Mild to severe: Dizziness, vivid dreams, insomnia, confusion, impaired concentration, amnesia, agitation, depersonalization, hallucinations, euphoria, somnolence (mild symptoms don’t interfere with daily activities; severe symptoms interrupt daily activities)
! Cardiac reactions (including ischemia, coronary artery vasospasm and MI) and noncardiac vasospasm-related reactions (such as hemorrhage and CVA) occur rarely, particularly in patients with hypertension, diabetes, or a strong family history of coronary artery disease; obese patients; smokers; males older than 40 yr; and postmenopausal women.
Rapidly and extensively absorbed from the GI tract. Excreted primarily in urine (86%) and, to a lesser extent, in feces (14%); 30% removed by hemodialysis. Unknown if removed by peritoneal dialysis. Half-life: 10 hr.
Antiretroviral agent, reverse transcriptase inhibitor (nonnucleoside); antiretroviral agent, reverse transcriptase inhibitor (nucleoside); antiretroviral agent, reverse transcriptase inhibitor (nucleotide)
Nonnucleoside, nucleoside, and nucleotide reverse transcriptase inhibitor combination; rilpivirine binds to reverse transcriptase, emtricitabine is a cytosine analogue, and tenofovir is an analogue of adenosine 5′-monophosphate. Each drug interferes with HIV viral RNA dependent DNA polymerase activities, resulting in inhibition of viral replication.
Emtricitabine: Rapidly and extensively absorbed after oral administration. Less than 4% plasma protein bound. Eliminated by a combination of glomerular filtration and active tubular secretion. Excreted primarily in urine (86%) and, to a lesser extent, in feces (14%). Rilpivirine: Rapid absorption after oral administration. 99% plasma protein bound. Hepatic metabolism via CYP3A enzymes. Eliminated in feces (85%) and urine (6%). Tenofovir: Moderate absorption following oral administration. Plasma protein binding less than 7%; minimal systemic metabolism; excreted by glomerular filtration and active tubular secretion. Half-life: Emtricitabine: 10 hr. Rilpivirine: 50 hr. Tenofovir: 17 hr.
! Lactic acidosis and severe hepatomegaly have been reported with nucleoside analogues (e.g., tenofovir), including fatal cases. Safety and efficacy during coinfection of HIV and HBV have not been established; acute, severe exacerbations of HBV have been reported following discontinuation of antiretroviral therapy.
This ACE inhibitor suppresses the renin-angiotensin-aldosterone system and prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor; may inhibit angiotensin II at local vascular, renal sites. Decreases plasma angiotensin II, increases plasma renin activity, decreases aldosterone secretion.
Therapeutic Effect: In hypertension, reduces peripheral arterial resistance. In CHF, increases cardiac output; decreases peripheral vascular resistance, B/P, pulmonary capillary wedge pressure, heart size.
Readily absorbed from the GI tract (not affected by food). Protein binding: 50%–60%. Converted to active metabolite. Primarily excreted in urine. Removed by hemodialysis. Half-life: 11 hr (half-life is increased with impaired renal function).