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DT3- EXAM 2 > Drugs- Mycobacterium (3)- Melissa** > Flashcards

Drugs- Mycobacterium (3)- Melissa** Flashcards

1
Q

Tuberculosis:
How common is it?
What is another term used to refer to this disease?

A 
#2 infectious cause of death worldwide; AIDs is #1; 
less common in US than rest of the world.

“The Consumption” –like in classic literature, or like in Moulin Rouge the 2001 Baz Luhrmann blockbuster…you decide.

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2
Q

Tuberculosis:
Causative organism? Which tissues does it infect?
Mode of transmission?
Describe active vs. latent.

A

Mycobacterium Tuberculosis
Infects LUNGS»> but can go anywhere!
Transmitted via respiratory droplets b/w humans

*Patients with Latent infections do not have symptoms and can be given px in order to prevent active infection, which is symptomatic and transmissable.

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3
Q

There are three types of resistant TB. Define them.

A
  1. Rifampin Resistant
  2. MDR (multi-drug resistant):
    Resistant to RIFAMPIN (RIF) + ISONIAZID (INH) (workhorse drugs)
  3. XDR (Extensive drug resistant) Rare:
    MDR resistance + FQN + either amikacin, kanamycin, or capreomycin (at least 1 injectable drug)
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4
Q

Describe the TB life cycle and when the infected individual is contagious:

A

TB inside MQ–> MQ walled off by leukocytes–>

granuloma LATENT–> immunocompromised/reactivation–> Granuloma rupture ACTIVE

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5
Q

What are the most important elements of mycobacterial cell wall? (4)

A
  • mycolic acid
  • murein
  • phospholipids
  • arabinogalactan
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6
Q

Describe the TB drug treatment regimen.
How are the drugs administered?
What defines therapeutic failure?

A

1 RIPE, RIPS (4 drug therapy unless resistance)

Failure= + sputum after four months of RIPE
Given orally for 6 months; may be daily or bi/tri weekly.

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7
Q

How long do patients with osteo/miliary/menengitis TB take RIPE/RIPS?

A

12-24mos for patients with osteo/miliary/menengitis

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8
Q

What is meant by DOT?

A

“Directly Observed Therapy”

Social worker meets patient and DIRECTLY observes him/her taking therapy 2-3x per week in order to assure compliance (esp in homeless, etc.)

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9
Q

What do RIPE and RIPS stand for anyway?

A

Rifampin
Isoniazid
Pyrazinamide
Ethambutol/ Streptomycin (less effective)

These are the drug combos used to treat TB

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10
Q

Rifampin:
MOA
Therapeutic Use; does it cross BBB? (3)
ADRS (3)

A

MOA:
Bactericidal
INHIBITS RNA synthesis by blocking DNA dep. RNAP

Therapeutic Use:

  • Active TB in combo
  • 2nd line for px
  • Crosses BBB*

ADRS:

  1. REVS up liver! (~Hepatotoxic)
  2. RED/Orange discoloration of body fluid
  3. Hypersensitivity (flu like)

Fun Fact: Rifampin is also commonly used as a prophylactic drug after n.meningitidis and h flu exposures!!!!

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11
Q

How does using rifampin in combo with isoniazid help treatment?

A

Synergism: allows for shortened therapy

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12
Q

Rifampin’s spectrum of activity covers some gram + and gram - organisms; how do we utilize this drug for treatment of said infections?

A

NEVER MONOTHERAPY BECAUSE BUGS WILL QUICKLY BECOME RESISTANT

*May use as supplemental therapy for MRSA infections that infiltrate bone etc. in order to facilitate penetration of tissue

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13
Q

List 3 important DD interactions with rifampin; why does this occur?

A

Rifampin revs up liver(^hepatocyte sER)–> CYP450 INDUCER –> ^Metabolism
May need up to 15-20 mg more of drug to be effective!

  1. Warfarin
  2. Narcotics
  3. OCPs & STEROIDS!!!💪
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14
Q

Isoniazid:
MOA (2)
Therapeutic use (2)

A

MOA:

  • INHIBITs mycolic acid synthesis–> weaken cell wall
  • Kills both actively growing and dormant organisms within granulomas

Therapeutic Use:

  • # 1 DOC for PREVENTATIVE therapy (latent infection)
  • combo tx for active infection
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15
Q

Isoniazid:

How is this drug metabolized?

A
  • Metabolized by acetylation in liver
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16
Q

Which populations are consistently slow acetylators of isoniazid?
What does this mean?

A

Egyptians
MORE drug in system at given time = MORE ADRs
(more neurotox!!)

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17
Q

Which populations are fast acetylators of isoniazid?

What does this mean?

A

Eskimos, Japanese

LESS drug in system at given time = LESS effective

18
Q

What are two important ADRs associated with Isoniazid use? How can we minimize them?

A
  1. Hepatotoxicity
  2. NEUROTOXICITY GIVE PYRIDOXINE (Vit B6)

(Isoniazid induces B6 metabolism)

19
Q

Pyrazinamide (PZA):
MOA
Therapeutic Use

A

MOA: Bactericidal towards DORMANT organisms; lives in acidic environment within MQs

Tx: Latent TB infections

20
Q

List two ADRs associated with Pyrazinamide use:

A
  1. hepatotoxicity

2. HYPERURICEMIA **NOT GOOD FOR GOUT PATIENTS*

21
Q 
Ethambutol: 
Bactericidal/static? 
Therapeutic use?
What is its most salient ADR?
When is it contraindicated?
A

BacterioSTATIC
Tx: Treats TB
ADR: OPTIC NEURITIS (dose related; can be reversible)
- loss of visual acuity// red green color blindness
Ethambutol=Eyes

DO NOT USE IN KIDS UNDER 5 BECAUSE THEY CAN’T TELL THEY CAN’T SEE!

