Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

DT4-Exam 1 > Pharm-OCP/MRT- Melissa *** > Flashcards

Pharm-OCP/MRT- Melissa *** Flashcards

1
Q

List the three estrogens in order of most to least potent:

A

17-B Estradiol –> Estrone–> Estriol

*estrione tri’s to be a good estrogen, but it just cant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where are the different types of estrogen formed in the body?
(Premenopausal women/ preggos/ men and post menopausal women…)

A

Premenopausal Women:
-Ovary, estradiol mainly

Pregnancy:
Placenta: Estrone, Estriol

Men and Postmenopausal women:

  • Liver
  • Adipose tissue
  • Primarily Estrone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the synthesis of 17-B Estradiol.

By which enzyme is the reaction catalyzed?

A

Cholesterol is the basis for ALL steroid hormones…

Androstenedione –>Testosterone–> 17B-Estradiol
*requires aromatase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe how the placenta forms Estrone and Estriol:

A

DHEA–> Estrone + Estriol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How are all three estrogens excreted?

A

Renal excretion as estrogens or glucuronide/ sulfate conjugates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the effect of estrogens on female sexual organs (4):

  • follicles?
  • endomertrium?
  • vaginal epi?
  • cervical mucous?
A
  • ^ follicular growth (ovarian atrophy in large doses)
  • ^ endometrial growth
  • cornify, thicken, stratify vaginal epi
  • decrease viscosity and ^ amount of cervical mucous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe 5 roles of estrogen outside the female reproductive system:

  • skin
  • bone
  • blood
  • cholesterol
A
  • ^ vascularization, softness, and suppleness of skin
  • ^ osteoblastic activity
  • ^ renal retention of Na, Cl, H2O (bloating)
  • maintain HDL/LDL balance = low CVD risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the three physiological effects of estrogen on men?

A
  • manage bone density
  • spermatogenesis
  • behavior
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What stimulates the production of progesterone in females?

Where is it produced?

A
  • LH –> corpus luteum production in 2nd half cycle
  • HCG –> corpus luteum production in early pregnany
  • HCG –> placenta + fetal adrenal gland production of P/E in late pregnancy

Also produced in adrenal cortex and testis (important intermediate in steroid synthesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is progesterone important in promoting pregnancy (2)?
What is the role of progesterone in endometrial cycle?
How does it affect cervical mucous?

A

-*Progesterone promotes IMPLANTATION/ Maintain pregnancy
by:
- ^ development of secretory endometrium
- Decrease amount and ^ viscosity of cervical mucous

(opposite of estrogen in terms of effects on endometrium/ cervical mucous)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Events of menstrual cycle follicular phase: (3)

A
  • Pulsatile: GnRH–> LH + FSH
  • follicle growth, granulosa cells secrete estrogen
  • Estrogen–> (-) feedback on hypothal.-> keeps FSH + LH in check.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Events of mid menstrual cycle surge:

What is required to maintain surge?

A

-^ Estradiol for 36hrs –> (+) Feedback on Hypothalamus–>
^ GnRH–> LH SURGE–> Follicle rupture + ovulation
-*Progesterone required to maintain LH surge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Events of menstrual cycle: luteal phase
What happens if implantation occurs?
No implantation?

A

Ruptured follicle–> Corpus luteum–> P + E released

  • No implantation–> DECREASE P + E–> menstruation
  • Implantation–> Embryo–> HCG–> P + E stay high
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What type of synthetic estrogen is used in combination oral contraceptives (COCs)?
How common are these drugs and what is one issue with their use?

A
  • Ethinyl estradiol
  • # 1 contraceptive in US
  • Strict oral dosing regimin= poor compliance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What type of synthetic estrogen is used in post-menopausal hormone replacement therapy (MHT)?
How does the dosing compare to that in COCs?

A

conjugated estrogens–dosing is much LOWER than that in COCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Monophasic COCs:
Dosing regimin?
What dose EE is considered low dose?

A
  • 21 days active hormone + 7 days placebo (Fe or nothing)
  • Take same amount EE + prog. for 21 days
  • Must be less than 35 ug EE to be considered low dose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Multiphasic COCs:
How do these work?
Why are they good?
What are the two types?

A

Hormone dose increases for 21 days (prevent ADRs)

Biphasic- prog varies.
-2 doses progesterone + constant E

Triphasic- either prog or EE vary

  • 3 doses progesterone + constant E
  • 3 doses E + constant progesterone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Extended COCs:
How do they work?
How long is the cycle always?

A

Dosing regimen alters # of pill free days –>
Decrease hypoestrogenism–> Fewer menstrual sx.

