Tuberculosis Flashcards

(55 cards)

1
Q

TB global scale

A

burden from TB globally is falling

- worldwide incidence rate is falling roughly at about 2% a year

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2
Q

what is the number 1 killer of communicable/ infectious diseases in the world?

A

TB

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3
Q

what is meant by a communicable disease?

A

one that can spread from one person to another through a variety of ways

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4
Q

TB kills more than ____ and ____ together

A

HIV and Malaria

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5
Q

examples of countries with high TB burden

A

India
China
Indonesia
Philippines

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6
Q

how many people on estimate are infected worldwide?

A

2 billion

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7
Q

TB in the UK

A

major problem in London- immigration from high incidence areas
2/3 of cases born abroad

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8
Q

vulnerable groups in the UK

A

those from high prevelence countries
HIV+ or immunosuppressed
elderly, neonates, diabetics
Homeless, alcoholics, injecting drug user, prisoners

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9
Q

Why are diabetics at risk of TB?

A

tuberculosis might induce glucose intolerance and worsen glycaemic control
-disease presentation and treatment can also be affected

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10
Q

mycobacteria

A

non-motile bacillus, very slow growing- long treatment
aerobic
unique thick fatty cell wall

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11
Q

what are a few diseases caused by mycobacteria infection

A

TB
non- tuberculous mycobacteria infections
leprosy

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12
Q

what is so important about the unique thick fatty cell wall in mycobacteria?

A

means it is resistant to acids, alkalis and detergents
resistant to neutrophil and macrophage destruction
acid- and alcohol- fast bacilli (but not all AAFBs are TB)

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13
Q

how is TB spread

A

airborne if pulmonary or laryngeal TB but others aren’t

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14
Q

TB bacteria in the air

A

attached to aerosol droplets which can remain suspended in air for many hours, especially if there is poor air circulation

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15
Q

what is outdoors mycobacteria eliminated by?

A

UV radiation

dilution

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16
Q

what is one exception to how TB is spread?

A

mycobacterium bovis - can be spread by consumption of unpasteurized infected cow’s milk (v uncommon in the UK)

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17
Q

What is the result of activated macrophages?

A

Damaged epithelioid cells
Langhan’s giant cells
Accumulation of macrophages, epithelioid & Langhan’s cells GRANULOMA
Central caseating necrosis (may later calcify)

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18
Q

what happens in the granuloma in TB

A

central caseating necrosis- tissues turn into a cheesy substance- this may calcify later

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19
Q

two edged sword of Th1 cell mediated immunological response

A

Eliminates / Reduces number of invading mycobacteria

Tissue destruction is a consequence of activation of macrophages

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20
Q

primary infection in TB

A

No preceding exposure or immunity

Mycobacteria spread via lymphatics to draining hilar lymph nodes

Usually no symptoms, can be fever, malaise. rarely chest signs

can be cleared/cured

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21
Q

what happens when primary infection progresses to tuberculous bronchopneumonia- 1% of people (3)

A

Primary focus continues to enlarge - cavitation

Enlarged hilar lymph compress bronchi, lobar collapse

Enlarged lymph node discharges into bronchus

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22
Q

Miliary TB (1-3% of people)

A

develops, with hematogenous (blood) spread of bacteria to multiple organs

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23
Q

CNS TB (affects 10-30%)

A

3 clinical categories:- foci of granuloma bursting causes tuberculous meningitis, intracranial tuberculoma, and spinal tuberculous arachnoiditis

24
Q

what is latent TB disease? (reactivated/ secondary TB)

A

usually occurs during the two years following the initial infection

  • TB enters a dormant stage with low or no replication over prolonged periods of time

balanced state of replication and destruction by immune mechanisms
only develops further in humans not animals

