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Menopause Practice > Ch10: Prescription Therapies > Flashcards

Ch10: Prescription Therapies Flashcards

1
Q

depo provera

Conditions when risks outweigh benefits (4)

A 
BP >160/95
Vascular disease
DM with vascular disease or DM >20 year duration
Stroke
Ischemic heart disease
Multiple risk factors for CVD
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2
Q

Most biologically active estrogen

A

Estradiol

primary source from ovarian follicle

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3
Q

Most abundant circulating endogenous estrogen in postmenopausal women

A

Estrone

converted from androstenedione secreted by adrenal cortex

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4
Q

Major estrogen in pregnancy

A

Estriol

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5
Q

Vaginal estradiol that exerts systemic effects

A

Femring

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6
Q

Marketed conjugated equine estrogens (CEE)

A

Prempro
Premphase
in combination with synthetic medroxyprogesterone acetate

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7
Q

Marketed synthetic conjugated estrogens

A

Cenestin (CE-A)
Enjuvia (CE-B)
no synthetic CE product is approved for osteoporosis

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8
Q

Marketed estradiol

A

Oral: Estrace, Gynodiol, Innofem
Transdermal: (gels)Divigel, Estrogel, Elestrin, (spray)Evamist, (emulsion)Estrasorb, (matrix patch)Alora, Climara, Estradot, Menostar, Minivelle, Vitelli, (reservoir patch)Estraderm
Vaginal: Estrace, Estring, Femring, Vagifem, Yuvafem, Imvexxy
considered bio identical

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9
Q

Marketed esterified estrogen

A

Menest, mixture containing 75-85% estrone

not indicated for osteoporosis

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10
Q

Marketed estropiprate

A

Ogen, oral form of estrone sulfate, solubility day and stabilized by piperazine
approved for prevention of osteoporosis

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11
Q

Marketed ethinyl estradiol

A

Femhrt

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12
Q

Tamoxifen

Indicated treatment and antagonist/agonist effect on tissue

A 
Primary prevention of breast ca in high-risk premenopausal and postmenopausal women (49% reduction in invasive ER pos breast ca)
Antagonist: breast
Agonist: bone, liver, uterus
Liver: decreases LDL, increases HDL
VMS: 50% women report hot flashes
VTE/PE: increased risk
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13
Q

Raloxifene

Indicated treatment and antagonist/agonist effect on tissue

A

Osteoporosis retention and treatment and prevention of invasive breast ca in high-risk postmenopausal women
Agonist: bone
Antagonist: breast (76% breast ca reduction after 3y use)
Neutral: uterus, vagina
VTE/PE risk: increased
VMS: hot flashes less intense than seen with tamoxifen

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14
Q

Bazedoxifene

Indicated treatment and antagonist/agonist effect on tissue

A 
Treatment of osteoporosis 
Agonist: bone
Antagonist: breast, uterus
Neutral: vagina
VMS: mild hot flashes
VTE: increased
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15
Q

Ospemifene

Indicated treatment and antagonist/agonist effect on tissue

A

Treatment of dyspareunia
Agonist: vagina, uterus
VTE: increased

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16
Q

Toremifene

Indicated treatment and antagonist/agonist effect on tissue

A

Treatment of advanced estrogen sensitive breast ca, adjuvant treatment of early breast ca
Agonist: weaker on uterus than tamoxifen, liver, bone
Antagonist: breast
Prolonged QT interval which may lead to ventricular arrythmia

17
Q

Lasofoxifene

A

Treatment of osteoporosis

Agonist: bone, vagina, uterus

18
Q

USPSTF recommends use of low to moderate dose statin therapy for primary preventions where all (3) these criteria are met:

A
  1. Age 40-75 years
  2. Presence of one or more CVD risk factors: dyslipidemia, DM, HTN, smoking
  3. Calculated 10-year risk of a CV event of 10% or greater
19
Q

AEs of statins (4)

A

Myalgias 3-5%
Myopathies 0.2-.2%
New-onset DM 9-27%
Hepatoxicity <1%

20
Q

Myalgias

A

Muscle pain
Flu-like symptoms
NL CK levels

21
Q

Myopathy

A

Muscle weakness

+/- elevated CK levels

22
Q

Myositis

A

Muscle tenderness due to inflammation
Elevated CK
Leukocytosis

23
Q

Myonecrosis

A

Muscle injury

Elevated CK levels

24
Q

Rate

A

Number of events per number of participants per time interval

25
Q

Relative risk

A

Rate of disease/outcome of interest in exposed group divided by rate of disease/outcome of interest in unexposed group

26
Q

Absolute risk or attributable risk

A

Risk difference between exposed and unexposed groups

“How many additional cases per year?”

