is pharyngitis

A

Endemic adenovirus infection, causing reddened oropharynx and soft palate and inflamed tonsils.

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16
Q

symptoms of pharyngitis

A

Sore throat
Tonsillar lymph nodes enlargement
Localised endemics of fever and
conjunctivitis

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17
Q

treatment of pharyngitis

A

phenoxymethylpenicillin or cefaclor if severe

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18
Q

what is acute laryngotracheobronchitis

A

Occasional complication of URTIs, particularly those caused by parainfluenza viruses and measles.
Most severe in children < 3yrs. Inflammatory oedema usually present which can spread to vocal cords.

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19
Q

symptoms of acute laryngotracheobronchitis

A 
Hoarseness
Barking cough (croup)
Stridor
Progressive airway obstruction
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20
Q

treatment of acute laryngotracheobronchitis

A

Nebulised adrenaline

Oral/IM corticosteroids (dexamethasone)

Oxygen and adequate fluids

Tracheostomy (rare!)

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21
Q

what is acute epiglottitis

A

Life-threatening airway obstruction in children aged 2-7yrs caused by H. influenzae.

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22
Q

symptoms of acute epiglottits

A

severe airflow obstruction

high fever

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23
Q

complications of acute epiglottitis

A 
mostly of H. influenzae
meningitis
diptheria
osteomyelitis
septic arthritis
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24
Q

treatment of acute epiglottitis

A

Urgent endotracheal intubation

IV antibiotics (ceftazidime, ceftriaxone)

Prevention vaccine given to infants
Do NOT inspect epiglottis until airway is
patent

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25
Q

what is influenza

A

Influenza A (pandemics) and Influenza B (localised outbreaks) incubate within 3 days. Not a cold!

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26
Q

symptoms of influenza

A

Abrupt fever
Shivering and aching
Severe headache
Sore throat + dry cough

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27
Q

complications of influenza

A

Secondary bacterial infection/pneumonia

Encephalomyelitis (rare)

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28
Q

investigations for influenza

A

Increase in complement-fixing antibody (hemagglutinin) between onset and after 1-2 weeks

Nasal/throat secretion analysis

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29
Q

treatment of influenza

A

Bed rest, fluids

Paracetamol

Neuraminidase inhibitors within 48hrs
(zanamivir, oseltamivir)

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30
Q

what is acute bronchitis

A

acute infection of bronchi causing them to become inflamed

Usually arises from Strep. pneumoniae/H. influenzae infections, or in people with COPD.

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31
Q

symtptoms of acute bronchitis

A

Irritating dry cough; becomes productive
Wheeze
Breathlessness
Mild fever

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32
Q

treatment of acute bronchitis

A

NO antibiotics unless there is underlying chronic lung disease (amoxicillin)

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33
Q

what is pneumonia

A

Acute infection of the lungs causing inflammation. Community, Hospital and Immunocompromised
-acquired pneumonia. Main causes: Strep. pneumoniae, H. influenzae, Staph. aureus, Influenza A.
Atypical causes: Mycoplasma, Legionella, Chlamydophila pneumoniae/psittaci, coxiella burnetti.
HAP only diagnosed after 48hrs in hospital

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34
Q

symptoms of pneumonia

A 
Fever and rigors
Pleuritic chest pain
Anorexia
Breathlessness
Cough – dry or productive
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35
Q

investigations for pneumonia

A

CXR consolidation, effusions,
collapse

FBC + U&Es, CRP

Sputum culture to detect organisms

CURB65 for CAP

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36
Q

treatment of pneumonia

A

CAP (see Antibiotic Man)
Mild/Moderate: (7 days) PO amoxycillin
If penicillin allergy PO doxycycline; if IV required IV clarithromycin

Severe: (10 days) IV co-amoxiclav + IV clarithromycin/PO doxycycline
If penicillin allergy IV levofloxacin

