Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Pharm- Contracept
contraception drugs
| Question | Answer |
|---|---|
| What estrogen is used in all COCs | (+what kind of estrogen is it) Ethinyl estradiol, which is a synthetic estrogen |
| What form of progestin is used in COCs | (that includes: 5 divided in 4 categories Synthetic: 1st gen - Estranes: norethinedrone, 2nd gen – Gonanes: levonorgestrel, 3rd gen – Gonanes w/o Andro : Desogestrel & Norgestimate, 4th gen – Spironolactone derivative w/ anti-andro and minero: Drosperin |
| What is diethylstilbestrol | (+kind of compound) A drug not used anymore that “prevents” miscarriage. Stopped cause it also causes cancer and infertility in offspring. Diethylstilbestrol is a non-steroidal estogen |
| What is medroxyprogesterone | (2 uses, kind of compound) Used in both hormonal replacement and depot (IM long-term release) contraception. It is a chemically modified progestin |
| COC are made of | (2, general) 1.Synthetic estrogen (ethinyl estradiol), 2.Synthetic progestin |
| HRT are made of | (2~3) 1.Conjugated Equine Estrogen (equilin sulfate, estrone sulfate), 2.Chemically modified progestin (medroxyprogesterone) |
| What phase of the menstrual cycle are COC trying to mimic | Luteal phase |
| Why are COC trying to mimic the luteal phase | Luteal phase has high E and high P, which prevents the release of GnRH, LH and FSH |
| By preventing the surge in LH and FSH (especially LH) of the luteal phase, COC prevent: | Ovulation |
| What predominates in COC: E or P | (be precise) P which is in mg, E is in µg |
| Which of E or P has much more complicated interaction in the body | (explain 4 things) E only binds ER. P binds PRs but also to a lesser degree AR (androgen), ER, GR (glucocorticoid). Furthermore PR are dependent on some E. |
| What is one explanation for P to be so promiscuous with other receptors | P is a the beginning of the pathways to make E (estradiol), A (testosterone), and G (cortisol) |
| What are the effects of estrogen on the body | (9) 1.secondary sex, 2.ovulatory cycle, 3.pregnancy, 4.increase thrombosis, 5.hypertension (increase Na retention), 6.Increase TGs, HDL, decrease LDL (no net effect), Stimulate cell proliferation: 7.breast cancer, 8.uterine (endometrial) cancer, 9.vasodi |
| What are the effects of progestin on the body | (2) 1.booby development, 2.maintains pregnancy (w/o P: lining softens like at the end of menstrual cycle) |
| The increase in thrombosis w/ E can lead to | (1~2) DVT then PE |
| Discuss the potency of the different types of E | (3) Synthetic > Conjugate Equine > Natural |
| Discuss the absorption of E | Good/rapid |
| Why aren’t natural E not used in COC or HRT (2) | 1st pass effect is huge (has to be IV) + short T1/2 |
| What is the only pharmacokinetic difference btw conjugated equine and synthetic | Synthetic have even longer T1/2 (they both have low first pass effect and can be taken orally) |
| Discuss the metabolism of estrogen (5) | Mostly in the liver: 1.-OH by P450, 2.conjugated to glucoronide, 3.E-glucoronide is extred in bile, 4.cleaved by bacteria back to E, 5.reabsorbed - remember this is called enterohepatic circulation |
| How can antibiotics use prevent the proper functioning of contraceptive | Block bacteria cleaving of E-glucoronide, thus E is excreted and you get lower serum levels |
| What other drug greatly influence E levels | Dilantin (in epileptic patients) activates Cyp 3A4, and thus decrease E levels |
| What has been the trend in the past 50 years in terms of COCs (2) | Decrease the amounts, and use mutliphasic COCs |
| What was the 1st generation of COCs problem | Blood clots |
| What was the 2nd generation’s COCs name + 2 problems | Sequential. They did not work well (too little P), and caused endometrial cancer |
| What was the 3rd gen’s COCs name | Lo-dose |
| What is the current 4st gen COCs | Multiphasic (to lower P levels) |
| What are OCs with only P called (2) | POPs or minipills |
| What is the dosing range of E in COCs | 20 to 50 μg |
| Name the P used in COCs in order of potency (4, don’t include drosperinone) | LNG > DSG > NGM > NE |
| What is the advantage of triphasics | 15% less exposure to P |
| When are monophasics preferred (2) | 1.late-cycle bleeding (need more progestin), 2.mood-swings on tri-cyclics |
| Usually COCs are started with average amounts on E (30μg), when is this not the case | Fat women probably need more E |
| What is the usually cycle of monophasic COCs, in terms of taking the pill | 21 days on, 7 days off |
| What is the point of starting the pill of Sunday | No periods during the weekends |
