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Advanced Pharmacology > Women's Health > Flashcards

Women's Health Flashcards

1
Q

First Phase: Follicular phase (proliferative phase)

A
  • endometrium builds up d/t estrogen which leads to production of estradiol
  • regulated by FSH which stimulates follicles to develop and mature
  • egg released after about 14th day of menstrual cycle
  • LH surges and leads to ovulation
  • after ovulation, endometrium proliferates
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2
Q

Second Phase: Luteal phase

A
  • progesterone produced by luteum and plays big part in this phase
  • temp increases 1/2 to 1 degree farenheit
  • ovum travels as a blastocyte via fallopian tube to uterus for implantation
  • after implantation, hCG starts to be produced to help maintain the corpus luteum to support the ovum/zygote
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3
Q

Polymenorrhea

A

21 day cycle

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4
Q

oligomenorrhea

A

cycle >35 days

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5
Q

amenorrhea

A

cycle >180 days (6 months)

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6
Q

Menorrhagia

A

heavy flow

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7
Q

metrorrhagia aka menometrorrhagia

A

prolonged bleedings with no clear pattern

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8
Q

What are used in replacement therapy, contraception, and/or management of menopause

A

gonadal hormone made from cholesterol

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9
Q

estradiol

A

—most potent estrogen; secreted in the ovary by the premenopausal woman

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10
Q

estrone

A

metabolite of estradiol; 1/3 of the potency of Estradiol; primary estrogen in the postmenopausal woman; generated from conversion of androstenedione in the peripheral and
adipose tissues

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11
Q

estriol

A

another metabolite of Estradiol; much less potent than Estradiol; principal estrogen produced by the placenta

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12
Q

Conjugated Equine Estrogen

A

sulfate esters of Estrone + Equilin is a common oral estrogen used as
HRT [Premarin]

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13
Q

Synthetic estrogens—ethinyl estradio

A

undergoes less liver metabolism than naturally occurring estrogens, so can be safely used at low doses

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14
Q

SERMs

A

Nonsteroidal compounds that bind to estrogen receptors [have both estrogen and anti-estrogen effects]
-ex: tamoxifene and raloxifene

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15
Q

MOA of estrogens

A

-activated steroid-receptor complex interacts with nuclear chromatin to initiate
hormone specific RNA synthesis

  • Used for postmenopausal hormone therapy, contraception, replacement in the
    premenopausal patients who are deficient [hypogonadism, premature menopause,
    surgical menopause
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16
Q

Postmenopausal Hormone Therapy

A

 Used in vasomotor instability, vaginal atrophy
 If the woman has a uterus, progestogen must be included to reduce the risk of
endometrial cancer
 If the woman has had a hysterectomy, unopposed estrogen is used—progestins may have
negative effects on the lipid panel
 ADE are less than in those using estrogens for contraception
 Estradiol by patch or gel is also effective for postmenopausal symptoms
 Risks of HRT—increased risk of CV events and breast cancer
 Women with only GU symptoms are best treated with vaginal estrogens

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17
Q

Other uses for postmenopausal hormone therapy

A

Contraception
- Combination of estrogen and progestogen is used

Primary Hypogonadism
- Estrogen that mimics natural cycle +
progestogen to stimulate development of
secondary sexual characteristics
- Must be continued until after growth has
been completed

Premature Menopause
- Estrogen + progestogen replacement is
used

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18
Q

Naturally Occurring Estrogens

A

 Absorbed though the GI tract, skin & mucous membranes
 Taken orally, estradiol is rapidly metabolized by the liver; micronized
estradiol is available and has better bioavailability

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19
Q

Synthetic Estrogen Analogs

A

 Ethinyl estradiol, mestranol & estradiol valerate are well absorbed after oral
ingestion
 These are fat soluble, they are stored in adipose tissues, from there they are slowly released
 Synthetic estrogen analogs have prolonged action & are more potent than natural estrogens

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20
Q

Metabolism of estrogens

A

 Estrogens are transported to the blood bound to albumin or SHBG;
bioavailability of oral estrogen is low [because of 1st pass metabolism]; to
reduce 1st pass effects—give the drug transdermally, intravaginally or by
injection

