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GYN > PCOS > Flashcards

PCOS Flashcards

1
Q

how common is PCOS

A

PCOS is the most frequently encountered endocrinopathy in women of reproductive age. Prevalence is 4-12%

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2
Q

common manifestation of PCOS

A

characterized by menstrual abnormalities

oligomenorrhea or secondary amenorrhea

if you don’t have this then you don’t have PCOS could have pre diabetes

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3
Q

PCOS usually occurs in this age group

A

usually manifest around menarche but can happen anytime

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4
Q

Hyperandrogenism effects of PCOS (3 broad systems)

A
  1. Clinically manifests as excess terminal body hair in a male distribution (Upper lip, chin, around the nipples and along the linea alba of the lower abdomen)
  2. Some have acne (typically its cystic acne) or male pattern hair loss
  3. Occasionally increased muscle mass, deepening of the voice and/or clitoromegaly due to excessive androgens
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5
Q

other than hyperandrogenism, what other symptoms do we see with PCOS

A 
infertility
obesity
DM
sleep apnea
acanthosis nigricans 
metabolic syndrome
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6
Q

why do you see infertility with PCOS

A
  1. A subset of women are infertile

2. Most women ovulate intermittently.

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7
Q

what % of PCOS are obese

A

This is present in nearly half of all women with PCOS

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8
Q

what % of women have DM2 and PCOS

A

10% of women with PCOS have Type 2 diabetes,

30-40% have impaired glucose tolerance by age 40.

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9
Q

classic dx of PCOS

A

can be diagnosed clinically in a woman with hirsutism, irregular menstrual cycles and characteristic ovarian morphology.
(Classic ultrasound findings often include multicystic ovaries
(10 or more on each ovary) with the follicle cysts lining the periphery of the ovary)

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10
Q

NIH Dx criteria

A

defined 2 minimum criteria for diagnosis

  1. Menstrual irregularities
  2. Evidence of hyperandrogenism either clinical (hirsutism, acne, male balding) or biochemical (elevated serum androgen level)
  3. Exclusion of other disorders that can results in menstrual irregularities and hyperandrogenism***
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11
Q

Rotterdam European Society of Human Reproduction/American Society for Reproductive Medicine (ESHRE/ASRM

A

2003 defined 3 criteria for diagnosis and indicated PCOS maybe present if 2 out of 3 criteria are met:

  1. Oligoovulation/anovulation
  2. Clinical or biochemical signs of hyperandrogenism
  3. Polycystic ovaries
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12
Q

Biochemical abnormalities w/ PCOS

Testosterone levels (3)

A

may be normal or elevated but usually <200ng/dl.

androstenedione and dehydropiandrosterone sulfate
DHEA-S are usually normal but may be elevated

FSH and LH are normal to high
LH to FSH is usually 3:1 or more

fasting gluscose would be high because of insulin resistance

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13
Q

TSH and prolactin are usually __ in PCOS

A

normal

need to rule out hypothyroid because can have similar symptoms or pituitary cause

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14
Q

if testosterone is > 150ng need to rule out

A

Adrenal tumors should be investigated if testosterone is > 150ng/dl. Rule out elevated Cortisol for Cushing’s (run screening ACTH/Cortisol)

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15
Q

rule out cushings by checking

A

ACTH and cortisol

If suspicious dexamethasone suppression test

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16
Q

Also can test for acromegaly if

A

no improvement look at IGF1 and growth hormone

can have pituitary tumor

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17
Q

rule out thyroid disorders

A

order TFTs

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18
Q

rule out Hyperprolactinemia

A

order prolactin

19
Q

Late onset Congenital Adrenal Hyperplasia (CAH) can be ruled out with

A

morning 17-OH progesterone

20
Q

Ovarian and adrenal tumors should also be considered with

A

testosterone over 150

21
Q

pathophys of PCOS

A

The basic pathophysiologic defect is unknown

Tends to cluster in families thought to be genetic

Abnormal metabolism of androgens and estrogen.–> lower estrogen and higher testosterone

PCOS is associated with peripheral insulin resistance and hyperinsulinemia, obesity amplifies the degree of both.

