FERTILITY AND REPRODUCTION MEDS

Card Set Information

Author:
ssilvis
ID:
198709
Filename:
FERTILITY AND REPRODUCTION MEDS
Updated:
2013-02-08 18:09:54
Tags:
MEDS
Folders:

Description:
MEDS
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user ssilvis on FreezingBlue Flashcards. What would you like to do?


  1. SEX STEROIDS-
    • -Present in males and females-diff. amounts
    • -Estrogens
    • -Androgens (Testosterone)
    • -Progestins (Progesterone)
  2. TESTOSTERONE-
    • -Development stimulated by LH
    • -Produced by:
    •       -Ovaries in females in small quantities
    •       -Testes in males in larger quantities
  3. ESTROGEN AND PROGESTERONE-
    • Estrogens- produced ovary and placenta, testes, and adrenal cortex.
    • Progesterone- produced in the adrenal glands, the gonads (specifically after ovulation in the CORPUS LUTEUM), the brain, and during pregnancy the PLACENTA.
  4. MENSTRUAL CYCLE-
    • -Begins with menstruation (3-6 days)
    • -Hypothalmus-
    •      -Releases gonadotropin-releasing hormone (GnRH) to act on  the anterior pituitary which stimulates FSH.
    • -Follicular phase-
    •      -FSH is released (ant. pit)
    •      -Estrogen secretion dominates and   increases.
    •      -Causes endometrium to proliferate
    •      -Stimulates ovulation at midcycle
    • Luteal phase-
    •      -Surge of LH started the luteal phase (ant. pit). LH SURGE TRIGGERS OVULATION!!!!!!
    •      -Triggers ovulation
    •      -LH surge causes Graffian follicle to swelland rupture resulting in ovulation
    •      -Graffian follicle turns into the corpus luteum
    •      -Preparation of uterus for pregnancy
    •      -Secretes estrogen and progesterone
    •      -If no pregnancy, corpus luteum decreases estrogen and progesterone and you menstrate.
    •      -If pregnancy, placenta secretes human chorionic gonadotropin.
    • -FSH AND LH ARE HORMONES FROM THE ANTERIOR PITUITARY!!!!!
  5. PHYSIOLOGIC EFFECTS OF ESTROGEN-
    • -Sensitize myometrium (in uterus) to oxytocin at parturition labor
    • -Stimulates secondary sex characteristics
    • -Affect mood andemotions
    • -Affect body feminine body fat distribution
    • -Enhances blood coagulation
    • -Inhibits bone resorption (STRENGTHENS THE BONES)
    • -Mild mineralocorticoid properties (SALT AND WATER RETENTION)
    • -Increase HDL (CHOLESTEROL LEVELS DECREASE)
  6. PHYSIOLOGIC EFFECTS OF PROGESTERONE-
    • -Increase basal body Temperature at ovulation and luteal phase
    • -Affects emotional state
    • -Mild mineralcorticoid properties
  7. PHYSIOLOGIC EFFECTS OF TESTOTERONE-
    • -Development of 2ndary sex characteristics in  males
    • -Growth of larynx, thickening of vocal cords
    • -Stimulates growth of penis, scrotum, seminal vesicle and prostate gland
    • -Stimulates and maintains sexual function
    • -Increases in lean body mass
    • -Stimulates skeletal growth
    • -Accelerate epiphyseal closure
    • -Incrases sebaceous gland activity and sebum production which produces acne
    • -Incrases erythropoietin in the kidneys
    • -Decreases HDL cholesterol
    • -Mild mineralcorticoid properties
  8. ESTROGENS- 2 TYPES-
    • 1.  Natural-
    • -Estradiol
    • -Conjugated estrogens (OBTAINED FROM THE URINE OF A PREGNANT MARE (HORSE)
    • 2.  Synthetic
    • -Ethinyl estradiol
    • -Mestranol
  9. PHARMACOKINETICS OF ESTROGEN-
    • -Well absorbed from GI tract
    • -Natural estrogens rapidly metabolized in the liver
    • -Synthetic estrogens are degraded (metabolized) less rapidly
    • -Most estrogens are readily absorbed from skin and MM, and vaginally
    • -Enterohepatic cycling- (ESTROGEN GOES TO LIVER AND IS BROKEN DOWN THEN GOES TO GI AND BACTERIA REACTIVATES ESTROGEN MOLECULES AND THEY ARE REASBSORBED BACK INTO THE SYSTEM)accounts for drug interactions, broad-spectrum antibiotic use alters bowel flora and rend OC ineffective.
