Respiratory Flashcards
Define aspergillus lung disease
Lung disease associated with Aspergillus fungal infection
Aspergillus infection is usually caused by Aspergillus fumigatus
How can aspergillus affect the lung
- Asthma (atopic)
- Allergic bronchopulmonary aspergillosis
- Aspergilloma (mycetoma)
- Invasive aspergillosis
- Extrinsic allergic alveolitis
Risk factors for aspergillus
ABPA: asthmatics (1-2%) and CF (25%)
Invasive aspergillosis: immunocompromised (see pg. 168)
Brief info about how each type of aspergillus lung disease is caused
- Asthma
- type 1 hypersensitivity rxn to fungal
spores - ABPA
- type 1 and type 3 hypersensitivity rxn to aspergillus fumigatus (early on bronchoconstriction, later bronchiectasis) - Aspergillioma
- Fungus ball within pre-existing cavity (often due to TB/sarcoidosis). Usually asymptomatic. - Invasive aspergillosis
-Invasion of Aspergillus into lung tissue and fungal dissemination
This occurs in immunosuppressed patients (e.g. neutropenia, steroids, AIDS) - Extrinsic allergic alveolitis
- May be sensitivity to aspergillus clavatus (malt workers lung)
Epidemiology of aspergillus lung disease
UNCOMMON
Mainly occurs in the ELDERLY and IMMUNOCOMPROMISED
Presenting symptoms of aspergillus lung disease
ABPA:
-Difficult to control asthma; wheeze; cough; sputum; recurrent pneumonia
Aspergilloma:
-Usually asymptomatic
-Cough, haemoptysis (can be torrential)
lethargy, weight loss
Invasive aspergillosis:
-Dyspnoea, rapid deterioration, septic picture
Signs of aspergillus lung disease
Tracheal deviation (only with very large aspergillomas)
Dullness in affected lung
Reduced breath sounds
Wheeze (in ABPA)
Halo sign (invasive aspergillosis… nodules surrounded by ground-glass appearance)
Cyanosis (possible in invasive aspergillosis)
Investigations for aspergillus lung disease
ABPA:
- CXR
- Aspergillus in sputum
- Aspergillus skin test and/or Aspergillus-specific IgE RAST
- Eosinophilia
- Raised serum IgE
- Positive preciptins
Aspergilloma:
- CXR (rounded opacity within cavity, usually apical… crescent of air)
- Sputum
- strongly positive serum preciptins
- Aspergillus skin test
Invasive aspergillosis
-Aspergillus is detected in cultures or by histological
examination
-Bronchoalveolar lavage fluid or sputum may be used
diagnostically
Pathophysiology of asthma
Asthma risk factors
Inflammaotry disease driven by Th2 cells. 3 processes:
1) Bronchial hyerresponsiveness
2) Bronchial inflammation (symptoms primarily due to inflammation of terminal bronchioles, lined with SM but not cartilage)
3) Endobronchial obstruction
Early phase (up to 1hr): xposure toinhaledallergens inapresensitized individual results in cross-linking of IgE antibodies on the mast cell surface and release of histamine, prostaglandin D2, leukotrienes and TNF-a. These mediators induce smooth muscle contraction (bronchoconstriction), mucous hypersecretion, oedema and airway obstruction.
Late phase (after 6–12h): Recruitment of eosinophils, basophils, neutrophil and Th2 lymphocytes and their products results in perpetuation of the inflammation and bronchial hyper-responsiveness.
Airway remodelling
GENETIC:
Atopy (=tendency for T lymphocytes to drive production of IgE on exposure to allergens)
Family history
ENVIRONMENTAL: House dust mites Pollen Pets Cigarette smoke Viral respiratory tract infections Aspergillus fumigatus spores Occupational allergens
Epidemiology of asthma
Affects 10% of children
Affects 5% of adults
Prevalence appears to be increasing
Asthma presenting symptoms
Episodic history
Wheeze
Breathlessness
Cough (worse in the morning and at night)
IMPORTANT: ask about previous hospitalisation due to acute attacks - this gives an
indication of the severity of the asthma
Precipitating factors for asthma
Cold Viral infection Drugs (e.g. beta-blockers, NSAIDs) Exercise Emotions Check for history of atopic disease (e.g. allergic rhinitis, urticaria, eczema)
Recognise the signs of asthma on physical examination
What is severe attach vs life threatening attack
What about near fatal
Tachypnoea Use of accessory muscles Prolonged expiratory phase Polyphonic wheeze Hyperinflated chest
Severe Attack: PEFR < 50% predicted Pulse > 110/min RR > 25/min Inability to complete sentences
Life-Threatening Attack: PEFR < 33% predicted Silent chest Cyanosis Bradycardia Hypotension Confusion Coma
Near fatal:
And/or requiring mechanical ventilation with raised inflation pressures
Asthma investigation
Acute setting vs diagnosis in chronic setting
1st line and second line test
If unsure of diagnosis?
If SpO2<94%?
What type of respiratory failure occurs in asthma
If you suspect allergic asthma?
Acute:
Peak flow, pulse oximetry, ABG, CXR, FBC (inceased WCC if infective exaerbation), CRP, U&Es, blood and sputum cultures
Chronic:
Diagnosis:
1) Spirometry + bronchodilator test is 1st line for confirming diagnosis.
-Signs of obstructive lung disease:
-FEV1/FVC ratio (<0.8 what is expected. FEV1 after bronchodilator should show at least 200mL and 12% IMPROVEMENT)
2) Methacholine challenge test is second line if pulmonary function testing is non-diagnostic:
- A >20% drop in FEV1 after administration of methacholine is diagnostic
*20% diurnal variation in PEFR on at least 3 days for a number of weeks can also diagnose asthma. An improvement by 20% of PEFR in response to a couple of weeks of asthma treatment is also diagnostic
3) Chest x-ray to exclude other diagnoses like pnuemonia and pneumothorax.
-Signs of pulmonary hyperinflation in cases of severe asthma
Low, flattened diaphragm
Wide intercostal spaces
Barrel chest
Monitoring: PEFR. Often a diurnal variation with a morning ‘dip’.
OTHER LAB
- IF SpO2 is less than 94%, do ABG.
- Initially there is reduced pCO2, raised pH, reduced pO2 so a T1RF
- Ultimately, there’s severe respiratory distress, leading to rising pCO2, low pH, very reduced o2 and T2RF.
Patients with acute asthma exacerbations initially have reduced PCO2 and respiratory alkalosis (raised pH) due to tachypnea. Rising PCO2 is a sign of respiratory fatigue and impending respiratory failure
Allergic asthma:
- Ab testing (total IgE)
- FBC may show eosinohilia
- Skin allergy tests
- Sputum sample (curschmann spirals, charcot-leyden crystals, and creola bodies)
Chronic
Peak flow monitoring - often shows diurnal variation with a dip in the morning Pulmonary function test
Bloods - check:
Eosinophilia
IgE level
Aspergillus antibody titres
Skin prick tests - helps identify allergens
Asthma management (chronic)
STEP 1
Inhaled short-acting beta-2 agonist used as needed
If needed > 1/day then move onto step 2
STEP 2
Step 1 + regular inhaled low-dose steroids e.g. beclamethasone (400 mcg/day)
STEP 3
Step 2 + inhaled long-acting beta-2 agonist (LABA)
If inadequate control with LABA, increase steroid dose (800 mcg/day)
If no response to LABA, stop LABA and increase steroid dose (800 mcg/day)
STEP 4
Increase inhaled steroid dose (2000 mcg/day)
Add 4th drug (e.g. leukotriene antagonist, slow-release theophylline or beta-2
agonist tablet)
STEP 5
Add regular oral steroids Maintain high-dose oral steroids
Refer to specialist care
Asthma management (acute)
Resuscitate, monitor o2 sats, ABG and PEFR
High-flow oxygen
Salbutamol nebulizer (5 mg, initially continuously, then 2-4 hourly) Ipratropium bromide (0.5 mg QDS)
Steroid therapy (100-200 mg IV hydrocortisone + 40 mg oral prednisolone for 5-7 days)
If no improvement –> IV magnesium sulphate. Consider IV aminophylline infusion
Consider IV salbutamol.
