Drug List Block 7 Flashcards
Ethinylestradiol and Oestradiol (natural form)
Both Oestradiol and Ethinylestradiol interact with the oestrogen receptor (ERaor ERb) present on female organs, breasts, hypothalamus and pituitary gland.
Upon ligand binding, the oestrogen receptor enters the nucleus, and regulates gene transcription.
This leads to an increase in the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and supresses(FSH) from the anterior pituitary.
Too much oestradiol has been linked to acne, constipation, loss of sex drive and depression. Conversely too little oestradiol, retards bone growth and development.
In men, proper oestradiol levels help with bone maintenance, nitric oxide production and brain function.
Nandrolone
Nandrolone is an anabolic steroid occurring naturally in the human body, albeit in small quantities.
Nandrolone increases production and urinary excretion of erythropoietin. It may also have a direct action on bone marrow.
Nandrolone binds to the androgen receptor to a greater degree than testosterone, but due to its inability to act on the muscle in ways unmediated by the receptor, has less overall effect on muscle growth. Nandrolone is unusual in that unlike most anabolic steroids, it is not broken down into the more reactive DHT by the enzyme 5a-reductase, but rather into a less effective product known as Dihydronandrolone.
Alprostadil
binds to the EP1 and EP2 receptors, leading to either an increase in cAMP and the activation of Protein Kinase A (PKA), or activation of Phospholipase C (PLC) depending on the receptor activated in the target cells.
When administered by intracavernosal injection or as an intraurethral suppository, alprostadil acts locally to relax the trabecular smooth muscle of the corpora cavernosa and the cavernosal arteries. Swelling, elongation, and rigidity of the penis result when arterial blood rapidly flows into the corpus cavernosum to expand the lacunar spaces. The entrapped blood reduces the venous blood outflow as sinusoids compress against the tunica albuginea.
Bicalutamide
Bicalutamide binds to the androgen receptor consequently blocking the action of androgens of adrenal and testicular origin which stimulate the growth of normal and malignant prostatic tissue.
Prostate cancer depends on the male sex hormone, testosterone, to grow. Bicalutamide stops testosterone reaching the cancer cells aiding shrinkage/slowing of growth of the cancer
Finasteride
Type II 5a-reductase converts testosterone to DHT. DHT appears to be the principal androgen responsible for stimulation of prostatic growth. Inhibition of Type II 5a-reductase with Finasteride, results in significant decreases in serum and tissue DHT concentrations, minimal to moderate increases in serum testosterone concentration, and substantial increases in prostatic testosterone concentration.
Decreases in DHT concentrations lead to a reduction in prostate size (approximately 20-30% after 6-24 months of continued therapy). Furthermore it is used as a surgical alternative for treatment of benign prostatic hyperplasia.
Goserelin
Goserelin is a luteinizing hormone releasing hormone (LHRH) super agonist. Super-agonists have higher efficacy than endogenous (full) agonists.
Goserelin is a decapeptide analogue of luteinizing hormone- releasing hormone (also known as gonadotropin releasing hormone [GnRH]). LHRH agonists (LHRHa) in acute administration initially stimulate the release of LH, resulting in a transient elevation in serum androgen (men) and serum oestradiol (women). However, chronic administration can cause down-regulation of the LHRH receptors, inhibiting LH (and other sex hormone) secretion. By decreasing the testicular production of androgen in men, LHRHa can inhibit the growth of androgen- dependent prostate cancer.
Sildenafil / Viagra
Nitric oxide (NO) causes the dilation of blood vessels. NO can cause this by the production of cGMP within the cell. PDE5 is an enzyme which breaks down cGMP and therefore reduces the cell response to NO. Therefore inhibition of PDE5 by Sildenafil slows the breakdown of the cGMP and therefore maintains the effectiveness of NO. Sildenafil also is used for erectile dysfunction as inhibition of PDE5 in the corpus cavernosum located around the penis causes smooth muscle relaxation and increased blood flow into the corpus cavernosum.
Desogestrel / Etonogestrel / Levonorgestrel: Synthetic versions of progesterone
These drugs are used as female contraceptives. They work by binding to the progesterone and oestrogen receptors present on the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Once bound to the receptor, progestins like desogestrel will slow the frequency of release of gonadotropin releasing hormone (GnRH) from the hypothalamus and blunt the pre-ovulatory LH (luteinizing hormone) surge, and maintain the high levels of progesterone
Medroxyprogesterone acetate
Medroxyprogesterone acetate (INN, USAN, BAN), also known as 17a-hydroxy-6a-methylprogesterone acetate, and commonly abbreviated as MPA, is a steroidal progestin, more potent than progesterone. It is used as a contraceptive, in hormone replacement therapy and for the treatment of endometriosis as well as several other indications. As a progestin it works as per Desogestrel.
Norethisterone
Norethisterone (INN, BAN), also known as Norethindrone (USAN), is a synthetic oral progestin with weak oestrogenic and androgenic properties. It has actions similar to those of progesterone but also functions as a more potent inhibitor of ovulation. The hormone has been used in treating amenorrhea, functional uterine bleeding, endometriosis, and for contraception.
Oestradiol sulphate / Oestradiol valerate (salts of oestradiol
Generally refers to the 17-b-isomer of oestradiol, which is the most potent form of mammalian oestrogenic steroids. In humans, it is produced primarily by the cyclic ovaries and the placenta. It is also produced by the adipose tissue of men and postmenopausal women. Oestradiol enters the female organs, breasts, hypothalamus, pituitary and interacts with the oestrogen receptor. The receptor then enters the nucleus and regulates gene transcription. Oestrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary.
Oestriol
Oestriol is only produced in significant amounts during pregnancy as it is made by the placenta. During pregnancy, oestriol levels can be measured to give an indication of the general health of the fetus.
DHEA-S is produced by the adrenal cortex of the fetus which is converted to oestriol by the placenta. If levels of “unconjugated oestriol” are abnormally low in a pregnant woman, this may indicate a problem with the development of the child. It has also been approved for the treatment of post-menopausal hot flashes. If it binds to the oestrogen receptor it acts as per oestradiol sulphate.
Mestranol
Mestranol is a 3-methyl ether of ethinyl oestradiol. Ethinylestradiol is orally bio-active and the oestrogen used in almost all modern formulations of combined oral contraceptive pills. It binds to the oestrogen receptor, increasing the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary. Mestranol is a biologically inactive prodrug of ethinylestradiol to which it is demethylated in the liver with a conversion efficiency of 70%. The combination of an oestrogen with a progestin suppresses the hypothalamic-pituitary system, decreasing the secretion of gonadotropin-releasing hormone (GnRH).
Mefanamic acid
NSAIDs are analgesic, anti-inflammatory, and antipyretic. Mefanamic acid inhibits the COX-1 and COX-2 enzymes, reducing the production of prostaglandin synthesis, by prostaglandin synthase. This
reduction in prostaglandin synthesis is the reason for the reduction in the symptoms of pain that are temporarily reduced.
Tranexamic acid
Tranexamic acid competitively inhibits the activation of plasminogen to plasmin (via binding to the kringle domain). Plasmin degrades fibrin clots, fibrinogen, and other plasma proteins, including the procoagulant factors V and VIII. Tranexamic acid binds to both the strong and weak receptor sites of the plasminogen molecule. In patients with hereditary angioedema, inhibition of the formation and activity of plasmin by tranexamic acid may prevent attacks of angioedema by decreasing plasmin- induced activation of the first complement protein (C1). Tranexamic acid also directly inhibits plasmin activity, but higher doses are required than are needed to reduce plasmin formation.
