Week 2 pt 2 Flashcards

1
Q

1) ___% or less of all women during menstrual lives (not caused by pregnancy) have amenorrhea
2) What are the 2 kinds of amenorrhea?

A

1) 5%
2) Primary and Secondary

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2
Q

1) Define secondary amenorrhea
2) Define oligomenorrhea

A

1) Menstruating women without menstruation for 3 months in individuals with hx of regular cycles or for 6 months in those with irregular cycles.
2) Bleeding occurring less frequently than every 35 days (>35days)

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3
Q

Menstruation ceases due to one of what 2 things?

A

1) Disrupted endocrine function along HPO axis or
2) Abnormality in genital outflow tract

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4
Q

What are 4 causes of amenorrhea?

A

1) Pregnancy (most common)
2) HP dysfunction
3) Ovarian dysfunction
4) Alteration in genital outflow tract

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5
Q

What are some Sx of pregnancy?

A

Breast fullness, weight gain, nausea, absent menses

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6
Q

1) Define Hypothalamic-pituitary (HP) dysfunction
2) What occurs with this?
3) What does this ultimately lead to?

A

1) Disruption or alteration of pulsatile GnRH secretion
2) Anterior pituitary gland not stimulated to secrete LH & FSH > Lack of folliculogenesis, no ovulation, & no corpus luteum
3) Leads to lack of increased sex hormone production & minimal endometrial proliferation > no menstruation

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7
Q

Hypothalamic-pituitary (HP) dysfunction: What are the causes of this?

A

1) Altered catecholamine (dop, epi, norepi) secretion & sex steroid hormone feedback
2) OR alteration of blood flow through HP portal plexus (i.e., tumor)

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8
Q

1) Define Primary ovarian insufficiency
2) What are some causes of this?

A

1) Follicles are exhausted or low in number
2) Chromosomal causes: Turner syndrome, X chromosome long arm deletion
Other causes: Savage syndrome, premature menopause, autoimmune ovarian failure

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9
Q

How can alteration of the genital outflow tract cause amenorrhea?

A

Obstruction prevents menstrual bleeding (if ovulation occurs)

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10
Q

Asherman syndrome:
1) What is it? What can it cause?
2) How do you Tx it?

A

1) Scarring of uterine cavity; amenorrhea
2) Most cases corrected with surgical lysis of adhesions
-Severe cases often refractory & require estrogen postoperatively to stimulate endometrial regeneration
-Balloon or IUD for some cases to prevent further adhesions (keeps the uterine walls separated)

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11
Q

What medical Hx should you take for amenorrhea?

A

Past illnesses
FHx of delayed puberty
LMP
h/o amenorrhea
Exercise amount (per day & week)
Dietary (restrictions, special diets)
Eating disorders
Medications
Illicit drug use
Psychiatric Hx
Other conditions

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12
Q

What should amenorrhea PE include?

A

-Tanner staging
-Breast development or no?
-Other stages of puberty met?
-Genital tract anatomy
-Uterus present?
-Hirsutism or acne (or both)
-BMI measurement
-Careful genital exam

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13
Q

1) What imaging can be done for amenorrhea?
2) What lab studies can be done for it?

A

1) Imaging with US, MRI, CT
2) Pregnancy (hCG), TSH, PRL, Estradiol, FSH

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14
Q

How do you Tx amenorrhea? Give examples

A

Correct the underlying pathology (if possible)
-Ex. Treat pituitary adenoma: hyperprolactinemia causing amenorrhea & galactorrhea
-Ex. Treat underlying cause of hypothyroidism with thyroxine replacement
-Ex. Oligo-ovulatory/anovulatory with PCOS: clomid (clomiphene citrate) to induce ovulation
-Ex. Hypogonadotrophic hypogonadism, induce ovulation with pulsatile GnRH

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15
Q

What are the goals of amenorrhea Tx? Give an example

A

Help the woman to achieve fertility (if desired)
Prevent of complications of the disease process
-Ex. estrogen replacement to prevent osteoporosis

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16
Q

Abnormal Uterine Bleeding (AUB):
1) Define Abnormal Uterine Bleeding (AUB)
2) Define Anovulatory Uterine Bleeding (AUB)
3) Give examples of Anovulatory Uterine Bleeding (AUB)

A

1) Abnormal uterine bleeding: vaginal bleeding not regular, not predictable, and not associated with premenstrual signs and symptoms that usually accompany ovulatory cycles.
2) Irregular bleeding that is associated with anovulation and unrelated to anatomic lesions of the uterus
3) PCOS, exogenous obesity, or adrenal hyperplasia

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17
Q

List and describe 2 etiologies of AUB (abnormal uterine bleeding)