*Cycle always 28 days, so 2 placebo days = 26 days hormone, 4 placebo days = 24 days hormone. Don’t memorize # of hormone days!!!!! Just know placebo and count.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Mircette: class + dosing regimen

A

Extended COC:

20 ug EE + desogestrel–>2 days placebo–>5 days 10ugEE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Yaz:
Dosing regimen
In addition to contraception, what was its clinical use? (2)
Salient ADR?

A

Extended COC:

  • EE + Drospiredone–> 4 placebo pills/ cycle
  • TREATS PMDD, reduces bloating (diuretic)
  • Worry about HYPERKALEMIA (dros= spiro derivative)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Yasmin: class + dosing regimen
How does it differ from Yaz?
Salient ADR?

A

Extended COC:

  • EE + Drospiredone–> 4 days placebo pills
  • Uses 10+ ug (30ug total) E to decrease w/drawal sx
  • Worry about HYPERKALEMIA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Drospirenone: What is it? Why is it important?

A
  • Derivative of spironolactone
  • Anti-mineralicorticoid activity (Hyperkalemia!)
  • Anti-androgen activity (prevent Progesterone ADRs like bloating)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Seasonale: class + dosing regimen

A

Extended COC:
Levonogestral + EE for 84 days–> 7 days placebo
*Bleed every 13 wks (3mos)

*Seasonal periods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Seasonique: class + dosing regimen

Advantages to this drug over seasonale?

A

Extended COC:
(Seasonale) but 10ug EE for 10 days instead of the 7 day placebo every three months

*Better follicular suppression + less breakthrough bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Lybrel: class + dosing regimen

A

Extended COC:
Levonogestral + EE for 365 days!
No bleeding!

*Not a coincidence that drug name is a play on the word “liberation”!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q 
*Patch (Xulane): 
Dosing regimin? 
ADRs (2)? 
Advantages?
In which population may Xulane not be as effective?
A

EE (more) + Norelgestromin (less) for 3 weeks–> 1 wk off

  • ADRs: ^ risk rash + thrombosis
  • Avoids hepatic first pass elimination
  • May not be as effective in obese patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

*Vaginal Nuvaring:
Dosing regimin?
Advantages? Disadvantages?

A

EE (more) + Etonogestrel (less) for 3 weeks–> 1 week off

  • Avoids hepatic first pass elimination
  • Better than patch for obese patients
  • Uterine first pass elimination instead!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the two synthetic estrogens? How are they used?

A
  • Mestranol: metabolized to active Ethinyl Estradiol
    (80ug M–> 50ug EE)
  • Ethinyl Estradiol: used in 2nd gen low dose COCs
    (more potent, more frequently used)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the 4 synthetic progesterone types?

A
  • Pregnanes
  • Estranes
  • Gonanes
  • Drospirenone

*These are altered in COCs while EE remains constant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Pregnanes: how are they used?

A

Injectable contraceptives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Estranes: how are they used?

A
  • Similar to 19-Norestosterone
  • hepatic metabolism
  • activity similar to E
  • used in COCs; shorter t 1/2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Gonanes: how are they used?

A
  • Similar to 19-Norestosterone but w ethyl vs. methyl group
  • Used in COCs
  • ^^^ t1/2 + bioavailability compared to estranes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Which progesterones have the MOST progestational and androgenic activity?

A

Levonorgestrel + Norgestrel

Norgestrel is in the name levonorgestrel!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Which progesterones have the LOWEST progestational and androgenic activity?
What population are these hormones good for?

A

Desogestrel + Norgestimate
Gestrodene + Drosperinone
*Good for patients with acne and PCOS

(just remember the progs are generally weak except levonorgestrel and norgestrel)

35
Q

Which progesterone has anti-androgen + anti-mineralocorticoid activity and can be used to reduce acne and weight gain?

A

Drosperinone– don’t forget hyperkalemia risk!

36
Q

What is the MOA for COCs?
How do the estrogen and progesterone influence ovulation? (3)
What are two effects of progesterone on the cervix and uterus that prevent pregnancy?

A
  • Negaitve FB on hypothalamus–> no LH/FSH surge
  • Estrogen–> Inhibit FSH
  • Progesterone–> Inhibit LH, also GnRH

Additional Progesterone Effects (prevail over estrogen)
Thicken cervical mucous–> Inhibit sperm entry
Endometrial atrophy–> Prevent implantation

37
Q

What are 3 factors leading to decreased contraceptive efficacy?

A
  • ADRs = non-compliance
  • ^ body weight
  • Drug interactions
38
Q

How long does it take for monophonic and triphasic drugs to become effective?
When do patients start a pack?