    • -Depends on the sexual maturity of the recipient
    • -Before puberty- Stimulate development of 2ndary sex characteristics
    • -Adult female- given cycliacally induce artificial menstrual cycle
    • -Used for contraception
    • -MUST BE GIVEN WITH PROGESTERONE DUE TO ENDOMETRIAL HYPERPLASIA
    • -At or after menopause- prevent s/s of menopause, MUST BE GIVEN WITH PROGESTERONE DUE TO ENDOMETRIAL HYPERPLASIA if patient has an intact uterus.
    • -Protects against Osteoporosis- but shouldn't be prescribed for this alone use Fosamax.
    • -THE ONLY TIME ESTROGEN CAN BE GIVEN ALONE IS IF PATIENT HAS NO UTERUS!!!
  10. PHARMACOLOGICAL PREPARATIONS- what it is used for:
    • 1.  Hormone replacement therapy- Estrogen/Progesertone preapartions
    • 2.  Oral contraception/acne/dysmenorrhea-
    • Estrogen/Progesterone prepartions
    • Progesterone preparations
    • 3.  Estrogen receptor antagonist
    • -hormonal therapy for breast cancer
    • 4.  Testosterone and adrogens
    • -replacement therapy- in men with decreased levels of testosterone.
  11. ESTROGEN S/S's-
    • -breast tenderness
    • -h/a
    • -edema (NA AND H20 RETENTION)
    • -n/v
    • -anorexia
    • -changes in libido
    • -HTN (NA AND H20 RETENTION)
    • -thromboembolic disorders
    • -gallbladder disease
    • -MONITOR PTS BP FREQUENTLY.
  12. CLINICAL USE OF ESTROGENS-
    • -Replacement therapy for -
    • Primary ovarian failure (Turner's syndrome)- Estrogen will stimulate sexual characteristics.
    • Secondary ovarian failure (menopause) for flushing, vaginal dryness and to preserve bone loss
    • Contraception
    • Male Cancer- decreases the aggressiveness of the cancer.
    • CONTRAINDICATED IN PREGNANCY, UTERINE FIBROIDS, HEPATIC DISEASE, ENDOMETRIOSIS, THROMBOEMBOLIC DISEASE, AND HYPERCALCEMIA.
  13. PROGESTERONE INDICATIONS-
    • -Suppress ovarian function
    • -Contraception
    • -Dysmenorrhe
    • -Endometriosis
    • -Uterine bleeding
    • -Mifepristone-termination  of pregnancy
    • -Cancers- breast, endometrial, and renal.
  14. PROGESTERINS DERIVATIVES-
    • -Megestrol
    • -Hydroxyprogesterone caproate
    • -Medoxyprogesterone acetate
    • Synthetic
    • BIRTH CONTROL PILL NAMES TO RECOGNIZE-
    • -19 norprogestines-
    •      -Estranes- Norethindrone and Norethynodrel
    •      -Gonanes- Levonorgesterol, Desogestrel, and norgestimate.
