Case 6- illness Flashcards
Pneumothorax
Air in pleural cavity, can result in a collapsed lung
Pleural effusion
Fluid in pleural cavity
Haemothorax
Blood in pleural cavity
Chylothorax
Lymph in pleural cavity
What causes a collapsed lung
Pneumothorax, pleural effusion, Haemothorax and Chylothorax. These all cause a collapsed lung which is unable to expand
How many cases of lung cancer are caused by smoking
90%
Lung cancer- when to refer for chest x-ray?
Findings are suggestive of cancer or they are over 40 with unexplained haemoptysis
Lung cancer- when to offer an urgent chest x-ray
In people over 40 with 2 or more of the following symptoms. The same is true if they have ever smoked and have one or more of the following unexplained symptoms: cough, fatigue, chest pain, weight loss, shortness of breath and appetite loss.
Lung cancer- what can happen to the tumours
Tumours may obstruct airways causing: persistent cough, shortness of breath and chest pain.
Tumours may also invade arteries causing bleeding: Haemoptysis (coughing up blood)
Tumours may compress mediastinal structures: Phrenic nerve compression (difficulty breathing), recurrent laryngeal nerve compression (hoarseness) and compression of the oesophagus (dysphagia).
Other side effects of lung cancer
Anaemia, bone pain, finger clubbing, fatigue, loss of appetite and weight loss
Paraneoplastic
Where seemingly false signs and symptoms are seen. The tumour may secrete hormones, antibodies and enzymes that affect sites far away from the tumour.
Symptoms of lung cancer associated Paraneoplastic syndrome
Neurologic, endocrine, dermatologic, rheumatologic, hematologic, and ophthalmological, nephrotic/glomerular symptoms.
Pancoast tumours
Tumour growths in the apical region of the lungs, typically squamous carcinoma. It presents with shoulder pain and Horner’s syndrome causing unilateral: ptosis (dropping of one eyelid), Miosis (pupil constricted in one eye) and Anhidrosis (loss of ability to sweat)
Small lung carcinomas
20% of lung cancers. An aggressive tumour with poor prognosis as it grows rapidly and metastases early. It develops centrally near the main bronchus. Neuroendocrine cells of the lung appear to have scant cytoplasm, the nuclei looks bigger by comparison. The cells appear indistinct. Associated with paraneoplastic syndrome.
Types of non-small cell lung carcinomas (80%)
1) Squamous cell carcinoma
2) Adenocarcinoma
3) Large-cell carcinoma
Squamous cell carcinoma
25% of lung cancers. Develops centrally near the main bronchus. Histological features include a change from columnar epithelium to squamous epithelial cells, deposition of keratin ‘pearls’. And it is surrounded by concentric circles of squamous epithelial cells.
Adenocarcinomas
35% of lung cancers. It develops peripherally. Histological features include mucoid glands. It is more common in woman and is the most common lung cancer in non-smokers.
Large cell carcinoma’s
10-15% of lung cancers. Epithelial tumours that lack the cytological features of small cell carcinoma and have no glandular or squamous differentiation
Symptoms of pleural effusion
Symptoms include chest pain, dyspnoea, cough, finger clubbing and symptoms of the underlying disease like weight loss. There must be a large effusion before it causes symptoms- 200ml for diagnosis (x-ray) and 500ml for it to be clinically evident.
How does pleural effusion present in examination
Inspect their hands for clubbing, you should also examine their breathing. During palpations you will see that chest expansion is reduced on the side of the effusion. During auscultation, the breath sound will be lower or absent and the vocal resonance will be lower or absent.
What can you see in an x-ray of pleural effusion
It will apear white, as it progresses the costophrenic angle disappears. As the fluid fills the lungs a meniscus will appear (curved upper surface of a liquid in a tube).
