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Exam 2- lecture 3 Flashcards

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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
PCOS results in
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
26
PCOS results in polyfollicular development which
becomes arrested and leads to polyovarian cysts
27
PCOS can present as
amenorrhea, menorrhagia and/or anovulatory bleeding
28
PCOS treatment
- metformin & thiazolidinedione | - progesterone or contraceptive hormones to maintain regular menstrual cycle & < androgen effects
29
causes of menorrhagia
systemic disorders or specific uterine abnormalities - prego - underlying bleeding disorders - von Willebrand's disease - hypothyroidism - intrauterine problems- fibroids, endometrial polyps, cancer
30
von willebran's disease
menorrhagia | factor 7 defect causing impaired platelet adhesion &increased bleeding time
31
cirrosis
menorrhadia | decreased estrogen metabolism, underlying coagulopathy
32
NSAID MOA
reduce production of PG involved in uterine contractions & in pain associated with menstruation - result in up to 50% reduction in blood loss
33
oral progesterone
reduces menstrual blood loss by 32-50%
34
IUD
reduces menstrual blood flow by >90%
35
tranexamic acid (IV or oral)
inhibitor of fibrinolysis
36
most common cause of anovulatory bleeding
PCOS
37
most adolescents will experience some anovulatory cycles in their first few years as HPO matures. should stabilize within
5 years of menarche
38
regardless of age evaluation of what with anovulatory bleeding should be done?
endometrial hyperplasia or cancer
39
in absence of ovulation in the normal menstrual cycle
progesterone is not produces & the endometrium continues to proliferate under estrogen production - becomes so thick it breaks off-> heavy anovulation bleeding
40
anovulatory bleeding treatment acute episodes
estrogen- promotes endometrial stabilization
41
long term stabilization of anovulatory bleeding
OC- surpress ovarian hormones & adrenal androgen production | also increase plasma levels of sex hormone binding globulins
42
dysmenorrhea is associated with
nausea, diarrhea, fatigue, HA
43
primary dysmenorrhea
pain with normal pelvic A&P | 90%
44
secondary dysmenorrhea
associated with underlying pelvic pathology | 10%
45
risk factors for dysmenorrhea
young age, heavy menses, nulliparity, early menarche, cigarette smoking
46
most important MOA of primary dysmenorrhea
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
uterine contractions
restrict blood flow to the tissue
48
prostaglandins sensitize
nerve endings to painful stimuli
49
secondary dysmenorrhea caused by
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
treatment for dysmenorrhea
NSAIDs OC depot MPA or IUD
51
premenstrual dysphoric disorder (PMDD)
severe form of PMS with strong mood alteration component that impairs normal life function & daily living
52
PMS/PMDD symptoms
depression, mood swings, chronic fatigue, anxiety, difficulty concentration, food cravings or binge eating, insomnia or hypersomnia
53
what improves PMS/PMDD symptoms?
suppression of ovulation
54
PMS/PMDD hypothesis
- low levels of centrally acting progesterone metabolite- allopregnanolone in luteal phase and/or reduced cortical GABA in follicular phase - low serotonin
55
endometriosis
presence or growth of endometrial tissue outside of the uterus - cause of pelvic pain & associated infertility - usually consists of glands & stroma
56
endometriosis tissue involement
ovaries> uterine ligaments> pelvic peritoneum > large & small bowel & appendix> mucosa of the cervix, vagina & fallopian tubes
57
endometriosis should be suspected in women with
dysmenorrhea or chronic pelvic pain
58
metastatic theory of endometriosis
most widely accepted. endometrial tissue implanted in abnormal location by various mechanisms
59
metaplastic theory of endometriosis
endometrial tissue arises directly from mesothelium of pelvis or abdomen
60
endometriosis & estrogen
enhances pain, promotes tissue growth, & stimulates release of inflammatory factors
61
endometriosis first line therapy
combined hormonal contraceptives- regress endometrial implants through induction of anovulatory or hypoestrogenic state & reduce menstrual flow or progestins- produce endometrial atrophy
62
endometriosis second line treatments
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
aromatase inhibitors
block formation of estrogen
64
endometriosis is a
chronic & relapsing disease

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