If PCO2 begins to increase, call anaesthetic help.
Ventilation may be needed on severe attacks.
Why is a normal pCO2 bad in an acute asthma episode
This is because during an asthma attack they should be hyperventilating and blowing off their CO2, so PCO2 should be low
A normal PCO2 suggests that the patient is fatiguing
What do you need to look out for with electrolytes during acute asthma treatment
Monitor electrolytes closely because bronchodilators and aminophylline causes a drop in K+
Complications of asthma
What complication of acute asthma treatment do you want to be careful about
Growth retardation Chest wall deformity (e.g. pigeon chest) Recurrent infections Pneumothorax Respiratory failure Death
Bronchodilators and aminophylline reduce potassium, so watch electrolytes closely for hypokalaemia
Define TB
Tuberculosis (TB) is a bacterial infection spread through inhaling tiny droplets from the coughs or sneezes of an infected person.
It mainly affects the lungs, but it can affect any part of the body, including the tummy (abdomen), glands, bones and nervous system.
Explain aetiology/risk factors for TB
(-names of the species causing it
- do they need o2?
- do they replicate inside or outside cells?
- What cell types does it infect
- How fast do they grow
- Gram stain?
- What staining method is used?
- t/f all those infected with TB develop active disease
Aeritiolgy: -Caused by 4 mycobacterial species, names the Mycobacterium tuberculosis complex (MTb) •Mycobacterium tuberculosis •Mycobacterium bovis •Mycobacterium africanum •Mycobacterium microti.
- These are obligate aerobes (i.e. need o2 to respire) and facultative intracellular pathogens (capable of living and reproducing inside or outside of cells)
- Usually infect mononuclear phagocytes
- Slow growing (12-18hr)
- relatively impermeable and stain only weakly with Gram stain
- they are termed ‘acid-fast bacilli’.
- F: Only a small number of bacteria need to be inhaled for infection to develop but not all those who are infected develop active disease. The outcome of exposure is dictated by a number of factors
Risk:
-Contact w high risk groups (origination/frequent travel to high risk country)
- Immune deficiency: corticosteroids, HIV, chemotherapy, nutritional deficiency, DM, CKD, malnutrition
- Lifestyle factors: drug/alcohol, homelessness, prison inmates
- genetic susceptibility (twin studies of gene polymorphisms)
Summarise epidemiology of TB
1/3 of world population infected
Co-infection with HIV remains a problem
Presenting symptoms of TB
Productive cough,sometimes systemic symptoms (weight loss, fevers, night sweats).
Hoarse voice and severe cough if laryngeal involvement,
Pleuritic chest pain if involving pleura
Signs of TB on physical examination
Pulmonary: Abnormal breath sounds, bronchial breathing, hoarse voice,
Extrapulmonary: confusion, neurological deficit, lymphadenopathy, cutaneous lesions, Weight loss,
Lymphadenopathy usually bilateral
Appropriate investigations for TB
Chest x-ray (onsolidation with or without cavitation, pleural effusion or thickening or widening of the mediastinum caused by hilar or paratracheal adenopathy). TB tends to affect the upper lobes
Smear and culture of:
- Sputum
- Induced sputum
- Brochoalevolar lavage fluid (if cough unproductive and induced sputum not possible)
- Aspiration of pleural fluid and pleural biopsy
- Gastric aspirates
BEST INVESTIGATION
The best investigation to
establish a diagnosis is a sputum sample, which should be tested for the presence of
acid-fast bacilli using Ziehl-Neelsen stain.
Differentiate primary TB, latent TB and reactivation TB
T/F people with latent TB are non infectious
In primary TB:
- Inhale bacilli and it reaches lymph nodes as innate immune system cannot clear it
- Proliferates inside alveolar macrophage
- Inflammatory infiltrate reaching lung and lymph nodes
- Macrophage present to T cell, causing type IV hypersensitivity reaction.
- Granuloma formation/tissue necrosis
- Some granulomas heal and become calcified (they still contain bacteria which can lie dormant here for many years). This is Ghon focus.
- ONLY 5% OF PATIENTS WILL HAVE ACTIVE DISEASE
Latent TB:
-Following infection (above) immune system contains the infection and the patient develops cell-mediated immune memory to the bacteria
T: people with latent TB are non infectious
About 10% of latent TB progress to:
Reactivation (active)TB:
-Majority of TB cases due to reactivation of latent infection decades after the initial contact. (in HIV patients, newly acquired TB also common)
Compare latent infection with active disease for TB:
- Location of bacilli
- Sputum smear
- Tuberculin skin test
- Chest x-ray
- Symptoms
- Infectious?
This is a key box
- Latent: In the ghon focus
Active: in the secretions/tissue - Latent: Negative
Active: frequently positive - Latent: Usually +ve
Active: usually +ve and can ulcerate - Latent: Normal (small calcified ghon focus frequently visible)
Active: consolidation/cavitation/effusion - Latent: None
Active: Night sweats, fevers, weight loss, cough - Latent: No
Active: Infectious to others if bacilli present in sputum
When are pulmonary/extrapulmonary disease most common out of primary active vs reactivation TB
In primary active TB, mostly pulmonary, extrapulmonary in minority. Remember most of the time, there is no active disease in primary TB (i.e. the initial infection)
In reactivation TB, pulmonary disease 55% of cases and extrapulmonary disease in 45% of cases
Define pneumoconiosis
The pneumoconioses are a large group of interstitial lung diseases, mostly of occupational origin, caused by the inhalation of mineral or metal dusts.
4 main types: asbestosis (covered separately); silicosis; coal workers pneumoconiosis (black lung disease) & chronic beryllium disease
Explain the aetiology / risk factors of pneumoconiosis
Pneumoconioses predispose you to which condition?
occupational exposure to silica
occupational exposure to coal
occupational exposure to beryllium
For silica and coal:
Ingested by macrophages and cause cytolysis of macrophage causing them to release their enzymes and cause fibrosis. In response to silica/coal, macrophages generate fibrogenic proteins and growth factors that stimulate collagen elaboration.
For beryllium:
A different pathophys. here. Does not have clear exposure response. Rather, following exposure to beryllium, T cells bind to beryllium, which changes the peptide binding ont he T cells so they react differently with other antigens.
Risk factors:
Coal workers pneumoconiosis: coal miners
Silicosis: Silica miners & sand blasters (increased risk of TB)
Asbestosis (construction workers and shipyard workers)
Occupational lung diseases, especially silicosis, are well established risk factors for the development of active tuberculosis (TB). Silicosis is also a risk factor for bronchogenic carcinoma
Summarise the epidemiology of pneumoconiosis
.
Recognise the presenting symptoms of pneumoconiosis
Differentiate coal miners from silicosis from asbestosis
Silicosis: Dyspnoea on exertion, cough, chest tightness
Coal workers pneumoconiosis asymptomatic, but co-existing chronic bronchitis is common.
Recognise the signs of pneumoconiosis on physical examination
Commonly a normal chest examination
Possibly:
crackles on chest auscultation,
wheezing/tightness, prolonged expiration, areas of dullness on chest percussion, cyanosis, weight loss etc.
Identify appropriate investigations for pneumoconiosis and interpret the results
Chest x ray finding of silicosis?
Chest x-ray:
silicosis and coal workers’ pneumoconiosis: progressive upper zone non-calcified, small, rounded opacities, ‘egg shell calcification of hilar nodes’ specific for silicosis;
chronic beryllium disease: progressive upper zone linear interstitial fibrosis
Spirometry (to determine severity and pharmacological treatment): may be normal or demonstrate restrictive changes; may show obstructive or mixed pattern
Beryllium lymphocyte prooliferation test (BeLPT):
If sensitised to beryllium will be +ve. Sensitive test. Blood sample first (confirmed with repeat test). If -ve, Brochoscopic lavage fluid tested
Differentiate the following types of breathing:
- Kussmaul
- Paroxysmal noctural dypnea
- Biot’s
- Cheyne-stokes
- Hyperventilation
- Usually deep breathing, in response to a metabolic acidosis, leading to hypocapnia
- Attacks of severe SoB and coughing generally at night. Common among patients with HF, and they wake patients from sleep
- Abnormal breathing pattern caused by quick, shallow inspirations followed by irregular periods of apnea, usualyl cuased by damage to the PONS due to strokes or trauma
- An abnormal breathing pattern characterized by an oscillation between apnea and hyperpnea with a crescendo-diminuendo ventilation pattern. Associated with heart failure. (look at the explanation here https://thorax.bmj.com/content/53/6/514)
- Hyperventilation (or over breathing) is an abnormal breathing pattern characterized by excessive alveolar ventilation resulting in elevated blood pH and respiratory alkalosis and hypocapnia
Should you give diuretics to somebody with cor pulmonale
In general, the use of diuretics in patients with cor pulmonale should be handled with caution due to an increased susceptibility to decrease the cardiac output, and thus cause acute renal failure.