 They are then hydroxylated in the liver to derivatives that are then
glucuronidated or sulfated

 The parent drugs and the metabolites are excreted into the bile and are then
reabsorbed through the enterohepatic circulation; inactive products are
excreted in the urine

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21
Q

Adverse effects of estrogen

A 
 Nausea
 Breast tenderness
 Elevation of BP
 Elevation of triglycerides
 Peripheral edema
 Increased risk of VTE and MI
 Increased risk of breast and endometrial cancer [endometrial cancer risk reduced by
concomitant use of a progestin]
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22
Q

Selective Estrogen Receptor Modulators

A

 Estrogen related compounds that display selective agonism or antagonism for estrogen
receptors—depending on the target tissue

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23
Q

SERM examples

A 
 Tamoxifen
 Toremifene [Fareston] not prescribed in US
 Raloxifene [Evista]
 Clomiphene [Clomid]
 Ospemifene [Osphena]
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24
Q

How does tamoxifen, toremifene, and raloxifene work?

A

By compete with estrogen for binding to the estrogen receptor in the breast tissue

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25
Q

Raloxifene (Evista) works by…

A

 Raloxifene also acts as an estrogen agonist in the bone, leading to decreased bone resorption, increased bone density and decreased vertebral fractures. Unlike
Tamoxifen and estrogen,
Raloxifene does not have appreciable estrogen receptor agonist activity in the endometrium [so no increased risk of endometrial cancer]
 Raloxifene also lowers total and LDL cholesterols

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26
Q

Clomiphene works by…

A

 Clomiphene acts as a partial estrogen agonist and interferes with the negative feedback of estrogens on the hypothalamus
 These effects increase secretion of gonadotrophin releasing hormone and gonadotropins—stimulating ovulation

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27
Q

What is tamoxifen used for?

A

in—metastatic breast cancer; add on therapy after mastectomy or XRT for breast cancer; prevention of breast cancer in those at high risk

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28
Q

What is Raloxifene used for?

A

prevention of breast cancer in those at high risk; prevention and treatment

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29
Q

What is Clomiphene used for?

A

used for infertility from

anovulatory cycles

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30
Q

What is Ospemifene used for?

A

—treatment of dyspareunia from

menopause

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31
Q

Pharmacokinetics of SERMs

A

 SERMs rapidly absorbed after PO administration
 Tamoxifen—metabolized by CYP450 isoenzymes
 Raloxifene—rapidly converted to glucuronide conjugates through 1st pass metabolism; undergoes enterohepatic cycling—main route is excretion through the bile into the feces

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32
Q

ADE of tamoxifen and toremifene

A

—hot flashes; nausea; endometrial hyperplasia and

malignancies have been reported with Tamoxifen

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33
Q

ADE of raloxifene

A

hot flashes and leg cramps; increased risk of DVT, PE and retinal vein
thrombosis; avoid use of Questran while taking Raloxifene

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34
Q

ADE of clomiphene

A

headache, nausea, vasomotor flushes, visual disturbances, ovarian
enlargement, increased risk of multiple births [these effects are dose related]

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35
Q

what is Progesterone

A

natural progestogen; produced in response to LH in women & by the testes in men; also produced by adrenal cortex in
both sexes

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36
Q

MOA of Progesterone

A

 In women—progesterone promotes development of secretory endometrium that
accommodates implantation of newly forming embryo
 High levels released during the luteal phase inhibit the production of gonadotropin and
prevent ovulation—if conception occurs, progesterone continues to be produced to
maintain the endometrium & reduce the uterine contractions
 If conception does not occur, release of progesterone from corpus luteum stops—this decline causes menstruation to take place

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37
Q

Therapeutic uses of progesterone

A

 Contraception

 Treatment of hormone deficiency

 Control of DUB (dysfunctional uterine bleeding), dysmenorrhea, endometriosis management and infertility

