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77 Cards in this Set

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First Line TB Drugs:
Rifampin
Isoniazid
Pyrazinamide
Ethambutol
"Streptomycin"
RIPE
First Line TB Drugs:
Rifampin
Isoniazid
Pyrazinamide
Ethambutol
"Streptomycin"
RIPE
Isoniazid (INH)MoA:
Inhibits synthesis of mycolic acids and mycobacterial cell wall
Isoniazid (INH)MoA:
Inhibits synthesis of mycolic acids and mycobacterial cell wall
Isoniazid (INH) Route:
PO/IM
Good PO absorption
Isoniazid (INH) Route:
PO/IM
Good PO absorption
Isoniazid (INH) Metabolism:
Metabolized by N-acetyltransferase in the liver

Slow acetylators have increased toxicity
Isoniazid (INH) AEs:
Hepatotoxic (AST, ALT)

Neurotoxicity (B6 defenciency; given prophyllaxis)
Rifampin MoA & PK
MoA: Inhibits DNA-dependent RNA polymerase and inhibits RNA synthesis

Extremely bactericidal (never monotherapy)

IV/PO
Well absorbed/widely distributed
Excreted into bile
Enterohepatic recirc.
Excretion via feces
Rifampin AEs:
Hepatotoxic
n/v
rash
Red-orange discoloration of fluids

POTENT 2D6 & 3A4 INHIBITOR
Pyrazinamide MoA & PK:
Prodrug converted to pyrainoic acid by mycobacteria

Bactericidal

PO Only (well absorbed)
Widely dist.
Extensive hepat. metab.
Metabolites renally excreted
Pyrazinamide AEs:
Hepatotoxic, hyperuricemia (gout), n/v
Ethambutol only TB agent not:
metabolized primarily metabolized in liver
Ethambutol MoA, PK:
Inhibits cell wall, bacteriostatic

PO only (well absorbed)
Primarily excreted in urine
Ethambutol AEs:
Optic neuritis (dose related)

Cat C
Streptomycin is an:
aminoglycoside
Streptomycin MoA, PK:
Inhibits protein synthesis

Bactericidal against rapidly dividing EC organisms

IM/IV
Eliminated renally
Streptomycin AEs:
Ototoxicity (can be permanent)
Nephrotoxicity (reversible)

Cat D
First Line TB Drugs:
Rifampin
Isoniazid
Pyrazinamide
Ethambutol
"Streptomycin"
RIPE
First Line TB Drugs:
Rifampin
Isoniazid
Pyrazinamide
Ethambutol
"Streptomycin"
RIPE
Isoniazid (INH) Metabolism:
Metabolized by N-acetyltransferase in the liver

Slow acetylators have increased toxicity
Isoniazid (INH) AEs:
Hepatotoxic (AST, ALT)

Neurotoxicity (B6 defenciency; given prophyllaxis)
Isoniazid (INH)MoA:
Inhibits synthesis of mycolic acids and mycobacterial cell wall
Rifampin MoA & PK
MoA: Inhibits DNA-dependent RNA polymerase and inhibits RNA synthesis

Extremely bactericidal (never monotherapy)

IV/PO
Well absorbed/widely distributed
Excreted into bile
Enterohepatic recirc.
Excretion via feces
Isoniazid (INH)MoA:
Inhibits synthesis of mycolic acids and mycobacterial cell wall
Rifampin AEs:
Hepatotoxic
n/v
rash
Red-orange discoloration of fluids

POTENT 2D6 & 3A4 INHIBITOR
Isoniazid (INH) Route:
PO/IM
Good PO absorption
Isoniazid (INH) Route:
PO/IM
Good PO absorption
Pyrazinamide MoA & PK:
Prodrug converted to pyrainoic acid by mycobacteria

Bactericidal

PO Only (well absorbed)
Widely dist.
Extensive hepat. metab.
Metabolites renally excreted
Pyrazinamide AEs:
Hepatotoxic, hyperuricemia (gout), n/v
Ethambutol only TB agent not:
metabolized primarily metabolized in liver
Ethambutol MoA, PK:
Inhibits cell wall, bacteriostatic

PO only (well absorbed)
Primarily excreted in urine
Ethambutol AEs:
Optic neuritis (dose related)

Cat C
Streptomycin is an:
aminoglycoside
Streptomycin MoA, PK:
Inhibits protein synthesis

Bactericidal against rapidly dividing EC organisms

IM/IV
Eliminated renally
Streptomycin AEs:
Ototoxicity (can be permanent)
Nephrotoxicity (reversible)

Cat D
Isoniazid (INH) Metabolism:
Metabolized by N-acetyltransferase in the liver

Slow acetylators have increased toxicity
Isoniazid (INH) Metabolism:
Metabolized by N-acetyltransferase in the liver

Slow acetylators have increased toxicity
Isoniazid (INH) AEs:
Hepatotoxic (AST, ALT)

Neurotoxicity (B6 defenciency; given prophyllaxis)
Isoniazid (INH) AEs:
Hepatotoxic (AST, ALT)

Neurotoxicity (B6 defenciency; given prophyllaxis)
Rifampin MoA & PK
MoA: Inhibits DNA-dependent RNA polymerase and inhibits RNA synthesis

Extremely bactericidal (never monotherapy)

