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1ST YEAR SYSTEMS: Respiratory > Tuberculosis > Flashcards

Tuberculosis Flashcards

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
Q

disease timeline TB

A

primary complex
progressive primary disease
Miliary, meningeal, pleural TB

latent disease
Pulmonary, skeletal

Genitourinary, Cutaneous TB

26
Q

clinical presentation of TB (9)

A 
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
Q

what is CRP?

A

c-reactive protein - produced by the liver in response to inflammation

28
Q

what is ESR

A

erythrocyte sedimentation
- indirect measure of the degree of inflammation present in the body
fall in RBC means increased ESR

29
Q

when to consider a CT scan in TB diagnosis

A

after carrying out CXR that appears normal
Miliary TB
cavitation and other differental
lymphadenopathy, alternative diagnosis

30
Q

what is lymphadenopathy?

A

disease of the lymph nodes, in which they are abnormal in size, number, or consistency

31
Q

diagnosing active pulmonary TB in CXR

A

mediastinal lymphadenopathy
pleural effusion
miliary - discrete foci of granulomatous tissue through the lung
pneumonic lesion with enlarged hilar nodes

32
Q

investigations for TB (8) N.B think different investigations for different types of TB

A

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
Q

what is NOT routinely used in diagnosing active TB

A

Mantoux or IGRA

34
Q

what is IGRA

A

Interferon Gamma Release Assay- blood test used to detect TB

35
Q

rules in treatment of TB (6)

A

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
Q

how many tablets does a standard 70kg patient take daily?

A

12 a day

37
Q

which drug can be paired with isoniazid to reduce risk of neuropathy

A

pyridoxine

38
Q

what is used to treat CNS, MIliar or pericardial TB

A

steroids

39
Q

side effects of rifampicin (5)

A 
orange urine/tears/lenses
induces liver enzymes 
hormonal contraception becomes ineffective 
hepatitis
rash
40
Q

side effects of isoniazid (3)

A

hepatitis
peripheral neuropathy
rash

41
Q

side effects of pyrazinamide (3)

A

hepatitis
gout
rash

42
Q

side effects of ethambutol (2)

A

optic neuropathy

rash

43
Q

BCG vaccination

A

given selectively since 2005

given to neonates or unvaccinated children under 5, whose parents/grandparents were born in a high risk country

44
Q

treatment of latent TB

A

different combos of Rifampicin, Isoniazide, Rifapentine

45
Q

What stimulates the macrophages to become activated?

A

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
Q

Which specific chemical activates Macrophages?

A

Interferon gamma CD40 - which is produced by Th1 cells in the lymph node

47
Q

What is the pathology for a susceptible host?

A

tissue destruction

Organism contained

Disease

48
Q

Who is normally affected by the primary infection?

A

Usually children, 80% Infected focus in alveolus, (lymph nodes, gut)

49
Q

How do we analyse sputum samples for TB?

A

ZN stain - immediate answer if AAFB

Culture

Sputum PCR

50
Q

what is the number 1 killer of infectious diseases?

A

TB

51
Q

key points of the WHO report on TB 2018

A
  1. 6 million TB deaths a year

0. 3 million of these also had HIV

52
Q

signs of TB

A

patches of crepitations (crackles)
shadowing on CXR
positive Mantoux test

53
Q

Diagnosis/investigation of TB

A 
high index of suspicion - mantoux test
3 sputum specimens on successive days
CXR 
PCR
histology - caseating granuloma (granuloma round necrotic tissue/cells)
54
Q

how long should treatment last for monoresistant TB ie resistance to one first-line anti-TB drug only

A

7-9 months

55
Q

how long should treatment last for CNS TB, H monoresistance extensive disease?

A

12 months

1ST YEAR SYSTEMS: Respiratory (38 decks)

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