 For contraception—they are combined with estrogens

 Synthetic progestogens—progestin used in contraception are more stable to first pass
metabolism
- Desogestrel, Dienogest, Drospirenone, Levonorgestrel, Norethindrone, Norethindrone acetate,
Norgestimate, Norgestrel
- Medroxyprogesterone acetate injection [this agent is used orally as part of HRT]

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38
Q

Pharmacokinetics of progesterone

A

 Micronized progesterone is rapidly absorbed after oral ingestion
 Metabolized by liver; glucuronidated metabolite is excreted by the kidney
 Oral medroxyprogesterone acetate has a ½ life of 30 days; when given IM or SC the ½ life is about 40-50 days and gives
contraceptive activity for approximately 90 days; other progestins have ½ lives of 1-
3 days allowing for once a day dosing

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39
Q

ADEs of progesterone

A

 ADEs

  • Headache
  • Depression
  • Weight gain
  • Changes in libido

 Progestins that are derived from 19- nortestosterone possess some androgenic
activity because of their similarity to
testosterone—can cause acne and hirsutism

 Those that are less androgenic—norgestimate
and drospirenone, are preferred in women
with acne [can raise K+]

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40
Q

Antiprogestins

A

Progesterone antagonist with partial agonist activity

Use of this drug early in pregnancy usually in abortion due to
interference with the progesterone

Often combined with the prostaglandin analog Misoprostol [PO
or intravaginally] to induce contractions—uterine bleeding and
the possibility of incomplete abortion

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41
Q

Example of antiprogestin

A

 Mifepristone [RU-486]
✹Progesterone antagonist with partial agonist activity
✹Use of this drug early in pregnancy usually in abortion due to
interference with the progesterone
✹Often combined with the prostaglandin analog Misoprostol [PO or intravaginally] to induce contractions—uterine bleeding and
the possibility of incomplete abortion

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42
Q

Major classes of contraceptives (COCs)

A

 Combination on an estrogen & a progestin
 Triphasic COC attempt to mimic the natural female cycle—most contain a constant dose
of estrogen with increasing doses of progestin given over 3 successive 7 day periods
 Active pills are taken for 21-24 days, followed by 4-7 days of placebo, for a total regimen of 28 days—withdrawal bleeding occurs during the hormone free period
 Extended cycle contraception [84 pills followed by 7 days of placebo] results in less
frequent withdrawal bleeding

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43
Q

Most common estrogen COC

A

ethinyl estradiol

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44
Q

Most common progestins im COCs

A

—norethindrone, norethindrone acetate, levonorgestrel, desogestrel, norgestimate and drosperidone

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45
Q

Contraceptive patches

A 
 Ethinyl Estradiol and Norelgestromin
 Patch is applied weekly for 3 weeks to
abdomen, torso or buttocks
 4th week no patch is worn
 Efficacy comparable to COCs in women
weighing <90 kg
 Total estrogen exposure greater than with
COCs
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46
Q

Contraceptive ring

A

 Vaginal ring of Ethinyl Estradiol and
Etonogestrel
 Ring left in place for 3 weeks, then left out
for r1 week
 Efficacy, contraindications & ADEs similar
to COCs

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47
Q

Progestin Pills

A 
 Norethindrone—called “Mini Pill”
 Taken daily
 Less effective than COCs; they may
produce irregular menstrual cycles
 Can be used while breast feeding, can
be used in those intolerant to estrogen,
those that smoke or those with
contraindications to estrogens
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48
Q

Progestin Injections

A 
 Medroxyprogesterone acetate given IM
or SC every 90 days
 ADE
 Weight gain
 Amenorrhea
 Bone loss/osteoporosis
 Return to fertility may be delayed for
several months after discontinuation
 Drug should not be used for >2 years
unless patient is unable to use other
methods
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49
Q

LARCs-progestin Based Implants

A 
 Subdermal Etonogestrel
 Ensures contraception for 3 years
 Effect totally reversible when surgically
removed
 ADEs—irregular menses; headaches
 Has not been studied in women >130% of
IBW
50
Q

LARCs-progestin based

A 
 Levonorgestrel releasing IUD system
 Lasts for 3-5 years
 Suitable for those who have
contraindications to estrogens; avoid in
patients with PID or hx of ectopic
pregnancy
51
Q