25
disease timeline TB
primary complex progressive primary disease Miliary, meningeal, pleural TB latent disease Pulmonary, skeletal Genitourinary, Cutaneous TB
26
clinical presentation of TB (9)
``` cough- haemoptysis SOB fever malaise sweats - mainly at night weight loss CRP normal in 15% ESR normal in 21% Erythema nodosum - fat swelling under skin ```
27
what is CRP?
c-reactive protein - produced by the liver in response to inflammation
28
what is ESR
erythrocyte sedimentation - indirect measure of the degree of inflammation present in the body fall in RBC means increased ESR
29
when to consider a CT scan in TB diagnosis
after carrying out CXR that appears normal Miliary TB cavitation and other differental lymphadenopathy, alternative diagnosis
30
what is lymphadenopathy?
disease of the lymph nodes, in which they are abnormal in size, number, or consistency
31
diagnosing active pulmonary TB in CXR
mediastinal lymphadenopathy pleural effusion miliary - discrete foci of granulomatous tissue through the lung pneumonic lesion with enlarged hilar nodes
32
investigations for TB (8) N.B think different investigations for different types of TB
sputum sample lumbar puncture in CNS TB urine in urogenital TB bronchoscopy with BAL (bronchoalveolar lavage - fluid is squirted into a small part of the lung and then collected for examination) induced sputum (for those that have trouble producing sputum- inhaled gas) Endobronchial ultrasound (EBUS) with biopsy aspirate/biopsy from tissue (lymph-node, bone, joint, brain, abscess) Endobronchial ultrasound (EBUS) with biopsy
33
what is NOT routinely used in diagnosing active TB
Mantoux or IGRA
34
what is IGRA
Interferon Gamma Release Assay- blood test used to detect TB
35
rules in treatment of TB (6)
multiple drug therapy is essential!!! as single agent treatment leads to drug resistant organisms within 14 days Therapy must continue for at least 6 months - Rifampacin, isoniazid, ethambutol and pyrazinamide for 2 months (given as one drug) - then Rifampicin and isoniazid for a further 4 months Legal requirement to notify all cases of TB Test for HIV, Hepatitis B and C
36
how many tablets does a standard 70kg patient take daily?
12 a day
37
which drug can be paired with isoniazid to reduce risk of neuropathy
pyridoxine
38
what is used to treat CNS, MIliar or pericardial TB
steroids
39
side effects of rifampicin (5)
``` orange urine/tears/lenses induces liver enzymes hormonal contraception becomes ineffective hepatitis rash ```
40
side effects of isoniazid (3)
hepatitis peripheral neuropathy rash
41
side effects of pyrazinamide (3)
hepatitis gout rash
42
side effects of ethambutol (2)
optic neuropathy | rash
43
BCG vaccination
given selectively since 2005 | given to neonates or unvaccinated children under 5, whose parents/grandparents were born in a high risk country
44
treatment of latent TB
different combos of Rifampicin, Isoniazide, Rifapentine
45
What stimulates the macrophages to become activated?
Th1 helper cells from the lymph node, these Th1 cells are activated by antigen presenting cells. These Th1 cells after receiving the signal from the antigen presenting cell then clonially proliferate in the lymph node
46
Which specific chemical activates Macrophages?
Interferon gamma CD40 - which is produced by Th1 cells in the lymph node
47
What is the pathology for a susceptible host?
tissue destruction Organism contained Disease
48
Who is normally affected by the primary infection?
Usually children, 80% Infected focus in alveolus, (lymph nodes, gut)
49
How do we analyse sputum samples for TB?
ZN stain - immediate answer if AAFB Culture Sputum PCR
50
what is the number 1 killer of infectious diseases?
TB
51
key points of the WHO report on TB 2018
1. 6 million TB deaths a year | 0. 3 million of these also had HIV
52
signs of TB
patches of crepitations (crackles) shadowing on CXR positive Mantoux test
53
Diagnosis/investigation of TB
``` high index of suspicion - mantoux test 3 sputum specimens on successive days CXR PCR histology - caseating granuloma (granuloma round necrotic tissue/cells) ```
54
how long should treatment last for monoresistant TB ie resistance to one first-line anti-TB drug only
7-9 months
55
how long should treatment last for CNS TB, H monoresistance extensive disease?
12 months