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MO2 > TB > Flashcards

TB Flashcards

1
Q

who identiried the infectious nature of TB?

A

robert Koch- Kochs postulates

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2
Q

what bacteria causes TB? what are its traits?

A
  • Mycobacterium tuberculosis.
  • Aerobic, gram positive, acid-fast bacilli.
  • Highly unusual cell surface made up of
    lipids and mycolic acid.
  • Intracellular - Able to survive inside
    macrophages.
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3
Q

how is TB transmitted?

A
  • Transmitted by aerosolised droplet from an
    infected patient
  • Inhaled into the alveoli of a new host
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4
Q

what are the outcomes of being infected with TB?

A

– Primary Tuberculosis (first infection)
– Complete clearance
– Post-primary Tuberculosis (re-infection)
– Active Tuberculosis
– Latent Tuberculosis

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5
Q

how does primary TB occur?

A

Mostly affects lungs – Pulmonary
Tuberculosis
* Results in an area of granulomatous
inflammation– Seen as a shadow on an x-ray, in TB it is called a Ghon focus

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6
Q

what is the result of 90% of primary TB?

A

90% of people will never develop active
disease due to a competent immune
response.

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7
Q

what is latent TB?

A

the bacillus may continue to reside trapped inside the granuloma.

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8
Q

how do you detect latent TB?

A
  • A skin prick test - the tuberculin
    test. Is able to detect this hypersensitivity
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9
Q

what can trigger reactivation to latent TB?

A

abnormalities in cell mediated immunity

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10
Q

what is used to eradiacte latent TB?

A
  • Extended antibiotic regimes used to
    eradicate latent TB
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11
Q

what is active or post-primary active TB?

A
  • Small percentage develop at first acquisition.
  • More commonly reactivation of latent TB infection.
  • May be induced if patient becomes immunocompromised
    – E.g. HIV, chemotherapy, high dose corticosteroids.
  • Results in an aggressive immune reaction which leads to large granulomas with a “cheesy” contents called caseation.
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12
Q

what does active TB look like on x-ray?

A
  • In the lungs this material is coughed up which leads to large cavitating
    lesions (observed on x-ray)
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13
Q

what is the 2-year mortality rate of untreated active TB ?

A

50%

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14
Q

where does extrapulmonary TB cause disease?

A

at almost ant site in the body

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15
Q

what usually causes extrapulmonary TB?

A

Usually caused by reactivation of latent infection

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16
Q

what are the most common sites of extrapulmonary tb?

A

– Lymph nodes; pleura; gastrointestinal tract; bone and CNS

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17
Q

what is disseminated disease?

A

(Miliary tuberculosis)
– Bacilli transported in blood or lymphatic system
– May develop as a primary infection or post primary reactivation.
– Can affect many organs and may cause diagnostic delay,
particularly if the lungs are not infected.
– More often presents in children and immunocompromised

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18
Q

what is the clinical presentation of active TB?

A

– cough, weight loss, fever, night sweats, fatigue, dyspnoea, chest pain, haemoptysis.

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19
Q

how do you diagnose active TB?

A
  • Respiratory
    – Chest X ray
    – Acid fast bacilli test and (multiple) sputum cultures.
    – Rapid diagnostic nucleic acid amplification tests (NAAT) often
    this is a PCR test (polymerase chain reaction)
  • Non respiratory
    – Biopsy / needle aspiration (culture)
    – Culture any surgical / radiological sample
    – MRI /CT / Ultrasound as appropriate
    – Chest X ray ( to confirm/exclude respiratory disease)
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20
Q

how do you initially manage pulmonary TB in hospital?

A
  • In hospital management – infection control measures required
    – Patient must be isolated (single room) if possible
    – Personal protective equipment (PPE), staff and visitors.
    – Negative pressure room if high risk of multi–drug resistant TB (MDR-TB)
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21
Q

how do you initially manage pulmonary TB in community?

A

– Advise patient the disease is highly contagious (When active)
– Avoid work / school / crowded places
– Wear face mask in public during first 2 weeks of treatment

22
Q

what are the two phases of treatment of pulmonary TB?

A

– Intensive (Initial) phase treatment- normally lasting two months with 4 drugs
– Continuation phase- usually 4-7 months, with 2 drugs

23
Q

what is the standard treatment for pulmonary TB?

A

– Initial - rifampicin, isoniazid (with pyridoxine), pyrazinamide and ethambutol for 2 months
– Continuation - rifampicin, isoniazid (with pyridoxine) for a further 4 months.

24
Q

what is rifampicin? how does it work?

A
  • Bactericidal, blocks RNA polymerase and therefore prevents protein formation.
  • Important member of the initial phase treatment
  • Kills slowly replicating bacteria throughout the whole course.
  • More active than isoniazid in the anaerobic environment of the caseous lesion
25
Q

when is rifampicin absorption reduced?

