Medicine- respiratory Flashcards
Signs and symptoms of lung cancer
Shortness of breath
Cough
Haemoptysis
Finger clubbing
Recurrent pneumonia
Weight loss
Lymphadenopathy – often supraclavicular nodes are the first to be found on examination
Signs of lung cancer on CXR
- Hilar enlargement
- “Peripheral opacity” – a visible lesion in the lung field
- Pleural effusion – usually unilateral in cancer
- Collapse
Horner’s syndrome triad
Which lung pathology is it associated with?
Partial ptosis, anhidrosis and miosis
Pancoast’s tumour
Classic clinical signs of pneumonia
-Bronchial breath sounds. These are harsh breath sounds equally loud on inspiration and expiration. These are caused by consolidation of the lung tissue around the airway.
- Focal coarse crackles. These are air passing through sputum in the airways similar to using a straw to blow in to a drink.
- Dullness to percussion due to lung tissue collapse and/or consolidation.
Legionella pneumophila (Legionnaires’ disease) can sometimes present with what?
Hyponatraemia
The rash associated with mycoplasma pneumonia
Erythema multiforme
Atypical pneumonia with Chlamydia psittaci is associated with what?
Bird keeping
The definition of atypical pneumonia
Pneumonia caused by an organism that cannot be cultured in the normal way or detected using a gram stain. They don’t respond to penicillins and can be treated with macrolides (e.g. clarithomycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline).
Typical asthma triggers
- Infection
- Night time or early morning
- Exercise
- Animals
- Cold/damp
- Dust
- Strong emotions
First line Ix in asthma
Fractional exhaled nitric oxide (FeNo test)
Spirometry with bronchodilator reversibility
Monitor serum what for pts on salbutamol?
Potassium
Typical sarcoid patient
Black Female Young or about 60y old
Blood abnormalities in sarcoid patients
- Raised serum ACE. This is often used as a screening test.
- Hypercalcaemia (rasied calcium) is a key finding.
- Raised serum soluble interleukin-2 receptor
- Raised CRP
- Raised immunoglobulins
Lung features of sarcoid
Lungs (affecting over 90%)
Mediastinal lymphadenopathy
Pulmonary fibrosis
Pulmonary nodules
Diagnosis of sarcoid
The gold standard for confirming the diagnosis of sarcoidosis is by histology from a biopsy. This is usually done by doing bronchoscopy with ultrasound guided biopsy of mediastinal lymph nodes.
First line treatment mild sarcoid
No treatment is considered as first line in patients with no or mild symptoms as the condition often resolves spontaneously.
The rash associated with sarcoid
Erythema nodosum. On the shins usually
Sarcoid histology
non-caseating granulomas with epithelioid cells.
Sarcoid treatment
Oral steroids are usually first line where treatment is required and are given for between 6 and 24 months.
Patients should be given bisphosphonates to protect against osteoporosis whilst on such long term steroids.
Second line options are methotrexate or azathioprine
Lung transplant is rarely required in severe pulmonary disease
Symptoms + signs of pulmonary hypertension
Shortness of breath is the main presenting symptom. Other signs and symptoms are:
Syncope
Tachycardia
Raised JVP
Hepatomegaly
Peripheral oedema.
The causes of pulmonary hypertension
The causes of pulmonary hypertension can split into 5 groups:
- Group 1 – Primary pulmonary hypertension or connective tissue disease such as systemic lupus erythematous (SLE)
- Group 2 – Left heart failure usually due to myocardial infarction or systemic hypertension
- Group 3 – Chronic lung disease such as COPD
- Group 4 – Pulmonary vascular disease such as pulmonary embolism (chronic thromboembolic disease)
- Group 5 – Miscellaneous causes such as sarcoidosis, glycogen storage disease and haematological disorders
ECG changes in pulmonary hypertension
-Right ventricular hypertrophy seen as larger R waves on the right sided chest leads (V1-3) and S waves on the left sided chest leads (V4-6) -Right axis deviation -Right bundle branch block
Rx primary pulmonary hypertension
IV prostanoids (e.g. epoprostenol)
Endothelin receptor antagonists (e.g. macitentan)
Phosphodiesterase-5 inhibitors (e.g. sildenafil)
Diagnosis of interstitial lung disease
Clinical features + high resolution CT scan of the thorax.
HRCT shows a “ground glass” appearance.