Emergency Contraception

A 
 Reduces chance of pregnancy after
an episode of unprotected or
ineffectively protected intercourse
 Reduces chance of pregnancy to
0.2-3%
 High doses of Levonorgestrel or high
doses of Ethinyl Estradiol +
Levonorgestrel
 Should be taken ASAP after the
intercourse—preferably within 72°
52
Q

Alternative for emergency contraceptive

A

 Progesterone agonist/antagonist—
Ulipristal [Ella] can be used as EC
within 5 days of unprotected
intercourse

53
Q

MOA of contraceptives

A

 Estrogens provide a negative feedback on the release of LH and
FSH by he pituitary—preventing ovulation
 Progestins thicken cervical mucous, interfering with the transport of
sperm
 Withdrawal of the progestin stimulated menstrual bleeding

54
Q

ADEs of estrogen contraceptives

A 
 Breast fullness
 Fluid retention
 Headache
 Nausea
 Elevated BP
 Thromboembolism
 Thrombophlebitis
 MI
 Stroke
55
Q

ADEs of progestin contraceptives

A

 Depression
 Changes in libido
 Hirsutism
 Acne

56
Q

COCs are contraindicated for:

A

contraindicated in presence of cerebrovascular and thromboembolic disease, estrogen dependent cancers,
liver disease and pregnancy

57
Q

COCs increase risk for what kind of caner

A

cervical

58
Q

COCs decrease risk for which cancers

A

endometrial and ovarian

59
Q

COCs should not be used in

A

> 36 years and are smokers

60
Q

Androgens

A

 Steroids that have anabolic and/or masculinizing effects in both men and women
 Testosterone—synthesized by Leydig cells in the testes & in smaller amounts by thecal cells in the ovaries and adrenal gland [in both sexes]
 Other androgens secreted by the testes—5 alpha dihydrotestosterone [DHT]; androstenedione dehydroepiandrosterone [DHEA]
 Testosterone secretion by Leydig cells is controlled by gonadotrophin-releasing hormone from
the hypothalamus, which stimulates the anterior pituitary to secrete LH and FSH
 Testosterone or its active metabolite [DHT] inhibits production of these specific trophic
hormones
 Androgens are needed for—normal male maturation, sperm production, increased production
of muscle proteins, Hbg. and decreased bone resorption

61
Q

MOA for androgens

A

 Testosterone must be reduced to its active derivatives, such as DHT
 The derivatives then diffuse into the prostate, seminal vesicles, epididymis and skin
 Testosterone is converted by 5 alpha reductase to DHT

62
Q

Therapeutic uses of androgens

A

 Used for males with primary hypogonadism or secondary hypogonadism [due to failure of the hypothalamus or pituitary]
 Anabolic steroids can be used to treat chronic wasting associated with HIV or cancer
 Unapproved uses—increased lean body mass, muscle strength and endurance in athletes; DHEA has been touted as an antiaging hormone
 Danazol, a weak androgen, used to treat endometriosis and fibrocystic breast disease

63
Q

ADEs of androgens

A 
 Weight gain
 Decreased breast size
 Deepening voice
 Increased libido
 Increased hair growth
64
Q

Pharmacokinetics of androgens: Testosterone

A

 Ineffective orally
 C17 esters of testosterone are given IM
 Transdermal patches, topical g

65
Q

Pharmacokinetics of androgens: testosterone derivates

A

 Alkylation of the 17 alpha position of
testosterone allows oral administration

-Fluoxymesterone [Androxy]—
hypogonadism or metastatic breast
cancer in the male

-Oxandrolone [Oxandrin]—orally active
testosterone derivative with anabolic
activity 3-13 times that of testosterone;
used for weight gain in those with HIV or
catabolic states; used for osteoporosis
related bone pain

66
Q

ADEs of androgens in females

A

masculization, acne, growth
of facial hair, deepening of voice, male
pattern baldness, excess muscle
development, menstrual irregularities