22
Q

pathophys –> hormones and PCOS

A

hyperinsulemia

Increases androgen production from theca cells.

Suppresses hepatic production of sex hormone binding globulin (SHBG).
—> This increases unbound levels of testosterone and free hormone.

Elevated androgen levels also lead to decreased levels of SHBG.

Amplifies the response of the granulosa cell to LH.

because of the decreased FSH relative to LH
can not create estrogen

Because of decreased FSH relative to LH the granulosa cells cannot aromatize androgens to estrogen.

This leads to decreased estrogen levels and consequent anovulation.

23
Q

goals of PCOS tx

A
  1. Restore ovulation
  2. Decrease the testosterone level
  3. Improve metabolic disturbances
  4. Protect uterine lining.

endometrial shedding at least once every three months (if the pt is not on birth control)

progesterone –> gets the lining mature

24
Q

first line tx for PCOS

A

First line therapy: Lifestyle modifications
can lower insulin level

  • reducing foods that require a lot of insulin
    1. Exercise
    2. Weight loss (low refined carbohydrate diet).
    3. Even a small amount of weight loss can establish menstrual cyclicity.
    4. Metabolic abnormalities also improve dramatically with weight loss.
25
Q

how is BC used to treat PCOS

A
  1. Can be used for women not interested in fertility.
  2. This cyclic withdrawal of estrogen and progesterone leads to complete endometrial shedding and lower LH, therefore lowering androgen levels.
26
Q

Intermittent Progestin therapy

A
  1. Protects uterine lining without estrogen risks.
27
Q

how do you assess the pt that looks like the could have PCOS

A

ask about HA to rule out prolactinoma

ask about hypothyroid sxs (constipation, dried skin

look for supraventricular fat pads (cushing’s)

28
Q

if you have a testosterone level >200 you want to start thinking about

A

tumors or adrenal issues

29
Q

LH

A

responsible for adrogen aspect

30
Q

what are you ruling out in a pt with PCOS

A

hyper or hypo thyroid can throw off period
insulin resistance and throw off ovaries

prolactin elevation and a tumor and fuck with cycle

PCOS symptoms but high IgF1 ended up having a pituitary tumor causing acromegaly

31
Q

this is the velcrow that decreases free floating hormone

A

Suppresses hepatic production of sex hormone binding globulin (SHBG).

32
Q

what if OCP fails as tx to produce a period

A

if birth control is not enough to have a period

will give progesterone for 10 days
Mimics luteal phase

protects the uterine lining

33
Q

how to treat PCOS in general

A

reduces metabolic disturbances
improving insulin withh decrease testosterone

metformin can help with this as well as diet and exercise
decreasing foods that require insulin (carbs and sugars)

34
Q

OCP work by

A

decrease LH levels and endometrial hyperplasia by restoring menses

estrogen stimulates the production of sex binding hormone

might increase insulin resistance

35
Q

what birth control should be avoided in PCOS

A

Avoid Norgestrel or Levonorgestrel

36
Q

metformin as tx for PCOS

A

not first line

200 mg of metformin is hte max for DM but can go up to 250mg for PCOS

37
Q

how does spironolactone work for PCOS

A

blocks testosterone receptors

this teatrogenic and must be used with OCP

38
Q

clomid for PCOS

A

usually given for infertility
clomiphene

could increase the risk of varian cancer?

39
Q

typical fasting insulin

A

10

40
Q

nml free testosterone

A

1-21

41
Q

DHEA

A

dehydroepiandrosterone. It is a weak male hormone (androgen) produced by the adrenal glands in both men and women

Ages 18 to 19: 145 to 395 micrograms per deciliter (µg/dL)

42
Q

17OH-progesterone

A

to rule out nonclassic congenital adrenal hyperplasia (NCCAH) due to 21-hydroxylase deficiency

43
Q

why would you have an MRI for a pt with PCOS

A

pituitary adenoma suspected

GYN (13 decks)

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