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Respiratory 2 > TB & TB Therapy > Flashcards

TB & TB Therapy Flashcards

1
Q

facultative intracellular bacillus, acid-fast pathogen that can cause chronic pneumonia and tuberculosis

A

Mycobacterium tuberculosis

  • transmitted through aerosols
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2
Q

Mycobacterium tuberculosis is facultative in what cell?

A

macrophages

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3
Q

Examples of facultative intracellular pathogens

A
  1. Mycobacterium tuberculosis

2. Legionella

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4
Q

Examples of obligate intracellular pathogen

A

Chlamydia

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5
Q

Why are antibodies not very helpful for intracellular pathogens?

A

Drugs must penetrate into cells to be effective; most antibodies can prevent infections though.

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6
Q

What plays a major role in the clearance of intracellular pathogens?

A

cell-mediated adaptive immune responses

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7
Q

Special characteristics of mycobacterium membranes

A
  • Has peptidoglycan but has mycolic acid in outer membrane (neither gram - or +)
  • No LPS
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8
Q

What stain is used for mycobacterium?

A

acid fast stains

  • Ziehl-Neelsen
  • Fluorescent Auramine-Rhodamin
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9
Q

Why is TB often undiagnosed in primary TB phase?

A

It takes about 6-8 weeks after exposure to mycobacterium for the PPD skin test to be positive; PPD skin test will be false negative if tested too early.

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10
Q

Studies suggest that some people can clear M.tuberculosis even after exposure because of

A

the clearance by their innate immune mechanism (still unclear why)

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11
Q

People with _______ have the highest risk for developing active TB

A

HIV

*TB-HIV Syndemic”

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12
Q

Why is HIV the strongest risk factor developing active TB?

A

Hastens progression from primary/latent TB infection to disease

*(TB accelerates the progression of HIV as well)

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13
Q

TB can be harder to diagnose in HIV infected individuals (True or False)

A

True (if you already have a depressed immune system, you won’t respond to the skin test as well)

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14
Q

People with HIV and latent TB have a 10% chance of reactivation EVERY year (True or False)

A

True

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15
Q

Long-lasting bad cough, Hemoptysis, Chest pain, Weight loss, Fever, and Night sweats are symptoms of

A

active TB

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16
Q

What causes the symptoms of active TB

A

the immune response (cytokines such as IL-1 and TNF-a, macrophages and T cells)

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17
Q

What can spontaneously occur in 6 months of TB?

A

spontaneous healing

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18
Q

How does TB survive in macrophages?

A

Arrest phagosome maturation (doesn’t get acidic enough to kill it)

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19
Q

TB-infected macrophages have what histological appearance?

A

foamy appearance due to lipid accumulation

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20
Q

Protection against TB is highly dependent on

A

TH1 mediated (CD4 and CD8) response

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21
Q

TB-infected macrophages induce TH1 response via

A

IL-12

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22
Q

CD4 and CD8 cells make what cytokine to activate infected macrophages, leading to oxygen/nitrogen radicals being produced and lysosome fusion

A

IFN-gamma

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23
Q

The end-product of TH1 immune response to TB

A

Formation of a multi-cellular granuloma that walls off the infection (making it not infectious)

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24
Q

What structure denotes latent TB infection?

A

granuloma (mycobacterium adopt a non-replication persistent states to survive in granulomas)

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25
Q

Reactivation of latent TB means

A

Granulomas has deteriorated and M. tuberculosis is reactivated, triggering overly robust T-cell response leading to lung damage.

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26
Q

Reactivation TB disease is highly

A

infectious

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27
Q

How does TB react in HIV patients?