How is COPD diagnosis confirmed
Definitive diagnosis requires spirometry, with a post-bronchodilator FEV1/FVC ratio of less than 0.7.
What should be used to differentiate URTIs that need further work up or Abx
The modified Centor score can also be used to help differentiate cases of URTI which require further work-up (nasopharyngeal swab) and/or antibiotics.
The risk factors used by the modified Centor score include age, tonsilar exudates, tender/swollen anterior cervical lymph nodes, fever, and cough.
A score of 1 requires no further testing (5-10% risk of Strep pharyngitis).
A score of 2-3 indicates rapid testing and culture is appropriate, and antibiotics should be used for positive tests/cultures only.
A score greater than 4 indicates that antibiotics should be used empirically, as the risk of Strep pharyngitis is greater than 50%.
The golden S sign is indicated what on chest x-ray
The Golden S sign can be seen with the collapse of all lobes of the lung but is most commonly seen in right upper lobe collapse. It is created by a central mass obstructing the upper lobe bronchus and should raise suspicion of a primary bronchogenic carcinoma.
non-small-cell lung carcinoma
What does a sail sign indicate
A left sided lower lobe collapse
(In the elbow, the fat pad sign, also known as the sail sign, is a potential finding on elbow radiography which suggests a fracture of one or more bones at the elbow. Often associated with elbow joint effusions).
What is silhouette sign
The silhouette sign refers to the loss of normal borders between thoracic structures.
It is usually caused by an intrathoracic radiopaque mass that touches the border of the heart or aorta.
It may occur, for example, in right lower lobe pneumonia, where the border of the diaphragm on the right side is obscured, while the right heart margin remains distinct.
What is spinnaker sign
The spinnaker sign is a sign of pneumomediastinum seen on neonatal chest radiographs. It refers to the thymus being outlined by air with each lobe displaced laterally and appearing like spinnaker sails.
What is the water bottle sign
The water bottle sign or configuration refers to the shape of the cardiac silhouette on erect frontal chest X-rays in patients who have a very large pericardial effusion.
Which drugs can cause pulmonary fibrosis
What are the x ray and CT findings of pulmonary fibrosis
It can be caused by a number of chemotherapy (busulfan, bleomycin, carmustine, methotrexate), cardiac (amiodarone), and antibiotic (nitrofurantoin) medications
The chest x-ray shows reduced lung volume and a bilateral increase in interstitial markings. Increased interstitial markings, with or without nodularity, are suggestive of pulmonary fibrosis.
Consistent computed tomography findings include honeycombing, traction bronchiectasis, lung architectural distortion, and interlobular septal thickening.
Soft tissue calcification when you suspect pulmonary fibrosis indicates what etiology?
What about pleural plaques
soft tissue calcification suggests an scleroderma while pleural plaques suggest asbestos inhalation.
Complications of obesity hypoventilation synrome
What defines this disease
This disease can put strain on the heart leading to heart failure, leg swelling, and other related symptoms.
Obesity hypoventilation syndrome is defined by the combination of obesity (BMI >30 kg/m2), hypoxemia during sleep, and hypercapnia during the day.
Which conditions can cause an anterior mediastinal mass
Lymphoma, thymoma, teratoma, thyroid masses, and a thoracic aorta aneurysm
What cells are seen in hodgkin lymphoma
a biopsy of the lymph nodes showing Reed-Sternberg cells.
What do the following types of consolidation indicate on chest x-ray:
- alveolar
- homogenous
- reticulo-nodular
Pneumonia “alveolar shadowing” + air bronchograms
Fibrosis “reticulonodular shadowing”
Pleural effusion “homogenous shadowing”
Distinguishing feature of squamous cell carcinoma
What about small cell
Squamous cell carcinoma –> causing cavitating lung lesions
Small cell –> causing paraneoplastic syndrome
Where do the different leads go on an ECG
Ride your green bike (Red is RA, yellow on LA, green on LL, black on RL)
Pneumonia treatment
You give amoxicillin (to cover strep) and a macrolyide (clari) for atypicals
Appearance of air under the diaphragm that isn’t free intraperitoneal air?
Normal large bowel can be seen interposed between liver and right hemidiaphragm. This is a normal variant and is known as Chilaiditis syndrome, do not confuse this appearance with free intraperitoneal air.
What causative organism of pneumonia is associated with AIDs
Pneumocystis jiroveci
Which additional symptom is caused by each of the following atypical pneumonias:
1) Legionella pneumophila
2) Mycoplasma pneumoniae
3) Chlamydia psittaci
They all present with vague symptoms like malaise, headache and diarrhoea.
1) It is associated with causing confusion (and found in bodies of water kept at temperatures below 60°C, such as air conditioning units)–> PRODUCED URINARY ANTIGEN (as does pneumococcus)
2) Mycoplasma pneumoniae causes red cell agglutination and is assocaiated with transverse myelitis
3) Chlamydia psittaci is parimarily found in birds but can cause atypical in HUMANS THAT ARE EXPOSED TO BIRDS
What antibiotic would be used to treat pneumocystis jiroveci?
Co-trimoxazole, a combination of trimethoprim and sulfamethoxazole, is used to treat
Pneumocystis jiroveci pneumonia in HIV patients. 14-21 days.
You need to give with antiemetic becasue it has SE of N&V. Check they don’t have G6PD as this drug can precipitate haemolytic anaemia
This drug is also used to treat some UTIs
When would metronidazole be used for respiratory infection
In aspiration pneumonia (as it is effective in treating anaerobes).
Note that for this reason it is also used to used to treat several GI infections (e.g. C. difficile colitis) and pelvic
inflammatory disease
Causes of air bronchograms on CXR
Air bronchograms refer to the appearance of bronchi (which are
radiolucent) that are made visible when something other than air is filling the
surrounding alveoli - such as pus in pneumonia, fluid in pulmonary oedema and
fibrosed tissue in interstitial lung disease.
What is the mantoux test?
The
Mantoux test is a technique in which an intradermal injection of tuberculin purified
protein derivative is administered and a reaction producing a raised, hardened area
around the injection site after 72 hours suggests that the patient has previously been
exposed to TB. Although it can identify patients who have been exposed to TB, it
does not distinguish between active and latent TB.
Pulmonary fibrosis symptoms and examination findings
Chronic dry cough, shortness of breath on exertion and sometimes weight loss
Signs: clubbing, fine inspiratory crackles (affecting both lower zones usually)
Causes of pulmonary fibrosis
Occupational toxins (asbestos) Systemic inflammatory conditions (rheumatoid arthritis) Certain medications (methotrexate)
Why can rheumatoid arthritis lead to pulmonary fibrosis
In rheumatoid arthritis the
pulmonary fibrosis may be a complication of the disease itself, and/or a complication
of its treatment (with methotrexate).
What kind of cough is found with COPD
Productive.
Lung cancer auscultation findings
Lung cancer usually presents with
haemoptysis and is likely to reveal bronchial breathing in a discrete lung zone, as
opposed to bilateral fine inspiratory crackles.
What might diffuse uptake on a thyroid uptake scan
Diffuse uptake throughout an enlarged gland is seen in Graves’ disease.
Diffuse uptake with a single cold nodule may be seen
in thyroid cancer.
