Bronchiectasis, Aspergilloma, Tuberculosis Flashcards
What is bronchiectasis [2]
- Permanent dilatation of the bronchi / airway due to
- a repeating cycle of infection and chronic inflammation.
Pathophysiology bronchiectasis [2]
- An initial insult, usually infective, damages airways > inflammatory response > further damage to the mucociliary apparatus.
- Renders susceptible to bacterial colonisation + vicious cycle of chronic inflammation and lung damage.
- Neutrophils are the most prominent cell type in the bronchial lumen and release mediators, particularly proteases and elastases, which cause bronchial dilation.
What causes bronchiectasis [8]
- Post-infectious: include TB, whooping cough, severe pneumonia, non-tuberculous mycobacterium and ABPA.
- Genetic: most common in childhood is CF
- Immunodeficiency: primary hypogammaglobinaemia, HIV, CLL and nephrotic syndrome.
- Aspiration and inhalation injury.
- Systemic conditions: RA, UC, yellow nail syndrome
- Mounier–Kuhn syndrome
- Williams–Campbell syndrome
- Swyer–James syndrome (MacLeod’s syndrome)
Bronchiectasis
Congenital causes [5]
- alpha-1-antitrypsin deficiency
- primary ciliary dyskinesia including Kartagener’s syndrome (dextrocardia, chronic sinusitis and bronchiectasis)
- Marfan’s syndrome
- Ehlers–Danlos syndrome
- Young’s syndrome (bronchiectasis, sinusitis and azoospermia)
Causative organisms [5]
Symptoms [3]
Signs [3]
H.influenza Pseudomona's Klebsiella S.pneumonia S.aureus
Symptoms:
- persistent cough
- copious purulent sputum
- +/- haemoptysis
Signs:
- Finger clubbing
- Coarse inspiratory crackles
- Wheeze (if co-existent asthma, COPD or ABPA)
Standard investigations [4]
Bloods - inflammatory markers, genetic tests
Sputum culture
CXR
Spirometry = obstructive
HRCT thorax
Investigations for congenital causes of bronchiectasis
CF genotype Serum total IgE Aspergillus precipitins Serum Ig Skin prick
CXR findings [3]
Thickened bronchial wall
Cystic shadows
Tram lines
Bronchiectasis - medical management
- Empirical treatment should be started while waiting for sputum culture. First-line treatment includes amoxicillin for 14 days (or clarithromycin if penicillin allergic) unless previous cultures have shown this to be inappropriate.
- IV antibiotics should be considered if the patient is very unwell, hospitalised or has a resistant organism that has failed to respond to oral therapy in the past (especially Pseudomonas aeruginosa). Prolonged use of antibiotics should be considered in patients who have >3 exacerbations per year or progressive lung function decline.
What is specific treatment for potential underlying causes [3]
Relieve obstruction
Iv Ig replacement
Steroids for APBA
What are complications of bronchiectasis? [5]
More prone to infection Pneumonia Pleural effusion Pneumothorax Cerebral abscess
What is allergic bronchopulmonary aspergillosis
Type 1 and 3 allergy to spores
What are the symptoms of ABPA [4]
- Wheeze, Cough, SOB
- May be labelled as asthmatic but prog worsening
- Bronchiectasis develops due to damage
- Recurrent pneumonia
What puts you at higher risk of ABPA [2]
Asthma
CF
How do you Dx ABPA [4]
CXR (transient segmental collapse, consolidation, bronchiectasis)
Sputum culture
Serum IgE (raised)
Aspergillis specific IgE RAST
How do you treat ABPA [4]
Steroid in attacks
Bronchodilator
Itracanazole
Bronchoscopy aspiration of pleural plugs
What are the complications of ABPA
Aspergilloma (fungal ball)
What is aspergilloma?
Fungal ball that forms from a pre-existing cavity (TB / sarcoid)
What are symptoms of aspergilloma [4]
Cough
Haemoptysis (MASSIVE)
Lethargy
Weight loss
How do you Dx aspergilloma [3]
CXR - round opacity
Sputum culture
Aspergillis skin test or serum precipitins
How do you Rx aspergilloma [2]
- Surgical excision
- Local instillation of amphotericin paste under CT guidance
What is invasive aspergillosis?
What puts you at risk of invasive aspergillosis [6]
Disseminated aspergillus infection starts in lungs and spreads to other tissues and organs haematogenously.
Immunocompromised HIV Leukaemia Wegners SLE Broad spec Ax
How do you Dx invasive aspergillosis [6]
BAL Sputum culture Biopsy = Dx CXR (nodules, cavitations) CT thorax (halo sign above nodules) Serial measurement of galactomannan (aspergillum antigen)
How do you treat invasive aspergillosis?
IV VORICONAZOLE
What are other fungal infections in the lung [4]
Asthma = type 1 hypersensitivity reaction to fungal spore
Extrinsic allergic alveolitis
Candida
Cryptococcus
Bronchiectasis
What is yellow nail syndrome?
