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PHARMACOLOGY: Pharmacodynamics: Pregnancy may be prevented through several mechanisms: Thickening of cervical mucus, which inhibits sperm through the uterus and sperm survival, inhibits ovulation from a negative feedback mechanism on the hypothalamus, leading to reduced secretion of follicle stimulating hormone (FSH) and luteinizing hormone (LH); altering the endometrium, which may affect implantation. Levonorgestrel is not effective once the implantation process has begun.
Pharmacokinetics: Absorption: Levonorgestrel is rapidly and completely absorbed after oral administration (Bioavailability about 100%) and is not subjected to first pass metabolism.
Distribution: The apparent volume of distribution of levonorgestrel is reported to be approximately 1.8 L/kg. It is about 97.5% to 99% protein-bound, principally to sex hormone-binding globulin (SHBG) and, to a lesser extent, serum albumin.
Metabolism: Levonorgestrel is conjugated at the 17 beta-OH position to form sulfate conjugates and glucuronide conjugates in plasma. Significant amounts of conjugated and unconjugated 3 alpha, 5 beta-tetrahydrolevonorgestrel are also present in plasma, along with much smaller amounts of 3 alpha, 5 alpha-tetrahydrolevonorgestrel and 16 beta hydroxylevonorgestrel. Levonorgestrel and its phase I metabolites are excreted primarily as glucuronide conjugates.
Excretion: About 45% of levonorgestrel and its metabolites are excreted in the urine and about 32% are excreted in feces, mostly as glucuronide conjugates.