 Pregnant women should NOT use because
of possible virilization of the female fetus

67
Q

ADEs of androgens in males

A

priapism, impotence, decreased sperm production, gynecomastia, cosmetic changes [like those seen in women], stimulate growth
of the prostate

68
Q

ADEs of androgens in children

A

abnormal sexual maturation and growth disturbances from premature closing of epiphyseal plates

69
Q

General effects of androgens are;

A

increased LDL,decreased HDL, fluid retention, edema

70
Q

ADEs of androgens in athletes

A

 In athletes—using anabolic steroids can cause premature closing of
epiphyses of the long bones—which will stunt the growth and interrupt development

 High doses may result in reduction of testicular volume, hepatic
abnormalities, increased aggression, major mood disorders

71
Q

What are antiandrogens

A

counter male hormonal action by interfering with the synthesis of
androgens or by blocking their receptors

72
Q

What antiandrogens can you take for prostate cancer

A

Flutamide [Eulexin], Bicalutamide [Casodex], Enzalutamide [Xtandi], Nilutamide
[Nilandron] act as competitive inhibitors of androgens at the target cell and
taken orally

73
Q

Antiandrogens use for BPH

A

 Finasteride [Proscar] and Dutasteride [Avodart] inhibit 5 alpha reductase resulting
in decreased formation of DHT

74
Q

What do progestins in COCs do?

A

—they suppress LH, FSH and cause the endometrium to be unfavorable for implantation

75
Q

Other scenarios where COCs can be used

A

 Regulating the menstrual cycle
 Reduction of heavy menstrual bleeding
 Management of acne
 Managing dysmenorrhea
 Managing PMS
 Reduce risk of ovarian, endometrial and colon cancers
 During perimenopause may prevent bone loss and reduce the risk of osteoporosis
 Products with Drospirenone—less like to have HTN, more likely to improve mood and lessen weight gain in those with PMS

76
Q

Overweight patients on COCs are at increased risk for…

A

stroke, MI and VTE

77
Q

COC Ring: 1 example

A

NuvaRing

78
Q

What are 3 IUDs

A

Skyla [3 years]
Liletta [3 years]
Mirena [5 years]

79
Q

Progestin alternatives

Oral Pills-35 mcg daily

A

 Norethindrone

 Many brand names—Camila, Errin, Heather, Jencycla, Jolivette, Nora-BE, Ortho Micronor, Nor-QD

80
Q

Progestin alternatives

Injectable

A

 Medroxyprogesterone acetate given IM every 90 days

 Depo-Provera; Depo-subQ Provera 104

81
Q

Progestin alternatives

Subdermal

A

 Etonogegstrel 68 mg every 3 years

 Nexplanon

82
Q

Nonhormonal contraceptive methods

A

 Vaginal spermicides [nonoxynol-9]
 Male condoms
 Female condoms
 Diaphragm [Rx required]—must be left in place 6°
 Cervical Cap [Rx required]—can be left in place 48°
 Sponge—must be left in place 6°
 Para-Guard Copper T380A IUD [RX required]

83
Q

Emergency Contraception

A

 3 FDA approved options for EC
 Progestin orally in high dose, progestin receptor modulator & Copper IUD Paraguard
 High dose estrogen/progestin combinations also can be used, but are not FDA approved—have more S/E and are not as effective as the FDA approved methods
 Progestin only options are OTC and are approved for use up to 72 hours after unprotected intercourse—Plan B, One-Step, Next Choice, One Dose, My Way
 Contain 1.5 mg of Levonorgestrol

84
Q

What is the first choice for a woman starting COCs

A

Cs should be a monophasic product, preferably with a 2nd generation progestin; cycle control may be better for some women with COCs containing 30-35 mcg of ethinyl estradiol

85
Q

Emergency contraceptive:

Ulipristal [Ella]

A

nearly 3 times more effective than the OTC options, can be
used up to 120 hours after the unprotected intercourse episode
 Requires a prescription
- effective in women up to 194 pounds

86
Q

Emergency contraceptive:

Ulipristal [Ella]

