Resp conditions Flashcards
Give examples of 2 organisms that cause TB
Mycobacterium tuberculosis
Mycobacterium bovis (unpasteurised milk)
+ africanum, microti
What makes TB a successful pathogen?
Thick waxy capsule cell wall is able to resist weak disinfectants and survive on dry surfaces for a long time.
Resistant to phagolysosomal killing by macrophages (- granuloma formation).
Able to remain dormant.
Describe the pathogenesis of primary tuberculosis
Inhaled into the lung and ingested by alveolar macrophages.
TB resists phagolysosomal killing and proliferates, releasting cytokines resulting in inflammatory involvement of hilar lymph node.
3 weeks later
Granuloma formation around TB (primary ghon focus) and associated lymph node, known together as the Ghon complex.
Caseous necrosis of complex occurs, and it undergoes fibrosis and calcification (Ranke complex)- visible on CXR.
TB is able to remain dormant within the Ranke Complex for many years = latent TB.
Cell-mediated immunity memory to TB is developed.
Reactivation occurs when the individual is immunocompromised.
Where in the lung is the primary Ghon complex usually found and why?
In the apex, as this is less well perfused so the TB comes into contact with fewer immune cells
Describe what may happen if an individual with a latent TB infection is immunocompromised?
How may the TB spread?
Reactivation occurs.
Memory T cells release cytokines and TB is able to spread to upper lobes (more O2) ans the immune cells contribute to more areas of caseous necrosis.
These areas cavitate, spreading to the rest of the lung (pulmonary TB) or to the vasculature –> systemic miliary TB.
Describe some features of systemic miliary TB - where is the infection likely to spread, with what effect?
Kidneys - sterile pyuria Adrenals - addisons Meninges - meningitis Lumbar vertebrae - Pott's disease Liver - hepatitis Cervical lymph nodes - scrofula
How could you diagnose CNS TB?
CSF would contain bacilli on lumbar puncture
What symptoms might be associated with extrapulmonary TB of the following systems? GI/abdominal GU Bone/spine CNS
GI/abdominal: ascites, ileal malabsorption
GU: epididymitis, frequency, dysuria, haematuria
Bone and spine: pain and swelling of joints, Pott’s
CNS: cranial nerve palsy, raised ICP due to meningeal inflammation, meningitis
Lymph node: swelling +/- discharge
How would you diagnose active TB?
CXR: patchy shadows/fibrosis, consolidation. Miliary - normal/miliary shadows.
Sputum/bronchoalveolar lavage: culture
Lumbar puncture for miliary/CNS
How is TB cultured and why?
It is acid fast due to waxy cell wall and gram stains weakly, so Ziehl-Nielson is used and appears red if TB.
How would you diagnose latent TB?
Mantoux:
Tuberculin injected, stimulates type 4 sensitivity reaction.
Interferon gamma release assays (IGRA) demonstrate exposure but not active infection.
What steps would you take immediately following histology + clinical picture consistent with TB?
Notify public health england.
Start treatment without waiting for culture results.
Begin contact tracing.
Isolate until non-infectious.
What is the treatment course for TB (apart from CNS)
Rifampicin for 6mo
Isoniazid for 6 mo
Pyrazinamide for first 2 mo
Ethambutol for first 2mo
DOTS: direct observed therapy - medication is taken under supervision.
Individuals must be isolated until no longer infectious, and it is crucial they take the whole course of medication.
Symptoms of pulmonary TB
Cough Haemoptysis Chest pain Breathlessness systemic features
Define pneumonia
lower respiratory tract infection - inflammation of lung parenchyma
Who is at risk of pneumonia?
Extremes of age Immunocompromised Individuals with COPD, CHD, diabetes Impaired swallow IVDU, alcohol abuse
Describe briefly the pathogenesis of pneumonia
Macrophages cannot phagocytose microbe
Release cytokines to recruit neutrophils, filling the alveolar space with dead bacteria + dead neutrophils + tissue fluid + inflammatory proteins = inflammatory exudate or ‘pus’.
This may lead to long term damage to lung parenchyma
symptoms of pneumonia
CHEST: Cough, potential rusty sputum (characteristic of s. pneumoniae), SOB, pleuritic chest pain
INFECTION: fever, sweats, rigors
SYSTEMIC: weakness, malaise
describe the features of pleuritic chest pain
Localised, sharp pain that worsens on ddeep breathing and when moving
Describe tests used to diagnose pneumonia
FBC shows raised WBC,
biochem U+E/LFTs show dehydration
Raised ESR and CRP indicate inflammation
Sample for culture -> microbio for targetted treatment, however management must start before results return.
Describe signs of pneumonia
Vitals: increased HR, resp rate, decreased BP, fever, dehydration, decreased sats
chest exam: signs of consolidation = dull to percussion, inc. vocal resonance, dec. air entry, crackles/wheeze
What scale is used to assess severity of pneumonia and therefore treatment course in CAP?
CURB>65 Confusion Urea Resp rate Blood pressure >65 0-1 = outpatient, amoxicillin 2 = admit, oral amoxicillin + clarithromycin 3-5 = IV coamoxiclav + clarithromycin
Principles of treatment with antibiotics for CAP vs HAP?
CAP: narrowest spectrum possible
HAP: start broad spectrum, more likely pt has come into contact with resistant microbes
what is parapneumonic effusion and how is it treated?
Parapneumonic effusion is any pleural effusion secondary to pneumonia (bacterial or viral) or lung abscess. Pockets of fluid are in the thoracic cavity. If these are filled with pus, it is known as empyema. Treated by drainage.