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Women's Health 2 > PCOS > Flashcards

PCOS Flashcards

1
Q

Describe the ovarian wedge resection procedures.

A
  • surgical removal of ½ to ¾ of each ovary (bilateral ovarian wedge resection)
  • many patients resumed regular menses and became pregnant s/p surgery
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2
Q

What type of cysts are characteristic of PCOS?

A

Follicular cysts

*growth arrested at antral stage

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3
Q

Describe the pathophysiology of PCOS

A
  • the cysts of PCOS are actually follicles
  • the follicles are arrested in development accumulate in the ovary

“PCOS women do not throw away their old follicles”

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4
Q

Follicle dynamics at birth

A
  • 2,000,000 primordial follicles
  • random development to 1o follicles
  • in absence of FSH, apoptosis, and resorption
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5
Q

Follicle dynamics at puberty

A
  • 200,000 primordial follicles
  • increased GnRH pulses
  • increased FSH
  • follicle development → ovulation
  • remaining follicles undergo apoptosis
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6
Q

Outline follicle growth

A
  • initial phase: gonadotropin-independent
  • recruitment and maturation:FSH dependent
  • FSH induces estradiol production and LH receptors
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7
Q

Appearance of ovaries in PCOS

A

“String of pearl” appearance

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8
Q

What factors contribute to anovulation in PCOS?

A
  • elevated testosterone suppresses FSH
  • FSH levels do not reach the level required to induce follicle maturity
  • follicle arrest, anovulation
  • absence of progesterone leads to elevated LH
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9
Q

What is the NIH major criteria for PCOS?

A
  1. Chronic anovulation (oligo- or amenorrhea)
  2. Clinical and/or biochemical evidence of hyperandrogenism
  3. Exclusion of other causes of anovulation and hyperandrogenism
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10
Q

What is the 2003 Rotterdam ESHRE/ASRM Consensus on PCOS?

A

** 2 of 3 required:
1. Chronic anovulation (Oligo- or anovulation)
2. Clinical and/or biochemical signs of hyperandrogenism (Unchanged)
3. Exclusion of other disorders (Unchanged)
4. Polycystic ovaries (minor criterion) –> Major
> or = 12 follicles measuring 2-9 mm, and/or
> 10 ml ovarian volume (0.5 x length x width x thickness)

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11
Q

Why is there controversy in PCOS diagnosis?

A

high prevalence (up to 68%) of PCOM in normal young women

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12
Q

What is the Androgen Excess and PCOS Society consensus on PCOS?

A
  • all 3 required:
    1. Hyperandrogenism (clinical and/or biochemical)
    2. Ovarian dysfunction (oligo-anovulation and/or polycystic ovaries)
    3. Exclusion of related disorders
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13
Q

So, what is PCOS??

A
  • A heterogeneous disorder of unclear etiology

- An important cause of menstrual irregularity and androgen excess in women

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14
Q

Describe “classic” PCOS when fully expressed.

A

manifestations include:

  • Ovulatory dysfunction
  • Androgen excess
  • Polycystic Ovaries
  • Obesity
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15
Q

Diagnostic tests for PCOS

A 
1. Anovulation: Menstrual history
(< 9 menses/year or > 3 consecutive months without menses)
2. Hyperandrogenism:  
-Physical exam: Hirsutism (note hair removal methods), acne
-Serum androgen levels: 
Testosterone (T), Free T, DHEA-S
3, Pelvic Ultrasound
4. DIAGNOSIS OF EXCLUSION***
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16
Q

What is the most common cause of secondary amenorrhea?

A

Pregnancy**

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17
Q

What are the exclusion diagnostic tests?

