Block 3: Pneumoconiosis, Pneumothorax Flashcards

1
Q

Asbestosis mangement

A
  • No specific cures
  • Avoiding further asbestos exposure
  • Smoking cessation
  • Annual influenza and pneumonia vaccination
  • Pulmonary rehabilitation
  • Screening for other asbestos-related diseases
  • Long-term oxygen therapy
  • Prognosis is better than in idiopathic pulmonary fibrosis (IPF)
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2
Q

Asbestosis features

A
  • dyspnoea and reduced exercise tolerance
  • clubbing
  • bilateral end-inspiratory crackles
  • lung function tests show a restrictive pattern with reduced gas transfer
  • typically causes lower lobe fibrosis
  • Treated conservatively
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3
Q

Types of asbestos

A
  • Serpentine- long curly whit fibres
  • Amphibole- blue and brown asbestos which are short needle like structures that lodge in the alveoli and cant be cleared
  • The lower sub-pleural zones are most affected
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4
Q

Other causes of asbestos related lung disease: BAPE and pleural plaques

A
  • Pleural plaques: benign and do not undergo malignant change, dont require any follow up. Typically asymptomatic but may cause pleural rub and reduce lung volume if extensive. They are smooth areas of hyaline fibrosis
  • Benign asbestos pleural effusion (BAPE): unilateral effusion, usually occurs within 10 years of exposure, will be exudate fluid and blood stained. Diagnosis of exclusion. Resolves spontaneously after a few months but might need aspiration or pleurodesis.
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5
Q

Other causes of asbestos related lung disease: mesothelioma and lung cancer

A
  • Mesothelioma: malignant disease of the pleura. Crocidolite (blue) asbestos is the most dangerous form. Offered palliative chemotherapy and limited role for surgery and radiotherapy, poor prognosis. Risk is not dose related. Diagnosis by biopsy, 50% die in the first year
  • Lung cancer: advised to stop smoking
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6
Q

Occupational exposure to asbestos

A

Construction, insulation, fireproofing, brake lining, ship building, boiler fitting, carpentry and electrical repair.

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7
Q

Malignant mesothelioma investigations

A
  • CXR: pleural effusion with associated pleural plaques
  • CT Thorax: would show pleural thickening, calcified pleural plaques and a pleural effusion
  • Pleural aspiration: sent for cytology, microbiology and biochemistry. Cytology would show reactive mesothelial cells, pleural fluid is exudate
  • VATS with pleural biopsy: gold standard, biopsy is needed to confirm diagnosis and allows pleurodesis to be performed at the same time.
  • Local anaesthetic thorascopy can be used to investigate cytology
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8
Q

Features of mesothelioma

A
  • Dyspnoea, weight loss, chest wall pain
  • Clubbing
  • 30% present as painless pleural effusion
  • Only 20% have pre-existing asbestosis
  • History of asbestos exposure in 85-90%, latent period of 30-40 years
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9
Q

Lights criteria for a pleural fluid exudate re:

A
  • Pleural fluid : serum protein ratio > 0.5
  • Pleural fluid : serum LDH ratio > 0.6
  • Pleural fluid LDH > 2/3 the upper limit of normal serum LDH
  • Causes of an exudate include: infection (lung and pleural), malignancy, connective tissue diseases, pulmonary embolism, chylothorax, ARDS and pancreatitis.
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10
Q

Management of mesothelioma

A
  • Symptomatic
  • Industrial Injuries disablement benefit is available for patients with diffuse pleural thickening, asbestosis, mesothelioma or lung cancer associated with asbestos exposure. Pleural plaques alone do not qualify.
  • The Diffuse Mesothelioma Payment Scheme: provides payouts when the employer is not contactable
  • Chemotherapy (cisplatin and pemtrexed), Surgery if operable
  • Prognosis poor, median survival 12 months
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11
Q

Pneumothorax risk factors

A
  • pre-existing lung disease: COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia
  • connective tissue disease: Marfan’s syndrome, rheumatoid arthritis
  • ventilation, including non-invasive ventilation
  • Menstruating women
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12
Q