HAP
Severe: (7-10days) amoxicillin + metronidazole + gentamicin

Non-severe: (7 days) amoxicillin + metronidazole

Specific
Staph. aureus flucloxacillin/vancomycin if MRSA

Klebsiella cefotaxime

Pseudomonas ceftazidime/ciprofloxacin + aminoglycide

Mycoplasma clarithromycin/ciprofloxacin

Legionella levofloxacin/moxifloxacin/consider rifampicin

Chlamydophila doxycycline/clarithromycin

Pneumocystis jiroveci co-trimoxazole

Fungal amphoterecin

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37
Q

what is COPD

A

encompasses 2 main clinical syndromes: chronic bronchitis and emphysema
characterised by airflow obstruction that is most reversible with bronchodilators

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38
Q

symptoms of COPD

A

productive cough
wheeze
breathlessness
infective exacerbations

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39
Q

complications of COPD

A

Hypertension
Osteoporosis
Weight loss
Cor pulmonale

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40
Q

investigations for COPD

A

Smoking history/chronic history of
symptoms

Family history (α1-antitrypsin
deficiency)

Lung function tests (↓FEV1/↓FVC,
↓PEFR)

CXR classically normal

ABGs de-saturate over time

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41
Q

treatment of COPD

A

Smoking cessation and lifestyle advice

SABA (salbutamol) mild COPD,
LABA (salmeterol) mod-sev COPD

SAMA (ipratropium) or
LAMA (tiotropium)

Inh. corticosteroid (beclometasone),
PO corticosteroid if severe
(prednisolone)

Seretide (salmeterol + beclometasone)

Xanthine (theophylline)

Anti-mucolytic (carbocysteine)

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42
Q

treatment of an acute exacerbation of COPD

A 
ISOAP 
ipratropium (neb)
salbutamol (neb)
oxygen (24%)
amocillin/doxyclycine is purulent sputum
prednisolone (PO)
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43
Q

what is asthma

A

chronic inflammatory condition where reversible obstruction of the airways occurs.
airflow limitation -> airway hyerresonsivemess -> bronchial inflammation

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44
Q

investigations for asthma

A

Allergen skin prick test

Lung function tests (↓PEFR: mod<80%,
severe<50%, life-threatening<30%)

Bronchial challenge testing (histamine,
methacholine)

CO transfer (normal in asthma)

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45
Q

treatment for asthma

A

SABA (salbutamol)

LABA (salmeterol)
\+ inhaled corticosteroid (beclometasone)
\+ sodium cromoglicate
\+ CysLT antagonist (montelukast)
\+ oral corticosteroid (prednisolone)
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46
Q

treatment of acute asthma

A 
O SHIT MAn 
oxygen 
salbutamol (neb)
hydrocortisone (IV)
ipratropium (neb)
magnesium sulpahte (IV)
prednisolone (PO)
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47
Q

characteristics of acute severe asthma

A

Unable to complete sentences
Respiratory rate >25 per minute
Pulse rate >110 beats per min
PEFR <50 % predicted

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48
Q

characteristics of life threatening asthma

A

PEFR <33% predicted
Bradycardia, hypotension, silent chest
Exhaustion, confusion, coma
ABG PaCO2 >5, PaO2 <8 or acidosis

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49
Q

what is OSA

A

airway becomes closed during sleep; muscles hypotonic during sleep and thus do not open airway. partial occlusion = snoring and complete occlusion = apnoea (cessation of breathing)

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50
Q

symptoms of OSA

A 
Loud snoring
Daytime sleepiness
Unrefreshed/restless sleep
Headache
Large neck and tongue
Small mandible
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51
Q

aetiology of OSA

A

Obesity
Narrow pharyngeal opening
Co-existent COPD
Respiratory depre

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52
Q

investigations of OSA

A

Epworth Sleepiness Scale
Overnight pulse oximetry
Diagnose if >10-15 apnoeas in any 1hr of
sleep

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53
Q

treatment of OSA

A

Nasal Continuous Positive Airway Pressure (via mask during sleep)

CNS stimulant (modafinil

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54
Q

what is bronchiectasis

A

Abnormal permanent dilatation of airways, resulting inflammation and thickening of walls.
Mucociliary transport mechanism is impaired and thus recurrent bacterial infections ensue.
Cystic fibrosis = most common cause.

