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GK F3E5 > ovarian disorders > Flashcards

ovarian disorders Flashcards

1
Q

PCOS is characterized by

A

chronic anovulation
polycystic ovaries
hyperandrogenism

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2
Q

PCOS is associated with these diseases

A 
hirsutism 
obesity 
DM 
CBD 
metabolic syndrome 
dyslipidemia 
NAFLD 
OSA
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3
Q

What is the pathophysiology behind PCOS

A

Abnormal androgen and estrogen metabolism
Unregulated androgen control
Insulin resistance= hyperinsulinemia
Decreased adiponectin

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4
Q

What are the hormonal inhibitions in PCOS

A

Inhibin (released from granulosa cells) inhibits FSH

Estrone (released from adipocytes) inhibits FSH= less aromatase= androgens NOT converted to estrogen

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5
Q

How does high insulin affect PCOS

A
  • Positive feedback on androstenedione, making more testosterone, and more estrone, therefor further inhibiting FSH
  • Increased LH secretion
  • Decreases SHBG and IGF= more free testosterone
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6
Q

How does decreased adiponectin affect PCOS

A

It is an insulin sensitizer, and regulates lipid metabolism and glucose levels

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7
Q

What does increased LH stimulate

A

Theca cells to produce androgens

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8
Q

What does adipose to to androgens

A

converts them to estrogen, which causes negative feedback to the anterior pituitary, decreasing FSH

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9
Q

How does PCOS present

A 
Infertility (PCOS is MCC***) 
Oligomenorrhea, Amenorrhea (anovulation) 
Obesity 
acne
hirsutism
male pattern baldness 
acanthosis nigricans
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10
Q

NIH 1990 criteria for PCOS (disorder of ovarian androgen excess) Dx says

A

Must have: oligomenorrhea + hyperandrogenism

Must exclude: hyperprolactinemia, CAH, and Cushing’s

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11
Q

Rotterdam 2003 crteria for PCOS says

A

Need 2/3: Ovulatory dysfunction, hyperandrogenism, or polycystic ovaries (12+ follicles)
Must exclude related disorders
(this criteria expands on the NIH criteria, does not replace it)

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12
Q

To have PCOS you must exclude

A 
premature ovarian failure 
physical stress 
obesity 
anovulation 2/2 d/c hormonal contraceptives 
pituitary adenoma/ hyperprolactinemia 
thyroid disorder
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13
Q

First line test if you suspect PCOS

A 
Ultrasound! you may see: 
12+ follicles, 2-9 mm in diameter 
"string of pearls" 
ovarian volume >10mL 
No evidence of dominant follicle or corpus luteum
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14
Q

To evaluate hyperandrogenism, start with

A

total testosterone. If normal (40-60), no further eval.

If >60, more testing

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15
Q

Further testing for hyperandrogenism (total testosterone >60) includes

A

17-OH progesterone (8AM): if >200, CAH
DHEA-S: >700, adrenal source of androgens
Cortisol: >10mcg, cushings
Prolactin: >25 is elevated. normal is PCOS (?)
TSH: Hyperthyroid causes oligo/amenorrhea
B-HCG: always order if amenorrhea!!

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16
Q

Other PCOS labs to get are

A

Fasting glucose
OGTT or HbA1c
Lipid profile

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17
Q

How do you treat PCOS

A 
Weight loss (increase SHBG, decrease free T) 
Metformin IF hyperinsulinemic 
COC (w/ low androgen) 
Fertility consult 
Provera (endometrial protection) 
Life-long lifestyle modification
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18
Q

What can you add to metformin to help treat infertility

A

Clomid!

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19
Q

How do you treat hirsutism

A

COC!

+/- antiandrogen (spironalactone), Topical vaniqa (anti-protozoal), mechanical hair removal

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20
Q

COC effects include

A

Increase SHBG= less free T

Decrease LH= decrease T production

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21
Q

Risks for PCOS include

A 
Endometrial hyperplasia 
T2DM 
HTN 
HLD 
CVD
stroke 
infertility 
metabolic syndrome 
sleep apnea
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22
Q

What should the ovaries feel like by age

A

Pre-menarche: not palpable
Reproductive: palpable 50% of time
Peri-menopause: very likely to have functional cysts
Post-menopause: not palpable w/in 3 years

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23
Q

What are characteristics of benign adnexal masses (US)

