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Respiratory > Bronchiectasis, Aspergilloma, Tuberculosis > Flashcards

Bronchiectasis, Aspergilloma, Tuberculosis Flashcards

1
Q

What is bronchiectasis [2]

A
  • Permanent dilatation of the bronchi / airway due to
  • a repeating cycle of infection and chronic inflammation.
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2
Q

Pathophysiology bronchiectasis [2]

A
  • 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.
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3
Q

What causes bronchiectasis [8]

A
  • 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)
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4
Q

Bronchiectasis

Congenital causes [5]

A
  • 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)
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5
Q

Causative organisms [5]
Symptoms [3]
Signs [3]

A 
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)
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6
Q

Standard investigations [4]

A

Bloods - inflammatory markers, genetic tests
Sputum culture
CXR
Spirometry = obstructive
HRCT thorax

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7
Q

Investigations for congenital causes of bronchiectasis

A 
CF genotype
Serum total IgE
Aspergillus precipitins
Serum Ig
Skin prick
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8
Q

CXR findings [3]

A

Thickened bronchial wall
Cystic shadows
Tram lines

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9
Q

Bronchiectasis - medical management

A
  • 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.
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10
Q

What is specific treatment for potential underlying causes [3]

A

Relieve obstruction
Iv Ig replacement
Steroids for APBA

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11
Q

What are complications of bronchiectasis? [5]

A 
More prone to infection
Pneumonia
Pleural effusion
Pneumothorax
Cerebral abscess
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12
Q

What is allergic bronchopulmonary aspergillosis

A

Type 1 and 3 allergy to spores

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13
Q

What are the symptoms of ABPA [4]

A
  • Wheeze, Cough, SOB
  • May be labelled as asthmatic but prog worsening
  • Bronchiectasis develops due to damage
  • Recurrent pneumonia
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14
Q

What puts you at higher risk of ABPA [2]

A

Asthma

CF

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15
Q

How do you Dx ABPA [4]

A

CXR (transient segmental collapse, consolidation, bronchiectasis)
Sputum culture
Serum IgE (raised)
Aspergillis specific IgE RAST

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16
Q

How do you treat ABPA [4]

A

Steroid in attacks
Bronchodilator
Itracanazole
Bronchoscopy aspiration of pleural plugs

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17
Q

What are the complications of ABPA

A

Aspergilloma (fungal ball)

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18
Q

What is aspergilloma?

A

Fungal ball that forms from a pre-existing cavity (TB / sarcoid)

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19
Q

What are symptoms of aspergilloma [4]

A

Cough
Haemoptysis (MASSIVE)
Lethargy
Weight loss

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20
Q

How do you Dx aspergilloma [3]

A

CXR - round opacity
Sputum culture
Aspergillis skin test or serum precipitins

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21
Q

How do you Rx aspergilloma [2]

A
  • Surgical excision

- Local instillation of amphotericin paste under CT guidance

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22
Q

What is invasive aspergillosis?

What puts you at risk of invasive aspergillosis [6]

A

Disseminated aspergillus infection starts in lungs and spreads to other tissues and organs haematogenously.

Immunocompromised
HIV
Leukaemia
Wegners
SLE
Broad spec Ax
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23
Q

How do you Dx invasive aspergillosis [6]

A 
BAL
Sputum culture
Biopsy = Dx
CXR (nodules, cavitations)
CT thorax (halo sign above nodules)
Serial measurement of galactomannan (aspergillum antigen)
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24
Q

How do you treat invasive aspergillosis?

A

IV VORICONAZOLE

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25
Q

What are other fungal infections in the lung [4]

A

Asthma = type 1 hypersensitivity reaction to fungal spore
Extrinsic allergic alveolitis
Candida
Cryptococcus

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26
Q

Bronchiectasis

What is yellow nail syndrome?

TRIAD

A

lymphoedema, yellow discolouration of nails, pleural
effusion

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27
Q

Bronchiectasis

Mounier-Kuhn syndrome [2]

A

tracheobronchial dilation associated with recurrent lower respiratory
tract infections

28
Q

Bronchiectasis

William Campbell syndrome

A

a congenital syndrome characterised by absence of cartilage in
subsegmental bronchi leading to bronchiectasis distal to the collapsed airways

29
Q

Bronchiectasis

Swyer James Syndrome

A

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.

30
Q

What would indicate bronchiectasis on HRCT? [3]

A
  • 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.
30
Q

What would indicate bronchiectasis on HRCT? [3]

A
  • 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.
31
Q

Additional medical treatments for bronchiectasis

A
  • 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.
32
Q

When would you consider long term nebulised antibiotics in bronchiectasis?

A

Long-term nebulised antibiotics or combination antibiotics, especially if chronically colonised with Pseudomonas, may be required.