  15. HORMONE REPLACEMENT THERAPY-
    • ESTROGENS-
    • -must be combinationwith progesterone
    • -giving estrogen alone to women who have not had a hysterectomy increases risk of endometrial cancer
    • -relieves vasomotor symptoms of meopause such as dizziness, h/a, tachycardia, palpitations, night sweats, atrophic vaginitis
    • -benefits in Osteoporsis and CV disease
    • -decreases levels of LDL and lipoproeinemia, increases levels of HDL - PROGESTERONE IS THE OPPOSITE!
  16. TREATMENT FOR HRT-
    • 1.  Oral preparations-
    •      -First pass metabolism
    •      -Hypertension
    •      -Thromboembolic d/o
    •      -gall bladder disease
    •      -induction of drug-metabolizing enzymes-metabolize other drugs faster..which we don't want...ex. seizure med.
    •      -uterine bleeding
    •      -increased r/f breast cancer-mild
    • 2.  Transdermal estradiol preparation-
    •      -physiologic levels of estradiol
    •      -consistent blood levels
    •      -Long duration of action
    •      -Convenience
    •      -Apply 1-2 x per week
    •      -Mild skin reactions
    • 3.  Vaginal administration- cream used primarily for vaginal s/s of menopause
    • 4.  Vaginal ring- releases estrogen for 3 months- helps atrophic vaginitis and releives menopause s/s
  17. WHY DOES ESTROGEN WORK FOR CONTRACEPTION?
    - It stops the pituitary gland from producing LH and FSH which causes a decreased level of estrogen.  It also supports the uterine ling to prevent BREAK THROUGH bleeding mid-cycle
  18. TREATMENT FOR HRT-
    • -cyclic or continuous replacement
    • -estrogen is for 25 days then progesterone starts on day 10 per cycle
    • -may or maynot have rx for 5-6 for menses
    • -progesterone suppresses risk of endometrial hyperplasia and r/f endometrial cancer.
  19. ORAL CONTRACEPTIVES-
    • -contain femail hormones
    • -prevent ovulation
    • -estrogen and progestin or progestin only
    • -progestin- long acting subdermal implants and Depot IM injections.
  20. ESTROGEN-PROGESTIN CONTRACEPTIVES-
    • -Monophasic
    • -same amt of progestin and estrogen throughout cycle
    • -biphasic and triphasic- mimic menstrual cycle- incrased amount after first 1/3 cycle
  21. USE OF CONTRACEPTIVES-
    • -prevent midcycle FSH/LH surge (big peak)
    • -stimulates ovualtion
    • -Indications- 21 cycle day pilss, start day 5 of menstural cycle or "Sunday start", acne, dysmenorrhea (is a result of increase in uterine prostaglandins which cause ischemia from small arteries in uterus at time of menstration.
    • -NSAIDS- prohibit prostaglandin synthesis
  22. ADVERSE EFFECTS OF ORAL CONTRACEPTIVES-
    • -risk of stroke
    • -MI, DVT
    • -thromoembolic complicaitons
    • -smokeer over age 35- do not give!
    • -caution- in GB disease, thromboembolic disease, and h/o MI or CAD
    • -contraindicated in active liver disease (where they are metabolized), breast cancer, or CA of reproductive tract
    • -increased r/f ovarian and endometrial ca
    • -increased r/f breast ca
  23. S/E OF ORAL CONTRACEPTIVES-
    • -acne better or worse
    • -hisuitism
    • -increased libido
    • -oily skin
    • -DVT
    • -nausea
    • -Mastalgia- painful breasts
    • -migraines better or worse
    • -no menses- amenorrhea
    • -weight gain
  24. POSTCOITAL CONTACEPTION RX-
    • -"The morning after pill- plan B"
    • -estrogen and progesterone
    • -not taking other contraceptives!
    • -taken 72 hours within intercourse
    • -followed by two doses 12 hours later
    • -inhibit transport of ova in fallopian tubes and later endometrium to prevent implantation of fertilized ovum
    • -adverse effects- N/V, h/a, dizziness, leg cramps, abdominal cramps
    • -comes with a pre-packaged uterine pregnancy test.
