1
Q
What are these:
- FEV1
- FVC
- KCO
- TLCO
What is obstuctive and restrictive pattern involving FEV1 and FVC?
A
- FEV1 = forced expiratory volume
- Volume that has been exhaled at the end of the first second of forced expiration
- FVC = focred vital capacity
- Volume that has been exhaled after a maximal expiration following a full inspiration
- KCO = Diffusion capacity of the lung per unit area for CO
- TLCO = Diffusion capacity of the total lung capacity for CO
Obstructive pattern:
- Normal (or increased) FVC, reduced FEV1:FVC ratio
- Reduced FVC, normal (or increased) FEV1:FVC ratio
2
Q
Define the classical features of asthma
(symptoms and signs)
A
Ashthma is a chronic inflammation condition of the airways, charactised by airway hypersensitivity to a number of factor.
Symptoms variable but recurring:
- Reverisible bronchospasm resulting in airway obstruction:
- Wheezing & SOB
- Classically worse during night or upon exercise
- Symptoms are typically worse in the morning (peak flow worse - ‘morning dipping’)
- Subjective feeling of chest tightness
- Cough, again classically nocturnal
Signs:
- Widespread expiratory wheeze
- Pulmonary function testing reveals a decreased FEV1 (peak flow) relieved by ß2 agonists
3
Q
How may the symptoms of asthma be differentiated from those of COPD?
A
In asthma airflow limitation is often fully reversible, either spontaneously or with treatment whereas COPD is a disease of progressive airflow limitation that is not fully reversible.
4
Q
Classify asthma into early and late onset and discuss the likely presenting characteristics of a typical patient who is likely to get each
A
Extrinsic asthma
- Type I hypersensitivity reaction
- ay occur in young patients with atopy (alergic diseases)
- Elevated IgE may be present, alongside eczema and/or rhinitis
- May disappear at age 15 but may recur.
Intrinsic asthma
- Non-immune mechanisms
- occurs in middle aged, with no causative agent can be identifie (no history of atopy - allergies)
- Skin tests are usually negative and IgE normal, remission is rare.
- They may present with shortness of breath and tight chest - more severe symptoms and associated with quicker deterioations in lung function
5
Q
Outline common precipitants of an asthma attack
A
Common precipitants:
- Environmental allergens: pets, grass pollen, dust mites
- Viral infections
- Cold air
- Emotion
- Drugs: NSAIDs particularly aspirin. Beta-blockers
- Atmospheric pollution
- Occupational pollutants: e.g. flour or chemicals
6
Q
What occupations may predispose to developing asthma?
A
Vehicle spray painting, woodworking, baking, soldering, healthcare workers, working with animals, working in agriculture, engineering, hairdressing
7
Q
Describe the clinical features of an acute asthma attack
A
Features of acute severe asthma:
- Tachycardia (HR > 110)
- Marked SOB (RR>25)
- Peak expiratory flow (PEF) 33-50% of best
- Cant complete sentences in one breath
May have pulsus paradoxus (abnormally large decrease in systolic BP during inspiration)
- Widespread bilateral expiratory wheeze in a hyper inflated chest
- Accessory muscle of respiration are often used
8
Q
Describe the blood gas abnormalities associated with severe asthma and highlight other clinical indices of severity
A
- In a mild attack, there may be low pCO2
- Due to hyperventilation
- A normal pCO2 with hypoxaemia suggests current deterioration (life threatening attack)
- In life threatening exacerbations there will be a high pCO2, severe hypoxia and low pH.
- PEF<50% indicates severity, and <33% life-threat.
9
Q
Describe how to use inhaler devices and other aids appropriately
A
Shake the inhaler, take a normal breath out, place the inhaler in your mouth and simultaneously breathe in and press the button to release the aerosol.
Hold the breath in for 10 seconds if possible.
Important not to just spray the inhaler into the mouth!
With the steroid inhaler, the patient should be counselled to rinse the mouth out after use.
10
Q
Describe the clinical features of life threatening asthma attack
A
-PEF less than 33% of best -SpO2 <92% -Silent chest, cyanosis or feeble respiratory effort -Bradycardia, hypotension or dysrhythmia -Exhaustion or confusion
11
Q
Describe the morphology and pathological consequences of acute asthma
A
Asthma is an inflammatory condition with both acute and chronic elements.
Acute asthma:
- Acute episodes of bronchospasm that are triggered by recognised triggers
- These triggers activate mast cells, which lead to two phases;
- An early phase of bronchospasm due to spasmogen production (histamine, prostaglandin D2 and leukotrienes)
- smooth muscle contraction narrows the airway
- A late phase due to chemotaxins attracting eosinophils and mononuclear cells
- cells infiltrates and muscosal oedema narrow the airway.
- There will also be airway hyper-reactivity in the late phase, which can lead to further acute deteriorations
- An early phase of bronchospasm due to spasmogen production (histamine, prostaglandin D2 and leukotrienes)
12
Q
Describe the morphology and pathological consequences of chronic asthma
A
Asthma is an inflammatory condition with both acute and chronic elements.
