1
Q
normal values of FEV1, FVC and FEV1/FVC?
A
FEV1 - <80% abnormal
FVC <80 abnormal
FEV1/FVC <0.7 = airway obstruction and normal FEV1/FVC but low FVC = airway restriction
2
Q
type 1 and type 2 respiratory failure?
A
type 1; hypoxia and normal or low co2 -> typically caused by PE
type 2; hypoxia and hypercapnia
3
Q
signs of hypercapnoea?
A
- Bounding pulse
- Flapping tremor
- Confusion
- Drowsiness
- Reduced consciousness
4
Q
obstructive lung disease?
A
- FEV1/FVC below 0.7
- FEV1 lower than FVC
- ASTHMA and COPD
5
Q
restrictive lung disease?
A
• FEV1/FVC above 0.7 • FVC & FEV1 below 80% predicted value • Due to restriction, lung volumes are small and most of breath is out in first second • Interstitial lung disease: - FIBROSING ALVEOLITIS - SARCOID
6
Q
transfer co-efficent?
A
• Measure of ability of oxygen to diffuse across the alveolar membrane
• Can calculate by inspiring a small amount of carbon monoxide (not too
much since can kill) then hold breath for 10 seconds at total lung
capacity (TLC) then the gas transferred is measured
low in; COPD and anaemia
high in; pulmonary haemorrhage
7
Q
COPD
A
• A disease state characterised by airflow limitation that is not fully reversible
• The airflow limitation is usually both progressive and associated with an abnormal
inflammatory response of the lungs to noxious particles or gases
8
Q
epidemiology of COPD?
A
- middle age
9
Q
aetiology of COPD?
A
- CIGARETTE SMOKING is the MAJOR cause of COPD and is related to the
daily average of cigarettes smoked and years spent smoking - Chronic exposure to:
• Pollutants at work (mining, building and chemical industries)
• Outdoor air pollution
• Inhalation of smoke from biomass fuels used in heating and cooking in
poorly ventilated areas
• These factors also play a role, particularly in developing countries - Alpha-1 antitrypsin deficiency:
• Causes early onset COPD (due to proteolytic lung damage)
• A rare cause of cirrhosis (due to accumulation of the abnormal protein
in the liver)
• Mutations in the alpha-1 antitrypsin gene on chromosome 14 lead to
reduced hepatic production of alpha-1 antitrypsin which normally
inhibits the proteolytic enzyme - neutrophil elastase
10
Q
pathophysiology of COPD?
A
- There is increased numbers of mucus-secreting goblet cells in COPD within
the bronchial mucosa, especially in the larger bronchi - In more advanced cases the bronchi become overtly inflamed and pus is seen
in the lumen - causes chronic bronchitis and emphysema
- The combination of emphysema (loss of elastic recoil of the lung with collapse
of small airways during expiration) and chronic bronchitis (airway narrowing)
results in severe airflow limitation - V/Q (ventilation perfusion) mismatch is partly due to damage and mucus
plugging of smaller airways from the chronic inflammation and partly due to
rapid closure of smaller airways in expiration owing to the loss of elastic
support - this mismatch leads to a fall in PaO2 and increased work or
respiration
11
Q
chronic bronchitis - COPD physiology
A
• There is airway narrowing and hence airflow
limitation as a result of hypertrophy and
hyperplasia of mucus secreting glands of
the bronchial tree, bronchial wall
inflammation and mucosal oedema
• Microscopically there is infiltration of the
walls of the bronchi and bronchioles with
acute and chronic inflammatory cells
• The epithelial layer may become ulcerated and, with time, squamous
epithelium replaces the columnar cells (squamous metaplasia) when
the ulcer heals
• The inflammation is followed by scarring and thickening of the walls,
which narrows the small airways
• The small airways are particularly affected early in the disease, initially
without the development of any significant breathlessness
• The initial inflammation is reversible and accounts for the improvement
in airway function if smoking is stopped early
• In the later stages, the inflammation continues, even if smoking is
stopped
• Patients chronic bronchitis are referred to as blue bloaters
12
Q
emphysema - COPD pathology
A
• Defined as dilatation and destruction of the lung tissue distal to the
terminal bronchioles
• Results in loss of elastic recoil, which normally keeps the airways open
during expiration
• Leads to expiratory airflow limitation and air trapping
• Premature closure of airways limits expiratory flow while the loss of
alveoli decreases capacity for gas transfer
• Patients with emphysema are referred to as the pink puffers
13
Q
types of emphysema
A
- Centri-acinar emphysema:
• Distension and damage of lung tissue is concentrated around
the respiratory bronchioles, whilst the more distal alveolar
ducts and alveoli tend to be well preserved
• Extremely common - Pan-acinar emphysema:
• Less common
• Distension and destruction affect the whole acinus and in
severe cases the lung is just a collection of bullae
• Associated with alpha-1 antitrypsin deficiency - Irregular emphysema:
• Scarring and damage that affects the lung parenchyma
patchily, independent of acinar structure
14
Q
pathogenesis of cigarette smoking?
A
- Causes mucus gland hypertrophy in the larger airways and leads
to an increase in neutrophils, macrophages and lymphocytes in
the airways and walls of the bronchi and bronchioles - These cells release inflammatory mediators (elastases, proteases,
IL-1,-8 & TNF-alpha) that attracts inflammatory cells (further
amplify the process), induce structural changes and break down
connective tissue (protease-antiprotease imbalance) in the lung
resulting in emphysema - Inactivates the major protease inhibitor alpha-1 antitrypsin
15
Q
clinical presentation of COPD?
A
- Characteristic symptoms are productive cough with white or clear sputum,
wheeze and breathlessness, usually following many years of a smokers
cough - Systemic effects include:
• Hypertension
• Osteoporosis
• Depression
• Weight loss
• Reduced muscle mass with general weakness - pulmonary hypertension due to hypoxic kidney
16
Q
investigations of COPD?
A
- Based on a history of breathlessness and sputum production in a chronic
smoker - In the absence of a history of cigarette smoking then asthma is a more likely
explanation, unless there is a family history suggesting alpha-1 antitrypsin
deficiency - LUNG FUNCTION TEST -> fev1/fvc <0.7
- CXR -> maybe normal or shower hyper inflated lungs
- ABG
17
Q
COPD treatment?