Define bronchiectasis
Obstructive or restrictive
Obstructive lung airway disease characterized by chronic bronchial dilation, impaired mucuociliary clearance and frequent bacterial infections
Obstructive because it causes mucus plugs to form in the airways
Explain the aetiology / risk factors of bronchiectasis
Severe inflammation in the lung causes fibrosis and dilation of the bronchi.
This is followed by pooling of mucus, predisposing to further cycles of infection, damage and fibrosis to bronchial walls.
CAUSES:
Idiopathic 50%
Post infectious (after severe pneomina, whooping cough, TB)
Host defect defects: PRIMARY CILIARY DYSKINAESIA (incl. Kartagener’s syndrome), cystic fibrosis, immunoglobulin deficiency
Obstruction of bronchi: foreign body, enlarged lymph nodes
Certain infections can worsen the chronic inflammation by causing a hypersenstivity response which results in even more inflammation in the airway
Gastric reflux disease
Inflammatory disorders
Summarise the epidemiology of bronchiectasis
Most often arises in childhood. Incidence reduced due to use of Abx.
Recognise the presenting symptoms of bronchiectasis
Productive cough with (foul smelling) purulent sputum/haemoptysis
SoB
Breathlessness, chest pain, malaise, fever, weight loss
Symptoms usually begin after an acute respiratory illness
Recognise the signs of bronchiectasis on physical examination
Finger clubbing;
Coarse creptitations (usually at the bases) WHICH SHIFT WITH COUGHING!!!!
Wheeze.
Identify appropriate investigations for bronchiectasis and interpret the results
Best method??
What would the following show:
CXR
CT chest
BEST DIAGNOSTIC METHOD:
-CT SCAN will show dilated bronchi and bronchioles
ALSO
- Sputum (culture and sensitivity, common organisms in acute exacerbation:
- Pseudomonas aeruginosa, haemophilus, staph aureus, strep pneumonia, moraxella catarrhalis, mycobacteria)
- CXR: Dilated bronchi may be seen as parallel lines radiating from hilum to the diaphragm (‘tramline shadows’). It may also show fibrosis, atelectasis, pneumonicconsolidations, or it may be normal.
- Pulmonary function testing showing reduced lung capacity and ability to force out air
- Broncography (rarely used)
- Sweat electrolytes (for CF), serum immunoglobulins, sinus X-ray (30% have concomitant rhinosinusitis), mucociliary clearance study
Genetic testing
Generate a management plan for bronchiectasis
ACUTE EXACERBATION:
-2 IV Abx with efficacy for pseudomonas. Phophylactic Abx for those with frequent exacerbations (>3/year)
LONG TERM:
Physiotherapy. Sputum and mucus clearance techniques are cornerstone of management (postural draiange). Patients taught to position themselves so the lobe to be drained is uppermost ~20 mins twice daily.
+
Bronchodilators may be considered in patients with responsive disease (salbutamol)
Inhaled corticosteroids (fluticasone) have been shown to reduce inflammation and volume of sputum, although it does not affect the frequency of exacerbations or lung function.
Maintain hydration with adequate oral fluid intake.
Consider flu vaccine
Bronchial artery embolization: For life-threatening haemoptysis due to bronchiectasis.
Surgical: Various surgical options include localized resection, lung or heart–lung transplantation.
Identify the possible complications of bronchiectasis and its management
Life threatening haemoptysis
Persistent infections
Empyema
Respiratory failure
COR PULMONALE
Multi-organ abscesses
Summarise the prognosis for patients with bronchiectasis
Most patients continue to have the symptoms after 10 years
What cardiac manifestation of bronchiectasis, explain why this occurs
RIGHT ventricular hypertrophy due to pulmonary hypertension (cor pulmonale)
There is a loss of elastin, and instead there is laying down of collagen by fibroblasts. The lungs become stiff and dilated and mucus filled leading to a pattern of obstructive lung disease.
Overtime there can be hypoxia which causes addaptive pulmonary arteriolar constriction, diverting blood away from the most damaged areas of the lungs.
But if damage is widespread, this leads to widespread pulmonary arteriole vasoconstriction which leads to pulmonary hypertension.
This increases pressure on the right ventricle.
This can cause a right ventricular heave
Miliary nodular lung densities (multiple small lung nodules)
Number of causes of miliary (=nodule appearance)
TB is the most likely in a young african or asian immigrant
Sarcoid, metastases, occupational lung disease and extrinsic allergic alveolitis can also cause military shadowing.
What are the features of pancoast syndrome
When Pancoast tumours compress or invade surrounding structures the resulting symptoms are known collectively as Pancoast syndrome.
Brachial plexus involved first –> shoulder and arm pain
Can be compression of spinal cord
Recurrent laryngeal nerve invasion can cause vocal cord palsy and hoarse voice
Which conditions are associated with horners syndrome
Diabetes mellitus Cerebrovascular disease Demyelination Trauma Carotid aneurysm Carotid dissection Skull base tumour
What are the most common causative organisms in community acquired pneumonia leading to hosp admission
What are the causes of HAPs
Strep pneumoniae (39%) Viral (13%) C pneumoniae (13%) Mycoplasma (11%) H influenzae (5%)
Moraxella catarrhalis, Chlamydia
and Legionella are all CAP atypicals.
HAPS:
Gram-negative
enterobacteriae (e.g. E. coli), S. aureus, Pseudomonas, Klebsiella, Bacterioides and
Clostridia.
What factors might be used to measure response to treatment in a pneumonia patient
Renal function (if impaired at presentation)
CRP
White cell count
What are the common subtypes of lung cancer
Adenocarcinoma approx 40% Squamous cell carcinoma approx 25-30% Small cell carcinoma approx 15% Large cell undifferentiated approx 10% Rare types are bronchoalveolar carcinoma and carcinoid, both approx 1% of all tumours, and unrelated to smoking
Define lung cancer
Specifically, define small cell carcinoma
Primary malignant neoplasm of the lung.
Non-small cell: 80%.
Includes squamous cell carcinoma, adenocarcinoma, large cell carcinoma and adenosquamous carcinoma
Small cell: 20%
Malignant neoplasm of neuroendrocrine Kulchistsky cells of the lung with early dissemintation.
Explain the aetiology / risk factors of lung cancer
RF:
Smoking –> genetic alterations causing neoplastic transformation
Also
-Occupational exposures and atmospheric pollution.
Small-cell lung cancers are usually central in the lung, in a main bronchus.
NSCLC are more of a mixed bag:
- Sqaumous cell carcinomas are centrally located
- Adenocarcinoma is peripherally located
- Large cell and bronchial carcinoid can be found centrally or peripherally
Summarise the epidemiology of lung cancer
Most common fatal malignancy in the west.
3x more common in men but increasing in women.
Recognise the presenting symptoms of lung cancer
May be asymptomatic with radiographic abnormality found
Due to the primary tumour:
NSCLC: cough, haemoptysis, chest pain, recurrent pneumonia
SCLC: cough, haemoptysis, dyspnoea, chest pain.
Due to local invasion (NSCLC):
- Brachial plexus (pancoast tumour) causing pain in the shoulder or arm
- Left recurrent laryngeal nerve (causing hoarseness and bovine cough)
- Oesophagus (dysphagia)
- Heart (palpitations and arrythmias)
Due to metastatic disease:
NSCLC: Weight loss, fatigue, fits, bone pain or fractures, neuromyopathies.
SCLC: weight loss, fatigue, bone pain.
Due to paraneoplastic disease: Weakness, lethargy, seizures, muscle fatiguability
Recognise the signs of lung cancer on physical examination
NSCLC:
-May be no signs or a fixed monophonic wheeze. Signs of collapse, consolidation or pleural effusion.
- DUE TO LOCAL INVASION: SVC compression (facial congestion, distension of neck veins, upper limb oedema). BRACHIAL PLEXUS (wasting of small muscles of hand. SYMPATHETIC CHAIN (Horner’s syndrome).
- DUE TO PARANEOPLASTIC PHENOMENA: hypertrophic osteoarthropathy (clubbing, painful, swollen wrist/ankles) and dermatological signs.
- DUE TO METS: supraclavicular lymphadenopathy, hepatomegaly
SCLC:
May be no signs or a fixed wheeze on auscultation of the chest.