| What are the 3 ways to start the pill | 1.Day 1 start (1st pill on 1st day of period), 2.Sunday Start, 3.Quick start (in doctor’s office) |
| What is the advantage of Day 1 start | You don’t need to use backup contraception for any time (you need 1 week for Sunday Start and Quick Start) |
| What should do if they missed one pill | Take two the next day |
| What should one do if they missed 2 pills | If week one or two: take two pill, then two pill again the next day. Supplement with a week of backup. If week three: start new pack (+ one week backup) |
| What P is used in POP (2) | Norethindrone or norgestrel |
| What doses are used in POP | The lowest needed for efficacy |
| What is very important with taking POP | You need to take it at the same exact time very day. |
| What is a very common time in a women life, when she would be told to use a POP | Lactating mother, the E in COCs can lead to vaginal bleeding in girls and gynecomastia in males |
| Other than POP (minipills) what are other P only contraceptions (3) (+ duration of each + P used in each) | 1. Depot shot (IM, medroxyprogesterone) – 3 months, 2. Implanon (subdermal implant, etonorgestrel) – 3 years, 3. IUD (levonorgestrel) – 5 years |
| What are the AE of P only OC (5 + 3 specific to one kind) | 1.higher failure, 2.irregular bleeding, 3.some women get amenorrhea (think they are pregnant), 4.acne (P activates AR), 5.depression, Depo-provera also has: 1.bone loss, 2.weight gain, 3.return to fertility delayed |
| How do COC and P-only prevent pregnancy (3) | 1.inhibit ovulation by inhibiting LH and FSH level, 2.they thicken the mucosa (physical barrier to sperms), 3.they alter the mucosal lining (sperm can’t stick) |
| How many COCs can you miss before being at risk | More than 2 and you are at risk |
| How many P-only can you miss before being at risk | Only be 3 hours late and you are at risk |
| Other than preventing pregnancies what are the other benefits of COCs | (5~6) 1.decrease ovarian cancer, 2.decrease endometrial cancer (thx to P, E does increase), 3.decrease fibrocystic disease/fibroadenomas, 4.decrease PID (blocks sperm and infections from sticking and passing through), 5.lower blood loss during menses, ~6 |
| What is the greatest AE of COCs (think back about the AE of E & P) (+ thus who should not get COCs) | Thrombosis, thus be careful or do not use in women older than 35 and smokers (this is due to Estrogen) |
| Other than thrombosis the main AE of COCs are: (5 for E, 3 for P – include name of drug for P) | Estrogen: 1.breast cancer, 2.hypertension (temporary), 3.gall bladder disease (stones, E increases stasis), 4.CVD/stroke, 5.cervical dysplasia/cancer Progesterone: 1.change HDL/LD |
| When is the increase in risk for breast cancer the highest when talking COCs | If taken before 1st pregnancy (remember: lifetime exposure to E is the reason for breast cancer) |
| What drug is linked to increase CVD/stroke risk in women taking COCs | Levonorgestrel |
| What two thinks correlate strongly with cervical cancer | Smoking, HPV |
| What are the mild AE of COCs (1 for E, 2 for P) | Estrogen: fluid retention (due to Na retention effect), Progesterone: acne/weight gain (androgen effects |
| Separate the bleeding cause by E deficiency and P deficiency: | E deficiency: early bleeding, P deficiency: late bleeding |
| What are the contraindication for COCs, (10) which ones can be fixed by using P-only (8) | 1.Hx of clots, 2.>35+smoke, 3.Hx of stroke/MI/CVD, 4.Hypertension, 5.Migraines, 6.Has to go through surgery (clots), 7.Lactating/had pregnancy, 8.high TGs, 9.has hormone sensitive cancer, 10.predispose for booby cancer |
| What is newer about Yasmin/Yaz (include 1 AE, and 1 advantage) | P is drospirenone, which is antimineralcorticoid thus less fluid retention. However K can become high. |
| Difference btw Yasmin and Yaz | Yaz is 24/4 schedule thus shorter period and thus less PMDD and less Acne |
| Describe orthe-evra (+ 1 contraindication + 1 AE) | It is patch (21/7). Does not work as well in heavy women, increase risk for clots. |
| Describe nuvaring | Ring (21/7) |
| What is the morning after pill (also called) (what is the timeline) | 2 pills containing High dose levo, also called Plan B. you have 72hrs after event (this is not an abortion pill, no ovulation, no implementation) |
| What is RU-486 (also called) (timeline) | Mifepristone, you have 49 days |
| What are the two extended cycle COCs, what is their 2 uses | Seasonale and lybrel: prevent painful periods/excessive bleeding as well as PMDD |
Created by:
mcafej02
Popular Science sets