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55
Q

symptoms of bronhiectasis

A 
Productive cough (yellow-green sputum,
can become haemoptysis)
Halitosis (bad breath)
Recurrent febrile episodes, malaise
Clubbing
Coarse crackles, pneumonic episodes
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56
Q

complications of bronchiectasis

A

Pneumonia, pneumothorax
Empyema
Metastatic cerebral abscesses
Life-threatening haemoptysis

57
Q

investigations of bronchiectasis

A

CXR dilated + thickened bronchi
CT thickened bronchi, cysts
Sputum S. aureus, Pseudomonas, HiB
IgA deficiency

58
Q

treatment of bronchiectasis

A

Postural drainage!

Antibiotics (mild: cefaclor/ciprofloxacin,
flucloxacillin if S. aureus;
persistent: ceftazidime)

Bronchodilators + anti-inflammatory
agents

59
Q

what are lung abscesses

A

Localised suppuration assoc. with cavity formation on CXR/CT

60
Q

aetiology of lung abscess

A

aspiration, TB, Stap/Klebs pneumonia, septic emboli, foreign body inhalation

61
Q

symptoms of lung abscess

A

persisting pneumonia, foul sputum, malaise, weight loss, raised inf. markers

62
Q

treatment of lung abscess

A

guided by culture results, surgical drainage

63
Q

what is cystic fibrosis

A

autosomal recessive disorder in which there is a defect in the CFTR gene, a critical chloride channel.
Failed opening of Cl channel -> ↑cAMP, resulting in ↓Cl and ↑Na -> ↑viscosity of airway secretions.

64
Q

symptoms of CF

A 
Recurrent infections
Sinusitis, nasal polyps
Breathlessness
Haemoptysis
Steatorrhoea
Meconium ileus (SI obstruction)
Malabsorption
Abnormal teenage milestones
65
Q

investigations in CF

A 
Family history 
Gene testing (sweat test)
66
Q

treatment of CF

A

Lifestyle (smoking, vaccines)

Antibiotics (as per bronchiectasis)

SABAs, ICS for symptoms

Inh recombinant DNAse (dornase)

67
Q

what is tuberculosis

A

Airborne infection spread by droplets by Mycobacterium species. Affects 1/3 of population.
Caseating granulomatous inflammation (necrotic centre; surrounded by epitheloid cells and Langhan’s
giant cells; formation of Ghon focus/complex). Primary=first infection. Latent=asymptomatic, smear –
ve

68
Q

symptoms of TB

A

Persistent productive cough (>3weeks) +
occasional haemoptysis
Weight loss, night sweats, fever, fatigue
Hoarseness, pleuritic pain

69
Q

investigations for TB

A

CXR consolidation +/- cavitation, fibrosis, calcification, pleural effusion, widening of
mediastinum

Latent: tuberculin skin test/Mantoux test (possible false –ve if previous BCG). If +ve do IFʎ test

Active: obtain tissue/fluid (induced sputum, bronchoalveolar lavage if unproductive cough,
aspiration of pleural fluid/biopsy, pus, ascites, urine, bone marrow, CSF)

Culture > PCR > ZN stain (but culture takes weeks, PCR is rapid so it is 1st line)

70
Q

treatment of TB

A

2 months RIPE, 4 months RI

Rifampicin SE discolouration of
urine/tears, hepatitis, flu-like illness

Isoniazide SE neuropathy,
agranulocytosis, allergic reaction

Pyrazinamide SE hepatic toxicity (rare),
reduced renal excretion of urate, gout

Ethambutol SE colour blindness
developing into blindness

71
Q

what is sarcoidosis

A

Multisystem non-caseating granulomatous Type IV hypersensitivity disorder of unknown aetiology

72
Q

symptoms of sarcoidosis

A

Erythema nodosum
Fatigue, weight loss
Uveitis
Peripheral lymphadenopathy

73
Q

investigations for sarcoidosis

A

CXR multiple abnormalities, BHL
Restrictive lung pattern
Hypercalcaemia, raised ACE level
Transbronchial biopsy

74
Q

treatment for sarcoidosis

A

corticosteroids (PO prednisolone)

75
Q

what is wegners granulomatosis

A

Granulomatous disease predominantly affecting small arteries. Lesions in URT, lungs, kidney

76
Q

symptoms of wegners granulomatosis

A

Severe rhinorrhoea ->nasal mucosa ulcer
Cough, haemoptysis, pleuritic pain
Occasionally involves skin and nervous
system.