A

1) Amenorrhea due to HP dysfunction with no genital tract obstruction: estrogen deficiency > no bleeding
2) Oligo-ovulation and anovulation with AUB: constant, noncyclic blood estrogen concentrations slowly stimulate the growth and development of endometrium
-Progesterone-induced changes do not occur > amenorrhea leads to intermittent sloughing over time

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18
Q

List and define 3 causes of abnormal uterine bleeding (AUB)

A

1) Ovulatory dysfunction (most common cause overall):
Relative estrogen deficiency due to HP dysfunction if no genital tract obstruction
2) Other nonstructural causes: Coagulopathy, endometrial factors (i.e. endometriosis), iatrogenic (breakthrough bleeding on hormonal contraceptives)
3) Structural Causes: Cervical or endometrial polyps,
Adenomyosis, Leiomyoma (uterine fibroid), Uterine or cervical cancer

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19
Q

How do you Dx AUB?

A
  1. Always rule out early pregnancy & its complications
  2. Exclude anatomic causes
    Pelvic exam (including speculum) +/- pelvic u/s to eliminate other sources
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20
Q

What labs can you use in the Dx of AUB?

A

1) hCG testing, CBC, TSH, cervical cancer screening, +/- STI testing (if high risk)
2) Basal body temperature chart or ovulation predictor kit also options

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21
Q

List and describe 2 diagnostics for AUB

A

1) TVUS: Can evaluate endometrial stripe (thickness) to evaluate for endometrial proliferation (can lead to endometrial cancer)
Normal: during menstruation 2-4mm
2) Endometrial biopsy: Do if anovulatory with abnormal bleeding; concern regarding endometrial hyperplasia

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22
Q

Define the following AUB terms:
1) Polymenorrhea
2) Menorrhagia
3) Metrorrhagia
4) Menometrorrhagia
5) Dysfunctional uterine bleeding

A

1) Abnormally freq. menses at intervals of less than 24 days
2) Aka hypermenorrhea; excessive and/ or prolonged menses (>80mL + >7 days) occurring at normal intervals
3) Irregular episodes of uterine bleeding
4) Heavy and irregular uterine bleeding
5) Bleeding caused by ovulatory dysfunction

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23
Q

Heavy menstrual bleeding (menorrhagia):
1) How common is it in healthy women of reproductive age?
2) It’s the reason for up to ____% outpatient clinic visits by women

A

1) Occurs in up to 14%
2) 20%

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24
Q

Acute AUB: How do you assess this?

A

1) Assess for hemodynamic stability (vitals), anemia, & pregnancy
2) Obtain description of current bleeding episode and recent & usual bleeding patterns
3) Complete history can help suggest PALM-COEIN categories
4) Rule out obvious causes requiring immediate surgery (trauma, lacerations, etc.)
5) Prompt control and organic pathology ruled out
6) Imaging usually delayed until bleeding controlled & patient is hemodynamically stable
-May need sooner for other symptoms (i.e., significant pain)

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25
Q

1) What are the initial labs for AUB?
2) What are the other labs?

A

1) HCG, CBC, coagulation tests (PT, PTT, INR), iron, ferritin, T&S
2) Thyroid, liver, creatinine, BUN

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26
Q

How do you Tx acute AUB?

A

1) Acute/Emergent: IVF, PRBCs
2) Heavy bleeding episode (intermittent): High-dose estrogen and progestin therapy; combo OCPs advocated for in the acute phase
-NSAIDs to normalize prostaglandins
3) Surgery

27
Q

When should you use surgery for acute AUB?

A

1) For failure of medical therapy & bleeding which precludes medical therapy
2) Failure of initial therapy (within 12-24 hours)

28
Q

Describe when to use the 5 different surgeries for acute and chronic AUB

A

1) Hysteroscopy with D&C to remove remaining endometrium
Selective embolization of uterine vessels (interventional radiology)
Balloon tamponade if emergent treatment required to stop bleeding
Endometrial ablation only if other treatments unsuccessful, the pt has no plans for future childbearing, and endometrial/uterine cancer r/o as cause of AUB
Hysterectomy (rarely) as last resort, for endometrial cancer/hyperplasia

29
Q

Chronic AUB:
1) What is the goal of Tx?
2) What is the main Tx?
3) What is an alternative Tx?
4) What if there’s no response to Tx?

A

1) Ensure regular shedding of endometrium and regulation of uterine bleeding
2) Progestational agent x >10days (progesterone challenge test)
-Most common: medroxyprogesterone acetate (Depo-Provera); when stopped, uterine withdrawal bleeding expected with 7-10days
3) Alternative: oral contraceptives (OCs)
Suppress the endometrium and establish regular, predictable withdrawal cycles
4) If no response to treatment, likely requires specialty (surgical) care.

30
Q

Hyperandrogenic disorders: What should you initially look into with these?