-Signs of lobar collapse of pleural effusion
-Signs of mets: supraclav. lymphadenopathy or hepatomegaly
-Signs of paraneoplastic syndrome
Identify appropriate investigations for lung cancer and interpret the results
NSCLC:
-DIAGNOSTIC= CXR (coin lesions, lobar collapse, pleural effusion). Sputum cytology, bronscopy with brushings or biopsy, CT- or USS guided percutaneous biopsy
-TM staging: Based on tumour size, nodal involvement and metastatic spread, using CT chest, CT or MRI head and abdomen (or ultrasound), bone scan, PET scan. Invasive methods like mediastinoscopy or video-assisted thoracoscopy may be used.
Bloods: FBC, U&E, Ca2+ (hypercalcaemia common), AlkPhos (increased with bone mets), LFTs. `
What are the common sites for lung cancer metastasis
Mediastinum and hilar lymph nodes
Other sites include the pleural, heart, breasts, liver, adrenals, branina dn bones
What cell type do small cell lung carcinomas arise from
Small cell carcinomas account for a small portion of lung cancers and originate from small, immature neuroendocrine cells.
What cell types do each of the following carcinomas arise from:
- Adenocarcinomas
- Squamous cell carcinomas
- Carcinoid tumours
- Large cell carcinomas
adenocarcinomas which frequently form glandular structures or have the ability to generate mucin; squamous cell carcinomas; which have squamous, or square shaped, cells that produce keratin; carcinoid tumors from mature neuroendocrine cells; and large cell carcinomas which lack both glandular and squamous differentiation.
Where does small cell carcinoma usually develop.
Is there an association with smoking
Small cell carcinoma is strongly associated with smoking and usually develops centrally in the lung, near a main bronchus.
YES there is a STRONG association with smoking
What is the fastest growing and rapidly metastasising lung cancer
In general, small cell carcinomas grow the fastest and more rapidly metastasize to other organs than the non-small cell lung cancers.
Because of this, by the time it’s diagnosed, it’s common to find large tumors in multiple locations both within and outside the lung.
What does “ limited mean” in small cell carcinomas
Typically when small cell carcinoma is within one lung, it’s considered limited, if it spreads beyond one lung it’s considered extensive.
Give 2 examples of a paraneoplastic syndrome in lung cancer (the typical examples)
When small cell carcinomas release ACTH, causing an increase in production and release of cortisol from the adrenal glands.
This causes Cushing’s syndrome, causing high blood pressure and blood glucose
Secondly when small cell cancers release ADH, which causes water retention leading to high BP, oedema and concentrated urine
Thirdly, when small cell carcinomas prompt the body to produce autoantibodies which bind and destroy neurons causing Lambert Eaton myasthenic syndrome
What type of antibodies are produced in lambert eaton syndrome
What type of immuological reaction is it
It is the result of antibodies against presynaptic voltage-gated calcium channels, and likely other nerve terminal proteins, in the neuromuscular junction
It’s a type II hypersensitivity reaction
Which lung cancers DO NOT have a link to smoking, and are therefore the most common type of lung cancer in a person who doesn’t smoke
Adenocarcinomas!
Which develop peripherally
Where are each of the non small cell carcinomas located
NSCLC are more of a mixed bag:
- Sqaumous cell carcinomas are centrally located
- Adenocarcinoma is peripherally located
- Large cell and bronchial carcinoid can be found centrally or peripherally
Which of the non small cell carcinomas have link to smoking
Adenocarcinoma (peripheral), NO LINK
Squamous cell carcinoma (central), STRONG LINK
Large cell (central or peripheral), STRONG LINK
Bronchial carcinoid (central or peripheral), NO LINK
Which types of carcinoma can form pancoast tumours
Both adenocarcinoma and squamous cell carcinoma
T/F only small cell lung cancers cause paraneoplastic syndrome
F
Give an example of a paraneoplastic syndrome caused by a NSCLC
Sqaumous cell carcinoma.
Paraneoplastic syndrome as PTH-like peptid is released which depletes calcium from the bones causing them to become brittle and increasing calcium in the blood
What causes haemoptysis in lung cancer
if cancer cells invade into a blood vessel then mucus can get blood tinged or blood clots can get coughed up.
How is lung cancer diagnosed
Initially lung cancer is usually identified as a coin-shaped spot, called a coin lesion on chest X-ray, or a non calcified nodule on chest CT.
Infections can also cause similar shaped spots, so a tissue biopsy from a bronchoscopy or a CT-guided fine-needle aspiration is typically done to make a histopathologic diagnosis.
In which situations is long-term oxygen therapy considered for COPD patients
1) Patients with PaO2<7.3 kPa despite maximal treatment
2) Patients with PaO2 7.3-8.0 kPa AND one of pulmonary hypertension,
polycythaemia, peripheral oedema or nocturnal hypoxia
3) Terminally ill patients
PE definition
Occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the vascular system from another site
PE RF and aetiology
Thrombus (>95% coming from DVT in lower limbs, and rarely from right atrium of patient with AF)
Other agents include amniotic fluid embolus, air embolus, fat embili, tumour emboli and mycotic emboli from right sided endocarditis.
RF: Having a deep vein thrombosis, the RF for which are: -Surgery (last 6 weeks) -Immobility including bed rest -Flight >8hrs -Malignancy -Pregnancy -Obesity -Heart failure
PE epidemiology
Relatively common, especially in hospitalized patients, they occur in 10–20% of those with a confirmed proximal DVT.
PE Hx
Depends on size
Small:
Asymptomatic maybe
Moderate:
Sudden onset dyspnoea, cough, haemoptysis and pleuritic chest pain.
Large (or proximal):
All of the above plus severe central pleuritic chest pain, shock, collapse, acute right heart failure or sudden death
Multiple small: pulmonary HTN
PE signs
Small: often none. Earliest sign is tachycardia or tachypnoea
Moderate: Tachypnoea, tachycardia, pleural rub, low saturation O2 (despite oxygen supplementation).
Massive PE: Shock, cyanosis, signs of right heart strain (RAISED JVP, left parasternal heave, accentuated S2 heart sound).
Multiple recurrent: Signs of pulmonary HTN and right heart failure
PE investigations
Well’s score to determine whether to do D dimer or CTPA.
Well’s score. <4 unlikely, >4,5 likely. Unlikely=consider D-dimer. Likely=consider CTPA
CTPA: first line. poor sensitivity for small emboli but very sensitive for medium to large
VQ scan. Not suitable if abnormal CXR or coexisting lung disease
A v/q scan preferred in pregnant women
GOLD STANDARD INVESTIGATION: is pulmonary angiography (this is invasive and rarely necessary)
Additional initial investigations:
Bloods- ABG
ECG- May be normal or more commonly show a tachycardia, right axis deviation or RBBB.
Classical SI, QIII, TIII pattern is relatively uncommon.
CXR: often normal (wedges shaped, westermarks sign)
PE management
If haemodynamically stable:
- O2,
- Anticoag with heparin or LMWH for 5 days
- Then changing to oral warfarin for minimum 3 months.
If haemodynamically UNstable (massive PE):
- Resp support
- 1st line is thrombolysis (alteplase, 50mg bolus of tPA)
- 2nd line is embolectomy
Prevent:
TEDs and Tinz (stockings and LMWH)
Screen for cancer after
PE complications and complications of management
Death, pulmonary infarction, pulmonary hypertension, right heart failure.
PE prognosis
Thirty percent untreated mortality, 8% with treatment (due to recurrent emboli or underlying disease). Patients have increased risk of future thromboembolic disease
What is the investigation of choice for diagnosis of PCP
Bronchoscopy is the investigation of choice for the diagnosis of PCP.
If safe to do, exercise oximetry is useful. An ambulatory oxygen saturation reading is deemed positive if the levels drop to 90% or below on exertion.
What are the CT findings of PCP
CT chest classically shows patchy areas of ground glass attenuation with background interlobular septal thickening, but is not a first line investigation.
What might legionella show on chest x ray
Bilateral pulmonary infiltrates, predominantly lower lobe in distribution
T/F a urine NAAT test can be used for legionella
F… that’s for the STI urine tests.