A
- SMOKING CESSATION IS MOST USEFUL,
- BRONCHODILATOR - LABA eg, salmterol or SABA eg, salutomal
- LAMA - eg, tiotropium bromide
- corticosteroid eg, prednisolone
18
Q
asthma? epidemiology
A
- Commonly starts in childhood between the ages 3-5 years and may either
worsen or improve during adolescence - Peak prevalence between 5-15 years
19
Q
3 key characteristics of asthma?
A
- Airflow limitation - usually reversible spontaneously or with treatment
- Airway hyper responsiveness (ADAM33)
• Bronchial inflammation with T lymphocytes, mast cells, eosinophils
with associated plasma exudation, oedema, smooth muscle hypertrophy,
mucus plugging and epithelial damage
20
Q
types of asthma?
A
• Allergic/eosinophilic asthma (70%):
- Allergens (e.g. fungal allergens and pets etc.) & atopy (readily develop IgE)
• Non-allergic/non-eosinophilic (30%):
- Exercise, cold air & stress
- Smoking & non smoking associated
- Obesity associated
21
Q
PATHOPHYSIOLOGY OF ASTHMA?
A
- Primary abnormality in asthma is narrowing of the airway which is due to
smooth muscle contraction, thickening of the airway wall by cellular
infiltration and inflammation and the presence of secretions within the airway
lumen - Inflammation: MAST CELLS bind to IgE and will respond if allergen binds to IgE; it releases histamine (bronchconstriction), tryptase, prostaglandin 2, cytokines
- Eosinophils release proteins and peroxidase which are toxic to epithelial cells
first bronchoconstriction then inflammation due to immune cell infiltration and then worsening inflammation due to eosinophil
remodelling - hypertrophy and hyperplasia causing excess airway narrowing
22
Q
clinical presentation of asthma
A
- Intermittent dysponea (difficulty breathing)
- Wheeze
- Cough (especially nocturnal) - frequent symptom in children
- Sputum
- Symptoms worse at night
23
Q
life threatening asthma attack?
A
- Silent chest
- Confusion & exhaustion
- Cyanosis (PaO2 less than 8kPa)
- Bradycardia
- PEFR less than 33%
24
Q
immediate management for asthma attack
A
• Oxygen therapy to maintain O2 sat (94%-98%)
• Nebulised 5mg salbutamol (+ ipratropium if life threatening) - repeat/IV
infusion
• Prednisolone (with or without hydrocortisone IV)
• Take arterial blood gases and repeat within 2 hours if severe attack or
patient deteriorating
• Chest X-ray if fails to respond to treatment
• Check PEFR within 15-30 mins/regularly
• Oximetry to ensure SaO2 is greater than 92%
25
investigations for asthma?
- take history - ADL
- lung function test; PEFR; if >15% improvement with bronchodilator = asthma
- exercise test
- blood and sputum test -> eosinophil
26
treatment of asthma?
- bonrchodilator -> SABA eg, salbutamol and LABA eg, salmeterol
- muscarinic antagonist -> short acting IPRATROPIUM and long acting TIOTROPIUM (M3 receptors)
- corticosteroids eg, prednisolone
- monoclonal antibody OMALIZUMAB
27
hypersensitivity pneumonitis?
• Previously called extrinsic allergic alveolitis
• Type of Interstitial Lung Disease (ILD) - distinct cellular infiltrates and
extracellular matrix deposition in lung distal to the terminal bronchiole i.e.
diseases of the alveolar/capillary interface
28
epidemiology of hypersensitivity pneumonitis?
- adults
- associated with specific occupations eg, farmers
- bird keeping
FARMERS LUNG MOST COMMON
29
pathophysiology of hypersensitivity pneumonitis?
- The allergic response to the inhaled antigen involves both cellular immunity
and the deposition of immune complexes (TYPE 3 HYPERSENSITIVITY REACTION) resulting in inflammation through the activation of complement
via the classical pathway
- These mechanisms attract and activate alveolar and interstitial macrophages
so that continued antigenic exposure results in the progressive development
of pulmonary fibrosis
- In the acute phase; the alveoli are infiltrated with acute inflammatory cells
- With chronic exposure, granuloma formation and obliterative bronchiolitis
(inflammation of bronchioles) occur
30
farmers lung?
• Fungus in mouldy hay is inhaled
• If individual is already sensitised to the organism, a type III immune
complex hypersensitivity reaction follows
• Clinically there is acute dyspnoea (difficulty breathing) and cough a few
hours after inhalation of the antigen
• One of the earliest features is bronchiolitis
• Later, chronic inflammatory cells are seen in the interstitium together
with non-caveating granulomas
• The inflammatory process may resolve on WITHDRAWAL of the antigen
but if there is chronic exposure then pulmonary fibrosis (build up of scar
tissue, makes lungs stiff) will develop
31
clinical presentation of hypersensitive pneumonitis
```
- Acute (4-6hrs post-exposure):
• Fever
• Rigors
• Myalgia
• Dry cough
• Dyspnoea
• Crackles (no wheeze)
```
- Subacute:
• Occurs with intermittent or lower-level exposure
• History or repeated acute attacks
• Signs same as acute, symptoms less severe and more gradual onset
- Chronic:
• Usually no history of preceding acute symptoms
• If the source of antigen is removed only partial improvement of
symptoms
• Cyanosis and clubbing may develop
• Weight loss
• Increasing dyspnoea
• Type 1 respiratory failure (low paO2, normal/low paCO2)
32
investigation of hypersensitivity pneumonitis
- Chest X-ray:
• Fibrotic shadow in upper zone of lung (upper zone mottling/
consolidation)
• Diffuse small nodules and increased reticular shadowing may be
present but not specific
- FBC; ESR and WCC raised
- Lung function test
33
treatment for hypersensitive pneumonitis?
- Acute:
• Remove allergen
• Give O2 (35-60%)
• Oral prednisolone (corticosteroid) followed by reducing dose
```
- Chronic:
• Avoid exposure to allergen
• Long term steroids can often achieve chest x-ray and physiological
improvement
• Corticosteroids e.g. prednisolone
```
34
occupational lung disorders?