A

nearly 3 times more effective than the OTC options, can be
used up to 120 hours after the unprotected intercourse episode
 Requires a prescription
- effective in women up to 194 pounds
***OTC EC are only good for up to 154 pounds

87
Q

Emergency contraceptive:

Copper IUD

A

it can be inserted up to 5 days after

the unprotected intercourse [will then give long term contraception for 7 years]

88
Q

What changes cause menopausal symptoms

A

 Changes in estrogen levels due to decreased production by the
ovaries are thought to cause an increase in neurotransmitters [Epinephrine & NE] released from hypothalamus

 This lowers the thermoregulatory set point—and then subtle changes in core body temperature can cause sweating and blood
distribution to the periphery
 Women who smoke or have a greater body mass experience more vasomotor symptoms

89
Q

What are approved for use for menopausal vasomotor symptoms

A

estrogen alone or in combination with
progestin

-used for 5 years or less

90
Q

Contraindications for estrogen/progestin to be used for vasomotor symptosm

A

**undiagnosed vaginal bleeding, estrogen dependent malignancy

  • Relative contraindications—past DVT, migraines with aura, active endometriosis, severe liver disease, strong FH of breast cancer
91
Q

17ß estradiol

A

Estrac

92
Q

Conjugated estrogens:

A

premarin

93
Q

Synthetic conjugated estrogens, A

A

Cenestin

94
Q

Synthetic conjugated estrogens, B

A

Enjuvia

95
Q

Esterified estrogens

A

Menest

96
Q

Estropipate

A

Ogen

97
Q

Biodentical hormone therapy

A 
 Hormone based medications that
are compounded by specialty
pharmacies
 FDA does not recognize this term
nor does it approve these
hormones for use
 Formulas are inconsistent
 Not evidenced based
98
Q

Nonhormonal options

A

 SSRIs & SNRIs—Paroxetine 7.5 mg daily [Brisdelle] is only nonhormonal FDA approved med for the treatment of menopausal vasomotor symptoms

 Clonidine/Gabapentin—neither is FDA approved for vasomotor symptoms
- Clonidine—centrally acting alpha agonist thought to elevate threshold at which the body will develop flushing—perhaps decreasing number of hot flashes;
0.05-.15 mg BID
- Gabapentin—anticonvulsant, helps to manage hot
flashes through an unknown mechanism; 900 mg daily

99
Q

Drugs to treat vaginal symptoms

A

 Lack of estrogen leads to atrophy of the vaginal tissues
 Before menopause, estrogen stimulated exfoliation of the vaginal cells; as the
cells exfoliate, glycogen is released, which is hydrolyzed into glucose
 Lactobacilli in the vaginal tissues convert this glucose to lactic acid, which
maintains the vaginal pH at 3.5-4.5; without estrogens, the pH increases to 5-7.5,
lading to symptoms that may include dryness, discomfort itching, burning,
discharge and painful intercourse

100
Q

What is the main treatment of vaginal symptms

A

estrogens

101
Q

Vaginal creams

A

conjugated estrogen: premarin

estradiol: estrace

102
Q

Vaginal tables

A

estradiol: vagifem
vaginal ring
estradiol: estring

103
Q

Ospemifene

A 
 Osphena is FDA approved
 Oral estrogen receptor
agonist/antagonist, for the treatment of
moderate to severe dyspareunia
 60 mg daily PO with food
 No dosage adjustments for renal
impairment or hepatic disease
 Fluconazole and Rifampin cannot be
taken while on Osphenia
 Side effects—hot flashes, vaginal
discharge, muscle spasms and
hyperhidrosis
104
Q

Vaginal options:

A

 Lubricants—can relieve sx of dyspareunia—use immediately before intercourse
 Water based or silicone based
 Yes, Astro-Glide, Replens
 Moisturizers—should be used routinely; at least every 3-4 days
 Replens moisturizer, Luvena, KY moisturizer
 Women should be encouraged to continue
sexual activity—helps maintain active blood
flow to the vagina, which can help with
lubrication and prevent atrophy