33
Q

Bronchiectasis

Interventional therapy and surgery [3]

A
  • 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.
34
Q

Tuberculosis terms

Primary TB
What is a Ghon focus
Re-activation TB
Latent TB

A

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

35
Q

Primary and latent TB

Transmission [3]

A
  • Mycobacterium TB are slow growing in water and soil
  • Spread by open pulmonary TB where coughing and sneezing
  • causes evaporated respiratory droplets
36
Q

Primary and latent TB

Pathophysiology [6]

A
  • 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
37
Q

Presentation of primary and latent TB [3]

A

Asymptomatic in majority
Erythema nodosum
Rarely chest sign

38
Q

Investigations of primary TB [2]

A

Mantoux test: +ve if >5mm

HIV test if mantoux positive

39
Q

What can happen after primary infection if don’t clear [6]

A

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

40
Q

Management of primary and latent TB [3]

A

Assess for active TB
If negative then treat as latent TB
Strict antibiotic regimen

41
Q

Other mycobacteria - name 3 other groups

A

Mycobacteria causing tuberculosis
Mycobacteria causing leprosy
Non-TB mycobacteria

42
Q

Name organisms:

Mycobacteria causing tuberculosis [5]

A

m. tuberculosis
m. bovis
m. africanum
m. microti
m canetti

43
Q

Name organisms:
Mycobacteria causing leprosy [2]
Non-tuberculosis mycobacteria [3]

A

m..leprae, m. lepromatosis

Non-TB mycobacteria:

  • M. avian complex
  • M. marinum
  • M. ulcerous
44
Q

Active TB: pathophysiology [4]

A
  • 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)
45
Q

Extra-pulmonary manifestations of TB
GU [5]
Bone and joint [3]

A

GU:

  • sterile pyuria
  • epididymitis
  • kidney lesions
  • salpingitis
  • abscesses and female infertility

Bone and joint:

  • pain, arthritis, osteoarthritis
  • abscess formation
  • nerve root compression
46
Q

Extra-pulmonary manifestations of TB
CNS [4]
GI [3]

A

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
47
Q

Extra-pulmonary manifestations of TB
LN [3]
Skin [3]
Pericadial [2]

A

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

48
Q

Active TB

Risk factor [6]

A

DM, hx TB, immunosuppression, HIV, alcohol abuse, IVDU, migration from high risk areas

49
Q

Active TB Presentation

Symptoms [7]

A

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
50
Q

Active TB Presentation

Signs [2]

A
  • crackles and reduced breath sounds if advanced
  • lower zone dullness, decreased percussion note > pleural effusion

- finger clubbing RARE (sign of chronic infection)

51
Q

Active TB Ix:

  • Pulmonary TB [2]
  • Pleural TB [2]
A

Pulmonary TB

  • CXR or CT thorax
  • 3 sputum samples

Pleural TB

  • CXR or bronchoscopy
  • Pleural biopsy > microscopy, culture and cytology
52
Q

Active TB management

A
  1. Notify public health and conduct contact tracing
  2. Antibiotic regimen
    - RIPE for 2 months
    - RI (Rifinah) for another 4m
53
Q

Management of active neurological TB [2]

A

RIPE for 2m

RI for 10m with steroids

54
Q 
Side effects of TB drugs:
Rifampicin [3]
Izoniazid [2]
Ethambutol [1]
Pyrazinamide [1]
A

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

55
Q

What do these results indicate?
6-15mm [2]
>15mm [1]

A

Sensitive to tuberculin
Shows past BCG vaccine or latent or active TB

Suggests very active TB - requires CXR

56
Q

What is prophylaxis treatment of TB

A

BCG vaccine protects children against TB and has stronger protection for TB meningitis in particular

57
Q

What could cause a false -ve Mantoux result [6]

A 
Immunosuppression - steroid / HIV 
Sarcoid
Lymphoma
Age extremes
Fever
Hypo-albumin
58
Q

Blood tests in TB and rationale [4]

A
  • 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.
59
Q

Sputum investigation in TB [5]

A
  • 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.
60
Q

Further investigations TB

When would bronchoscopy be indicated

A

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.

61
Q

If pleural fluid sampling was done on suspected TB, what might we find?

A

◆ Often an exudate.
◆ Organisms rarely cultured.
◆ Usually lymphocytic.
◆ Pleural adenosine deaminase (ADA), a lymphocytic enzyme, is often increased.

62
Q

What is the Xpert test

A

‘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.

63
Q

Pathophysiology of Primary Tuberculosis

What is a Ghon complex?

A
  • 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
64
Q

Which group of patients develop disseminated disease?

A

In immunocompetent people, the initial lesion usually heals by fibrosis. Those who are immunocompromised may develop disseminated disease (miliary tuberculosis).

65
Q

Surgical (historical) approaches to TB [4]

A
  • 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.

Respiratory (14 decks)

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