WEEK 2: Tuberculosis Flashcards

1
Q

what are the symptoms of tuberculosis? - late stage disease

A

Breathlessness​

Chest Pains​

Persistent cough​

Coughing up blood​

Night sweats​

Tiredness​

Loss of appetite​

Loss of weight​

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2
Q

what does TB look like in an x-ray?

A

Usually see clouded areas in upper lobe or superior segment of lower lobe​

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3
Q

name the bacteria causing TB

A

Mycobacterium tuberculosis complex

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4
Q

how many people globally are estimated to carry ‘latent’ TB?

A

2 billion people

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5
Q

what year was the first antibiotic effective against TB discovered?

A

1943

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6
Q

what was the first antibiotic effective against TB called?

A

streptomycin

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7
Q

how many people infected with Mycobacterium tuberculosis are asymptomatic?

A

an estimated 90%

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8
Q

how does TB infection process begin?

A

with the inhalation of droplet nuclei expectorated from the respiratory tract of active TB sufferer

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9
Q

what are the 4 potential outcomes of inhaling TB bacilli?

A
  1. Initial host response can kill all bacteria​. No chance of active TB ever developing​
  2. Organisms begin to multiply immediately causing primary tuberculosis.​
  3. Bacilli become dormant & never cause disease – Latent infection. Patient has positive tuberculin skin-test​
  4. Latent organisms eventually grow with resultant clinical disease – Reactivation TB​
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10
Q

why is infection of TB with HIV the strongest risk factor for progression?

A

TB increases levels of HIV-1 replication, propagation and genetic diversity​. Therefore, co-infection provides reciprocal advantages to both pathogens

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11
Q

what is lymphatic TB?

A

TB in the lymphatic system - often affects women and children

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12
Q

what is pleural TB?

A

just outside the lung in chest cavity

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13
Q

what is cutaneous TB?

A

infection of TB that shows in the skin

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14
Q

how does TB get around the body?

A

haematogenous spread (through blood)

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15
Q

what bacteria causes TB?

A

mycobacterium tuberculosis complex

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16
Q

what are actinomycetes?

A

the genus class related to the gram-positive bacteria

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17
Q

TB is described as a diderm - what does that mean?

A

it has 2 outer membranes

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18
Q

what do mycolic acids do for the TB bacteria membrane?

A

forms the bases for outer membrane lipid bi layer - these inter-collate with complex bio active lipids and form a really hydrophobic membrane. Protects bacteria from drugs and disinfectants and toxic agents

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19
Q

what are mycolic acids

A

made from 2 long fatty acids, and they form a very impermeable membrane

20
Q

how is mycobacteria stained?

A

with a Ziehl-Neelsen stain. Looks red

21
Q

how are TB cells recognised by the immune system?

A

CD1 genes (MHC i like proteins) present TB lipid antigens to T cells

22
Q

how many estimated deaths were caused by TB in 2020?

A

1.5 million

23
Q

is mycobacterium tuberculosis an extra or intracellular pathogen?

A

intracellular

24
Q

what usually happens when a macrophage engulfs a pathogen?

A

acidification occurs - pH is lowered

25
what happens when macrophages first engluf TB pathogen?
TB pathogen resists acid in macrophage
26
why is a granuloma formed?
after the bacteria are ingested by the macrophages, they survive inside. This internalisation triggers an inflammatory response and brings other wbc's to the area and forms a granuloma.
27
how is the caseous centre of a granuloma formed?
tissue inside granuloma dies and forms this caseous centre.
28
what attracts arrival of T lymphocytes?
IL-8
29
why does exponential bacterial growth slow down?
the area becomes solid so there's no access to nutrients and oxygen
30
if you have a good cell mediated (CMI) immunity, what is the outcome?
effective CD4+ and CD8+ T cell activation of macrophages, activated macros can better kill TB and any surviving dormant TB contained within microscopic granuloma.
31
if you have a poor cell mediated (CMI) immunity, what is the outcome?
macros around caseous legion stay poorly activated. TB continues intracellular growth, kills infected macros by delayed hypersensitivity response. Caseous necrosis, granuloma grows and is physically visible
32
how many outcomes of TB have a poor CMI?
5-10% infections - children and immunocompromised adults.
33
what is stage 4 for a poor CMI?
around 4-5 weeks, lung self damage. Infected macrophages spread, dissemination via lymphatics to thoracic lymph node and blood
34
what are the 4 stages of TB?
the initial macrophage response, the growth stage, the immune control stage, and the lung cavitation stage
35
what is DOTS?
directly observed treatment
36
what is the cause of drug resistant TB?
it is the result of interrupted, erratic or inadequate TB therapy
37
what are some requirements for DOTS?
political commitment from local government, standardised treatment with supervision (every drug dose to be observed by trained healthcare worker), effective drug supply and and management systems
38
what are some disadvantages to DOTS?
DOTS difficult to deliver, reliance on smear microscopy has only a 60% detection rate, efforts to control TB fail in high burden areas
39
what is latent TB?
a dormant enclosed infection that does not cause any symptoms.
40
what is MDR TB?
multi-drug resistant TB
41
what is XDR TB?
extensively drug resistant TB
42
how is TB treated effectively?
* make sure drugs work against specific strain * multiple medications used together * medications used for entire course of therapy
43
what drugs are used to treat TB infection?
- Rifampin ​ - Isoniazid​ - Ethambutol​ - Pyrazinamide
44
why does TB spread in the upper lobes of the lungs?
oxygen is greatest here and TB is a strict aerobe.
45
how is TB tested for?
purified protein derivative (PPD) intradermal skin test or interferon gamma release assay (IGRA)