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Pharm III > Lecture 10 (GYN)-Exam 5 > Flashcards

Lecture 10 (GYN)-Exam 5 Flashcards

1
Q

Cervical Dysplasia Summary: AGC
* What are they?
* Common or rare?
* Associated with what?
* What do you need to do?

A
  • Abnormal cells that original from the endocervix or endometrium
  • Rare - < 1% of cervical cytology
  • Associated with premalignant or malignant disease in 30% of cases
  • Colposcopy and endometrial biopsy
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2
Q

Polycystic ovarian syndrome (PCOS)
* Often presents as what?
* Too much of what?

A

Often presents as abnormal uterine bleeding
* Too much LH in follicular phase of menstruation (≥ 2x FSH secreted)

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3
Q

Polycystic ovarian syndrome (PCOS)
* Theca cells produce too much what? What does that cause?

A

Theca cells produce too much androstenedione
* Cannot all get converted to estradiol
* Some gets converted to estrone in fat cells
* Increases estrogen negative feed back stopping the release of FSH
* Continuous high levels of LH and no LH surge – NO OVULATION

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4
Q

Polycystic ovarian syndrome (PCOS)
* Why too much LH?

A

Why anterior pituitary produces too much LH not well known -> possible association with insulin resistance

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5
Q

PCOS
* What does high levels of androstenedione cause? (3)
* What does insulin resistance cause? (2)

A

High levels of androstenedione
* Hirsutism
* Male pattern baldness
* Acne

Insulin resistance
* Obesity
* Acanthosis nigricans

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6
Q

PCOS
* What happens because of lack of ovulation? (2)

A
  • Amenorrhea or oligomenorrhea
  • Heavy menstrual bleeding
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7
Q

PCOS
* How do you dx it?

A
  • High LH:FSH ratio
  • High androstenedione
  • Diagnostic imaging: ± ovarian follicles
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8
Q

Pcos - treatments
* Why weight lost?(4)

A

Goal: 5 to 10%
* Decreases insulin resistance
* Reduces hirsutism
* Regulates menstrual cycles
* Improved response to fertility treatments

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9
Q

Pcos - treatments
* Why metformin?

A

Improves insulin sensitivity and weight loss
* Regulates menstrual cycles
* No longer recommended as first-line for all patients

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10
Q

Pcos - treatments
* What is first line for androgen excess? How does it work?

A

CHC or progestin only contraception
* Provides progestin / suppress ovarian hormones
* Increases the concentration of sex hormone binding globulin (SHBG)
* Decreases concentration of circulating androgens
* Cycle regulation

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11
Q

Pcos - treatments
* What is second line of androgen excess? What does it not do? CI?

A
  • Spironolactone
  • Does not regulate the menstrual cycle
  • CI: pregnancy
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12
Q

Metformin in PCOS
* Can produce what? Alters what?
* Positive effect on what?
* How does it effect weight?

A

Can produce ovulatory cycles
* Alters insulin’s effect on ovarian androgen synthesis to allow return of ovulation

Positive effect on blood glucose and hyperinsulinemia
* Weight loss (10lbs)

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13
Q

Metformin in PCOS
* Inhibits what? What does that cause?
* Not as effective as what?

A

Inhibits ovarian gluconeogenesis and androgen synthesis
* Less androgens to convert into estrone that persistently promotes LH release

Not as effective as CHC therapy

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14
Q

Metformin in PCOS
* Recommended for patients with what?

A

Recommended for patients with
* Unsuccessful weight loss with diet and exercise
* Continued symptoms of high androgens after 6 months of CHC therapy

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15
Q

Pcos – Women not seeking pregnancy
* What is first line? What does it cause? (4)

A

CHCs first-line
* Provides daily progestin
* Antagonizes endometrial proliferative effects of estrogen
* Decreases effects of high androstenedione
* Provides contraception

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16
Q

Pcos – Women not seeking pregnancy
* What is the dosing guidelines for CHC?

A

≤ 35 mcg of ethinyl estradiol/day

Anti-androgenic progestins recommended
* Desogestrel
* Drospirenone
* Norgestimate

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17
Q

Pcos – Women not seeking pregnancy
* What do you give for patients with contraindications to CHCs?
* WHat are the routes?

A

Progestins only

Oral, IM, IUD:
* Oral: medroxyprogesterone 5 or 10mg for first 10 to 14 days every one to two months

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18
Q

Pcos – Women not seeking pregnancy
* How does progestins only work?

