Exam 2- lecture 3 Flashcards

1
Q

amenorrhea

A

absense of menstrual period

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2
Q

menrrhagia

A

abnormally heavy & prolonged menstrual period at regular intervals
>80mL per cycle

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3
Q

anovulatory bleeding

A

abnormal uterine bleeding that occurs w/out ovulation

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4
Q

dysmenorrhea

A

condition of pain during menstruation that interferes with daily activities
- begins at onset of bleeding & decreases over 12-72hrs

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5
Q

premenstrual syndrome (PMS)

A

collection of physical & emotional symptoms related to a woman’s menstrual cycle

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6
Q

need for treatment

A

reduced QOL
negative effects on reproductive health
potential long-term effects (osteoporosis, CVD)

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7
Q

primary amenorrhea

A
  • absence of menses by age 16 in presence of normal secondary sexual development
  • absence of secondary sexual development by age 14
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8
Q

secondary amenorrhea

A

absence of menses for 3 cycles or 6 months in a previously menstruating woman

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9
Q

most common secondary cause of amenorrhea

A

prego

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10
Q

secondary amenorrhea due to hormonal imbalance

A
  • hypothalamic suppression

- weight loss/eating disorder, PCOS, stress, thyroid malfunction

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11
Q

secondary amenorrhea due to hyperprolatinemia

A

abnormally high levels of prolactin produced by pituitary gland- drug induced, lactation, prego, hypothyroidism

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12
Q

secondary amenorrhea due to ovarian disorder

A

genetic disorders

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13
Q

secondary amenorrhea due to uterine disorder

A

uterine adhesions or abnormal development

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14
Q

secondary amenorrhea due to medications

A

antipsychotic, chemo, BP drugs, allergy meds

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15
Q

menses requires functional

A

uterus & vagina & normal ovarian function

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16
Q

primary amenorrhea can result from

A

congenital anomaly

imperforated hymen

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17
Q

secondary amenorrhea can result from

A

postsurgical adhesions

abnormal uterine development

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18
Q

lack of follicular development

A

can lead to amenorrhea

  • genetic abnormalities where estrogen production is inadequate to stimulate endometral growth (turner syndrome, gonadal dysgenesis)
  • chemo/radiation, where gonadal toxins are produced
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19
Q

altered FSH/LH secretion can be due to

A
pituitary prolactin-secreting adenoma
prego(>prolactin)
breast feeding (>prolactin
hypothyroidisn (>prolactin)
stress(<FSH/LH)
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20
Q

blockage of DA receptors

A

increases prolactin

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21
Q

stimulation of 5-HT recptors

A

increases prolactin

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22
Q

conditions that < GnRH & interfere with normal HPO axis-> blocking normal menstruation

A

weight loss, eating disorder, intense exercise, stress, PCOS

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23
Q

is PCOS genetic?

A

partially genetic

autosomal dominant

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24
Q

PCOS is a risk factor for

A
metabolic syndrom
obesity
insulin resistance
HTN
CV disorders
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25
Q

PCOS results in

A

anovulation or oligo-ovulation as a result of elevated androgen production by ovaries. Ovaries are stimulated to produce too much androgen by excessive secretion of LH or by elevated insulin

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26
Q

PCOS results in polyfollicular development which

A

becomes arrested and leads to polyovarian cysts

27
Q

PCOS can present as

A

amenorrhea, menorrhagia and/or anovulatory bleeding

28
Q

PCOS treatment

A
  • metformin & thiazolidinedione

- progesterone or contraceptive hormones to maintain regular menstrual cycle & < androgen effects

29
Q

causes of menorrhagia

A

systemic disorders or specific uterine abnormalities

  • prego
  • underlying bleeding disorders
  • von Willebrand’s disease
  • hypothyroidism
  • intrauterine problems- fibroids, endometrial polyps, cancer
30
Q

von willebran’s disease

A

menorrhagia

factor 7 defect causing impaired platelet adhesion &increased bleeding time

31
Q

cirrosis

A

menorrhadia

decreased estrogen metabolism, underlying coagulopathy

32
Q

NSAID MOA

A

reduce production of PG involved in uterine contractions & in pain associated with menstruation
- result in up to 50% reduction in blood loss

33
Q

oral progesterone

A

reduces menstrual blood loss by 32-50%

34
Q

IUD

A

reduces menstrual blood flow by >90%

35
Q

tranexamic acid (IV or oral)

A

inhibitor of fibrinolysis

36
Q

most common cause of anovulatory bleeding

A

PCOS

37
Q

most adolescents will experience some anovulatory cycles in their first few years as HPO matures. should stabilize within

A

5 years of menarche

38
Q

regardless of age evaluation of what with anovulatory bleeding should be done?