* Response to inhaling something at work
| * Can be; fumes, dust, gas or vapour
35
coal workers pneumoconiosis
- Pneumoconiosis means the accumulation of dust in the lungs and the
reaction of the tissue to its presence
- Common dust disease in countries that have or have had coal-mines
- Caused by the inhalation of coal dust particles over 15-20yrs
- These particles are ingested by alveolar macrophages in the small
airways and alveoli which then die, releasing enzymes and causing
fibrosis and simple pneumoconiosis where there is fine micro nodular shadow in CXR -> progress onto progressive massive fibrosis
progressive massive fibrosis -> fibrotic mass is in the upper lobes and RF and ANA are [resent in serum
- destruction in lung causing emphysema and airway damage
36
silicosis?
- Uncommon but seen in stonemasons, sand-blasters, pottery and
ceramic workers and foundry workers involved in fettling
- Caused by the inhalation of silica particles (silica dioxide) which is very
fibrogenic
- Silica is particularly toxic to alveolar macrophages and readily initiates
fibrogenesis
- CXR appearance show diffuse nodular pattern in upper and mid-zone
and thin streaks of calcification (egg-shell calcification) of the hilar
nodes
- Spirometry shows a restrictive ventilatory defect
- Patients have progressive dyspnoea and an increased incidence of TB
37
asbestos?
- Has widely been used in roofing, insulation and fireproofing due to its
resistance to heat, acid and alkali
- they are fibrogenic
- Significant time lag between exposure and development of disease,
particularly mesothelioma (20-40 years)
- Risk of primary lung cancers (usually adenocarcinomas) is increased
in people exposed to asbestos, even in non-smokers
38
bronchiectasis
• Chronic infection of the bronchi and bronchioles leading to permanent
dilatation of these airways
• Clinically the disease is characterised by productive cough with large
amounts of discoloured sputum and dilated, thickened bronchi detected on
CT
39
epidemiology of bronchiectasis?
W>M
- increasing age
- result of chronic infection -> damages lung -> scarring -> dilation
40
causes of bronchiectasis?
• Post infection (most common):
- Previous pneumonia
- Granulomatous disease e.g. Mycobacterium tuberculosis (TB)
- Measles, Whooping cough
• Congenital:
- Cystic fibrosis
• Mechanical bronchial wall obstruction:
- Foreign body
• Allergic bronchopulmonary aspergillosis (ABPA) - immunological over-
response
• HIV
41
pathophysiology of bronchiectasis?
- Failure of mucociliary clearance and impaired immune function contribute to
continued insult to bronchial wall, through the recruitment of inflammatory
cells and uncontrolled neutrophilic inflammation; bronchitis →
bronchiectasis → fibrosis
- Airways dilate due to pulmonary inflammation and scarring, as fibrosis
(surrounding scar tissue) contracts
- Secondary inflammation changes lead to further destruction of airways
42
clinical presentation of bronchiectasis?
- Usually the lower lobes are affected
- Chronic cough with production of copious amounts of foul smelling purulent
sputum (khaki coloured) - sometimes flecked with blood (intermittent
haemoptysis)
- Dyspnoea
43
investigation of bronchiectasis?
- CXR:
• Dilated bronchi with thickened walls (tramline and ring shadows)
• Multiple cysts containing fluid showing up as cystic shadows
- Sputum culture:
• To see bacterial colonisation status
- High resolution CT (HRCT):
• Thickened, dilated bronchi with cysts at the end of bronchioles
• Airways larger than associated blood vessels
44
bronchiectasis management?
- Improved mucus clearance:
• Postural drainage: Where physio tips patients so the affected lobes can
drain mucus- done 3 times a day for 10-20mins
• Chest physio
- Abs
- bronchodilators eg, nebulised salbutamol
45
cystic fibrosis?
• One of the most commonest lethal autosome RECESSIVE conditions in
CAUCASIANS, 25% condition and 50% carrier risk
46
cystic fibrosis, epidemiology
- more common in Caucasians
- family history
- pancreatic insufficiency
47
pathophysiology of cystic fibrosis
- CF gene located on long arm of ch7 as CFTR - cystic fibrosis transmembrane regulator protein
- CFTR - cl- channel and it actively imports negative ions causing an osmotic gradient of water moving out of cell into mucus
- mutation of this protein - F580 deletion causing defective cl- secretion and increased h20 absorption into cells -> thickened secretions
48
clinical presentation of cystic fibrosis
```
- Neonates:
• Failure to thrive
• Meconium ileus - bowel obstruction due to thick meconium (earliest
stool)
• Rectal prolapse
```
```
- Respiratory (upper & lower):
• Cough
• Thick mucus
• Wheeze
• Recurrent infections
• Bronchiectasis & airflow limitation
• Sinusitis
```
- Alimentary:
• Thick secretions
• Reduced pancreatic enzymes (due to mucus blocking pancreatic duct)
• Pancreatic insufficiency (diabetes mellitus & steatorrhoea (fatty stools
since enzymes not released to digest fat)
other
- clubbing
- osteoporosis
49
investigations for cystic fibrosis
- Clinical history
- Family history of disease
- One or more of these:
• Sweat test: will show high sodium & chloride concentrations greater
than 60mmol/L (Cl- will be higher)
• Absent vas deferens and epididymis (male urogenital abnormality)
• GI & nutritional disorders
- Genetic screening for known CF mutations
50
treatment for cystic fibrosis
- stop smoking
- Prophylaxis antibiotics:
• Flucloxacillin - Staphylococcus Aureus
• Amoxycillin - Haemophilus influenzae
- Regular chest physiotherapy (postural drainage, forced expiratory
techniques)
- B2 agonists (salbutamol) & inhaled corticosteroids (beclometasone) -
purely for symptomatic relief
- Mucolytics such as Dornase alfa (nebulised) or inhaled DNAse - to clear
airways of mucus
- Amiloride - inhibits Na+ transport thus less thick mucus
51
sarcoidosis
• Type of Interstitial Lung Disease - distinct cellular infiltrates and extracellular
matrix deposition in lung distal to the terminal bronchiole i.e. diseases of the
alveolar/capillary interface
• Typically presents with bilateral hilar lymphadenopathy, pulmonary
infiltration and skin or eye lesions
52
sarcoidosis epidemiology
- 20-40 yrs
- W>M
- first degree relatives
53
sarcoidosis pathophysiology
- Typical sarcoid granulomas consist of focal accumulations of epithelioid
cells, macrophages and lymphocytes - mainly T cells
- Generally unknown
54
sarcoidosis clinical presentation?