Urinary antigen testing cna be used for legionella. Serology is widely used, along with sputum culture
What type of bacteria is legionella
Weakly gram-ve bacillus
How does spread of legionella occur
The infection source can be air conditioning units
Spread is via droplets
What are the complications of legionnaires
Resp: respiratory failure, pleural effusion, pulmonary fibrosis
Heart: endocarditis, pericarditis
GI: Pancreatitis
Renal failure
What is the difference between type I and type II respiratory failure and what are the causes
Type 1 is PaO2 <8kPa and PaCO2 normal
Type 2 is PaO2 <8kPa AND PaCO2>6kPa.
Type 1 respiratory failure tends to be caused by focal lung diseases (i.e. affecting
only one part of the lung) such as pneumonia and PE.
Type 2 respiratory failure
tends to be caused by more diffuse lung diseases such as COPD and pulmonary
fibrosis.
Cause of hepatopulmonary syndrome
Rare complication of cirrhosis.
Failed clearance of vasodilators.
Causes microscopic pulmonary vasodilation, lead to hyper perfusion of lungs, and hypoxaemia.
This tends to occur at lung bases, so it received by lying
What is playpnoea
Dyspnoea relieved by lying flat. Opposite of orthopnea!
Skin lesions in TB?
Erythema nodosum and lupus vulgaris
Differentials for a cavitating lesion of the lung
INFECTIVE: S. Aureus, kleb, TB
MALIGNANCY: Squamous cell carcinoma
INFLAMMATION: Granulomatosis with polyangiitis
Which bacterial pnuemonia commonly follows influenza
S aureus.
Which antibiotic is used to treat HAP,
what if it’s specifically MRSA
What about H influenzae and N gonorrhoeae
HAP- tazobactam and piperacillin
MRSA- vancomycin
H influenzae/N gonorrhoeae- cefuroxime (a cephalosporin)
What is the most common type of lung cancer in smokers
Small cell
How might obstructive sleep apnoea be treated
Patients are advised to lose weight and severe cases may be
treated with CPAP (continuous positive airway pressure) via a nasal mask during
sleep.
Define pneumonia
Infection of distal lung parenchyma. Several ways of categorization:
community-acquired, hospital-acquired or nosocomial; .
aspiration pneumonia, pneumonia in the immunocompromised; .
typical and atypical (Mycoplasma, Chlamydia, Legionella).
Causes of CAP
Air conditioning? Recent flu? IVDU? Periodic epidemics? COPD?
TYPICALS:
Streptococcus pneumoniae,
Haemophilus influenzae and moraxella catarrhalis (COPD)
Staphylococcus aureus (recent influenza infection, IV drug users),
ATYPICALS (according to Amir Sam include
• Mycoplasma pneumoniae
• Chlamydia pneumoniae
• Legionella pneumophila)
Mycoplasma pneumonia (periodic epidemics),
Legionella (anywhere with air conditioning),
Chlamydia pneumonia and Chlamydia psittaci (contact with birds/parrots)
Coxiella burnetii (Q fever, rare),
TB (may present as pneumonia
(Klebsiella, in alcoholics, can be CAP but often HAP)
Causes of hospital acquired pneumonia
Gram-negative enterobacteria (Pseudomonas, Klebsiella),
(MRSA) Staphylococcus aureus
anaerobes (aspiration pneumonia).
Risk factors for pneumonia
Age, smoking, alcohol, pre-existing lung disease, immunodeficiency, contact with pneumonia.
Hx of pneumonia
- Which causes rusty sputum
- Which is known for causing confusion
Cough (productive, green/yellow, rusty (in S pneumoniae),
Fever, rigors, sweating, malaise
Breathlessness, pleuritic chest pain
Confusion (severe cases, elderly, legionella)
HEADACHE, DIARRHOEA, MYALGIA FOR ATYPICALS
Examination for pneumonia
Pyrexia, respiratory distress, tachypnoea, hypotension, cyanosis
Reduced chest expansion, dull to percuss, increased tactile/vocal fremitus, bronchial breathing (inspiration phase lasts as long as expiration phase), coarse crepitations on affected side.
Investigations for pneumonia
Hyponatraemia?
Agglutination on blood film?
Which particularly affects upper lobes
Bloods: FBC (abnormal WCC), hyponatraemia (particularly legionella), LFT, blood cultures, ABG, blood film agglutination (mycoplasma, caused by cold agglutins)
CXR: Lobar or patchy shadowing, may lag behind clinical signs, pleural effusion. Klebsiella affects upper lobe. REPEAT AFTER 6-8 weeks.
Sputum/pleural fluid. MCS (AFB?)
Urine: pneumococcus and legionella!
Atypical viral serology: increased antibody titres between acute and convalescent samples
Bronchoscopy: IF PNEUMOCYTIS CARINII pneumonia is susepcted, or when pneumonia fails to resolve, or clinical progression
Investigations for CAP specifically
Do not order microbiological tests routinely in patients presenting with CAP in the community. Blood cultures are usually only ordered for moderate- or high-severity CAP (as determined by the CURB-65 score) presenting in hospital.
DON’T do a chest x-ray in the community unless:
There is diagnostic doubt
Progress following treatment is not satisfactory at review
The patient is at risk of underlying lung pathology such as lung cancer.
See book for management
…..
Complications for CAP
Pleural effusion, empyema (pus in the pleural cavity), localized suppuration ! lung abscess1 (especially staphylococcal, Klebsiella pneumonia, presenting with swinging fever, persistent
pneumonia, copious/foul-smelling sputum), septicshock, ARDS, acute renal failure.
Pneumonia with erythema multiforme
M. pneumonia: Erythema multiforme, myocarditis, haemolytic anaemia, meningoencephalitis, transverse myelitis, Guillain–Barr!e syndrome.
Complications for pneumonia
Most resolve with treatment.
Markers of severe pneumonia: Confusion . Urea>7mmol/L . Respiratory rate>30/min . BP: Systolic <90mm Hg or diastolic <60mm Hg . Age >65 years
What type of organism is pneumocystis jirovecci
Fungus
How does PCP present
It presents with a dry cough, exertional
dyspnoea and fever.
What examination can be done for PCP
On examination, the patient is often asked to walk up and down
the room, whilst attached to a pulse oximeter, to demonstrate oxygen desaturation
on exertion.
What can chest xray look like for PCP
A chest X-ray may be normal, or it may show bilateral pulmonary
infiltrates.
How is PCP diagnosis confrimed
Diagnosis is confirmed by visualising the organism in a sputum, bronchoalveolar lavage or lung biopsy specimen.
Which lung condition affects HIV patients with a similar presentaton to TB
Mycobacterium avium complex (MAC) is a disease that affects HIV patients with very
low CD4 counts. It has a similar presentation to TB.
Diagnositc criteria for COPD
According to NICE, COPD can be
diagnosed when spirometry results show FEV1 < 0.8 and FEV1:FVC < 0.7.
What spirometry results are seen in restrictive lung disease
FEV1 < 0.8 and FEV1:FVC >0.7 is the typical pattern seen in restrictive lung
disease, in which both FEV1 and FVC are reduced, however, the decrease in FVC is
greater than that of FEV1, resulting in a normal or raised FEV1:FVC ratio.
What is hepatopulmonary syndrome triad
Liver disease, dilated pulmonary capillaries, hypoxaemia
How is hepatopulmonary syndrome diagnosed
Diagnosis is confirmed using
echocardiography
with contrast and agitated
normal saline
What are the symptoms of hepatopulmonary syndrome
Platypnea, dyspnea worse on sitting or standing than on lying, is characteristic but not pathognomonic . Other common symptoms include clubbing and the presence of spider nevi .
What is the cause of hepatopulnonary syndrome
HPS is a complication of chronic liver disease thought to be the result of increased levels of
nitric oxide
What is the management of hepatopulnonary syndrome
Definitive treatment is
liver transplantation
. Symptomatic relief with supplemental oxygen can be used in the interim.