105
Q

Bacterial Disease: Chancroid

A

caused by: Haemophillius ducreyi

RX:Prescriptions to Treat Zithromax 1 gram PO; Rocephin 250 mg IM

106
Q

Bacterial Disease: chlamydia

A

caused by: trachomatis

RX: Zithromax 1 gram PO; Doxycycline 100 mg BID x 7 days

107
Q

Bacterial Disease: Donovanosis

A

Caused By: Granuloma inguinale
Calymmatobacterium granulomatis

RX: Zithromax 1 gram PO x 2 1 days; Doxycycline 100 mg BID x
21days

108
Q

Bacterial Disease: Gonorrhea

A

Caused By: Neisseria gonorrhoeae PO

RX: 250 m g IM + Zithromax 1 gram PO
Suprax 400 mg PO + Zithromax 1 gram PO

109
Q

Bacterial Disease: Lymphogranuloma venereum

A

Caused By: Chlamydia trachomatis [serotypes L1, L2, L3]

RX: Zithromax 1 gram PO; Doxycycline 100 mg BID x 7 days

110
Q

Bacterial Disease: Nongonococcal urethritis

A

Caused By: Ureaplasma urealytium
Mycoplasma hominis

RX: 
Zithromax 1 gram or Doxycycline 100 mg BID for 7 days OR
Clindamycin 450 mg q 6° for 7days
Levaquin 500 mg for 7 days
Ofloxacin 300 mg BID for 7 days
111
Q

Bacterial Disease: Syphilis

A

Caused By: treponema pallidum

RX: r Aq. Penicillin G 2.4 million units IM
Doxycycline 100 mg BID for 14 days
[both +/- Prednisone 40-60 mg daily for 3 days]

112
Q

Bacterial Disease: Bacterial vaginosis

A

Caused By: Gardenerella vaginalis
Mobiluncus species

RX:
Flagyl 500 mg PO BID x 7 days
Flagyl gel 5 g. vaginally @ HS x 5d

113
Q

Viral Disease: CMV

A

Caused By: Cytomegalovirus

RX: Reassurance
If treatment indicated—Foscarnet or Cidofovir [with ID
consultation]

114
Q

Viral Disease: HSV

A

Caused By: Herpes simplex

RX: Acyclovir 400 mg TID for 7-10 days or 200 mg 5 times/day for
7-10 days
Valcyclovir 1000 mg BID for 7-10 days
Famcyclovir 250 mg TID for 7-10 days

115
Q

Viral Disease: HPV

A

Caused By: Human papilloma

RX:
-Podofilox 0.5% BID for 3 days [can repeat each week for 4 cycles]

  • Imiquimod 5% TIW @ HS for 16 weeks
  • Sinecatechins [Veregen] 15% ointment TID for 16 weeks
  • Local therapies may be indicated
116
Q

Viral Disease: Molluscum contagiosum

A

REFER TO DERMATOLOGY

Caused By: Pox virus

RX: 
Glycolic acid topically
Imiquimod 5% daily [leave on 6-10°]
Tretinoin topical [0.1% cream or 0.025% gel] @ HS Salicylic acid [50-80% compounded]
K+ hydroxide topical [compounded
117
Q

 Which of the following methods of hormonal contraceptive has the
lowest failure rate with typical use?

A

 Levonorgestrel IUD

118
Q

 When prescribing the sponge as a contraceptive option, the NP
should counsel the woman that after intercourse, the contraceptive
sponge must be left in place for:

A

6 HOURS

119
Q

 The estrogen component of combines oral contraceptives:

A

 Inhibits FSH production

120
Q

A 55 y/o woman reports that she had her LMP approximately 14 months ago. She had breast cancer that was treated with XRT and chemotherapy when she was 45 years old. She has no other
pertinent PMH or other surgical history. Her chief complaint is sever hot flashes that interfere with her ability to work. Which treatment option would be best for this patient?

A

 Paroxetine

121
Q

A 26 y/o female is using injectable MPA as a method of contraception. Which of the following adverse effects is a concern
if she wishes to use this therapy long term?

A

 Osteoporosis

Advanced Pharmacology (18 decks)

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