Pleural effusion- thoracentesis
Aspiration of fluid (removing) can be done to identify cause. This is done under the guidance of ultrasound and you insert the needle between the 7th and 8th rib. You then measure the protein to identify the type of effusion
Pleural effusion- Transudate
Pleural effusion caused by an increase in hydrostatic pressure due to venous outflow obstruction. This is caused by congestive heart failure. There will also be a drop in colloid osmotic (oncotic) pressure as not enough protein is made or too much is being lost. This causes the fluid to leak across but the proteins don’t. Most common causes include Heart failure, Hypoalbuminemia, Cirrhosis and Nephrotic syndrome. Less oncotic
How to identify pleural effusion caused by Transudate
Light criteria: pleural effusion to serum protein ratio should be <0.5
Pleural effusion- Exudate
Inflammation leads to increased permeability and protein and fluid leakage. Most common cause is Pneumonia and malignancy (breast and lung cancer). Large unilateral pleural effusions are probably due to malignancy. More oncotic then transudate
How to identify pleural effusion caused by Exudate
Pleural fluid protein vs. serum protein ratio >0.5
Types of Pneumothorax
- Primary spontaneous- occurs in health people (typically tall thin men).
- Secondary spontaneous- underlying condition (e.g. rupture of bulla in COPD).
- Traumatic- penetrating chest trauma (e.g. stab wound).
- Latrogneic- follows a procedure (e.g. mechanical ventilation.
How does Pneumothorax present
Unilateral pleuritic chest pain with breathlessness and possible cyanosis
Examination findings in Pneumothorax
In examination of the affected side there will be reduced chest expansion, decreased or absent breath sounds and hyper-resonance on percussion.
Chest x-ray of pneumorothorax
In a chest x-ray the collapse of lung tissue will be visible as the lung recoils and peels away from the chest wall.
Treatment of pneumorothorax
It is treated using a chest drain which when inserted into the pleural space can drain the air and fluid.
Features of tension pneumothorax
1) Tracheal deviation away from the site.
2) Tachycardia is >135bpm.
3) You get a pulsus paradoxus when there is an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration. The drop in blood pressure is more than 10mmHg.
4) Hypotension and a raised JVP.
5) It is a life threatening condition that requires instant action such as urgent decompression in the 2nd intercostal space. There is a mediastinal shift and signs of respiratory disease.
Haemothorax
Presence of frank blood in the pleural space. It can be caused by chest trauma, cancer or a pulmonary embolism.
Chylothorax
Presence of lymphatic fluid in the pleural space
Empyema
Presence of pus in the pleural space. Secondary to infection, usually pneumonia. Causes prominent systemic features and severe chest pain
Pleural Mesothelioma
Malignant mesothelioma affects the mesothelial lining but can also affect the pleura. This tumour rarely metastasises to distant sites and most patients present with locally advanced disease. It has a poor prognosis of approx. 1 year.
Signs and symptoms of pleural Mesothelioma
- Breathlessness.
- Pleural effusion or pleural thickening
- Chest pain is typically dull, diffuse, progressive.
- Palpable chest wall
- Weight loss, fatigue and fever.
- Finger clubbing (related to asbestosis).
What causes pleural Mesothelioma
Associated with asbestos in 70-80% of patients, may be many years after exposure of from another family members exposure
Pulmonary embolism
When one or more emboli (normally a blood clot) are lodged in and obstruct the pulmonary artery system
Risk factors for PE
Significant immobility and surgery
Causes of PE
- Emboli originating in the abdominal or axillary veins, or from the right ventricle.
- The most common type of emboli is DVT in the lower limbs (80%).
- Tumours.
- Fat emboli from long bone fractures.
- Amniotic fluid-pregnant woman
- Sepsis- i.e. infected catheters
- Foreign bodies, during IV drug use.
- Air- admitted during surgery.
Small and medium PE
Small and medium PE may not have any specific signs and symptoms. They may have dyspnoea, tachypnoea (abnormally rapid breathing), pleuritic chest pain or features of DVT. These features are present in most people with a PE even if they don’t have a DVT.
Signs and symptoms of PE
Dyspnoea, tachypnoea (rapid breathing), pleuritic chest pain, tachycardia, haemoptysis, syncope, hypotension (systolic BP less than 90 mmHg), crepitations (crackling sound), cough or fever.