When Dx is unclear lung biopsy can be used to confirm with histology.
Two medications that can slow the progression of Idiopathic Pulmonary Fibrosis
Pirfenidone is an antifibrotic and anti-inflammatory
Nintedanib is a monoclonal antibody targeting tyrosine kinase
Drug Induced Pulmonary Fibrosis (8)
- Amiodarone
- Cyclophosphamide
- Methotrexate
- Nitrofurantoin
- Bleomycin
- Amphoteracin B
- Carbamazepine
- Acebutolol
Secondary Pulmonary Fibrosis
- Alpha-1 antitripsin deficiency
- Rheumatoid arthritis
- Systemic lupus erythematosus (SLE)
- Systemic sclerosis
Primary spontaneous pneumothorax - associated conditions (4)
- Marfan syndrome
- Ehlers-Danlos syndrome
- Alpha-1-antitrypsin deficiency
- Homocystinuria
Management of primary spontaneous pneumothorax
- stable, small (<3 cm), minimal symptoms: observation + O2
- symptomatic or large (>3 cm): aspiration
- unstable/tension pneumothorax: needle decompression then chest tube, and VATS if unsuccessful (25-50%) Video-assisted thoracoscopic surgery
Management of tension pneumothorax
- Needle thoracostomy – large bore needle, 2nd ICS mid clavicular line, followed by
- Chest tube in 5th ICS, anterior axillary line
What is the target INR for warfarin post PE?
2-3
CXR signs of pleural effusion
Blunting of costophrenic angle
Fluid in lung fissures
Tracheal + mediastinal deviation
Large effusions might have a meniscus
Signs of tension pneumothorax
- Chest pain
- Tracheal deviation
- Absent breath sounds/ decreased air entry
- Hypotension
- Hypoxia
- Jugular vein distension
- Possibly hyperresonance
Characteristics of Lofgren’s Syndrome
- Bilateral hilar lymphadenopathy
- Erythema nodosum
- Arthralgia 95% diagnostic specificity for sarcoidosis (nb treated with NSAIDs rather than steroids)
Which drugs should not be used alone in the Rx of asthma?
Long acting beta2 agonists
First line investigations in asbestosis
Pulmonary function studies - restrictive picture seen
CXR- pleural plaques in the diaphragmatic pleura
Pulmonary function test typical of fibrosis
FEV1 decreased FEV1/ FVC normal or increased
Clinical signs of pleural effusion
- Decreased breath sounds
- Decreased fremitus
- DTP on the effusion side
- Deviation of the trachea to the opposite side
CXR signs of pleural effusion
- Blunting of the costophrenic angle
- Fluid in the lung fissures
- Larger effusions will have a meniscus.
- Tracheal and mediastinal deviation if it is a massive effusion
Characteristics of empyema aspirate
Low pH (<7.2) Low glucose Raised LDH
Severity of COPD
Stage 1: FEV1 >80% of predicted Stage 2: FEV1 50-79% of predicted Stage 3: FEV1 30-49% of predicted Stage 4: FEV1 <30% of predicted
Diagnosis of COPD
spirometry required for diagnosis (post-bronchodilator FEV1/FVC <0.70)
Airway changes in COPD
Airway changes include
- increased goblet cells
- fibrosis of bronchioles
- loss of tethering due to destruction of alveolar walls
Complications of COPD
- Hypercapnic respiratory failure
- Polycythaemia 2° to hypoxemia
- Chronic hypoxemia
- Pulmonary HTN from vasoconstriction
- Cor pulmonale
- Pneumothorax dt rupture of emphysematous bullae
- Depression
- Bacterial infections- leading to bronchiectasis
Management of stable COPD
PROLONG SURVIVAL
- Smoking Cessation
- Vaccination Annual influenza + pneumococcal vax
- Home Oxygen Prevents cor pulmonale and decreases mortality if used >15h/d; indicated if: (1) PaO2 <55 mmHg or (2) PaO2 <60 mmHg with cor pulmonale or polycythemia
First line Abc in COPD exacerbations
1st line: Amoxicillin-Clavulanic Acid
Diagnostic criteria for pleural effusion (Transudate vs exudate)
Transudate Protein <30 g/L (in patients with a normal serum protein level) Exudate Protein >30 g/L (in patients with a normal serum protein level)
High pleural fluid LDH is associated with what?
