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Year 3 > Week Two - Case Three > Flashcards

Week Two - Case Three Flashcards

1
Q

what is TB and what is it caused by

A

chronic infection disease, caused by mycobacterium tuberculosis. (MTB)

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2
Q

what are the three types that infect humans

A
  • M.tuberculosis (commonest)
  • M.bovis (bovine TB)
  • M.africanum
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3
Q

in how much of the global population is tuberculosis present in

A

about 30% of the global population, but in developed countries it is rate since the advent of TB inoculation

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4
Q

what happens to MTB when it is encountered by the immune system

A

it is engulfed by macrophages

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5
Q

what does the MTB and macrophages complex form

A

granulomas

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6
Q

where do these granulomas typically occur

A

the lungs, but the bacteria can also be carried to distant sites throughout the lymphatics, and granulomas can form at other sites

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7
Q

what is the test for latent TB

A

interferon gamma release assay (IGRA) or tuberculin skin testing (TST)

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8
Q

what is the test for active TB

A

XCR and microbiology (usually sputum) for acid fast bacilli

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9
Q

how is TB transmitted

A

via droplet spread - only the pulmonary form is infectious

usually needs sustained close contact with the infectious case

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10
Q

roughly how much of the worlds population has been infected with TB

A

roughly one third

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11
Q

in what patients do a signifiant amount of cases occur

A

those co-infected with HIV

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12
Q

how many cases are reported each year in the UK

A

9000 cases each year

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13
Q

what are the risk factors for TB

A

HIV (13% cases also have HIV)

Overcrowding/close contact with active case (1/3 chance of contracting from household member)

Ethnic minority groups

Malnutrition

IV drug use

Homelessness

Chronic lung disease

Immunosuppression

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14
Q

how many people will patients with active TB infect per year

A

on average 10-15

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15
Q

next few questions are on the pathogenesis

A
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16
Q

where does the mycobacteria go

A

the pulmonary alveoli

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17
Q

what happens to these mycobacteria

A

these are engulfed by alveolar macrophages and replicated within them

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18
Q

where is the primary site of infection

A

Primary site of infection (in the lungs) = “Ghon focus” (generally in upper lobe)

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19
Q

what surrounds the infected macrophages

A

lymphocytes and fibroblasts

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20
Q

what does this surrounding causes

A

granuloma formation

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21
Q

what does this granuloma formation prevent

A

dissemination of bacteria - prevents extra-pulmonary TB

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22
Q

what happens inside these lesions/granulomas

A

the bacteria may develop abnormal cell death in the centre (caseous necrosis) and can eliminate the bacteria

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23
Q

what is this sometimes called

A

LTBI - latent tuberculosis infection

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24
Q

what is the risk that LTBI will develop into active TB

A

there is a 10% chance that LTBI can develop into active TB during a patient’s lifetime.

the risk is greatest during the first two years of infection

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25
Q

how does active TB usually present

A

with fever, night sweats, weight loss and cough, usually lasting more than 2-3 weeks

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26
Q

what happens if there is a failure of the above mechanism

A

the bacteria may gain entry into the blood stream and spread throughout the body and set up many foci of infection (tubercles)

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27
Q

what is this called

A

extra-pulmonary TB

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28
Q

what happens to those tin less effective immune systems

A

progress to primary progressive TB

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29
Q

what happens to less immunocompetent people,

A

granulomas are formed but then the necrotic tissue undergoes liquefaction and the fibrous walls break down

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30
Q

what then happens to the necrotic material

A

it then drains into the bronchi and is coughed up and can infect others

drains into nearby blood vessels and seeds to other areas leading to extrapulmonary TB