- Acute sarcoidosis commonly presents with erythema nodusum (red lumps
form on the shins and less commonly thighs and forearms) with/without
polyarthralgia (aches in joints and joint pain) - it usually resolves
spontaneously
- Constitutional symptoms:
• Fever
• Weight loss
• Fatigue
```
- Respiratory symptoms:
• 90% have abnormal CXRs with bilateral hilar lymphadenopathy with/
without pulmonary infiltrates/fibrosis
• Dry cough
• Progressive dyspnoea
• Reduced exercise tolerance
• Chest pain
```
55
investigations of sarcoidosis
- CXR; bilateral hilar lymphadenopathy and pulmonary infiltrates
- FBC; raised ESR
- tissue biopsy; DIAGNOSTIC
56
treatment for sarcoidosis
- Acute sarcoidosis:
• Bed rest
• NSAIDs
- Corticosteroids:
• Prednisolone orally then gradually reduce dose
• In severe illness give IV methylprednisolone
• If steroid-resistant then:
- Methotrexate but close monitoring required
57
idiopathic pulmonary fibrosis
type of interstitial lung disease where there is patchy fibrosis or the interstitium and minimal or absent
inflammation, acute fibroblastic proliferation and collagen deposition
58
epidemiology of idiopathic pulmonary fibrosis
- A progressive chronic pulmonary fibrosis of unknown aetiology although
20% of patient give a history of occupational exposure to metals and wood
dusts
- Mean onset is in the sixties and presentation is very uncommon under the age
of 50
- Males are twice as likely to be affected
59
pathophysiology of idiopathic pulmonary fibrosis
- The pathogenesis of IPF is unknown
- It is thought that repetitive injury to the alveolar epithelium, caused by
currently unidentified environmental stimuli leads to the activation of
several pathways responsible for repair of the damaged tissue
- However in IPF, the wound healing mechanisms become uncontrolled,
leading to the over-production of fibroblasts and deposition of increased
extracellular matrix in the interstitium (fibrosis) with little inflammation
- The structural integrity of the lung parenchyma (functional tissue of organ) is
therefore disrupted; there is loss of elasticity and the ability to perform gas
exchange is impaired, leading to progressive respiratory failure
60
risk factors of idiopathic pulmonary fibrosis?
- cigarette smoking
- infectious agents CMV, HEP C and EBV
- occupational dust
- drugs eg, methotextrate
- GORD
- genetics
61
clinical presentation of idiopathic pulmonary fibrosis
- Dry cough with/without sputum
- Exertional dyspnoea
- Malaise
- Weight loss
- Arthralgia (joint pain)
- Cyanosis
- Finger clubbing
62
investigations of idiopathic pulmonary fibrosis?
- ABG; low pa02
- raised CRP and immunoglobulins
CXR; small volume lungs with increased reticular shadowing
HRCT - confirm diagnosis
lung biopsy
63
treatment of idiopathic pulmonary fibrosis
- oxygen
- pulmonary rehabilitation
- treat GORD and cough
- Pirfenidone - an antifibrotic agent that can slow the rate of FVC decline
(need to check eligibility)
64
pulmonary hypertension?
Pulmonary hypertension is defined as an mPAP of above 25mmHg as
measured at right heart catheterisation and secondary right ventricular
failure
65
aeatiology of pulmonary hypertension
• Pulmonary vascular disorders:
- Pulmonary embolism
• Diseases of lung and parenchyma:
- COPD
MSK:
- myasthenia gravis
• Cardiac:
- Mitral stenosis (narrowing of mitral valve of heart)
66
pathophysiology of pulmonary hypertension
- Hypoxic vasoconstriction, inflammation, cell proliferation resulting in
narrower vessels and increased right ventricular pressure caused
pulmonary hypertension
- Leads to the damage of the pulmonary endothelium resulting in the release of
vasoconstrictors such as endothelin which in turn increases pulmonary
vascular resistance (PVR) meaning the right ventricle must pump harder
causing right ventricular hypertrophy
- Increased platelet and leukocyte adhesion, elevated serotonin as well as
other factor cause further vasoconstriction and remodelling further
increasing PVR
- Patients with progressive pulmonary hypertension develop right ventricular
hypertrophy, dilatation and eventually failure resulting in death
67
clinical presentation of pulmonary hypertension?
- exertional SOB
- ankle swelling
- chest pain
- syncope
- features of cor pulmonale
68
investigations for pulmonary hypertension
- CXR:
• Enlarged proximal pulmonary arteries which taper distally
• Enlarged heart
- ECG; tall and peak p waves
- ECHO cardiogram -> right ventricular hypertrophy
69
investigations for pulmonary hypertension
- CXR:
• Enlarged proximal pulmonary arteries which taper distally
• Enlarged heart
- ECG; tall and peak p waves
- ECHO cardiogram -> right ventricular hypertrophy
70
treatment of pulmonary hypertension
- oxygen
- warfarin
- diuretics for oedema
- CCB
- - Oral endothelin receptor antagonist e.g. bosenten
- Phosphodiesterase-5 inhibitors
71
pleural effusion?
• A pleural effusion is the excessive accumulation of fluid in the pleural space
72
pleural effusion epidemiology
- Seen in adults and less commonly in children
- Recurrent pleural effusions are seen malignant mesothelioma
- Pleural effusions are transudates or exudates
73
pleural effusion pathophysiology?
- Transudates - transparent i.e. less protein:
Occurs when the balance of hydrostatic forces in the chest favour the
accumulation of pleural fluid i.e. increased pressure due to the backing
up of blood in left sided congestive heart failure
- Exudates - exudes proteins:
• Occurs due to the increased permeability and thus leakiness of pleural
space and or capillaries usually as a result of inflammation, infection or
malignancy
74
clinical presentation of pleural effusion
- Can be asymptomatic
- Shortness of breath especially on exertion
- Dysponea (difficulty breathing)
- Pleuritic chest pain
- Cough
- Loss of weight (malignancy)
- Chest expansion reduced on side of effusion
75
pleural effusion investigations?
- CXR -> detects larger fluids
- USS
- diagnostic aspiration
76
treatment of pleural effusion?