A
  • Pregnancy: Serum HCG!!!!
  • Congenital Adrenal Hyperplasia: 17-OH progesterone(in high-risk populations)
  • Hyperprolactinemia: Prolactin
  • Thyroid abnormalities: TSH
  • Androgen secreting tumor: DHEAS, Testosterone (suspected if T > 200 ng/dL or DHEAS > 700 mcg/dL)
    • Cushing’s syndrome: 24 hour urinary cortisol
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18
Q

PCOS prevalence

A
  • Affects 6-8% of reproductive age women
  • MCC of female infertility in the United States
  • Onset is likely pre-pubertal but difficult to detect until late adolescence
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19
Q

Which populations get PCOS

A
  • Multifactorial origin
  • Genetic predisposition (behaves like autosomal dominant trait)
  • Phenotypic expression determined by environmental factors that begin in utero (high AMH in mom might predispose female fetus to have PCOS in adulthood)
  • Factors that influence insulin secretion affect the phenotype
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20
Q

List the risk factors for PCOS in adolescents

A
  • Low birth weight: < or = 2500 g
  • Premature pubarche: Onset before 8yo
  • Family history (1st degree relative)
  • Obesity
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21
Q

What is the underlying problem in PCOS?

A
  • HYPERANDROGENISM**
  • Hypothalamic-pituitary-ovarian (HPO) axis disturbance
  • Insulin resistance and hyperinsulinemia

**primary

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22
Q

In PCOS, which organ primarily produces the excess androgen?

A

Ovaries

23
Q

Explain the hyperandrogenism pathophysiology in PCOS

A
  • Excess androgen production comes from the ovary
  • Increased thecal cell volume
  • Increased expression of LH receptors on theca cells
  • Exaggerated androgen production occurs when LH binds to receptors on the theca cells of the ovary
24
Q

Explain the HPO axis pathophysiology in PCOS

A
  • LH and FSH secretion abnormalities
  • Decreased FSH release
  • Increased LH release
  • Increased LH pulse frequency and amplitude
  • Increased LH:FSH ratio
25
Q

Elevated LH level and pulse frequency may be due to…

A

Lack of progesterone (anovulation): ↑LH

Feedback effect of androgens: ↓FSH

26
Q

What is the relationship between HPO and hyperandrogenism?

A
  • Disruption of hypothalamic-pituitary-ovarian axis (HPO) is believed to be a secondary defect
  • Hyperandrogenism (and anovulation) comes first
27
Q

Explain the insulin sensitivity (specifically hyperinsulinemia) pathophysiology in PCOS

A
  • Insulin resistance is a feature of PCOS in obese and non-obese women
  • Activation of insulin receptor (IGF) in the ovary: augmented thecal androgen response to LH
  • Suppression of hepatic SHBG production: increased free androgen proportion
  • Direct stimulation of LH secretion by insulin
  • Sensitization of LH secreting cells to GnRH
28
Q

Relationship between insulin resistance and PCOS

A
  • IR itself is not enough to cause PCOS (Only about 25% of reproductive-aged women with type 2 diabetes have PCOS)
  • Screening for IR is indicated in patients with PCOS
29
Q

What is the relationship between insulin resistance and hyperandrogenism?

A
  • Insulin resistance is believed to be a secondary defect
  • Hyperandrogenism comes first

*controversial

30
Q

PCOS and metabolic syndrome (MBS)

-relationship

A

Associated with significant risk for early cardiovascular disease

31
Q

PCOS and metabolic syndrome

-criteria for diagnosis

A
  • must have 3 of 5:
  • Abdominal obesity > 88 cm
  • Triglycerides > 150 mg/dl
  • HDL-C < 50 mg/dl
  • BP > 130/>85 mmHg
  • OGTT: 110-126 mg/dl and/or 140-199 mg/dl
32
Q

In PCOS patient, what are the screenings for long term health consequences?

A
  • 2 hour oral glucose tolerance test or Hemoglobin A1C (75gm glucose load – serum drawn before drinking it // blood drawn at 1 hr and 2 hr)
  • Lipid profile
  • Blood pressure
  • Endometrial biopsy (d/t increased risk for endometrial cancer)
  • Waist circumference
33
Q

What symptoms are you treating in PCOS?

