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EOR Exams- Review > Women's Health > Flashcards

Women's Health Flashcards

1
Q

absence of menstrual period

A

amenorrhea

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2
Q

light flow or spotting

A

cryptomenorrhea

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3
Q

heavy or prolonged bleeding @ normal menstrual intervals

A

menorrhagia

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4
Q

irregular bleeding between expected menstrual cycles

A

metrorrhagia

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5
Q

irregular excessive bleeding between expected menstrual cycles

A

menometrorrhagia

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6
Q

infrequent menstruation (prolonged cycle >35 days BUT less than 6 months)

A

oligomenorrhea

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7
Q

frequent cycle interval (<21 days)

A

polymenorrhagia

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8
Q

two types of dysfunctional uterine bleeding (DUB) and which one is more prevalent

A

1) chronic anovulation (90%)

2) ovulatory

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9
Q

what age group is chronic anovulation seen in

A

extremes of ages (early teens or periomenopausal)

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10
Q

what is chronic anovulation due to

A

disruption of the hypothalamus-pituitary axis

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11
Q

s/sxs of chronic anovulation

A

*IRREGULAR, unpredictable shedding (due to the unopposed estrogen because there is no progesterone to ovulate)

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12
Q

what is ovulatory DUB and what are the s/sxs

do you bleed?

do you ovulate?

what hormones play a part in the s/sxs?

A
  • *regular CYCLICAL bleeding
    • ovulation
  • prolonged progesterone (due to decreased estrogen levels) –> increased blood loss from endometrial vessel dilation & prostaglandins –> MENORRHAGIA
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13
Q

how do you dx DUB

A

dx of exclusion:
- must exclude organic causes (reproductive, systemic,
iatrogenic causes)
- if workup shows NO evidence of organic causes & -
pelvic exam –> DUB is dx

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14
Q

what is the workup for DUB

A

-hormone levels
-transvaginal US
-endometrial bx if endometrial stripe >4mm on
transvaginal or in women >35 y/o
- to r/o endometrial hyperplasia or carcinoma

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15
Q

tx for acute severe bleeding from dysfunctional uterine bleeding (DUB)

A
  • high dose estrogens OR
  • high dose OCPs
  • reduce dose as bleeding improves
  • dilation & curettage if IV estrogen fails
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16
Q

1st line for anovulatory dysfunctional uterine bleeding (DUB)

  • what do you use if estrogen is contraindicated
  • what another drug class that you can use to temporarily cause amenorrhea
A

-OCPs
- regulates the cycle, thins the endometrial lining &
reduces menstrual flow

  • Use Progesterone: if estrogen is contraindicated
    - e.g. medroxyprogesterone

-can use a GnRH agonist: Leuprolide (if given
continuously)

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17
Q

tx for ovulatory dysfunctional uterine bleeding (DUB)

A
  • OCPs
    -Progesterone (oral or IUD)–(e.g. Mirena reduces
    bleeding in 79-94%)
    -GnRH agonist: Leuprolide with add-back progesterone
    (to reduce SE of Leurprolide)
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18
Q

what is the last resort for dysfunctional uterine bleeding (DUB) is pharmacological medication does not work

A

Surgery:
- Hysterectomy: definitive management
-Endometrial ablation: endometrial destruction in pts
who dont want a hysterectomy

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19
Q

what is dysmenorrhea

A

painful menstruation that affects normal activities

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20
Q

primary vs secondary dysmenorrhea

A

primary:
- NOT due to pelvic pathology
- due to INCREASED PROSTAGLANDINS –> painful
uterine muscle wall activity
-Pain usually starts 1-2 yrs after menarche

secondary:
     -due to PELVIC PATHOLOGY 
     - e.g. endometriosis, adenomyosis, leiomyomas, 
       adhesions, PID
     - increased as women age (>25 y/o)
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21
Q

clinical manifestations of dysmenorrhea

A

-**diffuse pelvic pain right BEFORE or with the ONSET of
menses
- cramps last 1-3 days
- may be associated w/ HA, N/V
- +/- lower abdomen, suprapubic, or pelvic pain that may
radiate to the lower back & legs

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22
Q

what are PE findings of dysmenorrhea

A
  • can be normal
    -may have uterine tenderness but the findings are based
    on the cause
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23
Q