Chronic asthma
- Many asthmatics will have normal respiratory function between attacks, but some will develop persistent airway obstruction that can become indistinguishable from COPD (more common in intrinsic asthma)
- There is bronchoconstriction due to increased responsiveness of bronchial smooth muscle, and hyper secretion of mucus that plugs the airways
- Mucosal oedema further narrows the airways
- The sputum will contain Charcot-Leyden crystals (from eosinophil granules) and Curschman spirals (mucus plugs from small airways)
- In long-standing disease, the can lead to pulmonary hypertension
13
Q
How can you obtain an accurate peak flow rate (PEFR) from a patient
A
Stand tall, deep breath, encourage, and take the best of 3.
14
Q
Define chronic obstructive pulmonary disease (COPD)
A
- COPD is a disease of progressive airflow limitation that is not fully reversible, associated with an abnormal inflammatory response of the lungs to noxious particles or gases, predeminantly inhaled cigarette smoke
- The airflow limitation is due to decreased outflow pressure (emphysema) plus increased airway resistance (chronic bronchitis/bronchiolitis)
15
Q
Emyphysema causes COPD as causes decreased outflow pressure and therefore cause airflow limitation.
Describe the pathology of emphysema
A
Emphysema:
- Dilation of any part of the respiratory acinus (air spaces (air spaces distal to the terminal bronchioles) with destructive changes in the alvelor walls
- There is an absence of any scarring (fibrosis)
- Tissue destruction is caused by increased secretion and activation of extracellular proteases by inflammatory cells
- The inflammatory cells are stimulated by noxious particles e.g. smoking
- In centrilobular emphysema (most common cause) these changes are limited to the central part of the lobule directly around the terminal bronchiole, with normal aveoli elsewhere
- Panacinar emphysema leads to destruction and distension of the whole lobule, which can happen in smokers but is more common in a1-antitrypsin deficiency
- Dilated air spaces >1cm are termed bullae
- Loss of connective tissue in the alveolar walls leads to a loss of elastic recoil of the lungs, leading to air entrapment in the lungs and inadequate ventilation
- The reduction in the area available for gas exchange means there is reduced oxygen uptake
16
Q
Chronic bronchitis and bronchiolitis causes COPD as causes increases airway resistance and therefore causes airflow limitation.
Describe the pathology of Chronic bronchitis and bronchiolitis
A
Chronic bronchitis:
- Daily cough with sputum for at least 3 months per year for two years
- The primary abnormality seen is abnormal amounts of mucus, which causes plugging of the airway lumen
- The hypersecretion is associated with hypertrophy and hyperplasia of brochial mucus-secreting glands
- Shown by Reid indec: the ratio of gland: wall thickness
- Inflammation not typically present, although frequent LRTIs develop with secondary inflammation and squamous metaplasia
Bronchiolitis
- Cigarette smokers also develop inflammation of the airways <2mm in diameter, i.e. the bronchioles, with macrophage and lymphoid cell infiltration
- This is actually the first pathological change in COPD
- It may lead to scarring and narrowing of the airways
17
Q
Describe the typical history of a patient with COPD
(symptoms)
A
Clinical presentation:
- Productive morning morning cough, following many years of ‘smoker’s cough’
- Increased frequenced of lower respiratory tract infections
- Slowly progressive dyspnoea with wheezing
- Respiratory failure
- Chronic heart failure (cor pulmonale): occurs late
18
Q
On examination what would you find with a patient with COPD?
A
Signs:
Mild disease:
- widespread disease
Severe disease:
- Observations:
- Tachypnoea
- Cyanosis
- Flapping tremor of outstretched hands (if CO2 retainer)
- Inspection
- Hyperinflation
- Intercostal recession on inspiration
- Lip pursing on expiration
- Signs of respiratory distress (tracheal tug, paradoxical breathing, accessory muscle use)
- Palpation:
- Poor chest expansion
- Percussion:
- Hyper-resonant throughout, loss of cardiac/hepatic dullness
- Auscultation:
- Decreased breath sounds, prolonged expiratory phase
- Polyphonic wheeze (many pitches)
19
Q
What are complications of COPD?
A
- Acute exacerbations
- Polycthaemia (the bone marrow cells produces too many red blood cells)
- Respiratory failure
- Cor pulmonale (the enlargement and failure of the right ventricle of the heart)
- Pneumothorax
- Lung carcinoma
20
Q
What are risk factors for COPD?
A
- Cigarette smoke exposure:
- Stimulates neutrophils to produce elastase
- Can inactivate a1-antitrypsin
- Directly causes mucous gland hypertrophy
- Occuptional exposure to dust
- a1-antitrysin deficiency
- Recurrent chest infections
- Low socioeconomic status
- Asthma/atopy (allergies)
21
Q
Blue bloaters and Pink puffers are patients with COPD who exhibit specific phyical signs as a result of COPD
What are they? Why do they occur?
