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S2 Respiratory System > Tuberculosis > Flashcards

Tuberculosis Flashcards

1
Q

what other condition is related to TB?

A

HIV

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2
Q

how is TB prevalence/ morbidity evolving?

A

decreasing

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3
Q

environment for TB development?

A

poor nutrition, social distress

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4
Q

what does TB initially do in alveoli?

A

slow dev., consumption by macrophages

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5
Q

where do the macrophages go?

A

they go to lymph nodes

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6
Q

what happens in lymph nodes?

A

T cells get cloned and go back to alveoli to activate macrophages

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7
Q

why are activated macrophages a problem?

A

they attack TB as well as damage tissue (balance between destroying Ag and alveoli tissue)

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8
Q

under which conditions could you get TB as a primary infection in the UK?

A

if no immunity (to BCG vaccine)

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9
Q

advanced TB CXR top apex typical characteristics?

A

empty on CXR

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10
Q

in what areas is TB still a problem (Britain)? why?

A

London, because of immigration

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11
Q

what is the responsible organism for TB? what are the two main (70%) strains? where does TB come from?

A

mycobacteria tuberculosis, mycobacterium bovis, ubiquitous in soil, water

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12
Q

what organisms are responsible for the remaining 30%?

A

M. avium-intracellulare (HIV), M. kansasii, M. malmoense, M. xenopii

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13
Q

which organism is responsible for leprosy?

A

M. leprae

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14
Q

what type of bacteria is mycobacteria? how does that impact where it prefers to go to in the lungs?

A

non-motile bacillus, aerobic (predilection for apices of lung)

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15
Q

how fast is its growth?

A

very slow growing (disease is slow, treatment is long)

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16
Q

what is mycobacterium’s cell wall like? is this common?

A

uniquely has a very thick cell wall; lipids, peptidoglycans, arabinomannans

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17
Q

what is mycobacterium resistant to?

A

acids, alkalis, detergents, neutrophil, macrophage destruction

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18
Q

is mycobacteria an acid (an alcohol) fast bacilli (AAFB)? what test to find out?

A

yes, Ziehl Neilson stain

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19
Q

how does mycobacterium tuberculosis get transmitted (‘open’ pulmonary TB)?

A

coughing, sneezing; respiratory droplets evaporate, droplets nuclei contain mycobacteria (1 cough=3500 nuclei), remains airborne for very long periods

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20
Q

how can outdoor mycobacteria get eliminated?

A

UV radiation and infinite dilution

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21
Q

what happens to the larger droplets nuclei when inhaled?

A

impact on large airway and cleared

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22
Q

what happens to the small (<5 micrometer) droplets nuclei when inhaled?

A

1-3,organisms impact in alveoli slowly proliferate

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23
Q

how does mycobacterium bovis?

A

consumption of infected cow’s milk, deposited in cervical, intestinal lymph nodes

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24
Q

what is the immunopatholgy for TB?

A

activated macrophages -> epitheloid cells -> Langhan’s giant cells, accumulation of macrophages, epitheloid & Langhan’s cells -> GRANULOMA
also central caveating necrosis (may later calcify)

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25
Q

why is the Th1 mediated immunological response a “two edged sword”?

A
  • eliminates/ reduces number of invading mycobacteria

- tissue destruction is a consequence of activation of macrophages

26
Q

what factors change chance of infection?

A

virulence, number (of bacteria)

27
Q

what factors change susceptibility of being vulnerable to infection?

A

genetics, race, nutrition, age (susceptibility increased if elderly), immunosuppression

28
Q

how does TB affect a susceptible host? (as opposed to a resistant host)

A

increased tissue destruction, organism proliferates instead of being contained, turns into a progressive disease

29
Q

what is a primary infection?

A

infection when no preceding exposure or immunity

30
Q

who is normally affected by primary infection? where are they affected?

A

usually children, 80% infected focus in alveolus (lymph nodes, gut)

31
Q

how can TB spread from the alveoli?

A

spread via lymphatics to draining hilar lymph nodes; haematogenous seeding of mycobacteria to all organs of the body (lungs, bone, genitourinary (=reproductive) system)

32
Q

what is the outcome of an infection in 85% cases?

A

initial lesion + local lymph node (primary complex), heals with or without scars, may calcify (Ghon focus + complex)

33
Q

what are the symptoms for TB?

A

usually none, can be fever, malaise, Erythema nodosum, rarely chest signs

34
Q

what is the outcome for TB infection in terms of immunity?

A

infection is associated with development of immunity to tuberculprotein

35
Q

how do you test for tuberculin?

A

intra dermal administration of tuberculoprotein (PPD) results in lymphoctic and macrophage based areas of inflammation/induration after 48 hours

36
Q

what are the three outcomes of a primary infection?