1st line tx for dysmenorrhea

MOA

other tx

procedure if medical tx fails

A
  • NSAIDs = 1st line
    -MOA: inhibits prostaglandin-mediated uterine activity
    (best to start before s/sxs onset and given for 2-3
    days)

-Others:
- Supportive: local heat, Vit E started 2 days prior to &
for 3 days into menstruation
-Ovulatory suppression: OCP*/ depo provera/vaginal
ring significantly reduces symptoms
- Laparoscopy: if medication fails (done to r/o
secondary causes e.g. endometriosis or PID
- Endometriosis if MC secondary cause in
younger pts!!!!
- *Adenomyosis with increasing age

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24
Q

how is premenstrual syndrome characterized

A

cluster of physical, behavioral, & mood changes with CYCLICAL occurence during the LUTEAL phase

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25
Q

definition of PMDD

A

severe PMS with functional impairment

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26
Q

clinical manifestations of PMS

physical
emotional
behavioral

A

Physical:
- bloating, breast swelling/pain, HA, bowel habit
changes, fatigue, muscle/joint paint

Emotional:
- depression, hostility, irritability, libido changes,
aggressiveness

Behavioral:
- food cravings, poor concentration, noise sensitivity, loss of motor sense

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27
Q

dx of PMS

A

-Symptoms INITIATE during the LUTEAL phase (1-2 wks before menses) and is RELIEVED within 2-3 days of the ONSET OF MENSES + at least 7 symptoms free days during the follicular phase

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28
Q

management for PMS:

lifestyle modifications

medications

A

Lifestyle modifications:
-stress reduction, exercise, caffeine & Na restriction,
NSAIDs, Vit B6 & E

Mediations:
-SSRIs: for emotional symptoms
-OCPs: induces anovulation.
*PMDD: Drosperinone-containing OCPs
-GnRH: continuous dosing w/estrogen add back if no
response to SSRI or OCP
-Bloating: Spironolactone (androgen inhibitor taken
during the luteal phase to relieve breast
tenderness and bloating)
-Refractory Breast Pain that does not resolve w/
above:
-Danazol, Bromocriptine

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29
Q

what is the workup for amenorrhea

A 
HCG
serum prolactin
FSH
LH
TSH
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30
Q

primary vs secondary amenorrhea

A

Primary:
- failure of menarche onset by age 15 (in the presence
of 2ndary sex characteristics OR
- 13 in the absence of 2dary sex characteristics

Secondary:
-absence of menses for >3 months in a pt w/
previously normal menstruation OR >6 mos in a pt
who was previously oligomenorrheic

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31
Q

etiologies of primary amenorrhea:

with the uterus present (breast present/breast absent)

A

Breast Present:
-outflow obstruction: transvaginal septum, imperforate
hymen

Breast Absent:

  - ELEVATED FSH &amp; LH = ovarian causes 
       - E.g. Premature ovarian failure (46XX)
       - Gonadal Dysgenesis (Turner's 45 XO)
  - Normal/Low FSH &amp; LH
        - Hypothalamus-Pituitary Failure
        - Puberty Delay (ex. athletes, illness, anorexia)
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32
Q

etiologies of primary amenorrhea:

withOUT the uterus present (breast present/breast absent)

A

Breast Present:

 - Mullerian agenesis (46 XX)
 - Androgen Insensitivity (46 XY)

Breast Absent (RARE)
-Usually caused by a defect in testosterone
synthesis.
-Presents like a phenotypic immature girl with
primary amenorrhea (**will often have
intrabdominal testes)

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33
Q

Etiologies of secondary amenorrhea

A

Hypothalamus dysfunction

Pituitary dysfunction
Ovarian Disorders
Uterine disorder

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34
Q

Etiologies of secondary amenorrhea: MC etiology and 2nd MC

A

Ovarian (40%)

Hypothalamus dysfunction (35%)

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35
Q

Etiologies of secondary amenorrhea:

explain hypothalamic dysfunction: MOA

A
  • MOA: Disruption of normal pulsatile hypothalamic secretion of GnRH that directly lead to subsequent decrease in FSH and/or LH
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36
Q