- Depends on the underlying cause
- Exudates are usually drained if symptomatic
- Transudates are managed by treatment of underlying cause
77
pneumothorax
* Means air in the pleural space
| * Leads to partial or complete collapse of the lung
78
pneumothorax epidemiology
- Occurs spontaneously or secondary to chest trauma
- Spontaneous pneumothorax is most common in young males
- Generally a pneumothorax is MUCH MORE COMMON in MALES
79
pneumothorax epidemiology
- Occurs spontaneously or secondary to chest trauma
- Spontaneous pneumothorax is most common in young males
- Generally a pneumothorax is MUCH MORE COMMON in MALES
80
aetiology of pneumothorax
- bronchial asthma
- carcinoma
- TB
- pneumonia
- CF
- trauma
81
risk factors, pneumothorax?
- Being male
- Smoking increases risk
- Age - pneumothorax due to pleural bleb rupture is most likely to occur between
20-40yrs old, especially if person is very tall and underweight
- On mechanical ventilation
82
pneumothorax pathophysiology?
- Normally, the pressure in the pleural space is negative but this is lost once
there is communication with atmospheric pressure i.e. a breach in pleura,
the elastic recoil of the lung then causes it to deflate partially
- If the communication between the airways and the pleural space remains
open then a bronchopleural fistula results
- Once the communication between the lung and the pleural space is closed,
air will be reabsorbed slowly for example a 50% collapse of the lung will take
around 40 days to reabsorb completely once the air leak is closed
- About a third of patients will have a recurrence, for these patients chemical
pleurodesis with talc is used for patients when surgery is contraindicated
83
tension pneumothorax
- pneumothorax leads to significant impairment of respiration and or blood circulation
- tachycardia, tachypnoea, low 02, low BP and trachea deviation from affected side
84
clinical presentation of pneumothorax
- May be a sudden onset of dyspnoea and/or unilateral pleuritic chest pain
- As the pneumothorax enlarges the patients becomes more breathless and
may develop pallor and tachycardia
- There will be reduced expansion, hyper-resonance to percussion and
diminished breath sounds of the affected lung
85
investigations of pneumothorax
- CXR:
• DO NOT REQUEST IN TENSION PNEUMOTHORAX - WASTES TIME!
• Look for area devoid of lung markings, peripheral to the edge of the
collapsed lung
- Arterial Blood Gases (ABG):
• In dyspnoeic patients check for hypoxia
86
treatment for pneumothorax?
- Pneumothorax due to trauma, haemothorax or mechanical ventilation
requires a chest drain
- For tension pneumothorax do needle aspiration then chest drain - NEEDLE
ASPIRATION FIRST
- Needle aspiration to remove excess air
- Observation
- Oxygen for hypoxia
87
bronchial carcinoma, epidemiology?
M>F
| most common malignant tumour
88
risk factors for bronchial carcinoma?
- cigarette smoking
- occupational
- environmental
- pre existing lung disease
- HIV
- genetics
89
types of bronchial carcinoma?
- Broadly there are two main types of bronchial carcinoma:
• Small cell lung carcinoma (SCLC)
• Other types (non-small cell carcinoma):
- Squamous carcinoma
- Adenocarcinoma
- Large cell and differentiated carcinoma
- Carcinoid tumours
90
SCLC?
* STRONGLY ASSOCIATED with CIGARETTE SMOKING
* Has often spread by the time of presentation
* Often arises in a central bronchus
* Arises from endocrine cells
* Secretes polypeptide hormones
* Has early development of widespread metastases
* Chemotherapy is the primary treatment
* Poor prognosis
91
NSCLC
• Cigarette smoking association
• May have metastasised by the time of diagnosis
• Often treated best by surgical oblation with lymph node sampling
• Chemotherapy may be used and radiotherapy can be used as a follow
up for contamination margin
• More susceptible to new therapy such as tyrosine kinase therapy
92
squamous cell carcinoma
NSCLC
- most strongly associated with smoking
- Arise from epithelial cells, associated with the production of keratin
- Cause obstructive lesions of bronchus with post-obstructive
infection
- Local spread common
- Metastasise relatively late
93
adenocarcinoma?
MOST COMMON OVERALL:
- May be central or peripheral
- Usually single lesions but they can arise in a multifocal pattern,
sometimes bilaterally
- Originate from mucus-secreting glandular cells
- MOST COMMON CELL TYPE IN NON-SMOKERS
- associated with asbestos
94
carcinoid tumours?
- Usually associated with presentation at an earlier age (middle age)
and have characteristic neuroendocrine secreting cells and
relatively low rates of invasion and growth
- However they are still malignant
95
clinical presentation of bronchial cancer?
- Symptoms of local disease:
• Cough - most commonly encountered symptom, having a 3-week
cough merits a CXR
• Breathlessness - central tumours can occlude large airways resulting in
lung collapse and breathlessness on exertion
• Haemoptysis - fresh/old blood coughed up due to the tumour bleeding
in the airway
• Chest pain
- Symptoms of metastatic disease:
• Bone pain
• Headache
• Seizures
- Paraneoplastic changes:
• These are conditions which occur as a side effect of the tumour and
occur in 10% of patients:
- Secretion of parathyroid hormone (PTH)
- Syndrome of inappropriate ADH secretion (SIADH)
96
classification of bronchial cancer?
- TNM classification:
• Tumour - how big it is:
- T1 - < 3cm
- T2 - > 3cm
- T3 - Invades chest wall, chest wall, diaphragm & pericardium
- T4 - Invades mediastinum, heart, great vessels, trachea,
oesophagus, vertebra, carina
• Nodes - how many and where they are:
- N0 - No nodes
- N1 - Hilar nodes
- N2 - Same side mediastinal nodes or subcarinal
- N3 - Contralateral mediastinum or supraclavicular
• Metastasis:
- m1a - tumour on same side
- m1b - tumour is elsewhere
97
investigations of bronchial caner?
```
CXR:
• Appear as round shadow
• The edge has a fluffy spiked appearance
• Hilar enlargement
• Consolidation
```
CT
• To stage tumour
98
treatment of bronchial cancer?
- Non-small cell lung cancer (80% of lung cancers):
• Surgical excision
• Curative radiotherapy
• Chemotherapy +/- radiotherapy - e.g. CETUXIMAB
- Small cell lung tumours:
• combined chemotherapy and radiotherapy
• Endobronchial therapy - used to treat symptoms of airway narrowing:
99
mesothelioma?