  25. ORAL CONTRACEPTIVE DANGEROUS S/E'S-
    • ACHES
    • A- abdominal pain (GB disease)
    • C- chest pain (MI)
    • H- headache
    • E- eye problems
    • S- severe leg pain (DVT)
    • STOP TAKING IF ANY OCCUR!!!!
  26. ESTROGEN INTERACTIONS-
    • -drugs which increase heaptic metabolism of OC
    • -increases possiblitly of contraceptive failure- metabolized out of the system
    • -Phenytoin, barbituates, carbamazepine, antibiotics alter intestinal flora, warfarin, cyclosporine, anti-depressants, glucosteroids, increased hepatotoxic effects with dantrolene.
  27. PROGESTIN- ONLY CONTRACEPTIVES
    • -work against egg implantation  in the uterus
    • -blunts LH surge that produces ovulation
    • -thickens and decreases cervical mucous
    • -create thin, atrophic endometrium hostile to implantation of blastocyt
    • -IUD- localized effects on the endometrium
    • -higher failure rates with progestin-only contraceptives
    • -frequent spotting
    • -amenorrhea
    • -increased r/f ectopic pregnancy
    • -Norethindrone (minipills", Medroxyprogesterone acetate- depo shot, progesterone IUD's- release a small amount locally.
  28. ALL CONTRACEPTIVES SHOULD BE TAKEN?
    AT THE SAME TIME EACH DAY TO DECREASE THE R/F BREAK THROUGH BLEEDING.
  29. ANTIESTROGENS-
    • -Have tissue specific action- work against the estrogen in  the body- meds treat infertility.
    • -med has to bind to estrogen receptors to be effective if blocked can't connect
    • -FOOL the body into thinking not enough estrogen so FSH and LH are increased to stimulate ovaries for ovulation
    • -exert tissues-specific antagonist or partial agonist effects
    • 1. Clomiphene
    • 2.  Raloxifene
    • 3.  Tamoxifen
  30. 1.  CLOMIPHENE-
    • -taken day 5 of cycle- when ovulation occurs
    • -estrogen agonist and moderate estrogen antagonist
    • -indications- anovulatory infertility
    • -antagonizes estrogen receptors in hypothalamic-pituitary-ovarian axis- all of these need to be secreting normally for med to work- can't increase them if they are not functioning normally
    • -blocks estrogen negative feedback and incrases FSH and LH secretion helps ovarin follicle development and ovulation.
    • -anovulatory d/o; infertility
    • -inhibits GnRH by inhibiting neg feedbck effects of endogenous estrogen
    • -less successful in women with decreased estrogen levels
    • -unlikely to benefit women with FSH levals at or above 40.
    • -taken days 5-10 mesntrual cycle
    • -ovulation expected 5-10 days after last dose of clomiphene
    • -adverse effects- MULTIPLE BIRTHS
  31. 2.  TAMOXIFEN-
    • -breast tissue-estrogen receptor antagonist
    • -TREATS BREAST CANCER
    • -adverse effects- N/V, hot flashes, vaginal bleeding, menstrual irregularities
    • -possibly stimulates proliferation of endometrial cells-endometrial CA
    • -possibly stimulates proliferation of endometrial cells- endometrial CA
  32. 3.  RALOXIFENE-
    • -selective estrogen receptor modulator (SERM)
    • -TREATS OSTEOPOROSIS IN MENOPAUSAL WOMEN.
    • -but allows estrogen-like effects on bone and lipid metabolims- good for bones
    • -antagonizes effects of estrogen on breast tissue
    • -estrogen antagonist in uterine tissue
    • -
  33. ANTIPROGESTINS-
    • 1.  Mifepristone-
    • -an antagonist of progesterone receptors
    • -sentisizes uterus to action of prostaglandins
    • -inhibits ovulation
    • -alternative to surgical termination of pregnancy before 9 WEEKS of pregnancy
  34. ANDROGENS- TESTOSTERONE THERAPY-
    • TREATS-
    • 1.  Hypogonadism- primary testicular failure
    • 2.  Hypopituitarism- given with growth hormone to obtain maximal effect on skeletal growth.  Occassionally used in given in GYN d/o of endometrial bleeding and osteoporosis.