IV/PO
Well absorbed/widely distributed
Excreted into bile
Enterohepatic recirc.
Excretion via feces
Rifampin AEs:
Hepatotoxic
n/v
rash
Red-orange discoloration of fluids

POTENT 2D6 & 3A4 INHIBITOR
Rifampin MoA & PK
MoA: Inhibits DNA-dependent RNA polymerase and inhibits RNA synthesis

Extremely bactericidal (never monotherapy)

IV/PO
Well absorbed/widely distributed
Excreted into bile
Enterohepatic recirc.
Excretion via feces
Rifampin AEs:
Hepatotoxic
n/v
rash
Red-orange discoloration of fluids

POTENT 2D6 & 3A4 INHIBITOR
Pyrazinamide MoA & PK:
Prodrug converted to pyrainoic acid by mycobacteria

Bactericidal

PO Only (well absorbed)
Widely dist.
Extensive hepat. metab.
Metabolites renally excreted
Pyrazinamide MoA & PK:
Prodrug converted to pyrainoic acid by mycobacteria

Bactericidal

PO Only (well absorbed)
Widely dist.
Extensive hepat. metab.
Metabolites renally excreted
Pyrazinamide AEs:
Hepatotoxic, hyperuricemia (gout), n/v
Ethambutol only TB agent not:
metabolized primarily metabolized in liver
Ethambutol MoA, PK:
Inhibits cell wall, bacteriostatic

PO only (well absorbed)
Primarily excreted in urine
Pyrazinamide AEs:
Hepatotoxic, hyperuricemia (gout), n/v
Ethambutol AEs:
Optic neuritis (dose related)

Cat C
Ethambutol only TB agent not:
metabolized primarily metabolized in liver
Streptomycin is an:
aminoglycoside
Ethambutol MoA, PK:
Inhibits cell wall, bacteriostatic

PO only (well absorbed)
Primarily excreted in urine
Ethambutol AEs:
Optic neuritis (dose related)

Cat C
Streptomycin is an:
aminoglycoside
Streptomycin MoA, PK:
Inhibits protein synthesis

Bactericidal against rapidly dividing EC organisms

IM/IV
Eliminated renally
Streptomycin AEs:
Ototoxicity (can be permanent)
Nephrotoxicity (reversible)

Cat D
Streptomycin MoA, PK:
Inhibits protein synthesis

Bactericidal against rapidly dividing EC organisms

IM/IV
Eliminated renally
Streptomycin AEs:
Ototoxicity (can be permanent)
Nephrotoxicity (reversible)

Cat D
Amphotericin B MoA:
Bind to ergosterol in the fungal cell membrane (pokes holes)
Swiss Cheese
Amphotericin B PK:
IV in D5W sol over 2-4 hrs
Widely dist. in tissues
Excreted extremely slowly in urine (half life 24 hrs-14 days)
Amphotericin B AEs:
Infusion-related rxns (fever, chills, vomitting, headache)

Nephrotoxicity (lipid formulations less nephrotoxic)

Lowered Mg2+ & K+
Flucytosine (5-FC = 5-fluorocytosine) MoA, PK, AEs:
MoA: Inhibits DNA synthesis (nvr monotherapy)

PK: PO only; renal excretion

AE: Bone marrow suppression
Caspofungin, micafungin, anidulafungin are all members of what drug class?
Echinocandins
Echinocandins MoA, PK, AE:
MoA: Inhibit fungal cell wall synthesis; target Beta-(1,3)-D-glucan synthase enzyme

PK: IV only, hepatic metabolism

AE: Extremely well tolerated; Thrombophlebitis, abnormal liver enzymes possible
Terbinafine is what kind of antifungal?
Allylamine
Terbinafine MoA, PK, AEs:
MoA: Inhibits ergosterolsynthesis; Inhibits enzyme squalene epoxidase

PK: Topical and PO; 40% bioavailability due to first-pass metabolism; Long half-life of 200-400 hrs (slow release from tissues)

AEs: GI, hepatotoxicity
1st and Long
Azole antifungal MoA, PK:
MoA: Inhibit synthesis of ergosterol(fungal cell
membrane component); Inhibit enzyme 14-demethylase

PK: Variable absorption when administered orally Fluconazole>> voriconazole, posaconazole>>
itraconazole Most undergo hepatic metabolism via CYP450 3A4 Not posaconazolewhich is glucuronidatedin liver Exception = fluconazole(excreted in the urine)
Azole Interactions:
They're CYP450 inhibitors (including 3A4)
Azole AEs:
Hepatotoxicity, visual disturbances (voriconazole only)
Nucleoside Analogues MoA:
Prodrugs

Phosphorylated by viral and host kinases to form active triphosphateform (thymidinekinase)

Compete with endogenous nucleoside
triphosphatesand competitively inhibit
viral DNA polymerase

Inhibition of viral DNA polymerase
prevents the synthesis of viral DNA
Ganciclovir AE:
Bone marrow suppression
Cidofovir AE:
VERY TOXIC

Bone marrow suppression and nephrotoxicity

Probenecid and hydration are co-administered with each dose Probenecid decreases cidofovirsecretion into kidney
Foscarnet MoA:
Blocks pyrophosphate-binding sites on viral DNA polymerase and prevents attachment of nucleotide precursors to DNA

No activation needed
Foscarnet PK & AE:
IV only; renal excretion

Nephrotoxicity
WHich is the only IV NSAID?
toradol