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Yr 3 resp > tb > Flashcards

tb Flashcards

1
Q

definition of TB

A

Granulomatous disease caused by Mycobacterium tuberculosis.

primary - initial infection may be pulmonary (acquired by inhalation from the cough of an infected patient), or occasionally GI

miliary TB - results when there is haematogenous dissemination

post-primary - caused by reinfection/reactivation

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2
Q

aetiology of TB

A

recent travel

born in foreign country

family member exposed

M. tuberculosisis an intracellular organism (also known as acid-fast bacilli, AFB) which survives after being phagocytosed by macrophages.

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3
Q

pathophysiology fo active tb

A

when containment by immune system (T cells/macrophages) is inadequate

from primary infection or re-activation of previously latent disease

Transmission of TB is via inhalation of aerosol droplets containing bacterium.

This means only pulmonary disease is communicable.

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4
Q

pathophysiology of latent TB

A

infection without disease due to persistent immune system containment (ie granuloma formation prevents bacteria growth and spread).

+ve skin or blood testing shows infection, but no symptoms and pt non-infectious (normal sputum/CXR)

approx 2billion people expected to have latent TB

lifetime risk of reactivation 5-10%

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5
Q

RF for reactivation of TB

A

new infection (<2yr)

HIV

organ transplantation

high risk settings (homeless shelter, prison)

low socioeconomic status

haemodialysis

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6
Q

epi of TB

A

Annual mortality 3 million (95% in developing countries); annual UK incidence 6000.

Incidence in Asian immigrants>30 times native UK white population.

  1. 6 million new cases/yr of which 37% are unreported/undiagnosed
  2. 3% of new cases, and 20% of previously treated cases are drug resistant

Co-infection with HIV in 12% of new cases.

Leading cause of death worldwide, 1.5 million deaths/yr.

Effective diagnosis and treatment saved 43 million lives between 2000and2014.

UK ~8000/yr, ~12 per 100000. 73% born outside UK, 70% in deprived areas, 30% with pulmonary disease wait >4 months from symptoms to treatment.

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7
Q

sx of TB

A

haemoptysis

night sweats - B cell symptoms

fever

SOB

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8
Q

sx of primary TB

A

mostly asymptomatic

fever

malaise

cough

wheeze

erythema nodosum

phlyctenular conjunctivitis - allergic manifestations

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9
Q

miliary TB

A

Haematogenous dissemination leads to the formation of discrete foci (~2mm) of granulomatous tissue throughout the lung (‘millet’ seed appearance).

fever

weight loss

meningitis

yellow caseous tubercles spread to other organs (eg in bone and kidney - may remain dormant for years)

sputum may be -ve because spread is haematogenous = low threshold for LP

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10
Q

sx of post-primary tb

A
  • fever/night sweats
  • malaise
  • weight loss
  • breathlessness
  • cough - dry then productive
  • sputum
  • haemoptysis
  • pleuritic pain
  • signs of pleural effusion
  • collapse
  • consolidation
  • fibrosis
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11
Q

non-pul TB

A

in immunocompromised

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12
Q

TB LN

A

suppuration of cervical/supraclavicular nodes = abscesses or sinus = discharge pus and spread to the skin (scrofuloderma)

node firm to touch and not acutely inflammed - cold abscess

Skin can adhere to the underlying mass with risk of rupture and sinus formation

Investigate with fine-needle aspiration, AFB staining, and culture

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13
Q

CNS TB

A

Haematogenous spread leading to foci of infection in brain and spinal cord

foci can enlarge = tuberculomas.

Foci rupture = meningitis.

Increased risk with HIV, immune suppression and <3yrs

headache

meningism

confusion

seizures

focal neurological deficit

systemic symptoms

Needs LP and examination of CSF (leucocytosis, raised protein, CSF: plasma glucose <50%, AFB stain, PCR and culture). Look for TB elsewhere (CXR, etc), test for HIV. CT/MRI may show hydrocephalus, basal exudates. Tuberculomas are ring-enhancing.