Etiologies of secondary amenorrhea:

explain hypothalamic dysfunction: etiologies

A

Hypothalamic disorders

anorexia (or wt loss >10 ideal body weight), exercise, stress/nutritional deficiencies

systemic disease (e.g Celiac)

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37
Q

Etiologies of secondary amenorrhea:

explain hypothalamic dysfunction: Dx (labs)

A

Normal/decreased FSH & LH

LOW estradiol

*NORMAL PROLACTIN

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38
Q

Etiologies of secondary amenorrhea:

explain hypothalamic dysfunction: Tx

A

Stimulate gonadotropin secretion:

Clomiphene
Menotropin (Pergonal)

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39
Q

Etiologies of secondary amenorrhea:

Explain Pituitary Dysfunction: examples

A

Prolactin secreting pituitary adenoma

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40
Q

Etiologies of secondary amenorrhea:

Explain Pituitary Dysfunction: Dx labs

A

DECREASED FSH/LH

*INCREASED prolactin (galactorrhea)

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41
Q

what diagnostic study should you do if you suspect pituitary dysfunction (as an etiology of 2ndary emnorrhea)

A

MRI of pituitary sella turcica

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42
Q

Etiologies of secondary amenorrhea:

Explain Pituitary Dysfunction: tx

A

surgery for tumor removal

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43
Q

how does prolactin affect GnRH

A

prolactin INHIBITS GnRH

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44
Q

Etiologies of secondary amenorrhea:

Explain ovarian disorders: examples

A

PCOS

Premature ovarian Failure: follicular failure or follicular resistance to LH/FSH

Turner’s Syndrome

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45
Q

Etiologies of secondary amenorrhea:

Explain ovarian disorders: clinical manifestations

A
  • symptoms of estrogen deficiency: “like menopause”
    • hot flashes, sleep & mood disturbances,
      dyspareunia, dry/thin skin, vaginal dryness/atrophy
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46
Q

Etiologies of secondary amenorrhea:

Explain ovarian disorders: Dx (labs)

A

INCREASED FSH/LH

DECREASED estradiol –> ovarian abnormalities

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47
Q

Etiologies of secondary amenorrhea:

Explain ovarian disorders: what test should you order to see if it an ovarian etiology or hypoestrogenic or uterine etiology

A

Progesterone Challenge Test:

+ withdrawal bleeding = ovarain etiology

  • withdrawal bleeding = hypoestrogenic or uterine etiology
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48
Q

Etiologies of secondary amenorrhea:

Explain Uterine disorder: what is it

A

scarring of the uterine cavity

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49
Q

what is Asherman’s Syndrome

A

acquired endometrial scarring 2dry to postpartum hemorrhage

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50
Q

Etiologies of secondary amenorrhea:

Explain Uterine disorder: Dx

A

Pelvic US (absence of normal uterine stripe)

Hysteroscopy to dx & treat

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51
Q

Etiologies of secondary amenorrhea:

Explain Uterine disorder: management

A

Estrogen treatment to stimulate endometrial regeneration of the denuded area

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52
Q

definition of menopause

A

cessation of menses >1 yr due to LOSS OF OVARIAN function

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53
Q

average age of menopause in the US

A

51.5

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54
Q

what is premature menopause

A

menopause before age 40

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55
Q

who is at higher risk for premature menopause

A

DM

Smokers

Vegetarians

Malnourished patients

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56
Q

clinical manifestations of menopause

A

Estrogen Deficiency Changes:

  • menstrual cycle alterations
  • vasomotor instability (including HOT FLASHES)
  • mood changes
  • skin/nail/hair changes
  • increased cardiovascular events
  • hyperlipidemia
  • osteoporosis
  • dyspareunia
  • urinary incontinence
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57
Q

characteristics of atrophic vaginitis

A

thin, yellow discharge

pruritus

vaginal pH >5.5

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58
Q

PE for menopause

A
  • decreased bone sensitivity
  • skin: think/dry/decreased elasticity
  • vaginal: atrophy thin mucosa
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59
Q

Dx of menopause (labs)

A

FSH assay = most sensitive initial test (increased FSH
>30 IU/mL)

INCREASED serum FSH, LH

DECREASED estrogen (due to depletion of ovarian follicles)