TRIAD
lymphoedema, yellow discolouration of nails, pleural
effusion
Bronchiectasis
Mounier-Kuhn syndrome [2]
tracheobronchial dilation associated with recurrent lower respiratory
tract infections
Bronchiectasis
William Campbell syndrome
a congenital syndrome characterised by absence of cartilage in
subsegmental bronchi leading to bronchiectasis distal to the collapsed airways
Bronchiectasis
Swyer James Syndrome
caused by a childhood bronchiolitis obliterans infection, which may lead to bronchial wall damage with localised or generalised bronchiectasis, air-trapping and stunted pulmonary arterial development.
What would indicate bronchiectasis on HRCT? [3]
- lack of bronchial tapering
- airway dilatation to the periphery
- bronchial wall-thickening and the signet sign- where the airway is larger than the corresponding vessel due to dilatation.
What would indicate bronchiectasis on HRCT? [3]
- lack of bronchial tapering
- airway dilatation to the periphery
- bronchial wall-thickening and the signet sign- where the airway is larger than the corresponding vessel due to dilatation.
Additional medical treatments for bronchiectasis
- Chest physio - good for non-CF
- Mucolytic therapies (Carbocysteine) lack robust evidence but may help
- Postural drainage & nebulised hypertonic saline can help
- There is no evidence for the routine use of inhaled or oral steroid or bronchodilators unless there is evidence of airways obstruction.
When would you consider long term nebulised antibiotics in bronchiectasis?
Long-term nebulised antibiotics or combination antibiotics, especially if chronically colonised with Pseudomonas, may be required.
Bronchiectasis
Interventional therapy and surgery [3]
- Bronchial embolisation: indicated for massive haemoptysis.
- Surgical resection may be indicated for localised bronchiectasis once all medical measures have been
exhausted. - Lung transplantation is a common outcome in patients with CF, but is otherwise only routinely offered if there is rapid progressive respiratory deterioration despite optimum medical management.
Tuberculosis terms
Primary TB
What is a Ghon focus
Re-activation TB
Latent TB
Initial primary infection is mild febrile illness - Ghon focus develops and is contained.
10% will develop active disease after exposure
Active TB is when there are actually symptoms particularly resp sx
Re-activation TB - organism spreads from lungs haematogenously to bone and other organs
Latent TB refers to previous exposure but dont develop active disease, Mantoux test positive
Primary and latent TB
Transmission [3]
- Mycobacterium TB are slow growing in water and soil
- Spread by open pulmonary TB where coughing and sneezing
- causes evaporated respiratory droplets
Primary and latent TB
Pathophysiology [6]
- Macrophages ingest mycobacteria
- Th1 response create an inflammatory response
- Granulomas form with central caveating necrosis
- Mycobacteria focus on alveoli, lymphatic and gut
- Causing an initial lesion and local LN with(out) scar
- Scar calcifies and is contained in the scar
Presentation of primary and latent TB [3]
Asymptomatic in majority
Erythema nodosum
Rarely chest sign
Investigations of primary TB [2]
Mantoux test: +ve if >5mm
HIV test if mantoux positive
What can happen after primary infection if don’t clear [6]
Progressive consolidation
Bronchiectasis as bronchi collapse due to compression from LN
Bronchial spread
Pleural effusion
Bronchopneumonia if LN discharge
Haematogenous spread - miliary and meningeal TB
Management of primary and latent TB [3]
Assess for active TB
If negative then treat as latent TB
Strict antibiotic regimen
Other mycobacteria - name 3 other groups
Mycobacteria causing tuberculosis
Mycobacteria causing leprosy
Non-TB mycobacteria
Name organisms:
Mycobacteria causing tuberculosis [5]
m. tuberculosis
m. bovis
m. africanum
m. microti
m canetti
Name organisms:
Mycobacteria causing leprosy [2]
Non-tuberculosis mycobacteria [3]
m..leprae, m. lepromatosis
Non-TB mycobacteria:
- M. avian complex
- M. marinum
- M. ulcerous
Active TB: pathophysiology [4]
- reactivation of mycobacterium tuberculosis
- from latent disseminated primary infection OR new infection in previously infected susceptible source (now have different response as immunocompromised)
- causes tissue destruction after 1-5y
- in lungs, hips and spine and after 10-15y in kidneys and ureters and infertility (fallopian tube, uterus, vas deferens)
Extra-pulmonary manifestations of TB
GU [5]
Bone and joint [3]
GU:
- sterile pyuria
- epididymitis
- kidney lesions
- salpingitis
- abscesses and female infertility
Bone and joint:
- pain, arthritis, osteoarthritis
- abscess formation
- nerve root compression
Extra-pulmonary manifestations of TB
CNS [4]
GI [3]
CNS:
- N&V
- headache
- altered behaviour
- followed by reduced GCS +/- focal neuro deficit