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14
Q

skin TB

A

lupus vulgaris = persistent, progressive cutaneous TB: - jellylike reddish-brown glistening plaques

Scrofuloderma: skin lesion extended from underlying infection eg lymph node, bone; causes ulceration and scarring

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15
Q

heart TB

A

pericardial effusion

pericarditis/constrictive pericarditis

Myocardial involvement (arrhythmias, heart failure, ventricular aneurysm, or outflow obstruction) is rare.

Check chest imaging for other TB pathology, eg pulmonary disease, mediastinal lymph nodes.

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16
Q

GI TB

A
  • subacute obstruction - due to bowel wall thickening, stricture formation or inflammatory adhesions
  • change in bowel habit
  • weight loss
  • peritonitis
  • ascites
  • most disease is ileocaecal
  • colicky abdominal pain
  • biopsy needed for diagnosis
  • Caseation necrosis and an absence of transmural cracks/fissures distinguish from Crohn’s disease.
17
Q

GU TB

A

symptoms may be chronic, intermittent or silent

UTI symptoms

dysuria, frequency, loin pain, haematuria, sterile pyuria

renal failure

epididymitis

endometrial or tubal involvement

infertility

Granuloma may cause fibrosis, strictures, infertility, and genital ulceration.

18
Q

endo TB

A

adrenal insufficiency

19
Q

bone/joint TB

A

osteomyelitis

arthritis

paravertebral abscesses

vertebral collapse - Pott’s disease

spinal cord compression from abscesses

local pain and tenderness for weeks/mo

slow insidious progression

may not present until deformity or neurological symptoms

20
Q

systemic TB feature

A

low grade fever

anorexia

weight loss

malaise

night sweats

clubbing (bronchoectasis)

erythema nodosum

An aspergilloma/mycetoma may form in the lung cavities.

21
Q

Ix for latent TB

A

tubercilin tests - positive in previous exposure M. tuberculosis or BCG, strongly positive may indicate infection

mantoux test - Intradermal injection of purified protein derivitive (PPD) tubercilin, induration and erythema after 72 h. Size of skin induration is used to determine positivity depending on vaccination history and immune status (>5mm if risk factors, >15mm if no risk factors).

Heaf test - place drop of PPD on forearm, fire spring-loaded needled gun, read after3–7 days. Graded according to papule size and vesiculation.

INF-y test - in latent TB exposure of host T-cells to TB ag = release of INF. high specificity (negative with BCG vaccination) so can be used to diagnose latent TB if tubercilin is +ve

22
Q

ix for latent TB

A

CXR

HIV test - Recommended to coincident disease (2% may be HIV positive).

Sputum/pleural fluid/bronchial washings: Microscopy (Ziehl–Neelsen stain), culture (can assess drug sensitivity) (takes up to 6 weeks). Low sensitivity.

sputum smear - 3 specimens needed inc an early morning sample, stained for present of acid fast bacili (AFB). All mycobacteria are ‘acid-fast’ including M. tuberculosis. If AFB are seen, treatment should be commenced and the patient isolated (in hospital only if clinical indication, or public health reason for admission; or at home).

nucleic acid amplification test (NAAT) - Direct detection of M. tuberculosis in sputum by DNA or RNA amplifi cation. Rapid diagnosis (<8hrs). Can also detect drug resistance

CT, lymph nodes, pleural biopsy, sampling of other affected systems:(e.g. CSF).

23
Q

CXR for latent TB

A

primary - peripheral consolidation, hilar lymphadenopathy

miliary - fine shadowing

Fibronodular/linear opacities in upper lobe (typical), middle or lower lobes (atypical)

post-primary - upper lobe shadowing, streaky fibrosis and cavitation, calcification, pleural effusion, hilar lymphadenopathy

24
Q

why gets Tb testing

A

close contacts of those with pulmonary or laryngeal TB, those with immune dysfunction, healthcare workers, and high-risk populations, eg prison, homeless, vulnerable migrants.

25
Q

Ix for extrapulmonary TB

A

investigate for co-existing pul disease

Obtain material from aspiration or biopsy (lymph node, pleura, bone, synovium, GI/GU tract) to enable AFB staining, histological examination (caseating granuloma) and/or culture.

•NAAT can be carried out on any sterile body fluid, eg CSF, pericardial fluid.

Yr 3 resp (19 decks)

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