(androstenedione levels do NOT change)

predominant estrogen - estrone after menopause

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60
Q

what is the most sensitive initial test for menopause

A

FSH assay = most sensitive initial test (increased FSH

>30 IU/mL)

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61
Q

complications of menopause

A

Loss of estrogen:

  • increased osteoporosis
  • increased lipids
  • increased cardiovascular risk
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62
Q

Menopause: vasomotor insufficiency tx

A 
estrogen*
progesterone*
Clonidine
SSRIs
Gabapentin
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63
Q

Menopause: vaginal atrophy tx

A

estrogen (transdermal, intravgainal)

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64
Q

Menopause: osteoperosis prevention tx

A

Ca+ Vit D, weight bearing exercises

**bisphosphanates

calcitonin

**SERM (Raloxifen, Tamoxifen)

estrogen (w/w/o progesterone)

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65
Q

Menopause:

Risks/Benefits of ESTROGEN only HRT

A

Benefits:

- *MOST effective for symptomatic tx
- NO increased risk of breast cancer

Risk:
- INCREASED risk of endometrial cancer (due to
unopposed estrogen)
- often only used in pts with NO uterus
-Increased thromboembolism
-Increased liver disease

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66
Q

Menopause:

Risk/Benefits of estrogen + progesterone

A

Benefits:

- symptomatic relief
- decreased heart &amp; stroke risk 
- decreased osteoporosis &amp; dementia
 - ****PROTECTIVE against endometrial cancer 
- usually used with a women w/ intact uterus

Risk:

 - venous thromboembolism
  - controversial : higher risk of breast cancer
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67
Q

Leiomyoma aka…

A

uterine fibroid

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68
Q

MC benign gynecological lesion

A

uterine fibroid (Leiomyoma)

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69
Q

what type of tumor is a Leiomyoma (uterine fibroid)

A

benign uterus SM tumor

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70
Q

what hormone is a Leiomyoma’s growth associated with

A

estrogen

therefore it regresses after menopause***

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71
Q

Leiomyoma (uterine fibroid) are MC in (age group)

A

30s

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72
Q

Leiomyoma (uterine fibroid) are MC in (ethnicity)

A

AA

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73
Q

types of Leiomyoma (uterine fibroid)

A

intramural
submucosal
subserosal
parasitic

74
Q

MC clinical manifestations of Leiomyoma (uterine fibroid)

and others

A

bleeding = MC (menorrhagia)

  • most are asymptomatic, dysmenorrhea
  • abdominal pressure/pain related to size & location
  • bladder: frequency & urgency
75
Q

what would you see on PE during an abdominal or pelvic US during bimanual of a Leiomyoma (uterine fibroid)

A
  • Abdominal or pelvic US during bimanual:

- **large, irregular, hard palpable mass

76
Q

dx for Leiomyoma (uterine fibroid)

A

pelvic US

77
Q

management of Leiomyoma (uterine fibroid) for the majority

A

majority do not need tx

78
Q

most effective* management of Leiomyoma (uterine fibroid): medical tx

others

A

Goal: inhibition of estrogen (to decrease endometrial
growth)

Most effective: GnRH Agonist: Leuprolide (shrinks the
uterus)

Others:
-Progestins: causes endometrial atrophy

79
Q

3 types of management for Leiomyoma (uterine fibroid)

A

1) observation
2) medical
3) surgical

80
Q

definitive tx for Leiomyoma (uterine fibroid)

A

hysterectomy

81
Q

MC cause of hysterectomy

A

fibroids

82
Q

surgery for Leiomyoma (uterine fibroid) if fertility is desired

A

myomectomy

83
Q

what is adenomyosis

A

islands of endometrial tissue within the myometrium

84
Q

clinical manifestations of adenomyosis

A

**mennorhagia (progressively worsens)

**dysmenorrhea

+/- infertility

85
Q

PE findings for adenomyosis

A

**SYMMETRICALLY TENDER

**enlarged boggy uterus

86
Q

how is adenomyosis dx

A

dx of exclusion

87
Q

management of adenomyosis

A

ONLY effective therapy:

hysterectomy

88
Q

leiomyoma vs adenomyosis

A

Leiomyoma:
-asymmetric pain, firm, nontender

Adenomyosis:
-symmetric, soft, tender

89
Q

what is endometritis

A

infection of the uterine endometrium

90
Q

what is chorioamnionitis

A

fetal membrane infection

91
Q

T/F: endometritis is usually polymicrobial

A

True

92
Q

RF for endometritis

A
  • *postpartum or postabortal infection
  • *C-SECTION = biggest RF!**
  • prolong ROM >24 hrs
  • vaginal delivery
  • dilation/curettage
93
Q

what is the biggest RF for endometritis

A

c-section

94
Q

S/sxs & PE findings of endometritis

A
  • fever
  • tachycardia
  • abdominal pain & uterine tenderness after c-section/postabortal
  • may have fould smelling lochia/bleeding/vaginal discharge
95
Q

tx for endometritis post c-section

A

Clindamycin + Gentamicin

may add ampicillin for additional group B step coverage

Bactrim is an alternative

96
Q

tx for endometritis post vaginal delivery or chorioamnionitis

A

Ampicillin + Gentamicin

97
Q

prophylaxis during C section to reduce endometritis

A

1st gen cephalosporin x 1 dose

98
Q

what is endometriosis

A

presence of endometrial tissue (stroma & gland) outside the endometrial cavity

*the ectopic endometrial tissue responds to *cyclical hormonal changes

99
Q

MC site for endometriosis

A

ovaries

100
Q

sites of endometriosis

A 
*ovaries
posterior cul de sac
broad &amp; uterosacral ligaments
rectosigmoid colon
bladder
101
Q

RF for endometriosis

A
  • nulliparity
  • FH
  • early menarche
102
Q

when is the usual onset of endometriosis

A

usually <35 y/o

103
Q

classic triad of endometriosis

A

1) cyclic premenstrual pelvic pain
2) dysmenorrhea
3) dyspareunia

also dyschezia

104
Q

does endometriosis cause infertility

A

Yes, >25% of all causes of female infertility

105
Q

PE of endometriosis

A

usually normal, +/- fixed adenexal masses

106
Q

definitive dx of endometriosis and what will you see

A

laparoscopy with bx

raised, patches of thickened, discolored scarred or “powder burn” appearing implants of tissue

107
Q

what is an endometrioma and what is it associated with

A

it is endometriosis involving the ovaries large enough to be considered a tumor, usually fill with old blood appearing “chocolate colored”

***chocolate cyst

108
Q

medical management of endometriosis

A

-for premenstrual pain: *OCPs & NSAIDs
-progesterone: suppresses GnRH –> causes endometrial
tissue atrophy
-Lueprolide: GnRH analog causes pituitary FSH/LH
suppression
-Danazol: testosterone (supresses FHS/LH surge)

109
Q

surgical tx for endometriosis

A
  • conservative laparoscopy with ablation (if fertility is desired)
  • total abdominal hysterectomy with salpingo-oophorectomy (TAH-BSO)
110
Q

what is endometrial hyperplasia

A

endometrial gland proliferation

111
Q

what is endometrial hyperplasia a precursor to

A

endometrial carcinoma

112
Q

why does endometrial hyperplasia occur

A

due to continuous unopposed estrogen* by progesterone

113
Q

causes of endometrial hyperplasia

A

*chronic anovulation

PCOS, perimenopuase, obesity

114
Q

how does obesity cause endometrial hperplasia

A

conversion of androgen –> estrogen in adipose tissue

115
Q

what population is endometrial hyperplasia most common in

A

postmenopausal women

116
Q

clinical manifestations of endometrial hyperplasia

A

***bleeding: menorrhagia, metrorrhagia, postmenopausal bleeding, +/- discharge

117
Q

how to dx endometrial hyperplasia (and what will you see)

A

1) Transvaginal US (stripe >4mm)

2) Endometrial Bx (definitive dx)

118
Q

definitive dx for endometrial hyperplasia

A

endometrial bx

119
Q

tx for endometrial hyperplasia: withOUT atypia

A
  • *Progestin (PO or IUD-Mirena)

- repeat endometrial bx within 3-6 mos

120
Q

tx of endometrial hyperplasia: with atypia

A

**Hysterectomy

-progestin if fertility if wishes or if they are not a surgical candidate

121
Q

what is the MC gynecological malignancy in the US

A

endometrial cancer

122
Q

what age group is most at risk for endometrial cancer

A

postmenopausal (50-60 y/o peak)