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31
Q

what do 90% of the cases exhibit

A

90% of cases exhibit pulmonary features only

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32
Q

what do 10% of cases exhibit

A

extrapulmonary features

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33
Q

what are the differentials for TB

A

carcinomas
pneumonia
PUO
lymphoma
fibrosis lung disease

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34
Q

what is the big complication of TB

A

multi-drug resistant TB (MDR-TB) can develop if TB is not properly treated

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35
Q

what are the signs on a CXR seen with active TB

A

patchy nodal shadows in the upper zones

cavitating lesions

fibrous contractions

air space consolidation

typically apical lesions

36
Q

what would be seen on a CXR for milliary TB

A

multiple 1-10mm nodules throughout the lungs

37
Q

what sputum samples are carried out for TB

A

3 separate sputum samples in pulmonary TB including one early morning sample

38
Q

what is the stain used to test for TB

A

Ziehl-Neelsen (ZN) stain - rapid direct microscopy for acid-fast bacilli

39
Q

what percentage of cases does ZN detect on a single sample

A

detects about 50% of cases of TB on a single sample

40
Q

why does TB bacteria stain in a characteristic way

A

due to the waxy nature of their walls

41
Q

what is used to confirm TB diagnosis

A

culture

42
Q

what is the culture taken

A

Lowenstein-Jensen

43
Q

how long does the culture take

A

takes 4-8 weeks due to slow bacterial growth and sensitivities take 3-4 weeks more

44
Q

what do the molecular assays detect

A

detect MTB DNA

also detect if rifampicin resistant

45
Q

when should treatment be started

A

treatment should be started before culture results are back, and continued even if cultures are negative

46
Q

what is the skin test used to screen people at a high risk for TB

A

Mantoux tuberculin skin test (TST)

47
Q

what does the TST involve

A

tuberculin protein is injected into the dermis

48
Q

what happens after it is injected

A

patient re-presents after 48-72 hours and the level of inflammation at the inject site is assessed - by measuring the size of the induration

49
Q

what gives an indication of the likelihood of TB infections

A

The diameter of the induration (inflammation) gives an indication of the likelihood of TB infection

50
Q

what does positive TB results require

A

“Positive” (i.e. TB present) results require correlation with a patient’s risk factors

> 5mm induration – positive result for patients with HIV or other immunosuppression, recent contact with known TB

> 10mm induration – positive result for patients in high risk areas, or moved from high risk area
<5 years ago, IV drug users, residential care / hospital patients

> 15mm induration – positive result for patients with no underlying risk factors

51
Q

who are there false positives in

A

those previously immunised

52
Q

what conditions can potentially give false negatives

A

sarcoidosis, Hodgkin’s Lymphoma

53
Q

what does a positive test indicate

A

Positive test indicates that the patient’s immune system has prior recognition of TB antigens (not due to vaccination) and thus indicates previous, latent or active TB. Further testing is required (as above) to assess if test indicates latent or active disease

54
Q

what is the drug regimen for prolonged period in active disease

A

(isoniazid and rifampicin, pyrazinamide and ethambutol)

All 4 for 2 months, then,

55
Q

what is the treatment for latent TB

A

single antibiotic treatment for latent TB for 3-6 months

56
Q

how should MDR-TB be treated

A

with at least four effective antibiotics for 18-24 months is recommended

57
Q

what is the prevention for TB

A

vaccination (BCG)
public health measurements

58
Q

what is the mode of action of rifamycins

A

inhibits DNA transcription

59
Q

what kind of drug is rifamycins

A

bactericidal

60
Q

what are the side effects of rifamycins

A

Nausea, anorexia, pseudomembranous colitis, hepatotoxicity, orange colouration of excreted bodily fluids, toxicity syndromes, drug interactions

61
Q

what is rifamycins also used in

A

mycobacterial infections - these most commonly occur in those with HIV

resistance prevents widespread use

62
Q

what is the mode of action of isoniazid

A

inhibits synthesis of the cell wall

63
Q

what kind of drug is isoniazid

A

bactericidal

64
Q

what are the side effects of isoniazid

A

Nausea, vomiting, constipation, peripheral neuropathy, hepatitis, SLE-like-symptoms