Levels greater than 1000 IU/L are suggestive of empyema, malignancy or rheumatoid effusion.
A 52-year-old male presents with a cough, shortness of breath and fever. CXR shows a right-sided pleural effusion. A thoracentesis is performed and the results of the pleural fluid analysis are as follows: Colour: purulent Pleural/serum total protein ratio: >0.5 pH: 7.1 WBC count: 67,000 cells/µL Glucose: 1.5 mmol/l LDH: 1430 IU/L What is the most likely cause?
The most likely diagnosis is empyema. This gentleman has presented with, fever, shortness of breath and cough. The pleural fluid is purulent on inspection, the white cell count is significantly raised and glucose levels are low. The history and pleural fluid results are strongly suggestive of empyema and he should be treated empirically while culture results are awaited
A 56 -year-old, previously well woman was admitted with a 4-week history of a cough, night sweats and 1-week history of progressive breathlessness. She had never smoked and has no history of heart disease or rheumatological disease. Pleural fluid results are as follows: Colour: milky-white, odourless Triglyceride: 0.5 mmol/l Cholesterol: 12.4 mmol/l What is the most likely diagnosis?
The most likely diagnosis is pseudochylothorax. This woman has presented with a cough, night sweats and progressive breathlessness. A triglyceride level of less than 0.56 mmol/l and a cholesterol level of more than 5.18 mmol/l is indicative of pseudochylothorax. A pleural biopsy revealed chronic inflammation, and mycobacterium tuberculosis was isolated on a pleural fluid culture.
Potential ECG finding in COPD
ECG: cor pulmonale (peaked p waves and right axis deviation)
ABG evidence of CO2 retention in COPD
During stable disease: PaCO2 >6.0 and bicarbonate >30 indicates that the patient is a “CO2-retainer”
CXR findings in COPD
Chest X-ray: hyperinflation >6 anterior ribs or >10 posterior ribs visible in the mid-clavicular line Flattened diaphragm Hyperlucent lungs
COPD KEY POINTS
- COPD is a triad of emphysema, chronic bronchitis and small airway fibrosis.
- The main risk factors are tobacco smoking and inhaled pollutants. -COPD presents with progressive dyspnoea and productive cough. -Diagnosis is based on clinical features + spirometry (FEV1/FVC <70%).
- Management consists of conservative measures (such as smoking cessation) and inhaled bronchodilators.
- Complications include respiratory failure and cor pulmonale.
Winnipeg Criteria for antibiotics in COPD
Two of the following
- Dyspnoea
- Sputum production
- Sputum purulence
Hypoxaemia on ABG
If PaO2 is <10 kPa on air, a patient is considered hypoxaemic. If PaO2 is <8 kPa on air, a patient is considered severely hypoxaemic and in respiratory failure.
Type 1 Respiratory failure
Type 1 respiratory failure involves hypoxaemia (PaO2 <8 kPa) with normocapnia (PaCO2 <6.0 kPa). It occurs as a result of 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 lung tissue. As a result of the VQ mismatch, PaO2 falls and PaCO2 rises. The rise in PaCO2 rapidly triggers an increase in a patient’s overall alveolar ventilation, which corrects the PaCO2 but not the PaO2 due to the different shape of the CO2 and O2 dissociation curves. The end result is hypoxaemia (PaO2 < 8 kPa) with normocapnia (PaCO2 < 6.0 kPa). Examples of VQ mismatch include: Reduced ventilation and normal perfusion (e.g. pulmonary oedema, bronchoconstriction) Reduced perfusion with normal ventilation (e.g. pulmonary embolism)
Type 2 respiratory failure
Type 2 respiratory failure involves hypoxaemia (PaO2 is <8 kPa) with hypercapnia (PaCO2 >6.0 kPa). It occurs as a result of alveolar hypoventilation, which prevents the patient from being able to adequately oxygenate and eliminate CO2 from their blood. Hypoventilation can occur for a number of reasons including: Increased resistance as a result of airway obstruction (e.g. COPD). Reduced compliance of the lung tissue/chest wall (e.g. pneumonia, rib fractures, obesity). Reduced strength of the respiratory muscles (e.g. Guillain-Barré, motor neurone disease). Drugs acting on the respiratory centre reducing overall ventilation (e.g. opiates).