77
Q

investigations of wegners granulomatosis

A

CXR nodular masses/pneumonia infiltrates with cavitation

Renal biopsy reveals necrotising microvascular glomerulonephritis

78
Q

treatment of wegners granulomatosis

A

esponds well to cyclophosphamide or rituximab

79
Q

what is churg-strauss syndrome

A

Eosinophilic infiltration with high blood eosinophil count, vasculitis of small arteries and veins.
Predominately affects 40 year old males

80
Q

symptoms of churg-strauss syndrome

A 
Rhinitis and asthma, breathlessness
Systemic vasculitis (fever, sweats, fatigue,
weight loss, rash)
Cough
Difficulty passing urine
Cold peripheries
81
Q

investigations for churg-strauss syndrome

A

CXR pneumonic shadows (bilateral)

ANCA +ve

82
Q

treatment of churg-strauss syndrome

A

responds well to corticosteroids

83
Q

what is systemic lupus erythematosis

A

Chronic type III hypersensitivity disease that causes inflammation in various parts of body

84
Q

symptoms of systemic lupus erythematosis

A 
Joint pain, fatigue
Skin rash
Pleurisy with or w/o effusion
Effusions (usually small/bilateral)
Basal pneumonitis (restricted chest
movement due to pleural pain)
85
Q

what is idiopathic pulomary fibrosis

A

Patchy scarring of lung with collagen deposition and honeycombing. Late onset. Commoner in males.

86
Q

symptoms of idiopathic pulomary fibrosis

A 
Progressive breathlessness
Dry cough
Cyanosis
Fine bilateral end-inspiratory crackles
Clubbing
Assoc. with autoimmune diseases
87
Q

investigations for idiopathic pulomary fibrosis

A 
CXR initially ground-glass ->
honeycomb
CT bilateral changes, thick-walled cysts
Restrictive lung pattern, ↓CO transfer
Anti-nuclear antibodies
88
Q

treatment of idiopathic pulomary fibrosis

A

Corticosteroids (oral prednisolone)

Anti-fibrotic (pirfenidone)

89
Q

what is extrinsic allergic alveolitis

A

Widespread diffuse inflammatory reaction in small airways and alveoli due to inhalation of foreign
antigens, usually from animals. Cigarette smokers actually have decreased risk. Type III
hypersensitivity

90
Q

symptoms of extrinsic allergic alveolitis

A

Fever, malaise
Cough, breathlessness, wheeze
Coarse end-inspiratory crackles
Weight loss and IPF features (chronic)

91
Q

investigations for extrinsic allergic alveolitis

A

CXR fluffy upper zone nodular shadows
CT ground glass opacity
Restrictive lung pattern, ↓CO transfer
Raised leucocytes + T cells

92
Q

treatment of extrinsic allergic alveolitis

A

Prevent exposure

Oral prednisolone in early stages

93
Q

what is coal workers pneumoconiosis

A

Dust particles typically 2-5 micrometres in diameter are retained in small airways and alveoli

split into
simple pneumoconosis
progressive massive pneumoconiosis

94
Q

what is simple pneumoconiosis and symptoms

A

More common form; refers to deposition of coal dust in lung.

Symptoms usually COPD-related. CXR fine micro-nodular shadowing.

95
Q

what is progressive massive pneumoconiosis

A

Round fibrotic masses several cm in diameter develop in upper lobes -> apical destruction of lung.
Necrotic central cavities.