A
  • Infertility
  • Skin manifestations, hirsutism
  • Dysfunctional uterine bleeding, endometrial cancer prevention
  • Obesity, diabetes prevention (lifestyle changes)
34
Q

Infertility treatment

-ovulation induction

A
  • Weight loss (don’t have to be “normal” BMI to start ovulating again)
  • Clomiphene citrate (approx. 50-80% ovulate with clomid alone)
  • Aromatase inhibitors (first line, but off label)
  • Injectable gonadotropins
  • Laparoscopic ovarian drilling
  • Insulin-lowering medications - Metformin
35
Q

Insulin sensitizers

-metform action

A

*Oral biguanide anti-hyperglycemic approved for NIDDM (Glucophage)

  • Decreases hepatic gluconeogenesis
  • Increases peripheral glucose uptake (muscle, adipose tissue)
  • Increases insulin sensitivity at the post-receptor level
36
Q

Insulin sensitizers in women with PCOS

A
  • Improves menstrual cyclicity, restores spontaneous ovulation (up to 30% ovulate with metformin alone)
  • Improves symptoms of hyperandrogenism
  • May improve body composition (BMI, WHR) and lipid profile
37
Q

Skin manifestations, hirsutism treatment

A
  • Oral contraceptives

- Anti-androgens

38
Q

List the anti-androgens for hirsutism/skin manifestations

A
  • Spironolactone
  • Flutamide
  • Finasteride
  • GnRH agonists
39
Q

Oral contraceptives in PCOS

A
  • Currently considered first line therapy for those not currently desiring fertility
  • Use low dose estrogen (20-30 mcg ethinyl estradiol) and non-androgenic progestin (e.g. desogestrel or drospirenone)
  • Decreases risk of endometrial cancer
40
Q

Oral contraceptives action

A
  • Increases SHBG
  • Decreases bio-available androgen
  • Restores regular menstrual cycles
  • Decreases hirsutism, acne
  • Provides effective contraception
41
Q

PCOS and anti-androgens

A
  • Effectively reduces biochemical and clinical hyperandrogenism
  • May be more effective in treating hirsutism than metformin
  • Improves menstrual cyclicity
  • No improvement in metabolic abnormalities
42
Q

PCOS and anti-androgens

-Flutamide

A

non-steroidal antagonist acting at nuclear receptor

43
Q

PCOS and anti-androgens

-Spironolactone

A
  • K+-sparing diuretic with anti-androgen effect
  • MC choice in U.S.
  • 50-100 mg/day have been reported to be effective
44
Q

PCOS and anti-androgens

-Cyproterone acetate

A

anti-androgenic progestogen, combined with ethinyl estradiol

*not available in U.S.

45
Q

PCOS Symptom-dependent tx

-dysfunctional uterine bleeding

A
  • Endometrial biopsy

- Oral contraceptives or cyclic progestins

46
Q

PCOS Symptom-dependent tx

-obesity

A
  • Lifestyle management
  • Diet and exercise
  • Metformin
47
Q

Which of the following has been shown to be the MOST effective in prevention of diabetes in PCOS?

A

Diet and exercise

48
Q

Lifestyle intervention and weight loss in PCOS

A
  • Shown to effectively prevent diabetes in high risk groups*
  • Importance is emphasized, but difficult to achieve
  • Current recommendation is combination of lifestyle modification with pharmacologic therapy
49
Q

Effects of lifestyle intervention and weight loss

A
  • decrease testosterone
  • decrease insulin levels
  • increase SHBG
50
Q

Initial evaluation in PCOS

A
  • H&P
  • Total T, TSH, prolactin (could also consider: DHEA-S, 17-hydroxyprogesterone, LH, FSH)
  • Pelvic ultrasound
51
Q

PCOS periodic screening once diagnosis is established

A

-2 hour oral glucose tolerance test
-Lipid profile
-Blood pressure
+/- Endometrial biopsy

52
Q

Treatment in PCOS

-symptom dependent

A
  • Encourage healthy diet and exercise
  • Possibly do better with Low Carb diet
  • Ovulation induction with clomid if pregnancy is desired
  • Low-dose (20 mcg) OCPs if pregnancy is not desired
  • Obese and IR patients: Metformin
  • Marked hirsutism refractory to OCPs: Consider spironolactone

*lifelong therapy may be needed

53
Q

Which of the following is considered the primary pathophysiologic defect in PCOS?

A

Hyperandrogenemia

54
Q

PCOS: CONCLUSIONS

-pathophysiology

A

Primary defect: Ovarian hyperandrogenism

Secondary defects:

  • HPO axis disturbance
  • Insulin resistance

Women's Health 2 (9 decks)

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