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Pharmacology FINAL (2nd sem) > C2 > Flashcards

C2 Flashcards

1
Q

Antimycobacterial drugs؟

A 
1st line :
 Rifampin
   Isonazide
    Pyrazine.amide
     Ethambutol

2nd line :
Streptomycin
Cycloserine
Kanamycin

leprosy drugs :
Dapson
clofazimine
rifampin

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2
Q

Drugs for Tuberculosis?

A

RIPES

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3
Q

What is the MOA of antituberculotix?

what does it depends on?

A
  • Bactericidal or Bacteriostatic

- depending on drug concentration and strain susceptibility

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4
Q

Isoniazid MOA?

is it effective for dormant or growing bacilli?

A
  • Inhibits the synthesis of mycolic acids (cell walls)

- it is bactericidal for actively growing tubercle bacilli, but is less effective against dormants

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5
Q

Isonazid PharmacoKinetix?

A
  • absorption: well absorbed orally
  • metabolism: Liver (acetylation)
  • 1/2 life:
    *slow acetylators 3–4 h
    *fast acetylators 60–90m
    (for equivalent therapeutic effects fast acetylators require higher dosage)

inhibits CYP450

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6
Q

Isonazide clinical uses?

A
  • most important drug used in tuberculosis - component of most drug combination regimens
  • treats of latent infection
  • Prophylaxis
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7
Q

Isonazide Toxicity?

A
  • peripheral neuritis
  • insomnia
  • muscle twitching
  • inhibit the hepatic metabolism of drugs (eg, carbamazepine, phenytoin, warfarin)
  • Lupus-like syndrome
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8
Q

Rifampin MOA?

A
  • bactericidal
  • inhibits DNA-dependent RNApolymerase
  • if the drug is used alone, Resistance develops rapidly (changes in drug sensitivity of the polymerase)
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9
Q

Rifampin PharmacoKinetix?

A
  • absorption: well absorbed orally
  • distribution: most body tissues (even CNS)
  • metabolism: partially metabolized in the liver (enterohepatic cycling)
  • Elimination:خرا feces (free drug and metabolites)

inducer of CYP450

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10
Q

Rifampin clinical uses?

A
  • always in combination with others
  • solo: latent tuberculosis
  • in INH-intolerant patients or prophylaxis for INH-resistant strains
  • with dapson: leprosy
    (given monthly –> delays the emergence of resistance to dapsone)
  • with vancomycin: against MRSA or PRSP
  • meningococcal and staphylococcal carrier states
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11
Q

Rifampin Toxicity?

A
  • colors sweat, urine and tears orange
  • Rashes
  • thrombocytopenia
  • proteinuria
  • nephritis
  • liver dysfunction
  • induces liver drug-metabolizing enzymes
  • -> enhances the elimination rate of many drugs (anticonvulsants, contraceptive steroids, cyclosporine, ketoconazole, methadone, terbinafine, and warfarin)
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12
Q

Ethambutol MOA?

A
  • inhibits arabinogalactan synthesis
    (cell walls)
  • if used alone, resistance develops rapidly
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13
Q

Etham butol PharmacoKinetix?

A
  • absorption: well absorbed orally
  • distribution: to most tissues (also CNS)
  • elimination: unchanged in the urine

In renal impairment dose reduction is necessary

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14
Q

Ethambutol Clinical use?

A
  • tuberculosis

- always given in combination with other drugs

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15
Q

Ethambutol Toxicity?

A
  • visual disturbances
  • headache, confusion, peripheral neuritis.
  • hyperuricemia
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16
Q

Pyrazinamide MOA?

A
  • MOA is not known :)
  • its bacteriostatic
  • Resistance develops rapidly when the drug is used alone
17
Q

Pyrazinamide PharmacoKinetix?

A
  • absorbtion: orally
  • distribution:most body tissues (also CNS)
  • metabolism: Liver.
  • Elimination: urine (drug and metabolite)

Pyrazinamid avooooid in PPPPregnancy

18
Q

Pyrazinamide Clincal use?

A

short-course treatment in combo with others

19
Q

Pyrazinamide Toxicity?

A
  • non gout polyarthralgia (40% of patients)
  • Hyperuricemia (asymptomatic)
  • myalgia
  • maculopapular rash
  • G.I. irritation
  • hepatic dysfunction
  • photosensitivity
  • should be avoided in pregnancy*
20
Q

Streptomycin?

A
  • Aminoglycoside (Protein synthesis inhibitor)
  • Against resistant M tuberculosis strains
  • principally used in combos for life-threatening tuberculous diseases:
    meningitis
    miliary dissemination
    severe organ tuberculosis
21
Q

Streptomycin pharmacodynamic and pharmacokinetic?

A

similar to those of other aminoglycosides

22
Q

streptomycin uses?

A
  • meningitis
  • miliary dissemination
  • severe organ tuberculosis

-resistant TB, used in combo regimens

23
Q

cycloserine?
MOA
INDICATION
SE

A

cell wall active inhibitor ( inhibits peptidoglycan synthesis)

  • TB resistant to 1st line agent

drug of limited use because of its toxicity:

  • peripheral neuropathy
  • CNS dysfunction
24
Q

Antitubercular standard Drug Regimens

A
  • For empiric treatment of pulmonary TB:
    initial 3-drug regimen of RIP recommended
  • If the organisms are fully susceptible
    (and HIV negative) –> pyrazinamide can be discontinued after 2m and treatment continued for 4m with a 2-drug regimen!
25
Q

Antitubercular Drug Alternative regimens?

A
  • fully susceptible organisms:
    1. RI 9m,
    2. RE 18m
    3. Intermittent (2 or 3/week) high-dose 4-drug regimens
26
Q

Antitubercular Drug Regimens Resistance?

A
  • If resistance to Isonszide is > 4% –> the initial drug regimen should include ethambutol or streptomycin.
  • Tuberculosis resistant only to isonazide (most common) –> 6m with a regimen of RPE/S
  • Multidrug-resistant organisms (both Isonazide + Rifampin) –> 3 or more drugs for a period 18m (including 12m after sputum cultures become negative!)
27
Q

Drug for Leprosy?

A

Dapson

28
Q

What about Dapson?

A
  • DiAmino.diPhenyl.SulfONe) most active drug against M.Leprae.
  • it is recommended that the drug be used in combinations with Rifampin +/or Clofazimine (resistance)
29
Q

Dapson MOA?

A

inhibition of folic acid synthesis.

30
Q

Dapson PharmacoKinetix?

A
  • absorption: oral administration
  • Distribution: most tissues
  • metabolism: Liver (enterohepatic cycling)
  • elimination: urine
31
Q

Dapson Toxicity?

A
  • G.I. irritation
  • Fever
  • Skin rashes
  • methemoglobinemia

Pharmacology FINAL (2nd sem) (37 decks)

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