65
Q

what are the features of isoniazid

A

bactericidal on dividing organisms, static onrushing

66
Q

what is isoniazid only effective against

A

mycobacteria

67
Q

what is the mode of action of pyrazinamide

A

lowers intracellular pH, disrupting synthesis of fatty acids

68
Q

what kind of drug is pyrazinamide

A

bactericidal

69
Q

what are the side effects of pyrazinamide

A

Hepatotoxicity, nausea, vomiting, arthralgia, sideroblastic anaemia

70
Q

what is the only bacteria pyrazinamide is effective against

A

mycobacteria

71
Q

what is the mode of action of ethambutol

A

interferes with cell wall synthesis

72
Q

what type of drug is ethambutol

A

bacteriostatic

73
Q

what is the side effect of ethambutol

A

Optic neuritis – resulting in red/green colourblindness. neuritis

74
Q

what are the features of mycobacteria

A

This is its own genus of bacteria (like G+ or G-). The group include TB and leprosy. They are acid fast. They are also aerobic.

75
Q

what does acid fast mean

A

this means that the organisms are difficult to stain using normal staining techniques. the name refers to the fact that they can’t be stained by normal acid (ethanol) staining techniques. these bacteria are often particularly difficult to culture and identify
e.g TB takes around 6-8 weeks

76
Q

what samples do you take before prescribing IV co-amoxiclav

A
  • U&Es
  • sputum culture
  • respiratory viral swab
  • LFTs
  • blood cultures
  • HIV
  • lactate
  • FBC
77
Q

what are the common organisms that should be considered when dealing with a HAP

A

Staphylococci (including MRSA)
Enterococci
Gram negative bacilli (such as E-Coli or pseudomonas) or a mixed flora if aspiration pneumonia is suspected

78
Q

what is HAP defined as

A

defined as new onset of symptoms along with a compatible x- ray developing more than 48 hours after the patient’s admission to hospital. It occurs in around 1% of in-patients and its consequences can range from extending the patient’s hospital stay to increased mortality.

79
Q

what is a VAP

A

HAP occurring in patients on mechanical ventilation. The mortality rate from VAP can reach 50% or higher.

80
Q

how do you differentiate between an effusion and consolidation radiologically

A
  • In consolidation, the margins of opacification are not clear as compared to effusions.
  • In effusions the opacification is dense and there are no markings visible in the lung field. In consolidation you can see air bronchograms, so the opacification is not dense.
  • The diaphragm / costo-phrenic and cardio-phrenic angles are not visible in effusions. While these may still be visible in consolidation depending on areas of lung affected.
81
Q

what is the most common cause of fungal pneumonia

A

In the UK, Pneumocystis jirovecii is the most common cause of fungal pneumonia. It is mainly seen in patients with altered cell-mediated immunity (immunodeficiency incl. HIV, immunosuppression e.g. after transplantation) but can also occur in patients with a severe underlying respiratory condition (COPD, Cystic Fibrosis). Pneumonia is also a key symptom for so-called endemic mycoses (e.g. histoplasmosis, blastomycosis, coccidioidomycosis) that are limited to specific geographic areas (Americas primarily) and seen in fully immunocompetent patients.

82
Q

what is an environment mould that can also cause lung disease

A

Aspergillus is an environmental mold that can also cause lung disease. The type of disease is dependent on the host immune response.

83
Q

what type of TB has a high mortality rate

A

Disseminated TB (milliary TB) has high mortality despite treatment.

84
Q

what is the standard treatment for TB

A

While TB is a serious condition that can be fatal if left untreated, deaths are rare if treatment is completed. Active pulmonary TB requires a 6-month course of a combination of antibiotics. The standard treatment is 2 antibiotics (isoniazid and rifampicin) for 6 months and 2 additional antibiotics (pyrazinamide and ethambutol) for the first 2 months. It may take several weeks before the patient starts to feel better. Most patients become staining negative and non-infectious in 2 weeks.

85
Q

what kind of fungus is more likely in someone with an impaired immune system

A

Pneumocystis jiroveci (PJP) is a fungus that can cause pneumonia in anyone whose immune system is impaired by, for example, HIV virus or immunosuppressant drugs such as those used for rheumatoid arthritis and inflammatory bowel disease.

86
Q

what is the choice of treatment for PJP

A

Co-trimoxazole is the treatment of choice for PJP

87
Q
A

Year 3 (63 decks)

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