A

Use/abuse of androgenic drugs (anabolic steroids)

31
Q

Hirsutism:
1) Define it
2) What are the 2 origins you should consider?

A

1) Excess terminal hair (dark, thick, coarse) in a male pattern of distribution
2) Consider familial origin vs pathologic
a) Idiopathic: often familial; most common cause of non-pathologic
b) PCOC: most common cause of pathologic

32
Q

What does Hirsutism originate?

A

Starts on lower abdomen & around nipples, then chin & upper lip, then between breasts & lower back
+/- acne

33
Q

Hirsutism: What can you use to Dx it? Describe

A

Modified Ferriman-Gallwey scale: Score of 1-4 for 9 areas (next slide)
a) Normal: < 8
b) Mild: 8-15
>8 = hirsutism diagnosis
c) Moderate-severe: > 15

34
Q

Virilization: Where does it start? Where does it spread?

A

1) Starts with enlargement of the clitoris
2) Then temporal balding, deepening of voice, involution of the breasts, remodeling of limb-shoulder girdle, & hirsutism

35
Q

What are 4 causes of excess androgen production?

A

1) PCOS
2) Testosterone-secreting tumors
3) Adrenal disorders
4) Iatrogenic and idiopathic causes

36
Q

How do you define PCOS in a patient? Explain

A

Defined by Rotterdam Criteria (at least 2 of the 3 criteria):
Clinical or biochemical hyperandrogenism
Oligo-ovulation or anovulation (irregular menstrual cycles or oligomenorrhea)
Polycystic ovaries (ultrasound)
*Adolescent girls should meet all 3 criteria

37
Q

What must you rule out when diagnosing PCOS?

A

Other endocrine disorders that mimic PCOS: CAH, Cushing syndrome, hyperprolactinemia

38
Q

What approach should you use for PCOS evaluation?

A

Obtain history (hirsutism, acne, alopecia)
Identify underlying serious medical conditions in need of treatment
Assess emotional impact of hirsutism
Plan personalized approach

39
Q

What should PCOS eval PE include?

A

Assess degree of hirsutism, acne, androgenic alopecia
Thyroid
Breasts
Cushing syndrome (truncal weight gain, round face, limb muscle wasting)
Acanthosis nigricans
Bimanual pelvic exam

40
Q

List and describe the 3 labs used in PCOS Dx to rule out other disorders

A

Basal serum 17-hydroxyprogesterone levelto exclude late-onset CAH due to 21-hydroxylase deficiency
Serum prolactin & TSH levelsto exclude hyperprolactinemia (with or without thyroid dysfunction) and hypothyroidism
24-hour free urinary cortisolor overnight dexamethasone suppression test to exclude Cushing syndrome

41
Q

PCOS Evaluation:
1) What imaging and why?
2) What types of metabolic eval?(patients with classic PCOS and/or HAIR-AN) Why?

A

1) Pelvic ultrasound to exclude significant ovarian pathology
CT or MRI to detect androgen-secreting tumors of adrenals
2) 2-hour oral glucose tolerance test to exclude DM (or HbA1C)
Fasting serum lipid levels (checking for metabolic syndrome)

42
Q

1) What does PCOS Tx depend on?
2) What does initial therapy include? How long can it take to see improvement?

A

1) Patient presentation & desires
2) Combination oral contraceptive (COC) containing estrogen & progestin
Peripheral antiandrogen may be added to oral contraceptive to treat hirsutism (i.e., spironolactone – most common in U.S.)
May take 6 months to see improvement (maximum effect up to 2 years)

43
Q

81

A

Local hair removal usually required (cosmetic results)
Shaving, depilatory creams, electrolysis, laser therapy, and/or intense pulsed light
Plucking hairs discouraged (discomfort, scarring, folliculitis)

44
Q

Describe Tx of insulin resistance in PCOS

A

1) Occurs in up to 70% (95% of obese women)
2) T2DM risk
3) CVD risk
4) OSA risk
5) Counseling for weight loss, nutrition, exercise, & other lifestyle changes to reduce risk of DM & CVD
6) Consider metformin for some patients to reduce insulin resistance & anovulation

45
Q

Hyperandrogenic insulin resistance & acanthosis nigricans (HAIR-AN):
1) What is it? What does it cause?
2) What does it put you at increased risk for?

A

1) Inherited hyperandrogenic disorder; extremely high levels of circulating insulin
2) Increased risk of dyslipidemia, T2DM, HTN, & CVD

46
Q

Congenital Adrenal Hypertrophy (CAH):
1) What is it?
2) What is the most severe/ classic form?
3) Describe the milder (nonclassic) forms

A

Increased adrenal androgen production most commonly caused by 21-hydroxylase deficiency
Most severe form (Classic): virilization of female infant (ambiguous genitalia) or virilization + life-threatening salt wasting
Milder forms (Nonclassic) more common and may appear later in life
S/Sx: terminal body hair, acne, subtle alterations in menstrual cycles, and infertility, may also have polycystic ovaries on u/s

47
Q

1) How do you Tx nonclassic CAH?
2) What about classic?