Pneumothorax classification (primary/secondary)

A
  • Primary spontaneous pneumothorax (PSP): Occurs without underlying lung disease, often in tall, thin, young individuals. PSP is associated with the rupture of subpleural blebs or bullae.
  • Secondary spontaneous pneumothorax (SSP): Occurs in patients with pre-existing lung disease, such as chronic obstructive pulmonary disease (COPD), asthma, cystic fibrosis, or interstitial lung disease. Likely if >50 with significant smoking history
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13
Q

Pneumothorax classification: Traumatic/Iatrogenic

A
  • Traumatic pneumothorax: Results from penetrating or blunt chest trauma, leading to lung injury and pleural air accumulation.
  • Iatrogenic pneumothorax: Occurs as a complication of medical procedures, such as thoracentesis, central venous catheter placement, mechanical ventilation, or lung biopsy.
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14
Q

Pneumothorax features

A
  • Sudden onset pleuritic chest pain and dyspnoea, occasional dry cough
  • Primary: sometimes after exertion but not always
  • Examination: diminished breath sounds, hyper resonance on percussion, decreased vocal resonance and decreased chest wall movement on the affected side
  • Severe cases: hypoxia, tachypnoea, tachycardia and hypotension
  • Tensions pneumothorax; life threatening condition that presents with severe respiratory distress, tacheal deviation, jugular venous distension and haemodynamic instability
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15
Q

Pneumothorax investigations

A
  • CXR in posteroanterior (PA) and lateral view: reveals a visceral pleural line, absence of lung marking peripheral to the line
  • CT: can confirm diagnosis
  • Point of care ultrasound (POCUS): in rapid bedside diagnosis especially in tension pneumothorax and unstable patients
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16
Q

Primary pneumothorax management

A
  • if the rim of air is < 2cm and the patient is not short of breath then discharge should be considered: follow up over 2-4 weeks
  • otherwise, aspiration should be attempted
  • if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted
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17
Q

Secondary pneumothorax management

A
  • if the patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.
  • otherwise aspirate if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater then 1cm) a chest drain should be inserted. All patients should be admitted for at least 24 hours
  • if the pneumothorax is less the 1cm then give oxygen and admit for 24 hours
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18
Q

Other treatment for pneumothorax: iatrogenic, persistent, recurrent

A
  • Iatrogenic: majority will resolve with observation, if treatment required use aspiration. For ventilated patients and many with COPD use a chest drain
  • Persistent/recurrent pneumothorax: If a patient has a persistent air leak or insufficient lung reexpansion despite chest drain insertion, or recurrent pneumothoraces, then video-assisted thoracoscopic surgery (VATS) should be considered to allow for mechanical/chemical pleurodesis +/- bullectomy.
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19
Q

Treatment for pneumothorax: discharge advice

A

Sop smoking, don’t fly for 1-2 weeks and radiological resolution, ban on scuba diving unless the patient has had a bilateral surgical pleurectomy and now normal lung function and chest CT

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20
Q

Tension pneumothorax CXR

A

Loss of lung markings, trachea moves away from the pneumothorax. Treatment is needle decompression in the mid-clavicular line second intercostal space

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21
Q

Chronic thromboembolic pulmonary hypertension

A

Emboli are replaced over months or years by fibrous tissue, leading to chronic obstruction of the pulmonary arterial vasculature, progressive increases in pulmonary arterial pressure, and, if untreated, right heart failure. A rare complication of PE

22
Q

Complications of PE

A

death, right heart failure, Chronic thromboembolic pulmonary hypertension, recurrence of PE

Signs indicating central PE: hypotension and cardiogenic shock

23
Q

Pulmonary hypertension

A

An increase in mean pulmonary arterial pressure (PAPm) to ≥20 mmHg at rest as assessed by right heart catheterisation (RHC). The normal PAPm is 14+/3-mmHg

24
Q

Classification of pulmonary hypertension (by underlying cause)