A

primary infection is not controlled, so dissemination occurs throughout lungs (milliary TB)

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28
Q

miliary TB appears like _____ on CXR

A

millet seeds

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29
Q

Diagnostic tests for ACTIVE TB

A
  1. Acid fast bacillus (AFB) staining of sputum
  2. Culture bacilli from sputum on lowenstein-jensen agar
  3. Xpert MTB/RIF (allows detection of mycobacterium & rifampicin resistance)
  • 3 consecutive sputum samples are needed
  • culture takes weeks to grow in vitro
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30
Q

Which test is suggested by the WHO for initial diagnostic for people suggested of having MDR TB or HIV co-infection

A

Xpert MTB/RIF test (2 hour PCR test)

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31
Q

Diagnostic tests for TB exposure & complications

A
  1. PPD (aka TST) skin test
    - delayed-type hypersensitivity response
    - false + in ppl with BCG vaccine (M. bovis)
    - doesn’t work in HIV patients
  2. IGRA
    - measures IFN-gamma produced by T-cells
    - no BCG cross-reaction
    - doesn’t work in HIV patients
32
Q

MDR vs. XDR vs. TDR TB (what do they mean)

A

MDR: Multi-drug resistance
XDR: Extensive drug resistance
TDR: Total drug resistance

33
Q

Best method to ensure patient compliance with TB medication

A

DOTS (Directly Observed Treatment Short Course)

34
Q

Challenges of TB drugs are

A
  1. Access to M.tuberculosis in granulomas

2. efficacy on non-replicating M.tuberculosis that are in limited environments (nutrient-limited, hypoxic, acidic)

35
Q

Airborne precautions of TB

A
  1. Clean hands & wear PPE to protect against small droplets that remain airborne for hours
  2. Rooms with negative pressure (one way air; no recirculation)
36
Q

What is the vaccine against m.tuberculosis?

A

BCG (live attenuated M. bovis)

  • not used in the US
37
Q

Examples of Acid-Fast mycobacterium besides TB

A

M.bovis
M. avium complex
M.leprae (causes leprosy)
other NTMs (aka atypical mycobacteria)

38
Q

What are NTMs/atypical mycobacteria?

A

M. marinum
M. fortuitum
M. abscessus

39
Q

Describe M. avium complex

A
  • found in water supplies
  • form biofilms
  • causes pulmonary/disseminated diseases
  • more common in HIV patients
40
Q

What 2 forms of leprosy can be caused by M. leprae?

A
  1. Tuberculoid (Th1 response)
    - deformity due to nerve damage
  2. Lepromatous (Th2 response)
    - Active, nodulous
41
Q

What leprosy form is infectious?

A

Lepromatous (Th2 response)

42
Q

What is another name for leprosy?

A

Hansen disease

43
Q

Both forms of leprosy are treatable with multidrug therapy (True or False)

44
Q

acid-fast bacilli; normal inhabitants of soil and water; more common in southern and midwestern US; associated with Lady windermere syndrome (slender, older women); difficult to treat

45
Q

Why are NTMs difficult to treat?

A

TB drugs don’t work

46
Q

Describe M. abscessus?

A
  • Frequent in bronchiectasis, COPD, CF patients
  • Forms biofilms
  • causes chronic lung infection or skin/soft tissue infections
  • intrinsically resistant to drugs (poor outcome)
47
Q

NTM that is fast growing and recently associated with nail salons; causes bright red skin lesions

A

M. fortuitum

48
Q

First line drugs for TB (5 total)

A

Isoniazid
Ethambutol
Rifampicin/Rifampin, Rifabutin
Pyrazinamide

49
Q

What is WHO-approved TB therapy?

A

8 weeks of intensive phase (4 drug-combination) followed by 18 weeks of continuation phase (2 drug-combination) = total of 26 weeks

50
Q

MDR TB is defined as being resistant to what drugs?

A

Isoniazid

Rifampicin

51
Q

XDR TB is defined as being resistant to what drugs?

A

Isoniazid
Rifampicin
2 classes of 2nd-line

52
Q

TDR TB is defined as being resistant to what drugs?