A 
thin walls 
<3cm pre-menopause, <1cm post (simple cyst) 
hyperechoic (teratoma) 
linear curved pattern (hemorrhagic) 
homogenous echoes (endometrioma)
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24
Q

What are characteristics of malignant adnexal masses on US

A

Thick separations >2mm
solid, nodular
increased blood flow to solid component

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25
Q

Functional ovarian cysts include

A

Follicular cysts (MC**)
Corpus luteum cysts
Theca Lutein cysts

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26
Q

Non-functional ovarian neoplasms include

A

Epithelial cell: serous, mucinous, endometrioid
Germ cell: benign cystic teratoma
Stromal cell: granulosa, sertoli-leydig, ovarian fibroma

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27
Q

What is the normal ovarian cycle

A
  • At start of each cycle, many primordial follicles fill with follicular fluid.
  • ONE follicle in ONE ovary matures into Graafian follicle, and has the ovum (other non-dom follicles regress)
  • At ovulation, Graafian follicle ruptures and ovum is released, becoming corpus luteum
  • No fertilization= corpud luteum degenerates into corpus albicans
  • Fertilization= corpus luteum persists and secretes progesterone to support pregnancy
28
Q

Describe Follicular cysts

A

2-8cm
non-malignant
regress after 1-2 cycles
occur 2/2 failure of mature follicle to rupture and release ovum, or, failure of non-dom follicles to regress

29
Q

Describe a corpus luteum cyst

A

3-11 cm
Regress after 1-2 cycles
After ovulation, blood accumulates in cavity of corpus luteum stimulating resorption.
If resorption does NOT occur and CL is >3cm, it’s a cyst
If corpus does not rupture, you don’t get a drop in progesterone, and miss a period

30
Q

Describe Theca lutein cysts

A

Seen with high HCG levela (abn pregnancy) 2/2 Hydatidiform moles, choriocarcinoma, clomid therapy
Bilateral
Clear, straw fluid
Regress spontaneously w/ underlying d/o Tx
more likely to have septations

31
Q

Describe a Serous cystadenoma

A

MC epithelial cell neoplasm, MC in 30-50 y/o
70% benign, 20% malignant
Treat w/ surgery (cyctectomy or oopherectomy)

32
Q

Describe a mucinous cystadenoma

A

15% malignancy rate
get very large
US shows multiocular septations
Treatment is surgical

33
Q

Describe a benign cystic teratoma

A

MC in reproductive aged women (30)
Originate from primordial cells and found along the path of germ cells from yolk sac to gonads
Composed of well differentiated tissue from ectoderm, mesoderm, or endoderm (germ cell)

34
Q

Benign cystic teratomas contain

A

keratinized squamous lining with abundant sebaceous and apocrine glands
Ectoderm is MC origin (hair, teeth, etc)

35
Q

How do teratomas present

A

Asymptomatic! found via pelvic exam or incidentally on imaging
Pelvic pain (2/2 torsion or rupture)
Urinary frequency/urgency, back pain
*Pelvic mass on bimanual exam

36
Q

Labs for a teratoma should include

A 
Transvaginal US (unilateral, complex cyst) 
CEA, CA-125, AFP, bets HCG (should all be normal)
37
Q

How do you treat a teratoma

A

Laparotomy vc Laparoscopy
Ovarian cystectomy vs Oopherectomy
10% recurrence

38
Q

Describe Theca cell tumors

A

produce ESTROGEN!
develop along female cell types
can be malignant. develop across lifespan

39
Q

Describe Sertoli-Leydig cell tumora

A

produce ANDROGENS!
develop along male gonadal tissue type
can be malignant. develop across lifespan

40
Q

Describe how ovarian fibromas present

A

MC in middle age, NO hormone production
result from spindle cell collagen production
Small, solid tumors with smooth surface. Associated with ascites

41
Q

Ovarian cancer has the highest incidence among

A

women >63

42
Q

RF for ovarian cancer include

A 
nulliparity 
early menarche, late menopause 
infertility 
endometriosis 
FHx ovarian, colorectal, or breast CA (BRCA 1/2, Lynch) 
High saturated animal fat diet 
obesity 
talcum powder 
Turner's syndrome 
ERT 
caucasian
43
Q

How can you reduce the risk of ovarian cancer

A 
multiparity 
breast feeding 
long term oral contraceptive use (5 years) 
B/l tubal ligation 
low fat diet 
*B/l salpingectomy
44
Q