A
  • Readily absorbed from the gastrointestinal tract.
  • This is reduced if ingested with food.
26
Q

what are the adverse effects of rifampicin?

A

– Red orange discolouration of body fluid (stains contact lenses)
– Liver damage
* Common to see elevated liver enzymes, may reflect inflammatory response from disease or a reaction to treatment.
* Enzymes at 4x Upper Limit of Normal (ULN) suggest stopping drug treatment.
* Powerful enzyme inducer major possibility of drug interactions

27
Q

how does isonaizid work?

A
  • Inhibits the synthesis of the mycolic acids
    required for the cell wall.
  • Bactericidal and very effective at killing rapidly
    multiplying mycobacteria.
  • Acts rapidly to reduce initial bacterial load.
28
Q

when is isoniazid given?

A
  • Given throughout entire treatment phase to
    supplement rifampicin.
29
Q

where is isonaizid metabolised?

A
  • Metabolised in the liver.
  • Acetylation - can be fast or slower.
  • This can effect the half life
30
Q

who is most likely to have more adverse effects from isonaizid? why?

A
  • Slow acetylates and advance HIV more likely to have adverse effects.
31
Q

what are the adverse effects of isonaizid?

A

– Hepatotoxicity
– Nausea and vomiting
– Hypersensitivity reaction
– Peripheral neuropathy (PN)

32
Q

how do we try and avoid peripherap neuropathy with isonaizid?

A

supplement with B6 (pyridoxine)

33
Q

what is pyrazinamide? where does it work?

A
  • Bacteriostatic
  • Only works in acidic pH - which occurs inside
    macrophages in the tubercle
34
Q

why is pyrazinamide only effective for a short time?

A
  • Only works in acidic pH - which occurs inside
    macrophages in the tubercle.
  • The number of these decrease later in therapy, explaining why this is no longer effective.
35
Q

what are the side effects of pyrazinamide?

A

– Hepatotoxicity
– Rashes
– Urticaria
- gout

36
Q

what kind of drug is ethambutol?

A

Bacteriostatic

37
Q

what is the most signifigant side effect with ethambutol?

A

optic neuritis.
* Manifests as visual alteration, particularly loss of redgreen colour discrimination, progressing to a loss of
visual acuity

38
Q

what is the standard treatment for continuation phase?

A

Standard treatment is with rifampicin and
isoniazid for a further four months after
initiation.

39
Q

what is the risk of non-adherence with TB?

A
  • previous non-adherence, previous treatment failure, history of
    homelessness, drug or alcohol misuse, in prison/detention
    centre, cognitive or psychological disorders, MDR-TB
  • Also offer if significantly unwell or the patient requests.
40
Q

what are ways of promoting adherence?

A

– Includes Directly Observed Therapy (DOT)
* Medication provided in an appropriate form
* Patient reminders for appointments
* Extensive patient counselling + written information in appropriate language
* Home visits
* Random urine tests and other monitoring
* Access to free TB treatment for everyone
* Social and psychological support (including cultural case management and
broader social support)
* Incentives and enablers to help people follow their treatment regimen

41
Q

when would there be a treatment interruption?

A

At least 2 weeks missed or 20% of doses in
initial phase = “treatment interruption”
* Care needed to re-establish treatment

42
Q

what is multi-drug resistant TB?

A

– strains which are resistant to both rifampicin AND isoniazid

43
Q

what is extensive drug resistant TB?

A

– strains resistant to at least rifampicin and isoniazid, a fluoroquinolone and one
or more of the three available second line injectable drugs:
* kanamycin, amikacin, capreomycin

44
Q

who are at high risk of being resistant?

A
  • Previous TB drug treatment, particularly with poor adherence
  • Contact with a known case of multidrug resistant TB
  • Birth or residence in “WHO Hot Spots”
45
Q

what are examples of novel therapies for multi and extensive drug resistant TB?

A

Bedaquiline
Delamanid

46
Q

how does having HIV affect TB?

A
  • The risk of developing TB is estimated to be between 26 and 31 times
    greater in people living with HIV
47
Q

how do you manage HIV-related TB disease?

A

– Drug Interactions
* Rifampicin with antiretroviral agents (e.g. some of the protease
inhibitors and non-nucleoside reverse transcriptase inhibitors).

48
Q

how do you diagnose latent TB?

A
  • Mantoux test offered to:
    – Household contacts and non household close contacts of patients with active TB
    – people who are immunocompromised and at high risk of
    – new entrants from high incidence countries presenting for health care
49
Q

how do you treat latent TB?

A

3 months of isoniazid and rifampicin OR 6 months of isoniazid

50
Q

what is the vaccination against TB?

A

The Bacillus Calmette Guérin (BCG) vaccine

51
Q

who is BCG given to?

A
  • National programme withdrawn in 2005.
  • Now selective neonatal vaccination and those at high risk, under the age of
    35.

MO2 (55 decks)

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