  35. TESTOSTERONE-(MAIN NATURALLY OCURRING ANDROGEN)-
    • -first-pass metabolism extensive- if taken orally and some is reabsorbed so give IM or TD.
    • -given parenterally or transdermally
    • -ONLY ORAL ONE IS METHYLTESTERONE- IF NO OTHER CHOICE- RESISTANT TO HEPATIC METABOLISM BUT CAN CAUSE HEPATIC DAMAGE AND LIVER FAILURE WITH PROLONGED TX.
  36. ANDROGENS- TESTOSTERONE UNWANTED EFFECTS-
    • -infertility
    • -if given  for a long period the normal testosterone in your body will lose its effect
    • -salt and water retention with edema
    • -CA of liver
    • -impairs growth in children
    • -acne
    • -masulinization in girls
  37. SYNTHETIC ANDROGENS-
    • ANABOLIC STEROIDS-
    • 1.  Fluoxymesterone
    • 2.  Oxandrolone
    • -3 x more potent than testosterone
    • -promote wt gain and muslce development
    • -what athletes use- ABUSE
    • -counteract protein metabolism
    • -treat breast CA
    • -controlled substances
    • -increase body mass, strength, physical performance
    • -adverse eff-hepatic dysfunction, jaundice, aggressiveness, psychotic symptoms, acne, decreased testicular size and function, impotence
    • -women- masculinization, hirsuitism, deep vouce, menstral irregularities
    • -athlete abuse
  38. DANAZOL - look up what is- anabolic steroid?
    • -testosterone derivative
    • -weak androgenic and progestational activity
    • -po
    • -half life 5 hours: excreted in urine
    • -acts on pituitary gland to reduce secretion of GnRH, FSH, and LH, which leads to decreased estrogen production.
    • -RX- endometriosis, fibrocystic breast disease, gynecomastia, hereditary angioedema
    • -adverse eff.- mild hirsuitism, oily skin and acne, menstural irregulatities, hypercholsterolemia, hepatotoxicity, thromboembolic event, TERATOGENIC
    • -decreases growth rate of abnormal breast tissue
  39. ANTIANDROGENS-
    • -compete with estrogens and progesterones- inhibit gonadotropin secretion and/or compete with androgens in target organs
    • 1.  Cyproterone-
    • -androgen receptor antagonist
    • -adjunct in rx of PROSTATIC CA
    • -RX of precociuous puberty in males
    • -RX of masculinization and acne in women
    • 2.  Gonadotropin-releasing hormone analogues-
    • -decrease LH secretion which decreases testosterone synthesis by the testes
    • -Leuprolide- prostate cancer
    • -prolongs progression-free period and length of survival of men with advanced prostate cancer
    • 3.  Flutamide-
    • -androgen receptor antagonists
    • -competes with testosterone for androgen receptor
    • -RX of prostate CA
    • -adverse eff- mild gynecomastia, mild reversible hepatic toxicity
    • 4.  Finasteride-
    • -has affinity for androgen receptors in prostate gland
    • RX- BPH, and baldness
  40. ANDROGEN SYNTHESIS INHIBITORS-
    • KETOCONAZOLE-
    • -inhibit synthesis of testosterone
    • -antifungal drug
    • -inhibits CP450 enzymes inchluding those involved in steroidgenesis
    • -inhibits fungal infections and testosterone sythesis
    • -causes gynecomastia
    • -RX of prostate CA and Cushings syndrome- reduces steroid synthesis in the body.

What would you like to do?

Home > Flashcards > Print Preview