A

Antagonizes endometrial proliferative effects of estrogen

Does not decrease effects of high androstenedione
* Drospirenone with some effects

May or may not provide contraception

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19
Q

*

PCOS – Women seeking pregnancy
* What is first line?

A

First-line: weight loss

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20
Q

*

PCOS – Women seeking pregnancy
* What else can be first line besides weight loss? How does it work?

A

First-line: letrozole-> Aromatase inhibitor
* Inhibits the estrogen negative feedback
* Promotes follicle growth
* Stimulates ovulation

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21
Q

PCOS – Women seeking pregnancy: Letrozole
* replaces what?
* Highest what?
* What is the regimen?

A
  • Replaces historic clomiphene
  • Highest cumulative pregnancy and live birth rate (80% vs 30 to 40% with clomiphene)
  • Regimen: 2.5 to 7.5 mg PO daily on days 3 to 7 of the ovarian cycle
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22
Q

When is menarche, menstruation and menopause?

A
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23
Q

Prolactin
* Necessary for what?
* Synthesized and secreted from what?

A
  • Necessary for synthesis and maintenance of milk production
  • Synthesized and secreted from lactotrophs in the anterior pituitary
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24
Q

Prolactin
* How is it regulated?Inhibited? stimulated?

A

Regulated by the hypothalamus
* Inhibited by a constant release of dopamine (prolactin inhibiting factor)
* Stimulated by thyrotrophin releasing hormone (prolactin stimulating factor)

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25
Q

Galactorrhea
* What is it? What is the MCC?

A
  • Abnormal lactation
  • MCC - lesions of hypothalamus, pituitary
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26
Q

Galactorrhea:
* What are the other causes (besides lesions)(4)

A
  • Drugs – dopamine antagonists (antipsychotics, antidepressants metoclopramide, etc)
  • Hypothyroidism
  • Renal dysfunction
  • Manual stimulation
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27
Q

*

A
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28
Q
  • Evaluation of Galactorrhea
A
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29
Q

Galactorrhea treatments
* What are the different types of txt?(4)

A
  • Patient reassurance
  • Stopping or switching medications
  • Dopamine agonists
  • Surgery: Prolactinomas > 10 mm
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30
Q
A
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31
Q

*

Antipsychotic induced Galactorrhea
* What are the different treatment options?(3)
* MC occurs w/?

A

Treatment options
* Lower the dose
* Switch to alternative prolactin-sparing antipsychotic->Not ideal if clinically stable
* Add a full / partial dopamine agonist-> Aripiprazole

MC with risperiodone

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32
Q

Mastitis
* MC in what setting?
* WHat are initiating factors?

A
  • MC in the setting of breastfeeding
  • Initiating factor = milk stasis (prolonged engorgement, incomplete or inefficient feeding)
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33
Q

Mastitis
* What are the sxs?

A

Warm, erythema, edema, pain to breast plus systemic symptoms
* Fever, myalgias, chills, malaise, and flu-like symptoms

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34
Q

*

Mastitis
* What are MCC?
* May be complicated by what?

A

MCC Staphylococcus aureus (MRSA / MSSA)

May be complicated by abscess formation

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35
Q

*

Mastitis
* What is first line?
* Rarely requires what?
* What is the duration?

A

First-line: outpatient antibiotics (ex. Breastfeeding: cephalexin, clinda, augmentin, diclocycline) (No breastfeeding: Bacrtrim and doxy)
* Rarely requires IV antibiotics
* Duration – 10 to 14 days

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36
Q

Mastitis:
* Besides antibiotics, what are the additional txt?(4)

A
  • I and D abscesses
  • Cold compresses
  • NSAIDS
  • Pumping / breastfeeding
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37
Q

Breast cellulitis in non-lactating females
* Common or uncommon?
* What are the sxs?
* WHat is uncommon?
* What are the MC organisms?
* What is the txt?

A
  • Uncommon
  • Erythema, edema, pain to breast
  • ± axillary lymphadenopathy
  • Systemic symptoms uncommon
  • MC organisms Staph and Strep
  • Empiric treatment similar to mastitis
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38
Q

Breast cellulitis in non-lactating females
* What is the imaging?

A
  • ± ultrasound
  • Mammogram usually recommended
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39
Q
A
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40
Q

Fibrocystic Changes
* MC what?
* Ages?
* Thought to be due to what

A
  • Most common benign breast disease - ~50% of women of reproductive age
  • Most common ages 30-50
  • Thought to be due to hormonal imbalance: Estrogen
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41
Q

Fibrocystic Changes
* What are the sxs?

A
  • Multiple, usually bilateral TENDER mobile masses in the breast
  • Cyclical bilateral breast tenderness, most prominent just before menstruation
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42
Q

Fibrocystic Changes
* What are the red flags?

A

Red Flags – recurrent or severe symptoms, solid masses, nipple abnormalities, edema, skin changes, unilateral discharge

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43
Q

Fibrocystic breast disease treatment
* What is first line?(5)

A
  • Imaging
  • Patient reassurance
  • Physical support (bra)
  • Warm or cold compresses
  • Acetaminophen or NSAIDs
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44
Q

Fibrocystic breast disease treatment
* What is second line?

A

If 6-month trial of first-line therapies unsuccessful
* Tamoxifen 10mg PO daily
* Danazol
* Adjustment of CHC or hormone replacement therapies

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45
Q

*

Breast Cancer
* MC type and area?

A

MC ductal carcinoma / upper outer quadrant

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46
Q

SERMs vs aromatase inhibitors moa

A
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47
Q

Selective estrogen receptor modulator (Serm): Selective
* MC ones? (3)

A
  • MC tamoxifen, raloxifene, clomiphene
48
Q

Selective estrogen receptor modulator (Serm): Selective
* Antiestrogen effects on the breast decreases what?
* Important what?
* Estrogenic effects on bone?
* Tamoxifen increases risk of what?

A
  • Antiestrogen effects on the breast decrease breast cancer relapse after treatment
    * Important treatment component of estrogen and progestin receptor positive breast cancers
  • Estrogenic effects on bone decrease risk of osteoporosis
  • Tamoxifen increases risk of endometrial cancer
49
Q

Selective estrogen receptor modulator (Serm)

50
Q

Selective estrogen receptor modulator (Serm)

51
Q

Serms
* What are the MC SEs? (4)
* CI?(3)

A

MC adverse effects:
* Hot flashes
* Nausea/vomiting
* Increased risk of DVT/PE
* Abnormal vaginal bleeding (tamoxifen)

CI: history of DVT/PE, pregnancy, warfarin therapy (antagonism)

52
Q

Aromatase inhibitors
* What is the MOA?

A
  • Blocks conversion of androstenedione to estrogen
  • Decreases estrogen available for binding to hormone receptor positive breast cancer cells
53
Q

Aromatase inhibitors
* What are the SEs? (4)
* CI in who?

A

Adverse effects:
* Arthralgias, joint stiffness, bone pain
* Sexual dysfunction
* Decrease bone mineral density
* Hot flashes, flushing

CI: pregnancy

54
Q

Adjunct therapy for hormone receptor positive Breast cancer: Premenopausal women
* Low and + what?
* What is first line? (how long?, decreased what?, Transition?)

55
Q

Adjunct therapy for hormone receptor positive Breast cancer: Postmenopausal women
* Low what? + what?
* What is first line? What are the examples?
* Inactive in who?

56
Q

Terminology
* What is amenorrhea? Primary and secondary?

A

Amenorrhea - absence of menstruation
* Primary Amenorrhea- no menarche by 15 years old
* Secondary amenorrhea- amenorrhea for 3 or more months with previously regular menstrual cycles

57
Q

Terminology
* What is oligomenorrhea?

A

Oligomenorrhea - reduction of the frequency of menses: interval being more than 35 days but less than six months

58
Q

Terminology
* What is menopause and precocious menstruation?

A
  • Menopause - Amenorrhea for 12 months without other apparent cause
  • Precocious menstruation - Menarche before 9 years of age
59
Q

Amenorrhea etiologies

60
Q
  • Amenorrhea evaluation
61
Q
  • Amenorrhea Treatment:
62
Q

Primary ovarian insufficiency
* two what?
* MCC?
* Other causes? (4)

A

Two serum FSH levels in menopausal rage (taken 1 month apart)

MCC – idiopathic

Other causes:
* Chemotherapy / radiation
* Infection
* Auto-immune
* Abnormal karyotype (e.g., Turners variant)

63
Q

Primary ovarian insufficiency
* What is the first line txt? (general)
* What does it cause?(3)

A

First-line treatment = hormone replacement therapy (HRT)
* decrease vasomotor symptoms (hot flashes, flushing)
* decrease cardiovascular risks
* increase bone mineral density

64
Q

Primary ovarian insufficiency
* What are the first line choices?

A

Transdermal estradiol or Oral conjugated estrogens
Plus
Progesterone 7 to 12 days per cycle

65
Q

Primary ovarian insufficiency
* What is second line?

A

Second-line = CHC
* Patients seeking contraception

66
Q

Functional hypothalamic pituitary crisis
* What is it? What are the causes? (3)

A

Chronic anovulation secondary to suppression of the hypothalamus-pituitary axis (HPA)
* Stress
* Excessive exercise
* Body weight loss

67
Q

Functional hypothalamic pituitary crisis
* Why do you want to do txt? (4)

A
  • Restore HPA function
  • Preserve BMD
  • Restore ovulation
  • Improve fertility
68
Q

Functional hypothalamic pituitary crisis
* What is the first line txt?

A

Correct under lying cause
* Nutritional repletion / weight gain
* Stress reduction

69
Q

Functional hypothalamic pituitary crisis
* What is the second line txt?
* What is not recommended?

A

Pharmacologic treatment (short course)
* Transdermal estradiol and cyclic progesterone
* Second-line: CHCs (patients seeking contraception)

Bisphosphonates not recommended

70
Q

FYI

Amenorrhea – specific treatments

71
Q

FYI

Amenorrhea – specific treatments

72
Q

Heavy menstrual bleeding (HMB)
* What is it?

A
  • Menstrual bleeding > 80mL/cycle or > 7days
  • Bleeding that impacts quality of life (social, professional, familial, etc)
73
Q

Heavy menstrual bleeding (HMB)

75
Q

HMB treatments

76
Q

HMB treatments

77
Q

Tranexamic acid
* What is it?
* MOA?

A

Synthetic derivative of the amino acid lysine

MOA:
* High affinity for lysine binding sites of plasminogen
* Blocks these sites
* Prevents binding of plasmin to the fibrin surface
* Antifibrinolytic effect

78
Q

Tranexamic acid
* What are the SE?
* CI?

A

Adverse effects:
* N, V, D
* Myalgias
* Abdominal pain
* Headache
* Venous thromboembolism
* Color vision disturbance

CI: History of VTE

79
Q

Acute severe bleeding
* What do you need to do if hemodynamically unstable?

A
  • Stabilize – Fluids, blood
  • Emergent dilation and curettage initial treatment of choice
  • Alternative (patient expected to be stable for 3-4hours)->High-dose conjugated equine estrogen
80
Q

Acute severe bleeding: High-dose conjugated equine estrogen
* What is the dose?
* What does it cause? (2)
* Primary SE?

A
  • 25mg IV Q4-6 hours
  • Cessation of bleeding approximately 5 hours
  • Stabilization of endometrium
  • Primary adverse effect = nausea and vomiting
81
Q

Acute severe bleeding
* What is the txt of hemodynamically stable?

82
Q

dysmenorrhea
* What is it?

A

Crampy abdominal pain with or just before menses

83
Q
  • dysmenorrhea
84
Q
  • dysmenorrhea
85
Q

Dysmenorrhea treatment
* What is first line?

A
  • Topical heat
  • NSAIDs (IBU, naproxen, mefenamic acid)
  • Start 1-2 days prior to menses onset
86
Q

Dysmenorrhea treatment
* What is second line? What does it cause?

87
Q

Dysmenorrhea treatment

88
Q

Premenstrual syndrome vs premenstrual dysmorphic disorder
* What happens in both? (4)

A
  • Cyclic pattern of symptoms occurring in the last week of the menstrual cycle (luteal phase)
  • Resolves with menstruation
  • Cannot be attributable to other medical problem
  • Impacts normal daily functioning
89
Q

Premenstrual syndrome vs premenstrual dysmorphic disorder
* What is PMS?

A

At least one moderate to severe somatic or affective symptom must be present for at least 3 months

90
Q

Premenstrual syndrome vs premenstrual dysmorphic disorder
* What is Premenstrual dysmorphic disorder?

A
  • At least 5 symptoms must be present; 1 must be an affective symptoms
  • Occurs with the majority of cycles
91
Q

PMS / PMDD treatment
* What is the nonpharmacologic txt?

A
  • Limited efficacy
  • Mild to moderate PMS
  • Decrease intake of Caffeine, Refined sugars, Sodium
  • Increasing exercise
  • Cognitive behavior therapy
92
Q

PMS / PMDD treatment
* What is the first line txts?

A
  • SSRIs or venlafaxine (SNRI)
  • Combination hormonal contraception
93
Q

PMS / PMDD treatment
* What is the MOA of SSRI/venlafaxine?
* MOA of CHC?

94
Q

Ssris and SNRIs
* What are the dosing options?

A

Continuous vs Luteal Phase Dosing
Luteal:
* Start day 14 and discontinue with menses
* Decreased side effects
* Less effects on libido

95
Q

CHCs
* What is for PMDD? PMS?

A

PMDD
* Monophasic recommended
* 20mcg EE / 3mg drospirenone FDA approved indication
* Other monophasic combinations have similar efficacy

PMS
* Multiphasic regimens reduce physical symptoms but not mood symptoms

96
Q

What is last line for PMS/PMDD?

A
  • Severe symptoms not responding to first-line therapies
  • GnRH agonist - leuprolide
97
Q

Menopause
* What happens during perimenopause?

A
  • Menstrual cycles anovulatory
  • Irregular
  • Less estrogen and progesterone
  • Less inhibition on hypothalamus and pituitary
  • More GnRH, FSH, LH
  • High levels, erratic
98
Q

(PERI)Menopause symptoms
* What happens vasomotor?
* What happens on genitourinary?

A

Vasomotor
* Hot flashes, flushing
* > 25% of women
* Mean duration: 7.4 years

Genitourinary
* > 85% of women
* Vaginal dryness / atrophy / dyspareunia
* Increased risk of UTIs / urethritis / frequency/urgency

99
Q

(PERI)Menopause symptoms
* What happens psychological?
* Decreased what?
* Increased what?

A

Psychological
* Mood swings, poor memory, anxiety, depression

Decreased BMD

Increased risk of CVE

100
Q

Menopause treatment
* What is the nonpharm txt?

101
Q

Menopause treatment
* What is the pharm txt for mod to severe sxs?

102
Q

Menopause treatment review

103
Q

*

Hormonal therapy Contraindications

104
Q

Topical Hormone therapy
* What is the topical therapy for?
* What are the SE?(4)

A

Topical therapy
* Recommended if vaginal/GU symptoms only complaint
* More effective than oral hormone replacement
* 80-90% symptom improvement

Adverse effects:
* Vulvovaginal candidiasis, vaginal bleeding, breast pain, nausea

105
Q

Hormone therapy
* What is the oral ospemifene?

A
  • SERM – full estrogen agonist of vaginal epithelium
  • Decreases vaginal dryness and dyspareunia
106
Q

Menopausal hormone therapy (MHT): Overall consensus recommendations for MHT
* Most effective for what?
* May decrease what?
* What do you give for hysterectomy and if uterus is still present?

A
  • Most effective for vasomotor symptoms
  • May decrease all-cause mortality from heart disease
  • Estrogen only appropriate after hysterectomy; addition of progesterone required if uterus present
107
Q

Menopausal hormone therapy (MHT): Overall consensus recommendations for MHT
* Increased risk of what?
* Contraindicated in who?
* Dose, duration, routes of administration are personalized based on what?

A
  • Increased risk of VTE and stoke with estrogen-containing MHT->Risk is lower with transdermal MHT
  • Contraindicated in women with a personal history of breast cancer; highest association with progestin use
  • Dose, duration, routes of administration are personalized based on specific patient needs; age is not a sole indication of discontinuation
108
Q

FYI

Various MHT products

109
Q

Progestin only products
* What are the examples?

110
Q

Bioidentical therapy
* Personalized therapy based on what?
* Patient-specific what?
* Adjusted how?

A
  • Personalized therapy based on various hormone levels
  • Patient-specific doses compounded
  • Adjusted as needed for hormone fluctuations
111
Q

Bioidentical therapy
* Efficacy?
* Limited what?
* Same risks as what?
* Forms?

A
  • Efficacy equivalent to commercial products
  • Limited literature regarding superiority
  • Same risks as commercial products
  • Many dosage forms
112
Q

FYI

MHT Summary

113
Q

FYI

MHT Summary

114
Q

Ssris and SNRIs: First-line when MHT Contraindicated
* What is the continuous dosing effects?(4)

A
  • Decreases vasomotor symptoms
  • Decreases anxiety / depression
  • May worsen weight gain
  • May worsen sexual function
116
Q

Monitoring and follow-up

Pharm III (14 decks)

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