A
Blue bloaters:
- Patients with severe chronic bronchitis/COPD become insensitive to CO2 and thus rely on their hypoxic drive to stimulate respiratory effort
- These patients are not particularly breathless, but are cyanosed and oedematous
- Suggestive of cor pulmonale
- A blood gas will show type 2 respiratory failure (low oxygen, retaining CO2)
- Oxygen should be given with care in these patients
Pink puffers:
- These patients remain sensitive to CO2, thus keep a low CO2 and a near normal O2
- They are tachypnoeic and tachycardic, using accessory muscles to increase their ventilation and are breathless but not cyanosed
- The patients are very thin as large amounts f calories are used to breath
- This can progress to type 1 respiratory failure
22
Q
Outline the investigation of a patient with suspected COPD
A
- Lung function tests will show evidence of airflow limitation – decrease in both FEV and FVC, and a reduction in the ratio, to below 70%.
- CXR often normal - useful in ruling out other pathology
- CT may outline bullae
- Hb, PCV and CRP may be raised
- ABG may be normal at rest
- Sputum examination normally not required.
- ECG and Echo useful if heart involvement suspected
- Alpha-1 antritrypsin investigation may be required in younger patients or non-smokers.
23
Q
What spirometry data will show restrictive patterns?
obstructive patterns?
A
Restrictive pattern:
- Decrease in FEV and FVC but maintenance of normal ratio
Obstructive pattern:
- Decrease in FEV, normal FVC, and so decrease in ratio
24
Q
What is bronchiectectasis?
A
Chronic dilatation of the airways, leading to chronic infection/inflammation
25
Describe history of a patient with bronchiectectasis
(symptoms and signs)
**Symptoms:**
* Recurrent cough, producing copious quantities of infected sputum
* Intermittent haemoptysis (can be only symptom)
* Persistant halitosis (bad breath)
* Dyspnoea
* Reccurent febrile episodes and episodes of pneumonia
**Signs:**
* Clubbing is common (unlike in COPD)
* Coarse inspiratory crackles over infected areas, typically bibasal
* Wheeze
* Often low body habitus due to high energy demands
26
How do the symptoms and signs of brochiectasis differ from COPD?
* Clubbing is common, unlike in COPD.
* Sputum in COPD is not of the same quantity.
* Unlike in COPD, there is no wheeze.
27
Outline the pathology of bronchiectasis
* Any bronchi may be involved, but most commonly at the lung bases
* Airways are dilated, with purulent secretions and chronic inflammation in the wall with inflammatory granulation tissue
* Granulation tissue can bleed leading to haemoptysis
* With repeated exacerbations there can be fibrous scarring leading to respiratory failure
28
What are complications of bronchiectasis?
* Pneumonia
* Pneumothorax
* Empyema
* Lung abcess
* Haematogenous spread of infection
* Severe life threatening haemoptysis: more severe in cystic fibrosis
29
List risk factors for bronchiectasis
Most commonly no cause found, 'idiopathic bronchiectasis', however anything that interferes with drainage of brochial secretions or causes recurrent/persistent infection can lead to bronchiectasis:
* Post-infective: TB, measles, pertussis, pneumonia
* Cystic fibrosis
* Bronchial-obstruction: tumour/foreign body
* Allergic broncho-pumonary aspergillosis
* Ciliary dyskinetic syndromes: Kartagener's syndrome, Young's syndrome
* Immune deficiency: Specific IgA, hypoammaglobulinaemia
* Connective tissue diseases: 1/3rd of RA pts develop bronchiectasis
30
Elicit the physical signs of bronchiectasis
* Production of a khaki coloured, thick, foul-smelling sputum
* Haemoptysis may occur.
* Coarse inspiratory crackles can be heard over infected areas of the lung
* Halitosis (odorous breath) will persist
* Patients will often be febrile
* Clubbing is present.
31
What are the investigations required for a patient with suspected bronchiectasis?
* Sputum culture: atypical organisms
* CXR: cystic shadowing
* CT: to access distribution of disease, can see dilated airways with **signet ring** sign
* Spirometry: obstructive pattern, reversibility should be assessed
32
Describe the typical presentation of a patient with a community aquired pneumonia (CAP)
(symptoms and signs)
**Symptoms:**
* Acute systemic illness
* Fever
* Rigors
* Vomiting
* Cough
* Initally short, dry and painful progressing to a productive with mucopurulent sputum
* Dyspnoea
* Pleuritic chest pain - may be referred to shoulder or anterior abdominal wall
**Signs:**
* Tachypnoea
* Decreased chest expansion on the affected side
* Dullness to percussion over the affected area
* Coarse crackles and a pleural rub over the affected area, with bronchial breathing
* Increased vocal resonance
* 'Blue balloons' can be heard better: seen in consolidation, can't hear as well in effusions, pneumothorax or collapse
* Upper abdominal tenderness: in lower lobe pneumonia
33
How is the severity of pneumonia assessed?