27
Q

Number Needed to Treat (NNT)

A

Reciprocal of AR (absolute risk)

“How many people need to be treated to result in one less negative outcome?”

28
Q

Potential adverse events of estrogen therapy and estrogen-progesterone therapy (list 11)

A 
Uterine bleeding
Breast tenderness, sometimes enlargement
Nausea
Abdominal bloating
Fluid retention in extremities
Changes in the shape of the cornea, contact lens intolerance
Headache, sometimes migraine
Dizziness
Mood changes, particularly with progestin
Angioedema
Gallstones, pancreatitis
29
Q 
Coping strategies for ET or EPT adverse events:
Fluid retention (4)
A

Restrict salt
Maintain adequate water intake
Exercise
Try mild prescription diuretic

30
Q

Coping strategies for ET or EPT adverse events:

Bloating (3)

A

Switch to low dose non-oral continuous estrogen
Lower progestogen
Switch to another progestin or to micronized progesterone

31
Q 
Coping strategies for ET or EPT adverse events:
Breast tenderness (5)
A 
Lower estrogen dose
Switch to another estrogen
Restrict salt
Switch to another progestin
Cut down on caffeine and chocolate
32
Q

Coping strategies for ET or EPT adverse events:

Headaches (6)

A

Switch to non-oral continuous estrogen
Lower dose of estrogen or progestogen or both
Switch to continuous-combined regimen
Switch to progesterone or a 9-norpregnane derivative
Ensure adequate water intake
Restrict salt, caffeine and alcohol

33
Q 
Coping strategies for ET or EPT adverse events:
Mood changes (7)
A

Investigate pre-existing depression or anxiety
Lower progestogen dose
Switch progestogen
Switch from systemic progestin to progestin intrauterine system
Change to continuous-combined EPT regimen
Ensure adequate water intake
Restrict salt, caffeine, and alcohol

34
Q

Coping strategies for ET or EPT adverse events:

Nausea (4)

A

Advise taking oral estrogen tablets with meals or before bed
Switch to another oral estrogen
Switch to non-oral estrogen
Lower estrogen or progestogen dose

35
Q

Coping strategies for ET or EPT adverse events:

Bleeding (2)

A

Lower dose of estrogen or progestogen

Switch to a non-progestogen combined therapy (bazedoxifene SERM)

36
Q

contraindications for ET or EPT (9)

A

Undiagnosed abnormal genital bleeding
Known, suspected, or history of breast ca, except in appropriately selected patients being treated for metastatic disease or with oncology involvement
Known or suspected estrogen-dependent neoplasia
Active or history of DVT, PE
Active or recent (<1y) arterial thromboembolic disease (CVA, MI)
Liver dysfunction or disease
Known or suspected pregnancy
Known hypersensitivity to ET or EPT
Porphyria cutaneous tardis

37
Q

List 6 main types of estrogen

A

Human estrogen (17beta estradiol, estrone, estriol)
Animal-derived estrogen (conjugated equine estrogen)
Synthetic estrogen (CE-A, CE-B)
Synthetic estrogen analogs with steroid molecular structure (ethinyl estradiol)
Synthetic estrogen analogs without a steroid molecular structure (stilbesterol derivatives, not used for menopause-related therapy)
Plant-based estrogens without a steroid skeleton (phytoestrogens, not prescription products)

38
Q

Compare and contrast 4 human estrogens

A

Estradiol: 17 beta estradiol, most biologically active, secreted in ovaries, converts to estrone
Estrone: weaker, 50-70% less active, most abundant circulating endogenous estrogen in postmenopause, conversion of androstenedione secreted by adrenal cortex to estrone by peripheral tissues, converts to estriol
Estriol: weakest, only 10% as active as estradiol, major estrogen in pregnancy
Estetrol: synthesized exclusively during pregnancy by human fetal liver, very weak estrogen, not FDA approved for use in the US

39
Q

Bazedoxifene and CEE combination, good alternative for:

A

Women who do not tolerate progesterone therapy, history of irregular bleeding associated with a thickened endometrial stripe

Menopause Practice (5 decks)

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