A
  1. pulmonary arterial hypertension
  2. PH due to left heart disease
  3. PH due to lung disease
  4. chronic thromboembolic pulmonary hypertension
  5. PH with unclear / multifactorial mechanisms
25
Q

Signs and symptoms of pulmonary hypertension

A

SOB, fatigue, syncope, chest pressure/pain oedema, cyanosis, palpitations, raised JVP, right ventricular heave, systolic murmur, hepatomegaly

26
Q

Conditions that lead to PH

A

Liver disease, Connective tissue disease, lung disease, heart disease

27
Q

Investigations into PH

A
  • 1st line: TTE (transthoracic echocardiogram)
  • 2nd line: TOE (Transoesophageal echocardiogram)
  • Definitive: right heart catheter- inserted in jugular vein takes measurements at right atrium, right ventricle and the main pulmonary artery and wedge pressure
  • 6 minute walk test: measures how far someone can walk in 6 minutes, useful in gauging severity an response to treatment
28
Q

Capillary wedge pressure role in categorising PH

A
  • Pre - capillary = low wedge pressure i.e. arising before the capillary bed
  • Post Capillary = high wedge pressure i.e. Arising after the capillary bed - may be left sided heart failure / valvular disease
29
Q

Medical management of PH

A
  • diuretics (symptom control)
  • Oxygen
  • CCBs
  • prostacyclines
  • endothelial receptor agonists (bosentan, macicentan)
  • phosphodiesterase 5 inhibitors (sildenafil, tadalafil)
  • guanylate cyclase inhibitor (riociguat)
30
Q

Surgical management of PH

A

Only done for chronic thromboembolic PH:
- Pulmonary endarterectomy- best for proximal disease
- Balloon dilation: best for distal disease

31
Q

Lung disease causing cor pulmonale

A

Any lung disease or obesity (if causing Obstructive sleep apnoea or Obesity Hypoventilation syndrome

Pathophysiology: reduced blood flow to hypoxic alveoli. In significant hypoxia there is significantly increased pulmonary vascular resistance leading to hypoxia.

32
Q

Idiopathic pulmonary hypertension

A

Most common in young women, due to damage to capillary endothelium and remodelling, can be familial and most commonly associated with 2q 31-32, can be drug induced e.g. by SSRIs, St John’s Wort, pergolide, amphetamines, cocaine, appetite suppressants

33
Q

Management of chronic thromboembolic pulmonary hypertension

A

Lifelong anticoagulation, consider surgery, consider thrombophilias

34
Q

Management of acute exacerbation of COPD

A
  • A to E assessment
  • Controlled oxygen therapy- should be monitored with ABG’s to ensure they are not hypercapnic
  • Steroids (PO)
  • Salbutamol nebulisers (bronchodilator)
  • Ipratropium nebulisers (bronchodilator)
  • Consider antibiotics- if symptoms are severe or there are changes to the sputum
  • Non invasive ventilation- if there is hypercapnia and acidaemia
  • Intubation and ventilation can be considered in patients with severe exacerbations who don’t respond to treatment
35
Q

Pulmonary arterial hypertension

A

Characterised by progressive elevation of the mean pulmonary arterial pressure to more than 25mmHg at rest or more than 30mmHg on exercise. A subgroup of pulmonary hypertension

36
Q

Classes of Pulmonary hypertension

A
  • Class I: Pulmonary arterial hypertension
  • Class II: Pulmonary hypertension owing to left heart disease
  • Class III: Pulmonary hypertension secondary to Chronic Obstructive Pulmonary Disease (COPD)
  • Class IV: Pulmonary hypertension owing to chronic thromboemboli
  • Class V: Pulmonary hypertension owing to multiple miscellaneous causes
37
Q

Categories of PAH

A

1 - Idiopathic PAH
2 - Hereditary PAH
3 - PAH associated with other conditions (including connective tissue disorders, associated HIV infection, cirrhosis with portal hypertension congenital heart disease, schistosomiasis and chronic haemolytic anaemia)
4 - PAH associated with venous or capillary conditions (including pulmonary veno-occlusive disease and pulmonary capillary hemangiomatosis)
1.5 PAH of the newborn