CURB-65
* **C**onfusion: mini mental test score \<8
* **U**rea \>7mmol/l
* **R**espiratory rate \>30 per minute
* **B**lood pressure: hypotensive \<90/60
* **65** years or older
One point for each finding
0/1 = non-severe CAP
```
2 = moderately severe CAP
\>2 = severe CAP
```
34
How is hospital acquired pneumonia defined?
* Pneumonia that develops at least 48 hours after admission to hospital, with no signs of incubation on adission or develops in somebody in hospital in the past 10 days
35
List the common pathogens causing community acquired pneumonia
* Conventional bacteria (60-80%)
* Streptococcus pneunomia (most common)
* Haemophilus influenzae
* Atypical bacteria (10-20%)
* mycoplasma pneumonia
* Chylamdia pneumonia
* Legionella pneumonia
* Viruses (10-20%)
* Influenza/parainfluenza
36
List the common pathogens causing community acquired pneumonia
* Gram –ve bacteria (E Coli, Pseudomonas, Klebsiella)
* Staph Aureus
37
Who is more suspectable to pneumonia?
Patients at most risk are those following viral infection, hospitalized and ill, smokers, alcoholics, bronchiectasis, bronchial obstruction, immunosuppressed, IVDU, GORD.
38
How can pneumonia be classified with regard to the main site of the inflammatory response?
* Pneumonia can be classified into **lobar pneumonia** or **bronchopneumonia** based on the main site of inflammatory response within lung parenchyma (s the portion of the lung involved in gas transfer - the alveoli, alveolar ducts and respiratory bronchioles)
* Inflammatory exudate within the alveolar air spaces is what renders the infected areas of the lung macroscopically solid in 'consolidation'
39
Describe the pathology of bronchopneumonia
Who is it most common in? Why?
Where is the lobe does it mot commonly affect?
* Primary infection centres around the bronchi, spreading to involve adjacent alveoli which become consolidated
* The initial consolidation is patchy (involves lobules), but if untreated can become confluent (involves whole lobes)
* Most common in infancy and old age due to immobility and retention of secretions thus bronchopneumonia moster most commonly affects lower lobes due to effect of gravity
40
Describe the pathology of lobar pneumonia
* Organims gain entry to distal air spaces rather than colonising bronchi, thus there is rapid spread of infection through alveolar air spaces
* Macroscopically, the whole of the lobe becomes consolidated and airless
* These patients are normally adults, and become severely ill with associated bacteraemia
41
What investigations would you do for a patient presenting with community-acquired pneumonia
* Observations & oxygenation assessment
* Bloods: FBC, CRP, U&Es, LFTs
* Blood cultures
* CXR
* Sputum sample for culture
* Plus mycoplasma PCR if suspected
* Urine for legionella/pneumococcal antigen if moderate/severe (empiral treatment wont cover legionella)
* Serum mycoplasma IgM if suspected
* Throat swab in viral transport medium if sever pneumonia or suspected viral pneumonia
42
What antibiotic treatment woud you give for a patient with community acquired pneumonia?
* CURB 65 0/1: Non-severe CAP
* Oral amoxicillin
* Managed as outpatietn
* CURB 65 2: moderately severe CAP
* Oral amoxicillin and clarithromycin
* Usually admitting patient
* CURB 65 \>2: severe CAO
* IV clarithromycin plus co-amoxiclav
* Admit to high-dependency unit
Antibiotic treatment should be guided to sputum sensitivity results, microbiology advice, trust guidelines and patient’s allergy status.
43
Other than antibiotic how else should a patient with CAP be treated?
* Patients should stop smoking
* have physiotherapy to clear mucous and ensure no decline with regards to ADL once infection is resolved
* should be kept well oxygenated
* should have fluid balance maintained
* should be kept out of pain with pharmacological consideration of co-morbidities
44
What complications of pneumonia can occur?
* Parapneumonic effusion/Empyema (presence of pus in the pleural cavity)
* Post-infective bronchiectasis
* Lung abscess: clubbing
* Sepsis
45
Elicit the classical features of consolidation
Dullness, increased vocal fremitus and bronchial breathing are all a result of consolidation.
46
Recognise the radiological features of consolidation on CXR
Greyness - patchy in broncho, homogenous in lobar.
Middle lobe = heart border obscured
Lower lobe = diaphragm obscured
47
Describe the process of TB infection
| (Primary)
Primary TB
* Produced by M. Tuberculosis infection in those not previously infected
* Mild inflammatory response at site of infection followed by spread to regional lymph nodes
* Combination of infective focus and lymph node involvement is known as the primary complex
* The infective focus is known as the 'Ghon focus'
* 1-2 weeks after the infection, with the onset of immune sensitivity, the tissue reaction at both sites of the primary complex changes form characteristic caseating granulomas
* Pts usually asymptomatic
* Viable bacteria may remain walled off within the primary complex giving latent TB
48
What methods might primary TB become symptomatic?