123
Q

what type of hormone is endometrial cancer dependent

A

estrogen

124
Q

what is a major risk factor for endometrial cancer

A

endometrial hyperplasia

125
Q

RF of endometrial cancer (increased estrogen)

A
  • nulliparity
  • chronic anovulation
  • PCOS
  • obestiy
  • *estrogen replacement therapy
  • late menopause
  • htn
  • Tamoxifen
  • DM
126
Q

T/F: combination pills are protective against both ovarian & endometrial cancers

A

TRUE

127
Q

clinical manifestations of endometrial cancer

A

*****ABNORMAL UTERINE BLEEDING (postmenopausal bleeding)

128
Q

Diagnosis of endometrial cancer

A

1) Endometrial biopsy (MC = adenocarcinoma**)

2) US - usually endometrial stripe > 4mm***

129
Q

MC type of endometrial cancer on bx

A

adenocarcinoma (>80%)

130
Q

management of endometrial cancer

stage 1
stage 2,3
stage 4

A

Stage 1
- hysterectomy +/- post op radiation

Stage 2/3
-TAH-BSO + lymph node excision +/-post op radiation

Stage 4
-systemic chemotherapy

131
Q

1st thing to think of in a postmenopausal woman with abnormal bleeding

A

endometrial cancer (10% of abnormal bleeding cause)

132
Q

T/F: MOST postmenopausal bleeding is benign

A

True!

133
Q

Any postmenopausal bleeding in a woman NOT on HRT should raise suspicion for…

A

endometrial cancer
hyperplasia
leiomyoma

134
Q

what dx study can you use for postmenopausal bleeding and what is an indication for bx

A

Transvaginal US

stripe >4mm –> bx

stripe <4mm, repeat US in 4 months

135
Q

what diagnostic test do you use if you see focal thickening of endometrium in a postmenopausal woman

A

hysteroscopy

136
Q

after what does pelvic prolapse MC occur

A

childbirth

137
Q

RF for pelvic prolapse

A

multiple vaginal births
obesity
repeated heavy lifting
childbirth

138
Q

posterior bladder herniating int the anterior vagina

A

cystocele

139
Q

pouch of Douglas (small bowel) into the upper vagina

A

enterocele

140
Q

distal sigmoid colon herniates into the posterior distal vagina

A

rectocele

141
Q

clinical manifestations of pelvic organ prolapse

A
  • pelvic or vaginal fullness/heaviness “falling out” sensation
  • lower back pain (esp. w/ prolonged standing)
  • vaginal bleeding, purulent discharge
  • urinary frequency, urgency, stress incontinence
142
Q

PE of pelvic organ prolapse

A

bulging mass esp. w/ intrabdominal pressure

143
Q

tx for pelvic oran prolapse

A

-kegels
-pessaries
-surgical (hysterectomy, uterosacral or sacrospinous
ligament fixation)

144
Q

what are functional ovarian cysts (3 types)

Follicular

Corpus luteal

Theca Lutein

A

Follicular cysts: occur when follicles fail to rupture & continue to grow

Corpus luteal: cysts fail to degenerate after ovulation

Theca Lutein: excess BhCG causes hyperplasia of theca interna cells

145
Q

Clinical manifestations of functional ovarian cysts

A

MOST are asymptomatic!!!

Unilateral RLQ or LLQ pain if the cyst ruptures, undergo torsion, or become hemorrhagic

146
Q

PE for functional ovarian cysts

A
  • unilateral pelvic pain/tenderness

- may have a mobile palpable cystic adnexal mass

147
Q

Dx of funtional ovarian cyst

A

-Pelvic US
-Follicular: smooth, think walled uniocular
-Luteal: complex, thicker walled w/ peripheral
vascularity
-Order beta HCG to r/o pregnancy

148
Q

Management of functional ovarian cysts

A
  • supportive!!
  • most cysts <8cm are functional & usually resolve spontaneously
  • Repeat US in 6 wks
  • If cysts >8cm or persistent/found postmenopausal –> +/-laparoscopy or laparotomy
149
Q

what is the 2nd MC gynecological cancer

A

ovarian cancer

150
Q

what gynecological cancer has the highest mortality of all

A

ovarian cancer

151
Q

RF for ovarian cancer

A

**FH
**increased # of ovulatory cycles (infertility, nulliparity,
>50, late menopause)
***BRCA1/2
- Peutz Jehgers
-Turner’s syndrome