• Malignant mesothelioma is STRONGLY ASSOCIATED with ASBESTOS
EXPOSURE
• Tumour of the mesothelial cells of the pleura
• Other sites include the mesothelial cells of the peritoneum, pericardium and
testes
100
epidemiology mesothelioma?
M>F
40-70 yrs
latent period between exposure and development
101
pathophysiology of mesothelioma?
- It is a high grade malignancy of the pleura, that spreads around the pleura
surfaces, but can also start in the pericardial space, peritoneal space and in
the paratesticular space
- Tumour begonia as nodules in the pleura which extend as a confluent sheet to
surround the lung and extend into fissures
- The chest wall is often invaded, with infiltration of intercostal nerves, giving
severe intractable pain
- Lymphatics may be invaded, giving hilar node metastases
102
clinical presentation of mesothelioma?
- Chest pain
- Dyspnoea
- Weight loss
- Finger clubbing
- Recurrent pleural effusions
- Breathlessness
103
investigations of mesothelioma
```
- CXR & CT:
• Unilateral pleural effusion
• Pleural thickening
- Bloody/straw coloured pleural fluid
- Pleural biopsy
```
104
treatment for mesothelioma?
- Surgery for extremely localised mesothelioma
- Generally it is resistant to surgery, chemotherapy and radiotherapy
- Average time from diagnosis to death is around 8 months
105
good pastures syndrome?
• The co-existence of acute glomerulonephritis and pulmonary alveolar
haemorrhage and the presence of circulating antibodies directed against an
intrinsic antigen to the basement membrane of both kidney and lung
106
epidemiology of good pastures syndrome?
>16 yrs
| M>F
107
pathophysiology of good pastures syndrome?
- Specific autoimmune disease caused by a type II antigen-antibody reaction
leading to diffuse pulmonary haemorrhage, glomerulonephritis (and often
acute kidney injury and chronic kidney disease)
- There are circulating antiglomerular basement membrane (anti-GBM)
antibodies
108
clinical presentation of good pastures syndrome?
- Typically starts with symptoms of upper respiratory tract infection e.g.
sneezing, nasal discharge, nasal congestion, runny nose and fever
- Cough
- Intermittent haemoptyis
- Tiredness
- Anaemia - which may result from persistent intrapulmonary bleeding
- Acute glomerulonephritis
109
investigations of good pastures syndrome?
```
- CXR:
• Transient patchy shadows/pulmonary infiltrates due to pulmonary
haemorrhage often in lower zones
- Kidney biopsy:
• Crescentic glomerulonephritis
```
110
treatment of good pasture syndrome?
- Vigorous immunosuppressive treatment:
• Corticosteroids e.g PREDNISOLONE
• Plasmapheresis (where you remove blood and clean to remove
offending antibodies before inserting it back)
111
WEGENER’S GRANULOMATOSIS:
* Granulomatous disease of unknown aetiology
| * Type of ANCA-associated vasculitis
112
pathophysiology of wegeners granulomatosis
- Autoantibodies are made to neutrophil proteins
- As neutrophil rolls along blood vessels before it migrates into tissues,
autoantibodies bind to it and ACTIVATE NEUTROPHILS inappropriately
(before they have entered tissues where there a no pathogens)
- This results in the recruitment of more neutrophils and more activated
neutrophils when there is NO INFECTION
- This results in the production of reactive oxygen species (ROS) and
neutrophil degranulation
- Leading to the generation of microabscesses, recruitment of monocytes and
macrophages and lymphocytes to make granulomas
= INFLAMMATION
113
clinical presentation of wegeners granulomatosis
- Lesions involve upper respiratory tract, lungs and kidneys
- Starts with severe rhinorrhea (nasal cavity congested with significant amount of mucus) and subsequent nasal mucosal ulceration - characteristic ‘saddle- nose’ deformity
- Cough
- Pleuritic pain
- Haemoptysis
- May be skin purpura or nodules, peripheral neuropathy, arthritis/arthralgia
- renal disease
114
investigation of wegeners granulomatosis
```
- Bloods:
• c-ANCA is positive
• Elevated PR3 antibodies
• Raised ESR and CRP
- CXR:
• Nodular masses or pneumonic infiltrates with cavitation - clear
migratory pattern
- CT:
• Diffuse alveolar haemorrhage
- Urinalysis to check for proteinuria and haematuria - if present then consider
renal biopsy
```
115
treatment of wegeners granulomatosis
- Severe disease (biopsy proven renal disease) should be treated with
corticosteroid e.g. prednisolone and cyclophosphamide or rituximab to
induce remission
- Azathioprine and methotrexate are usually used as maintenance
116
pulmonary thromboembolus and infract?
• Bronchial circulation provides blood to the lung tissue itself - bronchial
circulation originates from the aorta
• ALWAYS SUSPECT PULMONARY EMBOLISM (PE) IN SUDDEN COLLAPSE
1-2 WEEKS AFTER SURGERY
117
pulmonary thromboembolus and infract?