96
Q

symptoms of coal workers pneumoconiosis

A

Considerable effort dyspnoea

Cough + black sputum

97
Q

investigations for coal workers pneumoconiosis

A

Rheumatoid factor and ANAs +ve; restrictive/obstructive pattern, ↓lung volume, ↓CO transfer

98
Q

what is asbestosis

A

Fibrosis causes by asbestos dust exposure

99
Q

symptoms of asbestosis

A

Progressive breathlessness, clubbing

Bilateral basal end-inspiratory crackles

100
Q

treatment of asbestosis

A

No treatment alters progression, but corticosteroids can help symptoms

101
Q

what is pneumothorax

A

Air in the pleural space. May be spontaneous (tall, thin males) or the result of trauma to the chest

102
Q

symptoms of pneuothorax

A 
Sudden onset pleuritic pain
Increasing breathlessness
Pallor, tachycardia
Mediastinal shift (tension
pneumothorax)
103
Q

treatment of pneumothorax

A

Needle aspiration (2nd IC space, midclavicular line)

Chest drain if recurs using large bore

104
Q

what is empyema

A

Pus in the pleural space. Usually complication of pneumonia. Exudate of pH< 7.2 very suggestive.

105
Q

symptoms of empyema

A

Ongoing fever

Persistent pneumonic symptoms

106
Q

treatment of empyema

A

surgical drainage

107
Q

what are pleural effusions

A

Excessive fluid in the pleural space.

can be split into
Transudate
protein < 30g/l LDH < 200
Heart failure, nephrotic syndrome, pericarditis

Exudate
protein > 30g/l LDH > 200
Pneumonia, cancer, TB, autoimmunity, MI, pancreatitis

108
Q

symptoms of pleural effusion

A

breathlessness, sometimes chest pain but rarely

109
Q

investigations of pleural effusion

A

Clinically detect when >500ml present

CXR detects when >300ml present, obliterated costophrenic angle, raised hemidiaphragm

Lights’ criteria (differentiates between transudate and exudate between 25-35g/l

110
Q

treatment of pleural effusions

A

treat underlying cause but drain if empyema (purulent fluid).

Thoracocentesis 5th intercostal space, mid-axillary line

111
Q

what is respiratory failure

A

Occurs when gas exchange is inadequate, resulting in hypoxia. It is defined as PaO2 <8kPa, subdivided
according to PaCO2 level

112
Q

what is type I respiratory failure

A

hypoxia (PaO2 < 8kPa) with normal or low PaCO2

113
Q

aetiology of type I respiratory failure

A

o Pneumonia
Pulmonary oedema
PE, fibrosing alveolitis
Asthma, emphysema, ARDS

114
Q

treatment of type I respiratory failure

A

Treat underlying cause

Oxygen (15L) non-rebreather (hypoxia)

Assisted ventilation if PaO2 < 8kPa
despite 60% O2

115
Q

what is type II respiratory failure

A

hypoxia (PaO2 < 8kPa) + hypercapnia (PaCO2 > 6.0 kPa)

116
Q

aetiology of type II respiratory failure

A

Pulmonary disease (asthma, COPD, pneumonia, fibrosis, obstructive sleep apnoea)

Reduced respiratory drive (sedation drugs, CNS tumour/trauma)

Neuromuscular disease (cervical cord lesion, diaphragmatic paralysis, poliomyelitis, MG,
Guillain-Barre Syndrome)

Thoracic wall disease (flail chest, kyphoscoliosis)

117
Q

treatment of type II respiratory failure

A

Oxygen (24%), recheck ABGs after 20min

If PaCO2 is steady/lower, increase O2 concentration to 28%

If PaCO2 rises > 1.5kPa and patient is still hypoxic, consider a respiratory stimulant (doxapram)
or assisted ventilation (NIPPV)

118
Q

what is ARDS

A

Respiratory distress due to stiff lungs (reduce pulmonary compliance) and gas exchange impairment.
Lung injury, severe sepsis and pneumonia result in fibrous exudate lining alveolar walls, impairing gas
exchange and destroying alveoli.

119
Q

symptoms of ARDS

A

Breathlessness
Tachypnoea
Increasing hypoxaemia, central cyanosis
Fine bilateral crackles

120
Q

treatment of ARDS

A

Treat underlying condition (sepsis,
pneumonia), position patient prone

Diuretics

Inhaled nitric oxide (vasodilator
improves V/Q)

Aerosolized surfactant

PEEP

Inspired oxygen

121
Q

what is pulmonary hypertension/cor pulmonare

A

Defined as mean pulmonary artery pressure of ≥25mmHg at rest.
Cor pulmonale = right heart failure due to pulmonary hypertension. Can occur in advanced COPD:
alveolar collapse (emphysema) results in hypoxia which causes vasoconstriction, increasing pressure in
the right side of the heart.