What is seen on echocardiography with hepatopulmonary syndrome
Echocardiogram with contrast and the injection of agitated normal saline is the gold standard for diagnosis. The bubbles in the saline are usually caught at the capillary level however in HPS the dilated capillaries allow passage of bubbles into the left atrium which can be seen using echocardiogram and contrast. The main differential is a right-to-left
cardiac shunt
which can also be identified using this technique.
Which 2 things can improve survival in COPD patients
Smoking cessation
and supplemental O2 titrated to maintain O2 saturation >90% for greater than 15 hours per day are the only interventions proven to improve survival in COPD patients.
What is asbestosis
A pneumoconiosis in which diffuse parenchymal lung fibrosis occurs as a result of prolonged exposure to asbestos
Which types of asbestos can cause asbestosis and which is more toxic
white asbestos and blue asbestos or crocidolite, the latter is more toxic
History of asbestosis
After a long latency period, this condition manifests with nonspecific symptoms, e.g., coughing and dyspnea, which are caused by fibrotic changes in the lungs.
Workers exposed to asbestos may develop pleuritic chest pain many years after first exposure as a result of acute asbestos pleurisy.
What is found on examination of asbestosis
Examination may be normal.
End-inspiratory crepitations and clubbing in asbestosis.
What is seen in the fibrotic areas of lung in asbestosis
Asbestos bodies consisting of fibres coated with an iron-containing protein are seen in fibrotic areas, especially in the lung base
What is seen on CXR in pulmonary fibrosis
In asbestosis, there is often
1) Bilateral lower zone reticulonodular shadowing and
2) Pleural plaques, visible as white lines when calcified, often most obvious on the diaphragmatic pleura or as ‘holly leaf’ patterns.
3) Rounded atelectasis Caused by pleural adhesions
4) Pleural effusion
What is mesothelioma
(malignancy of pleura, seen especially with blue asbestos, crocidolite, exposure).
Diagnosis of asbestosis
The diagnosis is established based on a history of occupational exposure (such as working with textiles, cement, ship-building, insulation) and characteristic changes on chest x-ray (reticular opacities and pleural plaques).
If unclear, bronchoalveolar lavage:
-Used when other noninvasive measures are unsuccessful. Useful in excluding concurrent infections and possibly carcinomas. This test also assists in quantitative asbestos fiber counts.
What are the long term complications of asbestos
Long-term exposure to asbestos can lead to complications like fibrosis, respiratory failure, and malignancy (especially bronchogenic carcinoma, and mesothelioma). Pleural effusion may be the first sign of a malignant mesothelioma.
Risk factors for asbestosis
Occupations involving the manufacture or demolition of ships, plumbing, roofing, insulation, heat-resistant clothing, and brake lining
Smoking
What are the 3 possible locations of mesothelioma
Pleural mesothelioma (most common) Peritoneal mesothelioma (rarely) Pericardial mesothelioma (very rarely)
Clinical findings of mesothelioma
Dyspnea and nonpleuritic chest pain (most common)
Fever, sweats, weight loss, fatigue
Features of pleural effusion: dull percussion; absent or reduced breath sounds on affected side
How is mesothelioma diagnosed
Pleurocentesis : bloody (exudative) pleural effusion (diagnostic in 30% of cases)
Imaging (CXR/CT): Multiple nodular, pleural lesions (pleural thickening-fluid in the space between the lungs and chest wall, or changes in the lungs,)
Ipsilateral hemothorax
Reduced size of ipsilateral lung fields
Obliteration of the diaphragm
GOLD STANDARD: Laparoscopy, thoracoscopy and pleuroscopy with stained biopsy:
-Mesothelioma cells and psammoma bodies (not specific to mesothelioma)
What effect can COPD have on the pulse and why
In addition, COPD can lead to
peripheral cyanosis (due to low oxygen saturation) and a bounding pulse (due to
carbon dioxide retention).
Sweat test diagnosis for which condition, and what makes diagnosis likely
crackles. A sweat test measures the chloride
concentration of the patient’s sweat. If the chloride concentration is > 60 mmol/L, a
diagnosis of CF is likely.
What is acute respiratory distress syndrome
Medical condition in critically ill patients, characterised by widespread inflammation in the lungs.
Sepsis is the most common cause, usually with a pulmonary origin (e.g., pneumonia)
Aetiology of ARDS
Common causes are pneumonia, sepsis, aspiration, and severe trauma
What are the features of ARDS
- Injury to cells forming alveolar barrier
- Surfactant dysfunction
- Activation of the innate immune response
- Abnormal coagulation
All this resulting in
-Impaired gas exchange
ARDS diagnostic
1) Acute onset (within a week)
2) Bilateral infiltrates consistent with pulmonary oedema
3) PaO₂/FiO₂ (arterial to inspired oxygen) ratio of ≤300 on positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H₂O
3 stages of ARDS
Exudative, prolferative, fibrotic
History of ARDS
Rapid deterioration of respiratory function, dyspnoea, respiratory distress, cough, symptoms of aetiolog
Examination for ARDS
Cyanosis, tachypnoea, tachycardia, widespread inspiratory crepitations.
Hypoxia refractory to oxygen treatment.
Signs are usually bilateral but may be asymmetrical in early stages.
Investigations for ARDS
1st:
CXR: bilateral infiltrates
ABG: A PaO₂/FiO₂ (inspired oxygen) ratio of ≤300 on positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H₂O is part of the diagnostic criteria for ARDS.
Sputum culture/blood culture/urine culture/amylase/lipase
May consider:
BNP (<100 nanograms/L), see if HF is more likely (<500 nanograms/L)
ECG
What type of emphysema is seen in COPD caused by smoking vs COPD caused by a1 antitrypsin
Centrilobular emphysema (centriacinar emphysema)
Most common type of emphysema
Classically seen in smokers.
Affects respiratory bronchiole
Panlobular emphysema (panacinar emphysema) Rare type of emphysema Associated with α1-antitrypsin deficiency. Affects whole acinar unit
Which part of the lung is affected by centrilobar vs panlobular emphysema
Centrilobular emphysema commonly affects upper lobe
Panlobular emphysema. Affects lower lobe
What is acute exacerbation of COPD caused by
80% of cases are caused by infection (especially in winter and fall).
Most commonly Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae and viruses such as influenza
Other causes include CHF, drugs (e.g. beta blockers), former Abx use, advances age etc.
Treatment for acute exacerbation of COPD
Sit patient upright
If hypoxic, administer oxygen and titrate to 88-92% (by nasal cannulae at 2L/minute or non-rebreather mask)
Salbutamol (5mg) delivered by a nebuliser driven by compressed air (not o2)
Ipratropium bromide 500mg if not responsing
Steroids should be used in all patients admitted with acute exacerbation of COPD e.g. prednisolone 30mg
If all of the above fail, consider non-invasive ventilation WITH BiPAP!!!!!, IV theophylline/
Antibiotic treatment is indicated for patients with ≥ 2 of the following cardinal symptoms:
- Increased dyspnea
- Increased cough
- Increased sputum production
The abx should be amox + clari as normal
What antibiotic should be given for hospital acquired pneumonia pseudomonas aeruginosa
piperacillin-tazobactam, cefepime, ceftazidime, or levofloxacin
What must be done after insertion of a central venous catheter
Pneumothorax may occur following central venous catheter (CVC) placement. Therefore, a chest radiograph should be obtained immediately to ensure adequate line placement and to assess for complications before the line is used.
When does a chest x ray not have to be done on a patient who has had a central venous catheter inserted?
The only exception to this rule is if a CVC is placed in a hemodynamically
unstable
or actively decompensating patient, as delay in using the CVC would result in potential patient death
What is extrinsic allergic alveolitis
Interstitial inflammatory disease of the distal gas-exchanging parts of the lung caused by inhalation of organic dusts. Also known as hypersensitivity pneumonitis
Causes of allergic extrinsic alveolitis
Inhalation of antigenic organic dusts containing microbes (bacteria, fungi or amoebae) or animal proteins induce a hypersensitivity response (a combination of type III antigen–antibody complex hypersensitivity reaction and a type IV granulomatous lymphocytic inflammation) in susceptible individuals.
Mixed type III and type IV immune reactions
What is farmer’s lung?
Allergic extrinsic alveolitis, due to Mouldy hay containing thermophilic actinomycetes.