A

Pack started on 5th day of menses or first Sunday after
Monophonic: 21 days
Triphasic: 7 day

39
Q

When is failure more common–at the start or end of a pack?

A

Failure is higher at beginning of pack and associated with varying time between doses

40
Q

What are two things that can happen if patients inappropriately vary time between doses?

A
  • failure

- ^ ADRs due to hormone flux

41
Q

List 5 ADRs associated with OCPs:

A
  • N/V/ HA (~migraine) / weight gain
  • ^ cholesterol sat in bile–> ^ Gall stones
  • ^ platelet agg + ^ clotting factor synth–> thrombosis
  • ^ RAAS activation–> ^ HTN
  • Breast cancer (controversial!!)
42
Q

What type of OCP would be safe for breastfeeding woman to take less than 6wks postpartum?

A

Progestin only formulation–NO E!

mini pill

43
Q

Contraindications to OCP use (5):

A
  • Hepatic/ Biliary Diseases
  • Cardiovascular/ clotting disorders
  • pregnancy/ breastfeeding
  • estrogen dependent cancers
  • HTN/ Diabetes/ Cigarette smokers over 35***
44
Q

When is the risk for venous thromboembolism on OCPs highest?

A

During first year of treatment

45
Q

At what dose is the risk for MI/Stroke highest on OCPs?

Which patient population is at highest risk?

A

50+ug ethinyl estradiol; women with HTN at highest risk

46
Q

What are some non-contraceptive benefits associated with OCP use?

A
  • ^ bone mineral density

- Decreased acne + hirsutism

47
Q

How do OCPs decrease acne and hirsutism? What condition are these drugs good to treat?

A

^ serum hormone binding globulins–> androgen sequestration

*Good to treat PCOS

48
Q

What are three ways we can adjust OCPs to manage ADRs?

A
  • Dose of E and P
  • Ratio of E:P
  • Type of P
49
Q

Which ADRs mandate adjustment to LOWER dose of estrogen? (5)

A
  • N/V/HA/ Migraine*** (you get sick)
  • CYCLIC weight gain, leg cramps, edema*** (you retain water)
  • HYPERmenorrhea
  • HTN
50
Q

Which ADRs mandate adjustment to HIGHER dose of estrogen? (3)

A
  • Vasomotor sx. (Hot flashes)***
  • EARLY Breakthrough bleeding
  • HYPOmenorrhea
51
Q

Which ADRs mandate adjustment to LOWER progesterone?

Aka what are the ADRs of progesterone?

A

Depression: of both your mood and your boobies.

You get sad about your small boobs. Like Leah and Stacee.

52
Q

Which ADRs mandate adjustment to LESS ANGROGENIC progesterone?

A
  • Acne/ oily skin

- consistent (non cyclic) weight gain

53
Q

Which ADRs mandate adjustment to HIGHER progesterone?

A
  • LATE breakthrough bleeding
  • HYPERMENORRHEA
    (low prog effects are similar to estrogen effects)

*Switch from norgestimate–> norgestrel

54
Q

When should you be concerned about a SINGLE missed dose and how would you manage it?
When is this most likely to cause failure?

A

Days 1-21 (non-placebo)

  • Take pill as soon as discovered
  • Do not take more than 2 per day
  • Most likely to fail within first 5 days
55
Q

How would you manage missing TWO doses?

How does this vary depending on when doses are missed?

A

Day 1-14: take extra pill for 2 days + additional method for 7

Day 15-21: stop pack, start new cycle + 7 days additional method

56
Q

What is the protocol for non-nursing new mothers on OCPs? (When can they start and why?)

A

May begin COC 4 weeks after delivery; must wait because thrombosis risk

57
Q

Describe the influence of smoking on OCP efficacy:

A

P450 INDUCERS!

  • Make OCPs LESS EFFECTIVE
  • Use supplemental method or ^ dose
58
Q

List some P450 inducing drugs that might cause OCP failure/ decrease efficacy:

A
  • Carbamazepine
  • Phenytoin
  • Phenobarbital
  • Pirimidone
  • Rifampin
  • St John’s wart

*Generally Think: Anticonvulsants, Antimicrobials

59
Q

Which ABX decrease OCP efficacy? How do they do this?

A

Tetracyclines,Erythromycin, PEN V, Ampicillin

  • DECREASE GI flora
  • Less GI flora = LOWER hormone enterohepatic circulation
60
Q

What is the primary contraceptive MOA for progesterone ONLY drugs?

A
  • Only 70-80% inhibition of ovulation

- Mostly thicken cervical mucous and cause endometrial atrophy

61
Q

Describe how the mini pill works; what is the active component?
When do you start the pills?
How long until they are effective?
How often do they inhibit ovulation?