GI:
- ileocecal lesions causing abdo pain, bloating
- and simulating appendicitis
- peritoneal spread causing ascites
Extra-pulmonary manifestations of TB
LN [3]
Skin [3]
Pericadial [2]
Lymph nodes:
- hilar, para-tracheal or superficial
- may later become matted
- and supprative with discharging sinuses
Skin:
- erythema nodosum (early immune response to infection)
- skin sinus formation,
- erythema induratum
Pericardial:
- pericardial effusion or constrictive pericarditis
Active TB
Risk factor [6]
DM, hx TB, immunosuppression, HIV, alcohol abuse, IVDU, migration from high risk areas
Active TB Presentation
Symptoms [7]
Symptoms:
- cough
- sputum
- haemoptysis (rare)
- SOB
- malaise
- fever, weight loss
- night sweats
- pleuritic or retrosternal pain
pleuritic pain may be secondary to a pleural effusion
retrosternal pain may be secondary to enlarged bronchial lymph nodes
Active TB Presentation
Signs [2]
- crackles and reduced breath sounds if advanced
- lower zone dullness, decreased percussion note > pleural effusion
- finger clubbing RARE (sign of chronic infection)
Active TB Ix:
- Pulmonary TB [2]
- Pleural TB [2]
Pulmonary TB
- CXR or CT thorax
- 3 sputum samples
Pleural TB
- CXR or bronchoscopy
- Pleural biopsy > microscopy, culture and cytology
Active TB management
- Notify public health and conduct contact tracing
- Antibiotic regimen
- RIPE for 2 months
- RI (Rifinah) for another 4m
Management of active neurological TB [2]
RIPE for 2m
RI for 10m with steroids
Side effects of TB drugs: Rifampicin [3] Izoniazid [2] Ethambutol [1] Pyrazinamide [1]
o RIFAMPICIN SE: orange coloured tears and urine, liver enzyme induction (prednisolone, anti-convulsants and OCP become ineffective), hepatitis
o IZONIAZID SE: hepatitis, peripheral neuropathy (pyroxidine B6)
o ETHAMBUTOL SE: optic neuropathy (check visual acuity)
o PYRAZINAMIDE SE: gout
What do these results indicate?
6-15mm [2]
>15mm [1]
Sensitive to tuberculin
Shows past BCG vaccine or latent or active TB
Suggests very active TB - requires CXR
What is prophylaxis treatment of TB
BCG vaccine protects children against TB and has stronger protection for TB meningitis in particular
What could cause a false -ve Mantoux result [6]
Immunosuppression - steroid / HIV Sarcoid Lymphoma Age extremes Fever Hypo-albumin
Blood tests in TB and rationale [4]
- Inflammatory markers (FBC and CRP).
- LFTs, U&Es (baseline required before treatment).
- Calcium and vitamin D levels: vitamin D plays an important role in the host response against TB. * HIV test: latent TB is more likely to be activated and more severe in presentation.
Sputum investigation in TB [5]
- Sputum culture is the gold standard investigation
- Acid-fast bacilli (AFB) are available within hours and confirms need for isolation.
- Cultures take up to 6–8 weeks and to determine full anti-mycobacterial sensitivities.
- If AFB are smear negative, treatment based on a clinical diagnosis may be necessary while awaiting culture results.
- identification of necrotising granulomas from lymph node or extra-pulmonary biopsy specimens.
Further investigations TB
When would bronchoscopy be indicated
Bronchoscopy is employed in cases where TB culture cannot be confirmed by sputum, but clinical suspicion is high, particularly where immunocompromise raises the possibility of other co-infections. Necrotising granulomas from EBUS are strongly suggestive of TB.
If pleural fluid sampling was done on suspected TB, what might we find?
◆ Often an exudate.
◆ Organisms rarely cultured.
◆ Usually lymphocytic.
◆ Pleural adenosine deaminase (ADA), a lymphocytic enzyme, is often increased.
What is the Xpert test
‘Xpert’ is a rapid (2 hours), point-of-care mycobacterium tuberculosis (MTB)/resistance to rifampicin (RIF) assay, offering diagnosis from sputum in 2 hours, as well as information on rifampicin resistance. This is of particular value for predicting multidrug resistance in high prevalence areas and heralds a new way of diagnosing TB.
Pathophysiology of Primary Tuberculosis
What is a Ghon complex?
- A non-immune host who is exposed to M. tuberculosis may develop a primary infection of the lungs.
- A small lung lesion known as a Ghon focus develops.
- The Ghon focus is composed of tubercle-laden macrophages.
- The combination of a Ghon focus and hilar lymph nodes is known as a Ghon complex
Which group of patients develop disseminated disease?
In immunocompetent people, the initial lesion usually heals by fibrosis. Those who are immunocompromised may develop disseminated disease (miliary tuberculosis).
Surgical (historical) approaches to TB [4]
- Thoracoplasty: marked volume loss on the affected side.
- Phrenic nerve crush: short supraclavicular fossa scar.
- Plombage: an inert substance (e.g. plastic balls) inserted into the pleural space, thus compressing the
adjacent lung.
