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.