• Bronchial circulation provides blood to the lung tissue itself - bronchial
circulation originates from the aorta
• ALWAYS SUSPECT PULMONARY EMBOLISM (PE) IN SUDDEN COLLAPSE
1-2 WEEKS AFTER SURGERY
118
risk factors of pulmonary thromboembolism/infarct
VIRCHOWS TRIAD
- change in blood flow/stasis -> immobility, obesity and pregnancy
- change in blood vessel; smoking and hypertension
change in blood constituents -> dehydration, polyctheamia
119
pathophysiology of pulmonary thromboembolism/infarct
- Arise from a venous thrombosis in the pelvis or legs, clots break off and
pass through the veins then through the IVC then through the right side of the
heart into the pulmonary circulation where it consequently becomes lodged
most likely in the small capillaries supplying the alveoli resulting in a
pulmonary embolism
- After PE, lung tissue is ventilated but NOT PERFUSED resulting in
intrapulmonary dead space and resulting in impaired gas exchange
- After some hours, the non-perfused lung NO LONGER PRODUCED
SURFACTANT resulting in alveolar collapse which in turn exaggerates
hypoxaemia
120
clinical presentation of pulmonary thromboembolism/infarct
```
- Sudden onset unexplained dyspnoea is most common and often only
symptom
- Pleuritic chest pain and haemoptysis are present only when infarction has
occured
- Dizziness
- Cyanosis
- Tachypnoea
- Tachycardia
- Hypotension
- Raised jugular venous pressure
```
121
investigation of pulmonary thromboembolism/infarct
- CT pulmonary angiography is the GOLD STANDARD TEST
- CXR:
• OFTEN NORMAL
- ECG:
• May be normal
• May show sinus tachycardia
- Blood gases:
• May be normal
• With significant pulmonary embolism there will be arterial hypoxaemia
i.e. low PaO2 with a low PaCO2 i.e. type 1 respiratory failure
- Plasma D-dimer:
• Type of fibrinogen degradation product that is released into the
circulation when a clot begins to dissolve
• D-dimer are elevated in other conditions e.g. cancer, pregnancy and
post-operatively and a positive result is NOT DIAGNOSTIC of PE and
requires further imaging
122
treatment of pulmonary thromboembolism/infarct
- High flow oxygen (60-100%) - give to all patients unless they have significant
chronic lung disease
- Anticoagulate with low molecular weight heparin e.g. Enoxaparin or Dalteparin
prevention
• Placed on vitamin K antagonist such as Warfarin (acts by preventing
Vitamin K being used by liver to produce clotting factors 2,7,9 & 10
(1972)) - Warfarin affects the Extrinsic pathway by the Prothrombin Time
(WEPT) for a period of 3-6 months
• Target INR is between 2-3
123
mucosal defences for URTI?
- Mucosal defences:
• Cough reflex (reduced by sedation, opiates, pain & mechanical
ventilation
• Mucus barrier & respiratory cilia - ‘mucociliary escalator’ (impaired
ciliary function can be caused by infection & primary ciliary dyskinesia
(genetic disorder that causes defects in cilia)
• Surface secretions e.g. defensins and complement
124
pharyngitis/tonsilitis?
* Both are infections in the throat that cause inflammation
* If the tonsils are primarily affected then its known as tonsillitis
* If the throat is primarily affected then its called pharyngitis
125
epidemiology of pharyngitis/tonsillitis
- The most common viruses to cause pharyngitis are adenoviruses of which
there are about 32 serotypes
- Can also be caused by rhinovirus, Epstein Barr virus and acute HIV infection
- Bacterial causes include:
• Lancefield Group A Beta-haemolytic streptococci e.g. streptococci
pyogenes
126
investigations for pharyngitis/tonsilitis?
- Fever
- Oropharynx and soft palate are reddened
- Tonsils are inflamed and swollen
- Within 1-2 days the tonsils lymph nodes enlarge
127
treatment of pharyngitis/tonsillitis
- Self-limiting disease
- Symptomatic treatment
- No antibiotics required
- Persistent and severe tonsillitis should be treated with
phenoxlymethylpenicilin or cefaclor
128
sinusitis?
• Infection of the paranasal sinuses that is bacterial or occasionally fungal
129
epidemiology of sinusitis?
```
- Bacterial:
• Streptococcus pneumoniae (40%)
• Haemophilus influenzae (30-35%)
- Most commonly associated with upper respiratory tract infection and
occasionally asthma
```
130
investigation of sinusitis?
- Frontal headache
- Purulent rhinorhoea (where nasal cavity filled with significant amount of
mucus fluid)
- Bacterial sinusitis presents with unilateral pain and purulent discharge with
or without fever for more than 10 days
- Facial pain with tenderness
- Fever
131
treatment for sinusitis?
- Nasal decongestants such as xylometazoline
- Broad spectrum antibiotics such as co-amoxiclav (H.influenzae can be
resistant to amoxicillin)
- Complications include; brain abscess, sinus vein thrombosis and orbital
cellulitis
132
acute epiglottis?
• Inflammation of the epiglottis (flap of cartilage behind the root of the tongue,
which is depressed during swallowing to cover the opening of the windpipe)
133
epidemiology of acute epiglottis?
- Formerly a life-threatening infection of the epiglottis, usually in children
under 5 years of age
-- Adults can also have the disease:
• Most severe due to Haemophilus influenzae
• Also from causes of pharyngitis and other bacterial infections of airway
• Caused by additional pathogens in immunocompromised e.g. AIDs
134
investigation of acute epiglottis?
- High fever
- Severe airflow obstruction - inspiratory stridor
- Meningitis
- Septic arthritis
- Osteomyelitis
135
treatment of acute epiglottis?
- Can be a life-threatening emergency and requires urgent endotracheal
intubation
- IV antibiotics e.g. ceftazidime
136
bordatella pertussis?
WHOOPING COUGH
137
whooping cough epidemiology?
- Caused by Bordatella pertussis, a GRAM-NEGATIVE COCCOBACILLUS
(ROD)
- Mainly a disease of childhood with 90% of cases occurring below 5 years of
age
- However, no age is exempt as the antibody levels fall over the years, although
in adults, mild infection may not be recognised
138
pathophysiology of whooping cough?
- Highly contagious and spread by droplet infection
- In early stages it is indistinguishable from other upper respiratory tract
infections
139
clinical sings of whooping cough?
- Catarrhal phase (1-2 weeks):
• Patient highly infectious
• Cultures from respiratory cultures are positive in 90% of cases
• Malaise
• Anorexia
• Rhinorhoea (nasal cavity congested with significant amount of mucus)
• Conjunctivitis
- Paroxysmal phase (1-6 weeks):
• Begins 1 week later from catarrhal phase
• Coughing spasms
• Classic inspiratory whoop is only seen in younger individuals in whom
the lumen of the respiratory tract is compromised by mucus secretion
and mucosal oedema
• These coughing spasms usually terminate in vomiting
• Cough for more than 14 days
140
investigations of whooping cough
- chronic cough and with er one clinical feature, history of contact or microbiological diagnosis confirms
- PCR
- nasopharngyeal swab - DIAGNOSTIC
141
whooping cough treatment?
- Antimicrobials such as macrolides e.g. clarithromycin will eliminate carriage
of bacteria and reduce symptoms in catarrhal stage and early paroxysmal
stage
142
croup?
• Acute laryngitis is an occasional complication of upper respiratory tract
infections, particularly those caused by parainfluenza viruses and measles
143
epidemiology of croup?