What are the 4 major histologic types of ovarian cancer

A

Epithelial
Germ cell
Sex cord and stromal
Neoplasm mets to ovary

45
Q

Epithelial ovarian cancer subcategories are

A
  • High grade serous carcinoma: MC, arise in fallopian tube
  • Endometrioid: arise from ovary, but look like endometrium
  • Clear cell carcinoma: arise from ovary, malignant transformation of endometriosis
  • Mucinous carcinoma: arise from cervix, but look like cervical epithelium
46
Q

What is the pathophys theory behind ovarian cancer (ovary theory)

A

Follicular rupture= ovarian epithelial trauma
Incessant ovulation and subsequent epithelial repair leads to malignant transformation
associated with endometrioid, clear cell, and mucinous ovarian cancer (not serous)

47
Q

What is the fallopian tube theory behind ovarian cancer

A

-Mutant p53 (tumor suppressor) creates a signature on the distal fallopian tube
-Distal fallopian tube is where epithelial stem cells are susceptible to DNA damage and malignant change
-Serous tubal intraepithelial cancer results
STIC is a precursor to high grade serous papillary cancer

48
Q

The fallopian tube theory confirms why

A

salpingectomy is considered a method to reduce risk of ovarian cancer
No fallopian tube= No signature= no STIC= no cancer

49
Q

What are the types of germ cell ovarian cancers

A 
Dysgerminoma
Endodermal sinus tumor
Immature teratoma 
Mixed 
Embryonal tumors
50
Q

How do germ cell ovarian cancers usually grow

A

quickly, with lymph spread, MC unilaterally, containing a mix of tumor types
*They make markers that help with treatment response!

51
Q

Describe a dysgerminoma

A

MC germ cell ovarian tumor
Unilateral
MC in women <30
Produce LDH, some produce hCG

52
Q

Describe endodermal sinus tumors

A 
Rare 
Bilateral 
Occur in childhood and teens
Most rapid growing of germ cell neoplasm
Produce AFP
53
Q

Describe an immature teratoma

A

MC <20
Unilateral
Produce AFP

54
Q

Describe Embryonal carcinomas

A

Rare
Occur in childhood and teens
Rapid growth, extensive spread
Produce AFP and HCG

55
Q

What are the sex cord/stromal ovarian cancers

A

Granulosa cell, and Sertoli-Leydig

56
Q

Describe a Granulosa cell ovarian cancer

A

MC
Causes hyperestrogenism= precocious puberty, post-menopausal bleeding
Seen in 50’s

57
Q

Describe a Sertoli-Leydig stromal cell ovarian cancer

A

Rare
Causes hyperandrogenism
Seen in 30’s-40’s

58
Q

MC ovarian cancer symptoms are

A 
Abdominal bloating or distention 
Abd/pelvic pain 
Decreased energy (lethargy) 
Early satiety 
Urinary urgency
59
Q

Other ovarian cancer Sx are

A 
increased abd size 
indigestion 
constipation 
back pain 
unexplained weight loss 
abnormal vaginal bleeding
60
Q

Acute symptoms associated with ovarian cancer are

A

Pleural effusion

Bowel obstruction

61
Q

On an ovarian cancer physical exam you MC see

A

Ascites
inguinal LAD
pelvic mass

62
Q

Ovarian cancer imaging should include

A

transabd/transvag US
mammogram/colonoscopy
CT
MRI
CXR
CA-125 (will be >65 is epithelial cancer)
hCG, AFP, LDH (will be high with germ cell tumors)

63
Q

Why don’t we screen with CA-125

A

-Because it can be elevated with other conditions, like:
endometriosis, uterine leiomyomata
PID
pregnancy
menstruation
cirrhosis
-Also, it is only elevated 50% of the time in early stage ovarian cancer, and even less in late stage

64
Q

How is ovarian cancer staged

A

FIGO!

65
Q

Treatment for ovarian cancer includes

A

Surgery (remove tumor and mets, peritoneal washing, remove nodes, hysterectomy)
Chemo (Paclitaxel and Carboplatin 6 cycles at 3 wk intervals)

66
Q

Why do we want to diagnose early (obvs, but like why)

A

you can preserve the contralateral adnexa and uterus

GK F3E5 (19 decks)

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