A
  • cleared (slight tissue damage, no impact)
  • contained latent (no progression but more tissue damage)
  • progressive disease
37
Q

what happens in 1% of primary infection which will lead to a very poor prognosis?

A

primary infection progresses, primary focus continues to enlarge -> cavitation, enlarged hilar lymph compress bronchi, lobar collapse, enlarged lymph node discharges into bronchus -> tuberculous bronchopneumonia

38
Q

how can a post primary disease happen?

A
  • reactivation of mycobacterium from latent primary infection disseminated by the blood stream around the body
  • new re-infection from outside source; different host response because of previous sensitisation, if insufficient immunity present: tissue damage, progressive
39
Q

what diseases are caused by a post primary disease?

A
  • pulmonary disease (1-5 years, maybe 30-40)
  • pleural TB, miliary, meningeal (6-12 month)
  • lymph nodes, usually cervical
  • bone and joint (spine, hip) (1-5 years, maybe 30-40)
  • genito-urinary
  • males; infertility- vas deferens (10-15 years, maybe 30-40)
  • females; infertility- uterus, Fallopian tubes (10-15 years, maybe 30-40)
  • pericardium; constrictive pericarditis
  • abdomen; ascites, ileal TB -> obstruction
  • adrenal -> Addison’s disease
  • skin; lupus vulgaris (10-15 years, maybe 30-40)
40
Q

what are the symptoms for post-primary pulmonary TB?

A

may be no symptoms for many months, respiratory: cough, sputum, haemoptysis, pleuritic pain, breathlessness, systemic: malaise, fever, weight loss (‘night sweats’)

41
Q

typical past medical history for a patient with post-primary pulmonary TB?

A

diabetes, immunosuppressive disease (HIV), previous TB, previous gastric surgery, malignancy

42
Q

typical drug history for a patient with post-primary pulmonary TB?

A

immunosuppressive drug (corticosteroid therapy)

43
Q

typical past social history for a patient with post-primary pulmonary TB?

A

alcohol, IV drug abuse (IVDA), poor social circumstances (malnutrition, vagrants), immigrants from high incidence areas

44
Q

typical signs for a patient with post-primary pulmonary TB?

A
  • may be none at all- extensive TB can be present without physical signs
  • if more advanced, may be crackles, bronchial breathing
  • finger clubbing is rare unless very chronic infection
45
Q

how do you diagnose TB on a CXR?

A
  • ‘patchy’ shadowing, often on apices/ upper zones or apex of lower lobes (related to high ventilation + poor perfusion of O2), often bilateral
  • cavitation if advanced
  • may calcify if chronic or healed TB
46
Q

how to investigate TB sputum?

A
  • sputum smear (Ziehl Neilsen stain, immediate answer if many AAFB)
  • sputum culture (up to 8 weeks)
  • sputum PCR
47
Q

how to get sputum if none is produced spontaneously?

A

induce production

48
Q

what further investigations are initiated if sputum negative?

A
  • CT scan of thorax
  • bronchoscopy with bronchoalveolar lavage, transbronchial biopsy, Z-N stain, culture, PCR, biopsy history
  • pleural aspiration and biopsy if pleural effusion, fluid cytology (lymphocytes), fluid for AAFB and culture, biopsy histology, 1 biopsy sent in saline for culture
49
Q

what was “the Sanatorium regime”?

A

improving immunity by offering fresh air, sunshine, bed rest and good food (vitamin D & cathelecidin (LL-37)

50
Q

how do you manage TB?

A

multi-drug therapy is essential, legal requirement to notify all cases, low threshold for HIV testing, AIDS defining condition

51
Q

what happens if you treat a patient with a single agent treatment?

A

drug resistant organisms within 14 days

52
Q

how long does TB therapy last?

A

6 months

53
Q

what drugs are used for TB treatment for the 2 months?

A

rifampicin, isoniazid, ethambutol, pyrazinamide

54
Q

what drugs are used for TB treatment for the 4 months?

A

rifampicin, isoniazid

55
Q

when is a patient following the treatment rendered non-infectious?

A

after 2 weeks

56
Q

what are the side effects of rifampicin?

A

orange ‘irn bru’ urine, tears, induced liver enzymes, prednisolone, anticonvulsants, oral contraceptive pill contraindication, hepatitis

57
Q

what are the side effects of isoniazid?

A

hepatits, peripheral neuropathy (pyridoxine B6)

58
Q

what are the side effects of ethambutol?

A

optic neuropathy (check visual acuity)

59
Q

what are the side effects of pyrazinamide?

A

gout

60
Q

why is contact tracing used for TB? how is first targeted?

A

identify source, identify transmission, duration of contact, close household contacts; casual contacts if close contacts have been infected with virulent organism/high transmission

61
Q

what does likelihood of infection with TB depend on?

A

duration of contact + intensity of contact

S2 Respiratory System (43 decks)

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