38
Q

Symptoms of PAH

A
  • Right ventricular dysfunction leads to reduced organ perfusion, present on exertion
  • Dyspnoea, fatigue, weakness, angina, syncope, cough (sometimes with haemoptysis), hypotension, hoarseness (sue to compression of the left recurrent laryngeal nerve)
  • As disease progresses: abdominal distention and peripheral oedema
39
Q

Signs of PAH

A
  • Cyanosis
  • Left parasternal heave
  • Signs on auscultation of the heart including
  • Tricuspid regurgitation murmur (pansystolic)
  • Pulmonary regurgitation murmur (diastolic)
  • Accentuation of the pulmonary component of the second heart sound
40
Q

PAH investigations

A
  • CXR: may show pulmonary arterial dilation and enlargement of the right side of the heart
  • ECG: in severe cases may show damage to the right side of the heart: right axis deviation, right bundle branch block, right ventricular hypertrophy, QTc prolongation
  • Pulmonary function tests
  • Echocardiogram: estimates the mPAP and looks at effects of PAH on the heart
  • High resolution CT or cardiac MRI
  • 6 minute walking distance: assess patients symptoms
  • BNP: will be elevated
41
Q

What is needed to diagnose PAH

A

Right heart catheterisation (RHC)

42
Q

What is used in stepped management for PH

A

1) CCB
2) Bosentan +/- sildenafil +/- ventavis
3) dietary Na restriction
4) aldactone and digoxin
5) IV meda (flolan)
6) combination therapy
7) inotropes
8) transplantation
9) paliative

43
Q

Treatment for PAH

A
  • Supportive therapy: diuretics, oral anticoagulants (for all patients), long term oxygen therapy ( consistently <8)
  • Treatment for conditions secondary to PAH like anaemias and atrial tachyarrhythmias
  • Calcium channel blockers
  • Severe cases: balloon atrial septostomy and lung transplant
44
Q

When can you prescribe CCB in apah

A

such as nifedipine, diltiazem, and amlodipine. if they have a positive response to acute vasoreactivity testing (where patients are administered a small dose of a short-acting vasodilator and have a decrease in mPAP of at least 10mmHg). Only a minority do

45
Q

Specific treatment for PAH

A
  • Endothelin receptor antagonists such as ambrisentan, bosentan or macitentan. Blocks endothelin on endothelin receptors, preventing vasoconstriction
  • Phosphodiesterase type 5 (PDE5) inhibitors such as sildenafil, tadalafil or vardenafil. Block the action of PDE5 on cyclic GMP in the smooth muscle cells of the arterioles in the lungs, reducing pulmonary blood pressure.
  • Prostacyclin analogues such as epoprostenol, iloprost or treprostinil. Vasodilator
46
Q

Complications of PAH

A
  • Cor pulmonale
  • Arrhythmias: atrial flutter and atrial fibrilation
  • Haemoptysis: associated with high mortality rate and may need emergency treatment
  • Dilation of the pulmonary arteries can cause: aneurysms, dissections, compression of the bronchi and recurrent laryngeal nerve
47
Q

PAH: factors that suggest poor prognosis

A
  • Deterioration in WHO/NYHC functional class
  • Increased serum uric acid level
  • Low 6 minute walking distance at initial assessment
48
Q

Metabolic syndrome definition

A

> 3/5
- Central obesity
- Raised TG
- Low HDL
- High BP
- High FBG

49
Q

Referral to tier 3 and bariatric surgery

A
  • Obesity class 3 goes straight to tier 3 services
  • A BMI >50 can be referred straight to bariatric surgery
50
Q

Cancer and diabetes

A

2ww for bladder= >60 with visible haematuria without evidence of UTI + dysuria or increased WCC

New onset diagnosis of diabetes in >60 send for CT scan to exclude pancreatic cancer

51
Q

Statins

A

20mg primary prevention, 80mg secondary prevention. LFT’s repeated after 4-6 weeks