Treatment for PE
Heparin and anticoagulants
PE
If untreated the risk of death is 23-87%, for clinically massive PE the risk of death is 50%. PE is the leading cause of maternal death in the UK
In PE when should the patient be admitted to hospital
- The patient is pregnant or given birth within the past 6 weeks.
- They have an altered level of consciousness.
- Systolic BP of less than 90 mmHg.
- Heart rate of more than 130 beats per minute.
- Respiratory rate of more than 25 breaths per minute.
- Oxygen saturation of less than 91%
- Temperature of less than 35 degrees
How does lung compliance change in emphysema
Compliance is higher because a lower pressure can cause a higher volume. There is less recoil due to the loss of elastic tissue
How does lung compliance change in alveolar fibrosis
The lungs are stiffer and have less compliance as the lung tissue gets replaced by fibrous tissue. A higher pressure causes a lower volume (right shift)
Pathway of care- lung cancer
GP -detection
Radiologist- diagnosing through investigations (CT scans, biopsy)
Multi-disciplinary team (including lung cancer specialist)- discussion of treatment plan
Surgeon- surgery to remove cancer
Oncologist- chemotherapy
May have to refer to palliative care
Airway resistance in COPD and asthma
It increases in asthma and COPD, the higher the resistance the harder it is to breathe. In asthma the resistance is reversible, in COPD the resistance is irreversible. In COPD small bronchioles offer the most resistance even though normally they offer the least.
Volume/Pressure graph in COPD
In inspiration a higher pressure is needed to increase the volume of the lungs. In expiration there is little reduction in volume as the airways collapse. At low pressure the airways do empty
COPD
Persistent respiratory symptoms due to airway obstruction which is not fully reversible. Includes bronchitis and emphysema
Emphysema
You get inflammation. There is an increase in elastase and metalloproteinase. Protein and elastin gets broken down and there is damage to tissues and capillaries. Less blood will move into the diffusion barrier. Less gases are able to diffuse across the alveolar membrane. As more tissue gets broken down elastic recoil decreases. You get enlarged alveolar which causes air trapping. There is lung hyperinflation. Air becomes trapped in the lungs as the alveolar membrane breaks down.
Risk factors for emphysema
Smoking, toxins, pollutants, Genetics ( a mutation in Alpha1- antitrypsin, which causes its deficiency)
Morphology of bronchiectasis
Permanent dilation of bronchi and bronchioles due to inflammation and scarring, usually the lower lobe
Symptoms of bronchiectasis
Persistent or recurrent cough and foul-smelling purulent sputum production. Recurrent respiratory infection and Haemoptysis
What is bronchiectasis associated with
It is associated with respiratory infection. This causes sustained epithelial injury and hypersecretion of mucus. If you have epithelial injury you are more likely to get chronic Bronchial infection. The lungs then become inflamed. There is a decrease in mucocilliary clearance. There is now permanent airway damage. Often associated with COPD.
Respiratory infections which can cause bronchiectasis
Congenital (diffuse)- Cystic fibrosis and Ciliary dysfunction.
Acquired (localised)- Pneumonia, TB and Bronchial tumours.
How is bronchitis diagnosed
A persistent productive cough for at least three consecutive months in at least two consecutive years
Morphology of chronic bronchitis
1) Cilia gets damaged so less mucus is removed.
2) Lumen blockage due to mucus hypersecretion.
3) There is an increase in goblet cells and an increase in mucus gland size and activity.
4) Increase in smooth muscle and bronchospasm
Where do you tend to get emphysema
In the upper two thirds of the lungs
Hyperinflation of lungs
Associated with air trapping as there is a bigger lung volume
Signs of emphysema
Barrel chest and progressive dyspnoea
Why do we see the signs and symptoms of chronic bronchitis
1) Mucus hypersecretion- productive cough
2) Bronchoconstriction- wheezing
3) Decrease in pO2- cyanosis
4) Alveolar hypoxia- pulmonary hypertension
5) Right sided heart failure- Cr pulmonale
Unlikely to have a fever or dullness to percusion.
Chronic bronchitis- bronchial spasm
There will be a degree of Bronchiolitis as there is inflammation of the Bronchioles. This causes bronchiole spasm which reduced the area of the lumen.