What is Pigeon/budgerigar fancier’s lung?
Allergic extrinsic alveolitis, due to Bloom on bird feathers and excreta.
What is mushroom worker’s lung
Allergic extrinsic alveolitis, due to Compost containing thermophilic actinomycetes.
What is humidifier lung
Allergic extrinsic alveolitis, due to Water-containing bacteria and Naegleria (amoeba).
What is maltworker’s lung
Barley or maltings containing Aspergillus clavatus. (link this above with the different aspergillus diseases)
Hx of acute extrinsic alergic alveolitis
Presents 4–12 h post-exposure. Reversible episodes of dry cough, dyspnoea, malaise, fever, myalgia.
Wheeze and productive cough may develop on repeat high-level exposures.
Hx of chronic extrinsic allergic alveolitis
Poorly reversible manifestation in some, slowly increased breathlessness and reduced exercise tolerance, weight loss.
Exposure is usually chronic, low level and there may be no history of previous acute episodes.
Examination of acute extrinsic allergic alveolitis
Rapid shallow breathing, pyrexia, inspiratory crepitations.
Examination of chronic extrinsic allergic alveolitis
Fine inspiratory crepitations (see Cryptogenic fibrosing alveolitis). Finger clubbing is rare.
How to investigate extrinsic allergic alveolitis
Bloods (FBC: neutrophilia, lymphopenia. ABG: reduced po2, reduced pco2)
Serology: Precipitating IgG to fungal or avian antigens in serum; however, these are not diagnostic as are often found in asymptomatic individuals (but good negative predictive value)… this is a 1st investigation according to BMJ.
CXR: Often normal in acute episodes. May show “ground glass” appearance with alveolar shadowing or nodular opacities inteh middle and lower zones. Chronic cases, fibrosis prominent in upper zones
High resolution CT-thorax: detects early changes before CXR. Patchy “ground glass” shadowing and nodules
Pulmonary function test: restrictive ventilatory defect (reduced FEV1, reduced FVC, but preserved ratio), reduced TLCO.
Bronchoalveolar lavage. Increased cellularity with increased CD8+ suppressor T cells.
Lung biopsy occasionally performed in patients with atypical features, or where there is an absence of an exposure history.
T/F COPD is a complication of asbestos exposure
F
The spectrum of asbestos-related thoracic diseases includes benign pleural effusion, pleural plaques, diffuse pleural thickening, rounded atelectasis, asbestosis (asbestos-related interstitial fibrosis), mesothelioma, and lung cancer. COPD is primarily caused by cigarette smoke.
What HR indicates severe asthma
Bradycardia is an ominous sign.
Tachycardia is normal in an asthma attach and may also be caused by salbutamol neb
Cause of collapsed lung in asthma attack?
This is likely to be due to a retained mucus plug – treat by physio and follow-up chest x-ray. Involve chest team (bronchoscopy) if collapse fails to resolve.
What electrical abnormlaity is aminophylline associated with
Hypokalaemia (and thus cardiac arrhtyhmias, so cardiac monitoring is needed0
MOA aminophylline
It is a phosphodiesterase inhibitor
CURB65 score?
Confusion and raised respiratory rate >30 are worrying signs that may indicate respiratory failure or sepsis.
Urea>10 and systolic BP<100 or diastolic <60 mmHg is sign indicating worse prognosis
Being over 65
What sign on examination might suggest a pneumonia is complicated by another pulmonary disease
Reduced lung volume on affected side suggests there may be a proximal lesion (most likely lung cancer), a parapneumonic effusion/pleural empyema, or there is old disease affecting that side
What is the approriate Abx therpay in community acquired management that doesn’t need hospital admission
Amoxicillin alone
What is the approprate Abx treatment for those with more severe illness that are admitted to hospital
Combination of co-amoxiclav (to cover resistant strains of H influenzae– approximately 15%) and a macrolide (clarithromycin, erythromycin, etc) is correct.
CURB65 score 3+ in hospital should be given what Abx?
dual therapy with an intravenous combination of a “broad spectrum ß-lactamase stable antibiotic such co-amoxiclav, together with a macrolide such as clarithromycin”.
What should those with mild penicillin allergy (just rash) be given instead of co-amoxiclav
Those with a mild penicillin allergy (rash only) may have a 2nd or 3rd generation cephalosporin instead of the co-amoxiclav
although patients with a history of severe allergy should avoid cephalosporins as there is a risk of crossover allergy
What is the risk of anaphylaxis for someone with penicillin allergy if given a cephalosporin like cefuroxime?
7%
In which infections does abscess formation occur in pneumonia
Staphylococcus aureus and Klebsiella infection
Patients with persistent fever despite Abx therapy should be assessed for what condition and how?
Patients with persistent fever despite appropriate antibiotic therapy should be assessed for possible empyema. Ultrasound can be very helpful as it distinguishes well between solid and fluid.
Normal Co2 in someone with an acute asthma attack is worrying
T
In a sick asthmatic, you would expect to see a low pCO2; if it’s normal or rising this suggests they are failing to keep up and will soon go into worse respiratory failure.
If somebody is on ICS and SABA and having frequent exacerbations, what is the next step in the management to reduce future exacerbations
Adding LABA (salmaterol)
Adding montelukast
(doubling steroid dose does not reduce exacerbation dose significantly)
Steroid side effects
cataracts, osteoporosis, diabetes mellitus, weight gain and increased rates of infection, including candida
What score is used to assess likelihood of group A strep infection in those with pharyngitis/tonsillitis
FeverPAIN score
Outline management of sore throat
If GAS confirmed or suspected (FeverPAIN 5-4), and throat cultures pending, consider prescribing Abx, particularly if in a vulnerable goup
For people not in a vulnerable group, and without severe symptoms, or who have a FeverPAIN score of 2 or3 consider a delayed antibiotic prescribing strategy.
Prescribe phenoxymethylpenicillin as the first-choice antibiotic.
What are the indications for tonsillectomy
A frequency of more than 7 episodes per year for one year, 5 per year for 2 years, or 3 per year for 3 years,
What medications are used in the management of PCP pneumonia
Co-trimoxazole (trimethoprim and sulfamethoxazole) in high dosage is the drug of choice for the treatment of mild to moderate pneumocystis pneumonia.
2nd line is pentamidine
What are the 2 key clinical features of ABPA
What blood marker is raised
This will cause episodes of bronchial obstruction leading to productive coughing (or coughing fits) and
asthma
, which are two classic symptoms in patients with ABPA.
Laboratory findings most notably show eosinophilia and elevated serum concentration of total IgE .
How can ABPA be eradicated from the airway
combination therapy with corticosteroids and ketoconazole is commonly used.
What is myasthenia gravis most commonly associated with
Thymic hyperplasia or thymoma
MG is associated with thymic hyperplasia in 70% or thymoma in 10%,
What happens to the tremor with parkinson’s with use of the limb
The resting tremor occurs at 4-6 Hz at rest which dissipates with the use of limbs, with generally asymmetrical onset
What is the most sensitive test for spinal MIR
MRI is a sensitive test but less specific than spinal MRI, however, spinal MRI is abnormal in fewer cases
Most specific test for carpal tunnel
The most sensitive and specific test for diagnosis is EMG and can confirm damage to the median nerve in the carpal tunnel and categorise the severity of the damage. There are specific tests for CTS such as Tinel’s test and Phalen’s test, though clinically these are not particularly useful due to sensitivity and specificity.
Screening of CF vs diagnosis
The most conclusive diagnostic test is the sweat test which is positive if sweat chloride is >60mmol/L.
Serum IRT used for screening
Which paraneoplastic syndrome is associated with each of the following:
Small cell carcinoma
Non-small cell lung cancer
Small cell lung cancer is treated with chemotherapy and is associated with SIADH and ectopic ACTH. Non-small cell lung cancer is more often associated with clubbing. Squamous cell carcinoma is associated with PTHrp release and is treated with radiotherapy. Adenocarcinomas are usually located peripherally in the lung and are more common in non-smokers although most cases are still associated with smoking. The paraneoplastic syndromes may include Lambert-Eaton myasthenic syndrome.
