| Hint | Answer |
|---|
| Use: Effective suppression of HBV DNA, normalization of ALT & reducing HBeAg. Adults only | |
| Telbivudine (Tyzeka) Class | |
| MOA: An adenosine analogue. Structurally similar to adefovir. | |
| P-kinetics: Synthetic (consensus). SC | |
| Group MOA cont: Associated with mitochondrial DNA toxicity (by inhibiting DNA polymerase gamma) | |
| SE: Increased pancreatitis in HIV/HBV pts. Emergence of resistance (mutations of DNA polymerase) | |
| Use: Improve therapeutic response in pts (>18 yo) w/ HCV genotype 1 when combined w/ IFN/ribavirin | |
| MOA: A thymidine analog | |
| Use: The most potent anti-HBV agent. Adults only | |
| SE: Flu-like symptoms (fever, chills, myalgias, malaise). Neurotoxicity, myelosuppression, fatigue (chronic use). Transient hepatic enzyme elevation. | |
| P-kinetics: Prolonged intracellular half-life in HBV (than in HIV). Rapid oral absorption; eliminated unchanged. Used at lower doses for hepatitis than for AIDS. | |
| Group MOA: 3 major enzymes are activated by IFN-JNK/STAT signaling pathway: (1) 2',5' oligo A synthase: produces 2'5' oligo A. | |
| P-kinetics: Clinical resistance is rare. Oral bioavailability decreased by food (taken w/ empty stomach). Renal elimination (serum concentration increased w/ altered kidney activit | |
| Group P-kinetics: Pills once a day for a year or longer | |
| PEG-IFN α-2a/2b class | |
| MOA: A prodrug of adefovir (adenosine analogue). Slows suppression of HBV DNA; least seroconversion | |
| Use: Lamivudine-resistant HBV. Adults only | |
| P-kinetics: Oral (TID). P450 substrates (potential rx interactions) | |
| P-kinetics: Oral bioavailability increased with high-fat meal, decreased with antacid. | |
| Drug MOA: PEG = polyethylene glycol | |
| IFN α-2b Class | |
| Lamivudine (3TC, Heptovir) Class | |
| P-kinetics:Oral bioavailability not affected by food. Emergence of resistance in long term use. | |
| Adefovir dipivoxil (Hepsera) Class | |
| Contraindications: Hepatic decompensation, autoimmune dz, cardiac arrhythmia, pregnancy | |
| | Hint | Answer |
|---|
| Use: HBV treatment adults only | |
| IFN α-2a/2b class | |
| Entecavir (Baraclude) Class | |
| P-kinetics: Slower clearance (less frequent dosing). Dosage adjustment is needed in renal dysfunction | |
| Group MOA cont. (2) Ribonuclease L (activated by 2'5' oligo A): degrades mRNA. | |
| Boceprevir Class | |
| Telaprevir Class | |
| P-kinetics: Higher rate of complete response & less resistance vs. adefovir | |
| SE: Dose-dependent hemolytic anemia. Depression, fatigue, irritability, nausea, insomnia. | |
| Contraindications: Pts w/ uncorrected anemia, ESRD, preggo. Teratogenic: avoid pregnancy for > 6 mos thereafter | |
| MOA: A prodrug (a guanosine nucleoside analogue). Phosphorylated by host cell enzymes; inhibits viral RNA-dependent polymerases. | |
| MOA: A guanisine analog. Inhibits all 3 functions of HBV RNA-dependent DNA polymerase (base priming, reverse transcription of the -strand, synthesis of the + strand of HBV DNA. | |
| P-kinetics: Natural. SC or IM | |
| PEG-IFN α-2a Class | |
| MOA: A cytosine analogue | |
| Group MOA cont. (3) Protein kinase (activated by dsRNA): phosphorylates/inhibits eIF-2, therefore blocking PRO synthesis | |
| P-kinetics: Lipophilic (pivoxil) moiety enhances oral bioavailability. | |
| Use: HBV: Safer for pts w/ decompensated liver dz. For both adults & peds | |
| MOA: Serine protease inhibitors. Bind to inhibit HCV non-structural protein NS3 | |
| Tenofovir Class | |
| SE: Nephrotoxicity (at high doses). Potential mitochondrial DNA toxicity | |
| SE: Anemia, neutropenia, dysgeusia, skin rash (esp. telaprevir), increased QT intervals (telaprevir) | |
| IFN alfacon-1 class | |
| Group MOA: Competively inhibit HBV DNA polymerase +/- incorporate into viral DNA causing chain termination. Phosphorylated to active forms intracellularly by cellular kinases. | |
| SE: HA, fatigue, nausea. Potential mitochondrial toxicity (lactic acidosis & hepatic steatosis) | |
|
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