122
Q

symptoms of pulmonary hypertension/cor pulmonare

A 
Progressive breathlessness
Ankle oedema
Parasternal heave, tricuspid regurgitation
Pulmonary hypertension
RV hypertrophy
Elevated JVP, ascites
123
Q

investigations of pulmonary hypertension/cor pulmonare

A

CXR enlargement of pul. arteries,
atrial/ventricular enlargement

ECG pattern of RVH

124
Q

treatment of pulmonary hypertension/cor pulmonare

A 
Encourage exercise, avoid overexertion
Oxygen (2l) during plane travel
Vaccination for influenza +
pneumococcal pneumonia
Oral anticoagulants
Diuretics
125
Q

what is PE

A

Thrombus, usually from systemic veins, lodges in pulmonary arteries.
Virchow’s triad: endothelial damage, abnormal blood flow or hypercoagulable blood -> clot formation.

126
Q

symptoms of PE

A

Sudden breathlessness
Sudden chest pain + haemoptysis
Tachypnoea
Fever, pleural rub, raised JVP

127
Q

investigations of PE

A

CXR usually normal, possible blunting of costophrenic angle

D-dimer – if undetected, exclude diagnosis of PE

V/Q scan shows underperfused areas

Geneva score to predict PE likelihood

128
Q

treatment of PE

A

Oxygen (60-100%) unless chronic lung disease

Anticoagulant (IM LMWH, IV heparin + warfarin)

IV fluids in massive embolus

Fibrinolytic (streptokinase

129
Q

what is pulmonary oedema

A

accumulation of fluid in the pleural space

130
Q

symptoms of pulmonary oedema

A

Breathlessness, orthopnoea
Cough + haemoptysis
Leg/abdominal swelling
Pale skin

131
Q

treatment of pulmonary oedema

A

oxygen

diureticss

132
Q

symptoms of lung cancer

A

Cough (3 week cough merits a CXR)

Breathlessness(central tumours occlude large airways)

Haemoptysis (tumour bleeding into airway)

Chest pain (peripheral tumour invade the chest wall/pleuritic pain

Wheeze (monophonic when due to partial obstruction of airway by tumour)

Hoarseness (compression of the recurrent laryngeal nerve)

Dysphagia (invasion of phrenic nerve/oesophagus)

133
Q

describe small cell carcinoma

A

Arise from APUD cells; secrete ACTH
Often centrally located
Rapid metastasis

134
Q

describe adenocarcinoma

A

Common in non-smokers; smoking can cause it
Arises from mucus-secreting glandular cells
Metastasises widely

135
Q

describe squamous cell caricinoma

A

Most common. Arise from epithelial cells
Occasionally cavitates; central necrosis
Local, slow metastasis. Hypercalcaemia, PTH

136
Q

describe large cell carcinoma

A

Poorly differentiated

Metastasises early on

137
Q

investigations for lung cancer

A

CXR may be initially normal due to small lesion/confined to central structures
Common presentations: mass lesions, pleural effusion (large, unilateral), mediastinal widening or
hilar adenopathy, slow resolving consolidation, collapse, reticular shadowing

CT indicates extent of disease. Includes liver, adrenal glands. TNM staging can be done

PET characterises extent of mediastinal nodal involvement or distant metastases (2nd line to CT)
PET + CT for best correlation

Assess fitness for surgery

138
Q

treatment of lung cancer

A

Surgery: early stage NSCLC surgery can be curative
If Stage III, treat with chemotherapy to downstage then surgical resection
Contraindicated if:
- Tumour is near hilum
- Evidence of metastasis
- FEV1 > 1.5 L
- Vocal cord paralysis

Radical radiotherapy: for patients with early stage NSCLC but adequate lung function, this is
ideal if surgery is not possible due to co-morbidities

Chemotherapy: effective against SCLC only

1MBChB Revision (12 decks)

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