152
Q

protective factors of ovarian cancer

A

OCPs**
high parity
TAH

153
Q

clinical manifestations of ovarian cancer

A

**rarely symptomatic until late disease course

  • abdominal fullness/distension
  • Back/abdominal pain, early satiety, urinary frequency
  • Irregular menses, menorrhagia, postmenopausal bleeding, constipation, intestinal compression
154
Q

what decades does ovarian cancer usually present in

A

40-60 y/o

155
Q

PE for ovarian cancer

A
  • Palpable abdominal or ovarian mass (*solid, fixed, irregular)
  • ***SIster Mary Joseph’s nodes: mets to umbilical LN
  • possibly ascites
156
Q

dx for ovarian cancer

what will you see on bx

A

90%= EPITHELIAL (esp. in postmenopausal)

Germ cell <30 y/o

157
Q

management of ovarian cancer

Early

Surgery

Chemo

A

Early:
-TAH-BSO + selective lympahdenectomy

Surgery:
- tumor debunking
-***serum CA125 levels used to monitor treatment
progress

Chemotherapy:
-Paclitaxel (Taxol) + Cisplatin or Carboplatin

158
Q

how do you monitor tx for ovarian cancer (surgery)

A

serum CA125 levels

159
Q

what is the MC benign ovarian neoplasm

A

dermoid cyst teratomas

160
Q

management of benign ovarian neoplasm

A

removal (due to increased risk of potential torsion or malignant transformation)

161
Q

in reproductive years, ___% of ovarian neoplasms are benign. Risk of malignancy ___ with age

A

90%

increases

162
Q

triad of PCOS

A

1) amenorrhea
2) Obesity
3) Hirsutism

163
Q

PCOS is due to…

A

insulin resistance

164
Q

___% of the population has PCOS

A

10%

165
Q

clinical manifestations of PCOS

A

1) menstrual irregularity (2ry amenorrhea/oligomenorrhea)
2) Increased androgen (hirsutism)
3) Insulin resistance (Type II DM, *OBESTIY-80%, Htn)

166
Q

what is the pathology os PCOS?

increased insulin & LH–> ?

A

increased ovarian androgen production

167
Q

PE for PCOS

A
  • *bilateral enlarged, smooth, mobile ovaries

- *acanthosis nigrans

168
Q

dx of PCOS

  • labs
  • imaging
A

-exclude other disorders
-Labs:
-increased testosterone**
-LH:FSH ratio >3:1*****
-GnRH agonist stimulation test: rise is serum
hydroxyprogesterone
-Pelvis US
** “string of pearls” appearance
- bilateral enlarged ovaries with peripheral cysts

169
Q

mainstay of PCOS tx

A

combination OCPs

170
Q

what type of OCP do you want to avoid in PCOS

A

androgenic progesterone (norgestrel or levonorgestrel)

171
Q

antiandrogen agents for hirsutism for PCOS

A

**spironolactone

172
Q

T/F: Spironolactone is teratogenic

A

TRUE! must be used w/ OCPs

173
Q

tx for inferitliy for PCOS

A

clomiphene

selective estrogen receptor modulator

174
Q

complications of PCOS (due to chronic anovulation)

A
  • increased risk of infertility
    -**increased risk of endometrial hyperplasia & carcinoma
    (due to unopposed estrogen)
  • insulin resistance –> increased risk of atherosclerosis &
    htn
175
Q

____ decreases amplitude of GnRH

A

Estradiol

176
Q

___ decreases frequency of GnRH

A

progesterone

177
Q

what level does progesterone have to be to ovulate

A

> 3

178
Q

neuropeptides that stimulate GnRH

A

NE
galanin
NYP

179
Q

neuropeptides that inhibit GnRH

A

GABA
dopamine
B-endorphins
corticotrophin releasing hormone

180
Q

what induces the FSH surge

A

low levels of progesterone

181
Q

FSH targets ____cells

A

granulosa cells

182
Q

LH targets ___ cells

A

thecal & stromal cells

EOR Exams- Review (1 decks)

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