A

ONLY norgestrel or norethindrone (progesterone)

  • Begin first day of menses; same dose throughout cycle
  • Inhibits ovulation 80%
  • Requires additional method for 3 weeks
62
Q

Indications for mini pill use: (3)

A
  • Breast feeding
  • Smokers over 35yoa + other situations w/ CI estrogen
  • Migraines and depression
63
Q

Disadvantages to mini pill use: (2)

A

Easy to FAIL!!

  • Low hormones = miss one dose = FAILURE!
  • Regimen off by 3 hours = FAILURE
  • Obviously use additional method if failure suspected
64
Q

Depot Preparation:
Active ingredient?
Treatment regimen?
MOA? (2)

A 
Medroxyprogesterone acetate (pregnane)
- IM injections every 3 mos

MOA

  • Stops LH surge
  • Induces endometrial atrophy–> delay fertility
65
Q

ADRs to Depot prep? (3)

A
  • weight gain
  • insomnia
  • decrease bone at 2 years +
66
Q

*Nexplanon:

ROA, duration of use

A
  • etonogestrel based implant

- good for 3 years

67
Q

Merena:

ROA, duration of use

A
  • levonogestrel IUD

- good for 5 years

68
Q

ParaGard:

ROA, MOA, duration of use

A
  • copper based IUD
  • causes inflammation and decreased sperm motility
  • good for 10 years
69
Q

Skyla:

ROA, duration of use

A
  • T shaped levonorgestrel IUD, smallest of them all

- good for 3 years

70
Q

Liletta:

ROA, duration of use

A
  • levonorgestrel IUD

- good for 3 years

71
Q

Progestin based Emergency Contraceptives:
Which synthetic hormone is used?
What are the two preparations available and when should they be taken?
What are some ADRS and limitations to use (2)?

A

Levonorgestrel

  • Plan B (2 doses 12 hours apart Levonorgestrel + EE)
  • Plan B one Step OTC (single dose levonorgestrel)
  • Should be taken within 72 hours of unprotected intercourse
  • May cause HA and abdominal cramps
  • Decrease efficacy with ^ BMI
72
Q

What is the most effective emergency contraceptive?

A

Copper IUD inserted within 5 days of unprotected sex

73
Q

Ulipristal acetate/ Ella:

Drug class, MOA, therapeutic regimen

A

Antiprogestin ECP

  • Selective progestin reuptake modulator
  • Take within 5 days unprotected intercourse
  • Prescription only
74
Q

Octoxynol-9/ Nontoxynol-9

Drug class, MOA, ADRs

A

Vaginal spermicide

  • nonionic detergent–> ^ leakiness in sperm cell wall
  • additives may cause irritation or allergy
75
Q

What are the goals of MRT? (2)

A
  • reduce vasomotor disturbance (hot flashes)

- reduce osteoporosis

76
Q

What is the most common hormone combo used in MRT?
When is a combination MANDATED?
What is the risk of using unopposed estrogen?

A

Estrogen + Progesterone

  • **Combo mandated in women WITHOUT HYSTERECTOMY
  • **Unopposed E = ^ risk endometrial cancer
77
Q

MRT Drug Regimens (3):

A
  1. 21 days estrogen + last 10 add progesterone + 1 week off
  2. Estrogen + progesterone for first 10-13 days
  3. Continuous E+ P
78
Q

Which synthetic estrogens and progesterones are used for MRT?

A

Estrogen: conjugated estrogen
Progesterone: medroxyprogesterone or norethindrone

79
Q

Premarin/ Prempro/ Premphase:

Therapeutic use and hormone constituents

A

MRT, primarily conjugated estrogen

80
Q

Duavee:
What is it?
Therapeutic use?

A

Conjugated estrogen + SERM (bazedoxifene)

  • SERM acts as estrogen AGONIST (osteoblast^) in bone
  • SERM acts as estrogen ANTAGONIST in uterus

Treats hot flashes and osteoporosis in post menopausal women w/o hysterectomy!

81
Q

What does SERM stand for?

A

selective estrogen receptor modulator

82
Q

General ADRs of MRT? (2)

CIs? (3)

A
  • ^ risk clots esp in first year
  • ^ risk HTN + CVD in higher doses

CIs: breast cancer, estrogen dependent cancer, thrombophlebitis

83
Q

When is unopposed estrogen mandated for MRT and why?

A
  • Women WITH HYSTERECTOMY should get E ONLY

- P associated with alteration of HDL/LDL ratio

DT4-Exam 1 (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions