Menopause Flashcards

1
Q

Menopause diagnosis

A

Diagnosed after 365 days of amenorrhea with no obvious pathologic cause

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2
Q

Average age of menopause

A

Average age 52 (+/- 7 years)
○ No relationship between menarche and age of menopause
○ Childbearing, height, weight, and prolonged use of OC’s do not influence age of menopause

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3
Q

_____ is associated with early menopause

A

Smoking

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4
Q

Lab values when diagnosing menopause

A

↓↓ Estradiol (<20 pg/mL) and ↑↑ FSH level (21–100 mU/mL) are helpful in
establishing the diagnosis

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5
Q

A large portion of the female population lives about one-third of their lives
without ______

A

estrogen

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6
Q

_______ = permanent cessation of menstruation after bilateral
oophorectomy or ablation of ovarian function (ie, by chemotherapy or radiation)

A

Induced menopause

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7
Q

_______ = menopause reached at or before age 40 and can be natural or induced

A

Premature menopause

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8
Q

_______ = menstrual cycle and hormonal changes that occur a few years
before and 12 months after the final menstrual period resulting from natural

A

Perimenopause

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9
Q

Cycle length _____ with age on average

A

decreases

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10
Q

Why does cycle length decrease with age?

A

The decrease is a result of shortening of the follicular phase, with the luteal phase length remaining constant

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11
Q

↓↓ estrogen levels trigger (via negative feedback loop) a _____ in FSH levels (diagnostic marker of menopause)

A

Increase

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12
Q

Perimenopause has two stages

A
  1. EARLY - (-2)
    a. Menstrual cycle = regular
    b. Cycle length changes by 7 days or more (i.e. length is now 24 days vs. 31)
  2. LATE - (-1)
    a. Interval of amenorrhea of > 60 days
    b. Increased variability in cycle length
    c. FSH is usually > 25 IU/L
    d. Most women begin to experience symptoms including
    i. Vasomotor symptoms
    ii. Sleep disturbances
    e. Duration typically 1-3 years
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13
Q

Premature Menopause/Premature Ovarian Failure

A

Spontaneous amenorrhea before age 40

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14
Q

Etiology of Premature Menopause

A

○ May have a familial component
○ 30% may be an autoimmune reaction against the ovary
○ Severe infections of the reproductive tract
○ Increased prevalence in genetic conditions affecting the X chromosomes
(i.e. fragile X syndrome, turner syndrome)

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15
Q

Can Menopause be Prevented?

A

No
Nothing can prevent menopause(ovarian function cannot be prolonged
indefinitely), nothing can be done to postpone its onset or slow its progress

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16
Q

Menopause - Physical Changes to the reproductive tract

A

a. Atrophic changes
i. Vaginal epithelium- can lead to Atrophic vaginitis
ii. Cervix - can lead to Dyspareunia
iii. Uterine - beneficial for those with endometriosis and uterine myomas (become asx)
iv. Ovarian - ↓↓ size

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17
Q

Menopause - Physical Changes to the urinary tract

A

a. Atrophic changes
i. Bladder - Atrophic Cystitis
ii. Urethra - Urethral Caruncle formation
b. Recurrent UTI’s

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18
Q

Menopause - Physical Changes to the breasts

A

Regression of breast size

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19
Q

Atrophic Vaginitis pathogenesis

A

■ Smooth, shiny, pale epithelial surface due to increasingly sparse
capillary bed
■ ↑in vaginal PH
■ ↑bacterial invasion due to disappearance of lactobacilli

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20
Q

Atrophic Vaginitis S/S

A

■ Pruritus, burning, soreness, dyspareunia
■ Leukorrhea
■ Easy to have mild vaginal bleeding from the walls

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21
Q

Atrophic Vaginitis

A

Based on patient SX and PE

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22
Q

Atrophic Vaginitis treatment

A

○ Water -soluble lubricants
○ Vaginal estrogen preparations preferred (vs. systemic combo’s)

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23
Q

Atrophic and Recurrent Cystitis

A

● Characterized by urinary urgency, frequency, incontinence, and
dysuria
● Marked estrogen deficiency may produce atrophic changes in these
organs similar to those of the vaginal epithelium
● Recurrent urinary tract infection may also develop as a result of
estrogen deficiency

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24
Q

Urethral Caruncle

A

● Benign fleshy outgrowth at the urethral meatus

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25
Q

Hot Flushes (Vasomotor Symptoms)

A

The most COMMON and characteristic symptom of peri-menopause
● Present in 75% of women

26
Q

The most COMMON and characteristic symptom of peri-menopause

A

Hot flashes

27
Q

Hot Flashes

A

● Begin with a sensation of pressure in the head, much like a headache
● Progresses in intensity until the physiologic flush occurs
○ Characterized as a feeling of heat or burning in the face, neck, and chest
● Followed immediately by an outbreak of sweating
● Palpitations may also be experienced

28
Q

Pathogenesis of hot flashes

A

○ Exact mechanism is unknown
○ Estrogen presence and then withdrawal
○ Excitation of sweat glands results from sympathetic cholinergic fibers, and
cutaneous vasodilation is under the control of tonic α-adrenergic fibers

29
Q

Hot Flushes treatment

A
  1. OCP= TREATMENT OF CHOICE (TOC)
  2. Progestins - Second line treatment
    a. Avoid in patients with breast disease
  3. Clonidine
  4. SSRI’s and SNRI’s - Second Line Treatment
    a. Most common vanlaxofine 35.7 mg
  5. Black Cohosh (herbal) - modest effects (concern with stimulation of breast
    and uterine tissues)
  6. Gabapentin - ↓↓ hot flashes by 50-80% (comparable to estrogen in studies!).
    However sedation is a major side effect limiting its use.
  7. Tibolone (synthetic steroid)
30
Q

TOC for hot flashes

A

OCP

31
Q

Osteoporosis

A

● Systemic skeletal disorder:
○ ↓↓ bone mass
○ Deterioration of bone tissue
○ ↑↑ in fragility of bone
○ Susceptibility to risk of fracture

32
Q

Women can lose up to ______% of their bone mass in the 5–7 years after menopause

A

10

33
Q

Most common site of fractures are

A
  1. Vertebral body
  2. Proximal femur
  3. Distal forearm/wrist
34
Q

Osteoporosis pathogenesis

A
  1. Bone resorption is ↑↑
  2. Bone formation is ↓↓
  3. Peak bone mass is ↓↓
35
Q

Estrogen administered postmenopausally is ______

A

protective against osteoporosis

36
Q

TOC for diagnosis and monitoring of osteoporosis

A
  1. DEXA scan
  2. Bone mineral density (BMD) reports via a T score:
    a. T score = # of standard deviations (SD) ↑↑ or ↓↓ the mean bone mineral density for
    sex-matched young normal controls
37
Q

Osteoporosis treatment

A

a. Calcium = Minimum 1200 mg
b. Vitamin D (800-1000 IU/d)
c. Smoking cessation
d. Avoid alcohol
e. Weight bearing and muscle strengthening exercise
f. Bisphosphonates
g. Calcitonin (peptide hormone)
h. Estrogen
i. Used to be the mainstay of therapy for prevention and treatment of postmenopausal
osteoporosis. However, health risks > benefits
i. Parathyroid hormone

38
Q

Sexual Dysfunction during menopause

A

Hypo-estrogenic state leads to atrophy of the vagina (atrophic vaginitis)

39
Q

Symptoms of vaginal atrophy include:

A

● Dyspareunia (painful intercourse)
● Reduced sexual functioning
● Diminished sensation
● Lessened secretions

40
Q

Sexual Dysfunction (vaginal atrophy) treatment

A

● Local estrogen cream (preferred vs. systemic)
● Testosterone - modest improvement in libido

41
Q

Postmenopausal Period (stage +1)

A

● The first 6 years following the final menstrual period (FMP)
● 12 months following the FMP marks the end of the
menopausal transition (MP at day 363?)
● FSH continues to ↑↑

42
Q

When do you treat women with menopausal symptoms?

A

No rx required = If ovarian function is maintaining some uterine bleeding
● If having hot flushes with ovarian function = rx low dose OCP’s

43
Q

Estrogen HRT Therapy - Indications

A

Some findings suggest estrogens prevent common conditions of aging, such as:
Alzheimer’s disease and Congestive Heart Disease
Estrogen therapy has only been proven to be effective in the following:
1. Prevention of osteoporosis
2. Treatment of vasomotor symptoms
3. Treatment of vulvovaginal atrophy

44
Q

HRT Complications

A
  1. Endometrial cancer
  2. Breast Cancer
  3. Thromboembolic Disease
  4. Stroke
  5. Uterine Bleeding
  6. Gallbladder Disease
  7. Lipid Metabolism
45
Q

Estrogen stimulation of endometrium unopposed by progesterone, causes _____

A

ENDOMETRIAL PROLIFERATION, HYPERPLASIA, and NEOPLASIA (AKA Hyperplastic endometrium).

46
Q

It is recommended that ____ be added to ET to reduce the risk of endometrial
hyperplasia or carcinoma

A

progesterone

47
Q

Risk Factors and protective factors for breast cancer

A

a. Risk Factors
i. Early age menarche
ii. Older age at menopause

b. Protective Factor
i. Early oophorectomy
c. Many studies have been published since 1974 regarding HRT and breast cancer.

48
Q

Thromboembolic disease risk with HRT

A

a. OCPs increase risk
b. Affects synthesis of coagulation factors via liver
○ Increased risk
c. Use of transdermal estrogens is probably associated with ↓risk when compared with oral estrogens

49
Q

Stroke risk with HRT

A

↑ risk noted in both EPT and estrogen-alone arm

50
Q

Uterine Bleeding risk with HRT

A

a. Estrogen-Progestin pts = Occurs in the majority of patients given estrogen/progestin
combos
i. Common in the first several months, does not indicate serious pathology
1. If the bleeding is heavy or prolonged, = biopsy

51
Q

Gallbladder Disease risk with HRT

A

A. Estrogens cause ↑↑ amounts of cholesterol to collect in bile
a. Results in ↑↑ synthesis of cholesterol
b. Bile normally has a 75–90% cholesterol
i. small ↑↑ = stone formation

52
Q

Hormone Replacement Therapy contraindications

A

a. Undiagnosed abnormal vaginal bleeding
b. Known, suspected, or hx of breast cancer
c. Active DVT, PE or hx of these conditions
d. Arterial thromboembolic disease (MI,
Stroke)
e. Liver dysfunction or disease
f. Estrogen-dependent neoplasia

53
Q

Indications for HRT use:

A
  1. Hot Flushes
  2. Atrophic Vaginitis
  3. Prevention of Osteoporosis
54
Q

Management Guidelines for Hot flashes using HRT

A

● Standard dosage of oral estrogen
○ 0.3–0.625 mg of conjugated equine estrogens (CEE’s) (ex- Premarin)
○ 0.5 mg oral estradiol
● 0.025 mg transdermal estradiol
● Higher doses may be necessary to relieve hot flashes

55
Q

Management Guidelines for HRT: Atrophic Vaginitis

A

● Vaginal preparations are preferred over systemic estrogens
○ These preparations are available in the form of:
■ Creams (ie, CEEs or estradiol 0.25–2g PM for 2 weeks, followed by 2x/wk)
■ Tablets (10 μg estradiol given nightly for 2 weeks, followed by 2x/wk)
■ Rings (estradiol releasing rings, which remain in place for 3 months at a time)

56
Q

Management Guidelines for HRT
3. PREVENTION OF OSTEOPOROSIS

A

ORAL
● PREVIOUS HIGHER DOSING
○ 0.625 mg of CEE
● Lower dosing also prevents bone loss, just not as well as higher doses
○ 0.3 mg of CEE’s, & 0.5 mg of micronized estradiol
■ TRANSDERMAL
● 0.05- 1mg of transdermal estradiol
● 0.025-mg transdermal patches
● low-dose(0.014 mg/d) estradiol approved for prevention of osteoporosis

57
Q

80–90% of women will experience some vaginal bleeding initially with _____

A

Progestin-Estrogen Therapy

58
Q

HRT benefits

A

● Reduce sexual dysfunction
● Improve sleep problems
● Improve hot flushes and night sweats
● Reduce aching joints/muscles
● Improve vaginal dryness
● Prevents bone loss and osteoporotic fractures
● HRT may reduce colorectal cancer risk

59
Q

Bioidentical Hormones (BHT)

A

Many women express a preference for bioidentical hormones (BHT), with the expectation that they are safer, with comparable efficacy.
● Bioidentical hormones are plant-derived compounds that have the same chemical and molecular
structure as those of hormones produced by the human body.
● Pharmacists can custom prepare and package (compound) bioidentical hormones according to a
physician’s specifications.

60
Q

Synthetic ESTROGEN

A

These are hormones that are made from chemical sources that approximate the hormones the human body makes.
Also refers to Premarin (CEE), although made from a natural source (horse urine), it isn’t bio-identical (i.e. the same structure as endogenous estrogen)

61
Q

Bio-identical Hormone Therapy

A

Forms of estradiol, estone, and estriol which are synthesized from a plant chemical extracted from Yam’s and Soy. They do not approximate your hormones; they have the same exact chemical structure as endogenous estrogen. The body can’t distinguish the difference