A

Isoniazid
Rifampicin
2 classes of 2nd-line
Others

53
Q

Second line drugs for TB (10 total)

A
  1. -Manids
  2. Cycloserine
  3. -Mycins (+Amikacin)
  4. Linezolid
  5. -Floxacins
  6. Bedaquiline
54
Q

Drugs that blocks the synthesis of mycolic acid

A

1st line: Isoniazid

2nd line: -Manids

55
Q

MoA of Isoniazid

A

Isoniazid gets converted into its active form by bacterial KatG enzyme. The active form inhibits bacterial InhA enzyme that produces mycolic acid.

56
Q

MoR (Mechanism of resistance) against Isoniazid

A

Mutations in KatG and InhA enzymes confer resistance

57
Q

Toxicities of Isoniazid

A
  1. Hepatotoxicity (inc. w/age but 3% overall)
    - associated with NAT 2 acetylation
    - associated with CYP2E1 enzyme
  2. Peripheral Neuropathy
    - associated with Vitamin B6 deficiency
58
Q

Explain association between NAT2 acetylation and hepatotoxicity

A

More NAT 2 acetylation = fast acetylators (less prone to toxicity)

Lower NAT 2 acetylation = slow acetylators (more toxic metabolites)

  • NAT 2 polymporphisms differ among races
  • 50% of Americans are slow acetylators
59
Q

With Isoniazid, ethanol can promote what enzyme, causing more toxic metabolites and worse hepatotoxicity

60
Q

Since _____ is similar to Isoniazid in structure, its production decreases.

A

Vitamin B6

  • vitamin B6 supplements are taken with Isoniazid
61
Q

What drug has advantages over older drugs because it has no significant CYP-associated drug interactions?

62
Q

Drugs that blocks the synthesis of galactan portion of the cell wall

A

1st line: Ethambutol

2nd line: Cycloserine

63
Q

MoA of Ethambutol and Cycloserine

A

The drugs inhibit arabinosyl-transferase enzyme necessary to make galactan in cell wall

64
Q

MoR of Ethambutol and Cycloserine

A

Mutations in arabinosyl-transferase confer resistance

65
Q

Toxicities of Ethambutol

A

Optic neuritis (inflammation of optic nerve) that can cause R-G color blindness

  • reversible
66
Q

Toxicities of Cycloserine

A

Various neurologic symptoms

  • Don’t Memorize (headache, vertigo, drowsiness, etc)
67
Q

Drug that is a RNA Polymerase inhibitor

A

Rifampin, Rifabutin (both 1st line)

68
Q

MoR of Rifampin and Rifabutin

A

Mutations in RNA polymerase confer resistance

69
Q

Toxicities of Rifampin/Rifabutin

A
  1. Orange coloration of skin, urine, feces, saliva, tears
  2. Nephrotoxicity (inflammation of nephron tubules)
  3. Drug Interactions
    - Induces CYP enzyme therefore decreases HIV drug effects
70
Q

Drug that converts into its negative form by PZase enzyme and uses pH trapping to disrupt cell energetics

A

Pyrazinamide (1st line)

71
Q

MoR of Pyrazinamide

A

Mutations in PZase

72
Q

Toxicities of Pyrazinamide

A
  1. Hepatotoxicity

2. Pregnancy risk category C (still can be used)

73
Q

Drugs that are protein synthesis inhibitors

A
  1. Aminoglycosides
    - Mycins (+Amikacin)
  2. Oxazolidenone
    - Linezolid

*they are 2nd lines

74
Q

Drugs that are DNA synthesis inhibitors

A

Fluoroquinolones (-floxacins)

- 2nd line

75
Q

Drug that inhibits ATP synthase

A

Bedaquiline (2nd line)

76
Q

Toxicity of Bedaquiline

A

Drug interactions

- co-administration with rifampin reduces HIV drug effects by inducing CYP enzyme

Respiratory 2 (6 decks)

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