Antibodies assoc with Wegener’s Granulomatosis (Granulomatosis with polyangiitis)
anti-neutrophil cytoplasmic antibodies (ANCAs) - but not exclusively
Diagnosis of Wegener’s Granulomatosis (Granulomatosis with polyangiitis)
Tissue biopsy from affected area
The only treatment for COPD that prolongs life (2)
- Smoking cessation 2. O2 therapy in chronic hypoxaemia
Indications for home oxygen in COPD
Pa02 <55mmHg Sp02 <88%
First line therapies for an acute exacerbation of COPD
- Supplemental 02 (88-92%)
- Short acting bronchodilators SABA (albuterol) and anticholinergics (Ipratropium)
- Systemic corticosteroids (prednisone)
- Abx if increased dyspnoea, cough or sputum
Antibodies which are pathognomic for Goodpasture Syndrome
Anti-glomerular basement membrane
Lung nodules- suspicious features
- >8mm
- Irregular borders
- Ground glass opacity
- Doubling in size in one month to one year
- Hx smoking
- Old age
- Extra-pulmonary malignancy
Signs of acute respiratory distress syndrome
- Typical CXR appearance of widespread bilateral pulmonary infiltrates
- Acute onset
- PCWP <18 or no evidence of increased left atrial pressure - Pa02/ Fi02 <200
Acute glomerulonephritis and pulmonary haemorrhage
Goodpasture syndrome
Respiratory side effect of ACE inhibitors
Dry cough
Coarse crackles are associated with what? And fine crackles?
Coarse- bronchiectasis Fine- interstitial lung disease + fibrosis
What is the most serious complication of systemic sclerosis?
Pulmonary hypertension
Causes of bronchiectasis
- Cystic fibrosis
- Pneumonia
- Respiratory infections
- TB
- Rheumatoid arthritis
- Sjogren’’s syndrome
- Inflammatory bowel disease
- Marfan’s
- Alpha-1 antitrypsin
- Allergic bronchopulmonary aspergillosis
Bronchiectasis presentation
Productive cough + foul green sputum - lasting months to years Rarely- clubbing
Bronchiectasis diagnosis
High resolution CT Radiographic findings include airway dilation, bronchial wall thickening, and atelectasis
FEV1/FVC ratio > 70% suggests what?
Restrictive ventilatory defect
Typical ABG pictures in an asthma attack (early and late)
Early: respiratory alkalosis caused be hyperventilation (PaC02 decreased, pH increased, mild hypoxaemia) Late: Respiratory muscle fatigue results in respiratory acidosis caused by inability to ventilate (normalizing PaC02, normalizing pH, reduced Pa02)
Consider what in a patient who is < 60 with COPD and no smoking history?
Alpha-1 antitrypsin deficiency
The most common malignancy associated with asbestos exposure
Bronchogenic carcinoma
Complications of silicosis (2)
1) Increased risk of TB (screen annually)
2) Progressive massive fibrosis
With what are ferruginous bodies in the alveolar septum associated?
Asbestosis
What does acute respiratory distress syndrome most commonly follow?
Sepsis
What is the classical CXR appearance of ARDS?
Ground glass appearance due to bilateral alveolar infiltrate consistent with pulmonary oedema
Best investigations to diagnose pulmonary hypertension
Echo can estimate pulmonary artery pressure + assess RV function = best initial Ix
Most accurate test is right heart catheterization showing mean arterial pulmonary pressure over 25mmHg
Best investigation if a patient with suspected PE has a modified Wells score <4
D-Dimers- normal dimers exclude PE
Best investigation if a patient with suspected PE has a modified Wells score >4
CTPA
Which anticoagulant is contraindicated in pregnancy?
Warfarin
Which lung cancer is most strongly associated with smoking?
Small cell
Management of small cell cancer ie surgery/chemo or radio?
Unresectable. Sometimes respond to chemo + radio then recur. Poor prognosis.
Pleural effusions: best first Ix and then best next step
First Ix CXR Then thoracentesis
Obstructive sleep apnea- best initial test
Polysomnography
Pleural effusion
Sarcoidosis
Erythema nodosum
Horner’s syndrome
Bronchiectasis
Virchow’s triad
Stasis
Endothelial injury
Hypercoagulability
Do what to loculated pleural effusions before thoracentesis?
Localise by US or CT prior to drainage
In thoracentesis where is the needle passed in relation to the rib and why?
Over the top to avoid the neurovascular bundle