22
Q

How do we monitor patients on ethambutol to avoid ADRs?

A

Get baseline visual acuity and follow up every 4-6 weeks to catch impairment early

23
Q

Streptomycin:
MOA
ROA
Relevant therapeutic use

A

MOA:
Aminoglycoside: STOPS protein synth–> BacteriCIDAL; treats active NOT latent organisms

ROA: IV/IM ONLY!

Tx: Replaces Ethambutol when treating TB in kiddos and patients who are ethambutol intolerant!

24
Q

What are Streptomycin’s ADRs (2):

A 
#1: Damage CN VIII (Vestibular>>>ototoxic) 
2. Hepatotoxic
  • A note about aminoglycosides:

They all effect kidneys and CN VIII, but streptomycin specifically is a little less ototoxic/ nephrotoxic

25
Q

RIFABUTIN
MOA
Therapeutic Use (2)
ADRs (2)

A

Rifamycin derivative (MOA = Rifampin)

Tx: TB in rifampin intolerant pts.; MAC active and latent infxn ((rifaButin= people rifampin is BAD for.))

ADRs: Red secretions, Hepatotoxicity, NEUTROPENIA
(Same as rifampin)

26
Q

RIFAPENTINE:
MOA
Therapeutic Use
Advantage to use?

A

Rifamycin derivative (MOA = Rifampin)

Tx: HIV NEGATIVE patients WITHOUT cavitation lesions in CONTINUATION PHASE of TB treatment

Once Weekly dosing = convenient

27
Q

Clofazamine:
MOA
Therapeutic use
ADRS (2)

A

MOA: binds mycobacterial DNA–> INHIBITS transcription

Tx: Leprosy»>TB and other mycobacterial infections

ADRs:

  1. Crystal deposition–> LIFE THREATENING organ damage/ abdominal pain
  2. GI upset
  3. Discoloration of eyes and skin
28
Q

How are macrolides used to treat mycobacterial infections?

A
  • Used in combo with other agents to treat MAC
  • Not effective against TB

“MACrolides are for MAC (and so are fluoroquinolones)”

29
Q

How are FQNs used to treat mycobacterial infections?

A
  • Cipro + Oflox treat TB in combo with other agents

- FQNs inhibit MAC in vitro

30
Q

What is another term for Leprosy?
What are the two types of leprosy infection?
How is the disease transmitted?

A

Hansen’s Disease

  1. Lepromatous- disseminated; multibacillary; lost specific cell mediated immunity
  2. Tuberculoid- localized; paucibacilliary; specific cell mediated immunity intact

Transmission via direct skin-skin contact

31
Q

Describe briefly the high yield symptoms of leprosy and how it is diagnosed:

A
  • skin lesions, hypo pigmentation, loss of sensation (esp extremities)
  • Dx with acid fast stain of skin biopsy (can’t culture)
32
Q

What is the drug treatment regimen for leprosy?

How long does treatment usually last?

A

“Treat LEP-RO-CY with DOC-TOR-C (Dr. C)”

  • Dapsone
  • Rifampin
  • Clofazimine
  • Treat px for close contacts
  • Treatment lasts 3-5 yrs
33
Q

Dapsone:
MOA
ADRs

A

MOA:
BacterioSTATIC
Competitive inhib folic acid synthesis (dihydropteroate synthase)

ADRs:
1. HYPERSENSITIVITY “SULFONE SYNDROME”
Fever, malise–> Jaundice
ADMIN STEROIDS AND CONTINUE THERAPY

  1. Dose dependent hemolytic anemia
34
Q

Describe the cluster of symptoms associated with TB, Cancer, HIV, MAC (4):

A

Fever, NIGHT SWEATS, weight loss, anemia

like malignancy

35
Q

When do AIDS patients get prophylaxis for MAC?

Describe the regimen.

A

CD4 LESS THAN 50!

  • Clarithromycin BID or…
  • Azithromycin weekly in large dose
36
Q

What drugs do we use to treat MAC?
How quickly do patients begin to feel better?
How long for sterile cultures?

A

Clarithro»> Azithromycin + Ethambutol
+/- Clofazamine or Rifampin/Rifampin derivative

Patients will feel clinical improvement within 1-2 mos (longer than long term treatment for other mycobacterium infections)
- Sterile Cultures after 3mo treatment

37
Q

Drug of choice for TB Px?

A

isoniazid

38
Q

Drug specifically targeting DORMANT organisms?

A

pyrazinamide

39
Q

Drug specifically targeting ACTIVE organisms?

A

streptomycin

40
Q

WHO IN THE HECK IS ZEIHL NEELSEN?

A

Actually, He’s two people. Two scientists. Or maybe a I should say its a THING.

–This is a very cruel synonym for “acid fast”, essentially.
Acid fast organisms like TB grow on ZEIHL NEELSEN medium.

MTB also grows on LOWENSTEIN JENSEN!

DT3- EXAM 2 (19 decks)

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