- Mainly due to parainfluenza viruses
| - Most severe in children under the age of 3 years
144
pathophysiology of croup?
- Inflammatory oedema extends to the vocal cords and the epiglottis, causing
narrowing of the airway; there may be associated tracheobronchitis
- Progressive airway obstruction may occur, with recession of the soft tissue
of the neck and abdomen during inspiration and in severe cases central
cyanosis
145
investigations of croup?
- Voice become hoarse with a barking cough (croup)
| - Audible stridor (high pitched wheezing when breathing in)
146
treatment of croup?
- Nebulised adrenaline gives short-term relief
- Oral or intramuscular corticosteroids e.g. dexamethasone should be given
with oxygen and adequate fluids
147
pneumonia?
• Defined as inflammation of the substance of the lungs
• An acute lower respiratory tract infection
• Usually caused by bacteria but can also be caused by viruses and fungi
• Usually due to infection affecting distal airways and alveoli with the formation
of an inflammatory exudate
148
CAP - community acquired
• In a person with no underlying immunosuppression or malignancy
• Occurs across all ages but commoner in extremes of age
• May be primary or secondary to underlying disease
• Streptococcus pneumoniae is the COMMONEST CAUSE
• Followed by Haemophilus influenzae and Mycoplasma
pneumoniae
149
HAP - hospital acquired?
• Defined as new onset of cough with purulent sputum, along with a
compatible X-ray demonstrating consolidation, in patients who are
beyond 48hrs of their initial admission to hospital or who have been in a healthcare setting within the last 3 months (including
nursing/residential homes)
• Seen mostly in; the elderly, ventilator-associated and post operative
```
- Aerobic GRAM-NEGATIVE bacilli/rods are MOST COMMONLY
involved:
- Pseudomonas Aeruginosa
- Escherichia coli (E.coli)
- Klebsiella Pneumoniae
```
150
pathophysiology of pneumonia?
- Bacteria ‘translocate’ to the normally sterile distal airway
- Where they overwhelm resident host defence (particularly alveolar
macrophages and neutrophils)
- Normally alveolar macrophages will ingest the bacteria and produce
humoral factors
- Antibodies would be produced as well as microbial factors and the bacteria
will be destroyed
- HOWEVER when the host defence is overwhelmed the alveolar
macrophages change roles and instead coordinate response where they fill alveolar space with inflammatory exudate
151
clinical presentation of pneumonia?
- Symptoms of; fever, night sweats, raised respiratory rate, productive cough
and ABSENCE OF UPPER RESPIRATORY TRACT SYMPTOMS makes
pneumonia more likely
- dull percussion
- pleuritic chest pain
152
investigations of pneumonia?
- CXR:
• Radiological abnormalities can lag behind clinical signs
• A normal CXR on presentation should be repeated after 2-3 days if CAP is
suspected clinically
153
treatment of pneumonia?
- Maintain O2 sats between 94-98% (provided the patient is not at risk of CO2
retention, due to loss of hypoxic drive in COPD)
- First dose of antibiotics should be administered within 4 hours of
presentation in hospital and treatment should not be delayed whilst
investigations are awaited
- Narrow spectrum antimicrobials if mild = amoxicillin 5-7days
- IV antibiotics if severe = co-amoxiclav or clarithromycin 7-10 days
154
TB, epidemiology?
- Majority of cases are seen in Africa and Asia (India and China)
- Cause of death for most people with HIV
- Caused by 4 main mycobacterial species:
• Mycobacterium tuberculosis - most common cause
• Mycobacterium bovis - where milk is unpasteurised
• Mycobacterium africanum
• Mycobacterium microti
155
TB microbes?
• Aerobic, non-motile, non-sporing, slightly curved rods/bacilli with a
thick waxy capsule
• Acid-fast bacilli (resist decolorisation) - go red/pink with Ziehl-neelsen
stain
• Only stained weakly with Gram stain due to high lipid content in their cell
wall
• Slow growing - generation time is 15-20 hours
• Resistant to phagolysosomal killing by macrophage, hence
granulomata
• Able to remain dormant
156
TB, pathophysiology?
- TB is an airborne infection spread via respiratory droplets
- Only a small number of bacteria need to be inhaled for infection to develop
- However, NOT ALL INFECTED actually develop ACTIVE DISEASE
- The outcome of exposure is dictated by a number of factors, including the
host’s immune response
* primary TB -> bacilli proliferate inside macrophage and causes inflammatory cell infiltrate causing delayed hypersensitivity type reaction (granuloma). If bacteria cannot be contained then TB diseases and spreads to other organs
* latent TB - when person develops cell mediated immunity memory
157
clinical presentations of TB?
```
- Systemic features:
• Weight loss (most predictive of TB)
• Low grade fever
• Anorexia
• Night sweats (most predictive of TB)
• Malaise
```
```
- Pulmonary TB:
• Can be asymptomatic
• Productive cough with occasional haemoptysis
• Chest pain
• Breathlessness
```
• Bone:
- Pain or swelling of joint
• CNS TB:
- Bacilli in CSF and on meninges
158
investigations for TB?
- CXR:
• Patchy or nodular shadows in the upper zones with loss of volume, and
fibrosis with or without cavitation
• Consolidation
- Sputum:
• Stained with an auramine-phenol fluorescent test (more sensitive but
less specific), it highlights bacilli as yellow-orange on a green
background
- Latent TB diagnosis:
• Tuberculin skin test ‘Matnoux’:
• Interferon gamma release assays (IGRAs):
- Use antigens specific to M. tuberculosis e.g. ESAT-60 and CFP10 to
distinguish between this and BCG vaccine or environmental
mycobacteria
159
TB treatment?
• Rifampicin for 6 months:
- Bactericidal, blocks protein synthesis - effective throughout
treatment course
- Side effects; red urine, hepatitis and drug interactions
• Isoniazid for 6 months:
- Bactericidal for rapidly growing bacilli (blocks cell wall
synthesis) , most effective in initial stages
- Side effects; hepatitis and neuropathy
• Pyrazinamide for first 2 months:
- Bactericidal initially, less effective later
- Side effects; hepatitis, arthralgia/gout and rash
• Ethambutol for first 2 months:
- Bacteriostatic, blocks cell wall synthesis
- Side effects; optic neuritis
• Remember by “RIPE”
Phase 2a
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