Interstitial lung disease (parenchymal lung disease)
A heterogeneous group of restrictive lung disease. An initial injury to the epithelium or endothelium leads to diffuse chronic inflammation and fibrosis with end stage honeycomb appearance. Lung volume and compliance decreases. In pulmonary fibrosis a trigger causes repeated inflammation. This causes the release of cytokines which promote fibrogenesis. Eventually this cycle leads to the dilation of airways.
Interstitial lung disease- fibroblasts
Pulmonary fibrosis is a pathological feature of interstitial lung disease. The fibroblasts lay down fibrous tissue, this makes the tissue stiffer reducing compliance.
Pulmonary fibrosis- Pathogenesis
1) Inflammation causes leukocyte induced cytokine release i.e. from inhalation of dust, drugs or idiopathic conditions.
2) Stimulation of fibrosis via increased fibroblasts
3) Alveolar epithelial cell damage.
4) Decreased surface area for gas transfusion.
5) Increased stiffness and decreased compliance
Types of interstitial lung disease
Huge range of conditions linked by pulmonary fibrosis
What can cause interstitial lung disease
1) Occupation/Environment- asbestosis, Coal miners pneumconiosis.
2) Hobbies- wine making, glass blowing.
3) Pets- pigeon fancier’s lung
4) Past medical history- connective tissue diseases, lupus, sarcoidosis, rheumatoid arthiritis.
5) Drugs- Amiodarone (heart medication), Nitrofurantoin (antibiotic), Methotrexate.
Idiopathic pulmonary fibrosis
Accounts for 15-25% of chronic interstitial lung disease where the cause of inflammation is unknown
Types of restrictive lung disease
Interstitial lung disease
Types of obstructive lung disease
COPD, asthma and bronchiectasis
Obstructive lung disease
Limitation of airflow due to obstruction Total lung capacity- Normal Forced vital capacity (FVC)- Normal Expiratory flow (FEV1)- decreased FEV1:FVC ratio- decreased
Restrictive lung disease
Fibrosis reduces ability of parenchyma to expand Total lung capacity- decreased Forced vital capacity (FVC)- decreased Expiratory flow (FEV1)- decreased FEV1:FVC ratio- normal
Vital capacity (VC)
The greatest volume you can expire starting from a position of maximal inspiration = IRV + VT + ERV = 4600 ml. The vital capacity is affected by posture, is proportional to height, decreases with age and is generally higher in males than females.
Tidal volume (VT)
The volume breathed in or out at rest (500ml)
Inspiratory Reserve Volume (IRV)
The volume of air that can be inspired in addition to normal resting (tidal) inspiration = 3000 ml.
Expiratory Reserve Volume (ERV)
The volume of air that can be expired following a normal (tidal) expiration = 1100 ml.
Residual volume (RV)
The volume of air remaining in the lungs at the end of a maximal expiration (i.e. it is the air that cannot be expired) = 1200 ml.
Functional residual capacity (FRC)
The volume of air remaining in the lungs at the end of a normal resting expiration = ERV + RV = 2300 ml.
Forced Expiratory Volume in one second (FEV1)
The greatest volume of air which the subject can expire in the first second starting from the position of maximal inspiration and expiring as hard and fast as possible.
Forced vital capacity (FVC)
The greatest volume of air the subject can expire starting from a position of maximal inspiration and expiring as hard and fast as possible
Peak expiratory flow (PEF)
The maximum flow rate during forced expiration
FVC and FEV1 in restrictive
FEV1 - <80% predicted
FVC- <80% predicted
FEV1/FVC ratio- >0.7
FVC and FEV1 in obstructive disease
FEV1- <80% predicted
FVC- unchanged, drops in severe disease
FEV1/FVC ratio- <0.7
Classification gained from FEV1 % predicted value:
- FEV1 80% or above of predicted: Mild disease
- FEV1 50-79 % of predicted: Moderate disease
- FEV1 30-49% of predicted: Severe disease
- FEV1< 30% of predicted: V. severe disease