A

1) Nonclassic CAH: may not require tx or may need supplementing glucocorticoids (prednisone)
Classic (dx in childhood): hormone replacement therapy (hydrocortisone/cortisol; aldosterone replacement)

48
Q

Infertility:
1) ____% fertile couples conceive after 1 year of frequent attempts
2) _________% couples in U.S. infertile (15% unexplained)

A

1) 85%
2) 10-15%

49
Q

1) Define primary infertility and give an example
2) Define secondary infertility

A

1) Occurs without any prior pregnancy
-Ex: azoospermia (absence of sperm), endometriosis, tubal occlusion
2) Occurs following previous conception

50
Q

Successful conception requires what 6 things?

A

1) Ovulation of a competent oocyte
2) Production of competent sperm
3) Subsequent fertilization
4) Generation of a viable embryo
5) Transport of the embryo into the uterine cavity
6) 1Successful implantation of the embryo into the endometrium

51
Q

Describe the cervical factors of infertility

A

1) Spinnbarkeit: Profuse, watery mucus produced by the cervix during few days before ovulation
2) Patient seen during immediate preovulatory phase (day 12-14 of 28-day cycle) to assess quality
3) Amount & clarity recorded
4) Should stretch to at least 6.5 cm
5) pH should be > 6.5

52
Q

Male infertility (20-40%):
1) What should Hx include?
2) What about exam?
3) What initial lab?

A

1) coitus frequency, pregnancies sired, genital tract infections (mumps, prostatitis), genital/inguinal surgery or trauma, exposures, excessive alcohol/cigarettes, environmental heat, meds (ex CCBs)
Exam:
location of urethral meatus, testicular size estimated, assess for varicocele
Labs:
Semen analysis after 2-4 days of abstinence
Sperm production and development: ~70 days
Abnormal spermatogenesis 40% of male fertility causes

53
Q

Describe further testing for male infertility (depending on DDX)

A

Genetic evaluation (if azoospermia or very low #)
FSH, LH, testosterone levels (primary vs secondary hypogonadism)
Prolactin level
Epididymal sperm aspiration
Testicular biopsy

54
Q

Describe Tx for male coital factors

A

1) “Scheduled intercourse” every 1-2 days during periovulatory period (days 12-16 of 28-day cycle)
2) Avoid lubricants toxic to sperm
3) Reduce (or cease) use of alcohol & smoking
4) Discourage use of saunas, hot tubs, & tight underwear

55
Q

IVF-ET with ICSI (effective for male factor) requires what?

A

1 motile sperm for each egg

56
Q

List and describe 3 treatments for ovulation factors

A

1) Fertility drugs: correct luteal insufficiency in unexplained infertility
-clomiphene (Clomid) most commonly used
2) U/S & carefully timed hCG administration: if no ovulation with clomid
3) Induction of more frequent ovulation for oligomenorrhea (menses > 35 days): Technique depends on diagnosis (i.e., thyroid disease, hyperprolactinemia, PCOS, etc.)

57
Q

Describe the main complication of ovulation induction

A

1) Excessive stimulation of ovaries ovarian hyperstimulation syndrome (OHSS)
2) Multiple pregnancy (8-10%) may occur with ovulation induction treatment (clomiphene)

58
Q

1) Describe uterine factors if infertility
2) What do all the tubal factors of infertility have in common?

A

1) Seldom the cause; ex fibroids or endometrial polyps
2) Occlusion

59
Q
A

Fimbrial end (most common)
Mid-section – postoperative or TB infection
Isthmus-cornual – congenital, mucus plugs, endometriosis, tubal adenomyosis, or prior infection

60
Q

Evaluation of uterine & tubal factors:
100

A

Hysterosalpingography (HSG) or laparoscopy to diagnose tubal abnormalities (click me)
Helps check patency of fallopian tubes
Hydrosalpinges (singular = hydrosalpinx)
Damage & blockage of end of fallopian tubes (fluid-filled & edematous)

61
Q

Treatment of tubal factors

A

May require surgical treatment
>10% conceptions after repair of diseased tubes = ectopic pregnancies
*Overall, for women, if HSG normal or abnormal and further workup required, hysteroscopy and/or laparoscopy are the next options.

102

62
Q

103

A

Laparoscopy identifies unsuspected pathologic conditions in ~30% unexplained fertility
Preferred for substantial adhesions or endometriosis
Endometriosis most common finding
Other possible causes/findings: pelvic inflammatory disease (PID), appendicitis, adhesions
Often IVF preferred over surgery (because of high success