A

endometrial hyperplasia or cancer

39
Q

in absence of ovulation in the normal menstrual cycle

A

progesterone is not produces & the endometrium continues to proliferate under estrogen production
- becomes so thick it breaks off-> heavy anovulation bleeding

40
Q

anovulatory bleeding treatment acute episodes

A

estrogen- promotes endometrial stabilization

41
Q

long term stabilization of anovulatory bleeding

A

OC- surpress ovarian hormones & adrenal androgen production

also increase plasma levels of sex hormone binding globulins

42
Q

dysmenorrhea is associated with

A

nausea, diarrhea, fatigue, HA

43
Q

primary dysmenorrhea

A

pain with normal pelvic A&P

90%

44
Q

secondary dysmenorrhea

A

associated with underlying pelvic pathology

10%

45
Q

risk factors for dysmenorrhea

A

young age, heavy menses, nulliparity, early menarche, cigarette smoking

46
Q

most important MOA of primary dysmenorrhea

A

release of prostaglandins & other mediators in menstrual fluid which initiate inflammatory response->uterine contractions (PGF2alpha) & vasoconstriction

  • LK C4 & D are also elevated
  • elevated vasopressin
47
Q

uterine contractions

A

restrict blood flow to the tissue

48
Q

prostaglandins sensitize

A

nerve endings to painful stimuli

49
Q

secondary dysmenorrhea caused by

A

cervical stenosis (cervical narrowing/closure)
endometriosis (abnormal uterine tissues)
pelvic infections
pelvic congestion syndrome (varicose veings in abdomen)
uterine or cervical polyps or firboids
genital outflow obstructions
pelvic adhesions

50
Q

treatment for dysmenorrhea

A

NSAIDs
OC
depot MPA or IUD

51
Q

premenstrual dysphoric disorder (PMDD)

A

severe form of PMS with strong mood alteration component that impairs normal life function & daily living

52
Q

PMS/PMDD symptoms

A

depression, mood swings, chronic fatigue, anxiety, difficulty concentration, food cravings or binge eating, insomnia or hypersomnia

53
Q

what improves PMS/PMDD symptoms?

A

suppression of ovulation

54
Q

PMS/PMDD hypothesis

A
  • low levels of centrally acting progesterone metabolite- allopregnanolone in luteal phase and/or reduced cortical GABA in follicular phase
  • low serotonin
55
Q

endometriosis

A

presence or growth of endometrial tissue outside of the uterus

  • cause of pelvic pain & associated infertility
  • usually consists of glands & stroma
56
Q

endometriosis tissue involement

A

ovaries> uterine ligaments> pelvic peritoneum > large & small bowel & appendix> mucosa of the cervix, vagina & fallopian tubes

57
Q

endometriosis should be suspected in women with

A

dysmenorrhea or chronic pelvic pain

58
Q

metastatic theory of endometriosis

A

most widely accepted. endometrial tissue implanted in abnormal location by various mechanisms

59
Q

metaplastic theory of endometriosis

A

endometrial tissue arises directly from mesothelium of pelvis or abdomen

60
Q

endometriosis & estrogen

A

enhances pain, promotes tissue growth, & stimulates release of inflammatory factors

61
Q

endometriosis first line therapy

A

combined hormonal contraceptives- regress endometrial implants through induction of anovulatory or hypoestrogenic state & reduce menstrual flow
or
progestins- produce endometrial atrophy

62
Q

endometriosis second line treatments

A

GnRH agonists- goserelin, leuprolide, nafarelin
- create GnRH receptor down regulation & function oopharectomy of FSH & LH secretions. this diminishes endometrial implants
or
- danazol- syntheic steroid analogue of testosterone; induces anovulation, amenorrhea & endometrial atrophy through suppression of LH & FSH & induction of high androgen, low estrogen

63
Q

aromatase inhibitors

A

block formation of estrogen

64
Q

endometriosis is a

A

chronic & relapsing disease