* The Ghon focus can erode through the visceral pleura to discharge organisms and cause TB pleurisy/pleural effusion
* Enlarged hilar lymph nodes can also erode into the bronchus and rupture, causing TB bronchopneumonia
* The enlarging nodes can also erode into vessels, giving miliary dissemination to the lung (pulmonary arteries) or systemic dissemination (pulmonary vein)
* Erythema nodosum (red lumps on skin) is also common in primary disease
49
Describe how post-primary (secondary) TB infection occurs
* M. Tuberculosis re-infection in tuberculin-sensitive individuals
* Infection can be from exogenous sources, or more commonly 'reactivation' from a healed primary complex
* There is an immediate granulomatous response to the disease, thus regional lymph node involvement is not common
* In the lung, this creates a classical apical lesion termed Assmann focus, with destruction of lung parenchyma leading to caviation
* Again the lesion may heal with fibrosis and calcification if the immune system is strong or will progressively enlarge in those with poor immune systems
* This has greater risks of eroding into vessels/airways and causing complications
50
What are symptoms of post-primary TB?
Signs on examination?
* Earliest symptoms non-specific:
* malaise, night sweats, anorexia, weight loss
* Specific symptoms occur late (only in establish disease)
* Productive mucoid cough
* Repeated small haemoptysis
* Pleural pain
* Can present with pleural effusion
Signs on examination:
* Fever and apical crepitations with late signs of consolidation or pleural effusion
* May be clubbed in advanced disease
51
What are common predisposing factors for a TB infection?
* High risk patients are those
* born in endemic areas
* Previously treated for TB (can come back - post-primary)
* Close contacts with TB
* Immunosupressive co-morbidites or drug treatments
* Live in overcrowded conditions
* Alcohol/drug abusers
52
What investigations would you do if a patient has suspected active pulmonary TB?
* Sputum samples: take at least 3, including one morning sample
* Microscopy: for acid-fast bacilli, results within 24h
* PCR: if rapid diagnostic results are required or suspected MDR-TB (however this will not differentiate between active & latent TB)
* Culture: gold standard diagnostic test, but takes 6 weeks, on Lowenstein-Jensen medium
* If sputum samples negative, bronchoscopy with biopsy
* CXR
* upper lobe cavitation
* pleural effusions
* lymphadenopathy
53
What investigations would you do for a patient with suspected latent TB?
* Mantoux test
* TB antigen injected, size of wheal reaction monitored (is there a reaction)
* Interferon-gamma release assay: IGRA blood test also required to diagnose latent TB in immunocompromised individuals, as they can have false negatives in skin tests
* Always do standard bloods
* FBC, U&Es, LFTs to rule out other causes and will affect treatment given
54
List the common sites and pathological features of non-pumonary TB
When small numbers of tubercle bacilli escape into the blood, most die if host defence mechanisms are effective, yet for unknown reasons some bacilli settle in specific organs and may remain dormant for many years, appearing later to cause disease:
* Painless lymphadenopathy: lymphatic TB
* Monoarthritis: joint/spinal TB
* Sterile pyuria: renal TB
* Meningitic syndrome: TB meningitis
* Erythema nodosum/lupus vulgaris: cutaneous TB
* Chest pain: TB pericarditis
55
What is a pneumothorax?
Collection of air in the pleural space that causes an uncoupling of the lung from the chest wall
56
Describe the clinical presentation of a pneumothorax
* May be aymptomtic in young patients with a small pneumothorax
* May present with a sudden onset of unilateral pleuritic pain, with progressive breathlessness
* There may the physical signs:
* Reduced expansion
* Increased resonance to percussion
* Decreased breath sounds
* Reduced vocal resonance
57
What are the causes of a pneumothorax divided into?
What are the causes?
* Spontaneous pneumothorax
* Primary: lung parenchyma otherwise normal, caused by rupture of the apical bleb, often in tall, thin young men
* Secondary: underlying lung disease/abnormalitiy, e.g. COPD, pneumonia, cystic fibrosis, asthmatic, malignancy
* Traumatic pneumothorax
* penetrating trauma e.g. rib fractures
* Iatrogenic pneumothorax
* lung biopsy
* endoscopy
* subclavian cannulation
* postive pressure ventilation
58
What is the difference between a simple and tension pneumothorax?
**Tension pneumothorax**
* Air in the pleural space leading to cardiac compromise
* Caused by a valvular mechanism allowing air entry to the pleural space during inspiration, but no exit during expiration
* The intrapleural pressure is very high, deflating lung and decreasing venous return to the heart
* Suggested by:
* tracheal deviation away from the affected side
* respiratory distress
* pallor
* haemodynamic compromise
* distended neck veins
59
What investigations would you do for a patient with a suspected pneumothorax?
