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Anti-microbials > Anti-Tb Drugs > Flashcards

Anti-Tb Drugs Flashcards

1
Q

Discuss the characteristics of mycobacteria

A
  • resistant to most antibiotics- lipid-rich cell wall
  • Lay dormant
  • Intracellular pathogens- drugs need to penetrate the cell
  • High chance of developing resistance which is why multi-drug tx. is used
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2
Q

What are the fist line agents and which agent is no longer part of this

A

H (INH) RZE
Inoniazid
Rifampicin
pyraminazide
ethambutol

Streptomycin

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3
Q

Explain the relationship between ioniazid and pyrazinamide

A

When ioniazide used alone it cures 95 to 98% of TB cases over 9 months. When pyrazinamide is added for the first 2 months, case reduced in 6 months

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4
Q

Explain the fist line TB regimen for uncomplicated TB in adults/children >8 years and younger= 8 years

A
  1. 2HRZE/4HR
  2. 2HRZ/4HR
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5
Q

Explain the drug regiment for complicated TB in children =< 8 years old

A

2HRZE/4-7HR

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6
Q

Explain some characteristics of Isoniazid and MOA

A
  • Structurally similar to pyridoxine
  • Most active drug treatment of TB
  • Bactericidal against multiplying bacteria
  • Bacteriostatic against non-dividing bacteria
  • Penetrate into macrophages

Inhibits the synthesis of mycolic acids (essential for cell walls) unique to mycobacterium
- Prodrug activated by KatG

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7
Q

explain the mechanisms of resistance regarding Ioniazid

A
  1. Mutation mechanisms
  2. Mutation or deletion of KatG gene (ioniazid won’t be activated)
  3. Cross resistance with ethionamide
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8
Q

Explain the pharmacokinetics of ioniazid

A
  • rapidly absorbed from the GIT within 1-2 hrs
  • Diffuses into all bodily fluids and tissue (CNS and CSF)
    Acetylation by N acetyl-transferase
    Inhibits metabolism of phenytoin and carbamazepine
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9
Q

Discuss the clinical uses of ioniazid

A

max 10mg/kg, 300 mg day for adult
Primary tuberculosis, miliary TB
single agent in latent TB
Pyrioxidine supplementation is essential to prevent neurotoxicity

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10
Q

Discuss the adverse effects of ioniazid

A
  1. SLE (immunological reaction and skin rashes)
  2. Hepatotoxicity (20-40%)
  3. Peripheral neuropathy
    4 CNS toxicity- psychosis, memory loss and seizures

SHIPP

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11
Q

Discuss the characteristics of rifampicin

A

Semisynthetic derivative of rifamycin
Rifamycin is produced by streptomyces mediterranei

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12
Q

Explain the antimicrobial activity of rifampicin

A

Gram positive and gram negative cocci
Some enteric bacteria
Mycobacteria , H. influenzae, Staph aureus,
Chlamydia, certain viruses

Leprosy, severe legionaires’ disease, chemoprophylaxis of meningococcal meningitis, severe staphylococcal infection

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13
Q

Explain the mechanism of action of rifampicin

A
  • Inhibits RNA synthesis
  • Penetrates most tissues including phagocytotic cells
  • Kill organisms inaccessible by other drugs (lung cavities)
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14
Q

Explain the pharmacokinetics of rifampicin

A
  • well absorbed orally
  • Distributes widely in body fluids
  • highly protein bound
    Even with renal or hepatic failure, dosage does not need to change
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15
Q

Explain the mechanism of resistance for rifampicin

A
  • RNA polymerase mutations that prevent the binding of rifampicin to the RNA polymerase
  • Drug-resistant mutants present in the mycobacterial population
    NO CROSS RESISTANCE WITH OTHER DRUGS ONLY TO RIFAMYCIN DERIVATIVES
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16
Q

Explain the clinical uses of rifampicin

A

Latent tuberculosis (monotherapy or combination with pyrazinamide
Bacterial
- Single drug prophylaxis in place of ioniazid
infections (Staph aureus, H influenza, legionella, chlamydia
Prophylaxis against H. influenza type B

17
Q

explain the adverse reactions of rifampicin

A

FAT HI
Flushing
Acute tubular necrosis
Thrombocytopenia
Hepatic toxicity
Influenza-like symptoms e.g. chills, fever, wheezing
Red orange discoloration of urine or tears

18
Q

Explain the drug interactions with rifampicin

A
  1. strong enzyme inducer
  2. Increases elimination of many drugs
  3. Warfarin, steroid contraceptives, analgesics, antidiabetic agents, phenytoin, and protease inhibitors. elimination is enhanced. The drug does need to be increased
  4. Induces its own metabolsim, half life decreases as weeks progress
19
Q

Explain the properties of pyrazinamide

A
  • Derivative of nicotinamide
  • Only treatment of TB
  • Inactive at neutral pHm activated at pH of 5.5
  • converted to pyazinoic acid (active form)–> mycobacterial pyrazinamidase
  • Effective against persisters, prevents relapses
20
Q

Explain the MOA of pyramid

A
  • exact mechanism of action not known
  • Inhibits synthesis of fatty acids required for synthesis of mycolic acid
  • Inhibits mycobacterial cell wall
  • resistance develops easily
21
Q

Explain the adverse reactions with pyrazinamide

A
  • Hepatotoxicity
  • Hyperuricemia (gouty attacks and high uric acid levels)
  • Nausea, vomiting and fever

CONTRAINDICATED IN PREGANCY

22
Q

Explain the antimicrobial action of ethambutol

A
  • No effect on other organisms other than mycobacteria
  • Crosses the blood-brain barrier when meninges are inflamed
  • Used only for the treatment of tuberculosis and meningitis
23
Q

Explain the MOA of ethambutol, when does resistance develop, when does it accumulate?

A
  • inhibits mycobacterial cell wall synthesis
  • Inhibits arobinosyl transferase (important in polymerisation of aribinoglycan)
  • When used alone
  • renal failure
24
Q

Explain the adverse effects of ethambutol and the testing that needs to take place as well as contraindications

A

Optic neuritis
- loss of visual acuity
- red-green colour blind
- Peripheral vision loss

regular visual acuity tests is required

Avoided in patients with impaired vision or children too young for visual testing

25
Q

Explain the MOA, Pharmacokinetics and adverse effects of streptomycin

A

Inhibits protein synthesis by binding to the S12 ribosomal unit

Active extracellularly

IM or IV

Ototoxicity and nephrotoxicity, vertigo and hearing loss

26
Q

When will second-line agents be used?

A
  • Resistance to first line agents
27
Q

List the second line agents, their MOA and adverse effects

A
  1. Ethionamide
    - Similar to ioniazid
    - Inhibits synthesis of mycolic acid
  2. Amikacin and kanamycin
    Multidrug resistant TB
    Amikacin= MAC (mycobacterium avium complex)

Macrolides
Limited activity against TB, used for MAC prevention

Fluoroquinolones
TB and MDR TB

28
Q

What are the principles of TB treatment

A

Kill a large number of actively multiplying bacilli

Treat persisters (semidormant bacilli)

Prevent drug resistance with multiple therapy

Anti-microbials (8 decks)

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