* Expiratory CXR
* trace outline for areas devoid of lung markings and always look for tracheal deviation
* ABG:
* Signs of respiratory distress or chronic lung disease
60
What is the emergency treatment for a pneumothora?
**Aspiration:**
Insert large bore needle attached to syringe partially filled with saline into the 2nd intercostal space in the mid-clavicular line on the side of the suspected lesion. Pull back on the syringe to allow air the bubble out until a chest drain can be inserted. Alternatively, insert a cannula at the same location, and allow air to flow out.
**Chest drain:**
Pneumothoraces may be aspirated using a chest drain. Chemical pleurodesis with talc is used for patients with contraindication to surgery. Video-assisted thoracoscopic approach may be used to resect a bleb and achieve pleurodesis.
61
What are the major pathological classifications of lung cancers?
(list)
Split into small cell disease (20%) and non-small cell disease (80%)
* Non-small cell lung cancer (80%)
* Squamous cell carcinoma - 50%
* Adenocarcinoma - 20%
* Large cell anaplastic tumours - 10%
* Small cell anaplastic carcinoma (20%)
* AKA oat cell carcinoma
62
Describe the pathology of squamous cell carcinoma (SCC) of the lung
* SCCs arise from squamous metaplasia of the normally psuedostratified ciliated columnar epithelium, in response to cigarette smoke exposure
* They are usually central, and close to the carina, thus frequently present with collapse/infection secondary to obstruction
* They may secrete PTH, causing hypercalcaemia
* They are friable tumours so can often be diagnosed with sputum cytology
* They are relatively slow growing compared to other tumours, and may be resectable
63
Describe the pathology of adenocarcinoma of the lung
* Equal gender incidence unlike the other (3:1 male: female)
* Characteristically orginate in peripheral locations, potentially in areas of previous lung scarring
* Bronchoalveolar carcinoma is a special type of adenocarcinoma, accounting for less than 5% but associated with a better prognosis
64
Describe the pathology of large cell anaplastic carcinoma of the lung
* Features showing SCC or adenocarcinomatous origins may be seen, but they are not differentiated enough to be classified
* They have a poor prognosis, and are often widely disseminated at diagnosis
65
Describe the pathology of small cell anaplastic carcinoma of the lung
* Aka oat cell carcinoma, as the cell nuclei resemble oat grains
* Arises from neuroendocrine "Kulchitsky" cells, and expresses markers e.g. NCAM-1
* Usually centrally located, and rapidly growing
* The most highly malignant of lung cancers, often metastasied at diagnosis
* Originate from the bronchial epithelium, but differentiate into neuroendocrine cells to secrete active products:
* ADH: symptoms of SIADH - dillutionall hyponatraemia due to retention of water but not solute, leading to muscle weakness, cheyne-stokes respiration and neurological signs
* ATCH: Cushing's syndrome
* They can also rarely cause Myasthenia Gravis like symptoms in 'Eaton-Lambert syndrome'
* Reduced tendon reflexes
* Dry eyes, sexual inpotence and neuropathy
* Symptoms get better with usage unlike MG
66
Describe the risk factors for lung cancer
* **Smoking**
* Passive smoking (1.5x)
* living in an urban area
* Asbestos
* petroleum products
* radiation
* coal tar
* multiple other occupations exposures - Most occupational exposures related to adenocarcinoma, with less of a link with smoking.
* Family history (genetics) and fibrosis may also play a role in cancer development
67
Outline the epidemiology of lung cancer in developed countries
Lung cancer represents 13.6% of cancer load in the UK, but 22% of cancer-related deaths. The male:female ratio is 3:1
68
Describe the common clinical presentation of lung cancer
Symptoms and signs
Clinical features: (symptoms)
* Persistant cough: due to distal infection
* Haemoptysis: due to ulceration of the tumour
* Dyspnoea: due to ulceration of the tumour
* Chest pain: due to pleural/chest wall involvement
* B symptoms: e.g. fever, night sweats, weight loss
On examination: (signs)
* Clubbing
* Cachexia
* Signs of anaemia
* Hypertrophic pulmonary osteoarthropathy
* Paraneoplastic syndrome: clubbing and painful periosteitis of small joints of the hand
* Chest signs of collapse/consolidation/effusion
* Signs of metastases
69
What can local invasion of lung cancer cause?
i.e. what stuctures are affected?
* Recurrent laryngeal nerve palsy
* Change in voice, left cord paresis
* If present, indicates inoperability
* Phrenic nerve palsy
* asymptomatic if unilateral
* SVC obstruction
* Raised JVP
* raised arm BP/swelling
* facial swelling
* Often due to lymph nodes rather than the tumour itself
* Pancoast syndrome
* Malignant neoplasm of the lung apex, leading to destructive lesions of the thoracic inlet, often involving the brachial plexus
* Horner's syndrome (miosis-pupil constrition, ptosis-drooping of upper eyelid, anhydrosis-inability to sweat in forehead)
* Shoulder pain, radiating along the ulnar forearm and hand
* Atrophy of hand/arm muscles
* Oedema (due to blood vessel compression)
* Pericarditis
* Atrial fibrilation
70
What paraneoplastic syndrome can local metastic manifetions of lung cancer cause?
* Hypertrophic pulmonary osteoarthropathy
* clubbing and periostitis of the small hand joints
* Distal expansion of the long bones as well as painful, swollen joints and synovial villous proliferation are often seen
* Lamert-eaton syndrome - resulting in muscle weakness
* SIADH
* Secondary Cushing's
* HyperPTH
71
What investigation would you do for a patient with suspected lung cancer?
What might you find if they did have lung cancer?
* FBCs:
* anaemia/secondary polycthaemia (too many RBCs)
* LFTs:
* signs of liver metastases
* U&Es:
* hypercalcaemia, hyponatraemia
* CXR
* Sputum/pleural fluid cytology
* Staging CT: head to pelvis
* Biopsy: CT guided if peripheral, via bronchoscopy if central
* Pulmonary function tests: useful if planning surgery
* PET scan/radionucleotide bone scan if suspected metastatic diesease
72
Describe a bronchoscopy procedure to a patient
Fibre optic tube is passed through the nose, then the oropharynx and finally the pharynx, larynx, trachea and is able to visualise the carina and bronchioles. The patient may be offered a local anaesthetic spray, or, it may be done in the anaesthetic room pre-operatively.
73
What is a pleural effusion?
A pleural effusion is excess fluid that accumulates in the pleural cavity, the fluid-filled space that surrounds the lungs
74
What are the types of collections which may accumulate in the pleural space?
* Empyema/pyothorax:
* accumulation of pus, due to infection
* Chylothorax:
* accumulation of lymph due to thoracic duct leakage
* Haemothorax:
* accumulation of blood, due to trauma
* Fluid effusion: transudates or exudates
75
How are the causes of a pleural effusion classified?
**Transudative effusion causes:** (occur due to increased hydrostatic pressure or decreased oncotic pressure)
* Cardiac failure:
* LHF leading to increased hydrostatic pressure
* Liver failure:
* decreased protein production decreasing oncotic pressure
* Renal failure:
* nephrotic syndrome decreasing oncotic pressure
* Peritoneal dialysis
**Exudative effusion causes:** (occur due to increased capillary permeability)
* Infections
* bacterial pneumonia
* TB
* Neoplasm
* lung prumary or secondary
* mesothelioma
* Pulmonary infarction
* PE
* Autoimmune disease
* RA/SLE
* Abdominal disease
* pancreatitis
* subphrenic abscess
76
Describe the clinical features and examination features of a pleural effusion
(symptoms & signs)
Symptoms:
* May be asymptomatic or present with dysponea and pleuritic pain
Signs (on examination):
* Descreased chest expansion, tracheal deviation away if large
* Stony dull to percussion
* Decreased breath sounds
* Can be bronichial breathing above effusion due to compressed lung
* Reduced vocal resonance
* Mediastinal deviation (in massive effusion)
77
Describe the aetiology and clinical features of an empyema
* An empyema is the presence of pus in the pleural space
* it is caused by bacterial invasion of the pleural space , either spreading into an exudative effusion from adjacent pneumonia, or from direct inoculation (e.g. poor aseptic technique in a chest drain)
Clinical presents:
* As fever plus signs of pleural effusion
* fever, rigors, malaise, pleuritic pain, SOB
* Aspirated fluid is yellow and turbid, with pH \<7.2, low glucose, high lactate dehydrogensase
78
What investigations would you do for a unilateral pleural effusion?
What would they show?
Unilateral effusions are more likely to be exudative, with bilateral effusions more likely to be transudative
Investigations:
* CXR:
* Can be detected when \>300ml fluid is present, a flat upper border implies there is also a pneumothorax
* USS (to guide aspiration)
* Aspiration:
* Fluid sent to sent microbiology (for MCS)
* Clinical chemistry (protein, lactate dehydrogenase (LDH), glucose)
* **_Cytology_**
* **Exudates have a protein level of \>30g/L**
* **Transudates have a protein level of \<30g/L**
79
Describe the main conditions associated with asbestos inhalation
**Mesothelioma:**
* Caused by light exposure, with an interval of 20-40 years between exposure to disease onset
* There will be pleuritic pain, increasing dyspnoea and a unilateral pleural effusion on CXR
* Survival is poor, with median survival of 2 years from diagnosis
**Asbestosis:**
* Caused by heavy exposure, with an interval of 5-10 years from exposure to disease
* There will be progressive dyspnoea, with diffuse bilateral streaky strikes on CXR with honeycombing
* The outcome is poor and can progress after exposure ceases
There can also be asbestos-related carcinoma of the bronchus, with features above plus those of bronchial carcinoma
80
What is pneumoconiosis?
Pneumoconiosis is disease of the lungs caused by inhalation of dusts, generally used to refer to pathology caused by coal dust
81
Describe the pathology of simple and complicated pneumoconiosis
* The coal dust is toxic to macrophages (normal defence for inhaled dusts), thus there will be a local inflammatory response similar to that seen in COPD
* If this becomes chronic, there will be fibrosis leading to restructive lung disease
* Silicates are the main dusts causing industrial pulmonary fibrosis, often mixed with coal
**Simple coalworker's pneumoconiosis:**
* Presence of small nodules (2-5mm) on CXR, not associated with any clinically significant impairment of respiratory function
* May develop progressive massive fibrosis
**Progressive massive fibrosis:**
* Presence of large nodules (\>10mm) on CXR, and the disease progresses relentlessly leading to a mixed obstructive and restrictive pattern
* It may present long after active exposure to coal dust, and culminates in COPD (dyspnoea and cough productive sputum, sometimes black)
* This can progress to respiratory failure
82
# Define restrictive lung disease
Causes?
Restrictive lung disease involves processes that reduce the patient’s total lung capacity, without loss of ability to inspire and expire adequately.
**Causes:**
* Recurrent exogenous injury and responsive endogenous stimuli lead to transformation, disruption and apoptosis of epithelial cells in the lung.
* Cytokines are released, stimulating angiogenesis and myofibroblast proliferation: leading to collagen construction and development of “fibrotic foci”.
83
Define obstructive lung disease
Obstructive deficits involve maintenance of normal total lung capacity, but a decline in ability to inspire and expire as easily
84
What are the main groups of disease leading to pulmonary fibrosis?
* Localised fibrosis may be caused by:
* systemic sclerosis
* sarcoidosis
* tuberculosis
* asbestosis
* berylliosis
* Diffuse fibrosis may be caused by:
* Idiopathy pulmonary fibrosis
* Rheumatoid lung
* Tuberous sclerosis
* neurofibromatosis
* Langerhans’ cell histiocytosis
85
How does is fibrosis classified?
How do they differ in presentation and on X-ray?
Localised or generalised fibrosis
* Localised fibrosis physical signs at the chest wall include:
* reduced chest wall movement on affected side
* mediastinal displacement towards the lesion
* dull to percussion
* bronchial breath sounds
* increased vocal resonance
* coarse crackles
* Generalised fibrosis will lead to:
* reduced global expansion
* increased vocal resonance
* fine crackles.
Localised fibrosis gives streaky shadowing on CXR, whereas generalised fibrosis gives a honeycomb lung picture.
86
How can you distinguish between type 1 and type 2 respiratory failure?
**Type I Respiratory failure:**
* PaO2 low (\<8kPa)
* PaCO2 normal or low
It is typically caused by a ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs
caused by diseases of the lung parenchyma
**Type II Respiratory failure:**
* PaO2 low (\<8kPa)
* PaCO2 high (\>6kPa)
Type 2 respiratory failure is caused by inadequate alveolar ventilation; both oxygen and carbon dioxide are affected
87
What are the implications of having a high arterial pCO2?
Hypercapnia results in a respiratory acidosis. This may eventually lead to unconsciousness and death
Clinical features of hypercapnia are:
* Headache, tachycardia, bounding pulse, CO2 retention flap and papilloedema as well as feature of acidosis:
* Kussmal respiration: air hunger, giving deep and laboured breathing
* Cardiovascular dysfunction
* Potassium abnormalities: acidosis leads to potassium loss from cells, leading to hypokalaemia if renal function is good, or hyperkalaemia if impaired
* Cerebral dysfunction: confusion or coma
* Peripheral vasodilation & increased permeability: leadiing to oedema
88
Distinguish between acute and chronic type II respiratory failure and respiratory and metabolic causes of acidosis
Chronic type II respiratory failure is caused most commonly by COPD.
Acute causes include morphine overdose, airway collapse, foreign body, etc.
Chronic respiratory acidosis will exist alongside metabolic compensation, whereas acute respiratory acidosis will not – the metabolic compensation is not a fast process.
Respiratory acidosis is caused by a high pCO2, whereas metabolic acidosis is caused by a negative base excess
89
What are the causes of ventilatory failure?
(type 2 respiratory failure)
Occurs when alveolar ventilation is insufficient to excrete the volume of CO2 being produced by tissue metabolism
* Severe pulmonary disease:
* asthma
* COPD
* pulmonary fibrosis
* obstructive sleep apnea
* Reduced respiratory drive
* CNS pathology
* sedative drugs
* Thoracic wall disease
* rib fracture (pain)
* kyphoscoliosis
* flail chest
* Neuromuscular disease
* diaphragmatic paraylsis
* Myasthenia gravis
* Guillian-Barre
* cord lesions
* Poliomyelitis
90
What is the effect of chest wall and spinal deformity on respiratory function?
Deviation in the shape of the chest wall away from normal is going to have logical effects on respiratory function, through change/limitation in the ability of the chest to expand
CP1
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