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Female Repro Physiology > Female Path 2 > Flashcards

Female Path 2 Flashcards

1
Q

What are the common sx of PCOD (polycystic ovarian disease). What are you at risk for if you have this?

A
  1. Infertility
  2. Oligomenorrhea
  3. Hirsutism
  4. Type 2 DM

At risk for endometrial carcinoma (^ estrone)

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2
Q

What is the hormonal imbalance involved with PCOD?

A

LH:FSH>2
There is increased androgen production from theca cells that leads to hirsutism and estrone production in adipose tissue.
Increased estrogen causes neg feedback on FSH leading to degeneration of follicles

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3
Q

Ovarian tumors come in 3 flavors. What are they and how common is each one?

A
  1. Surface epithelium (75%)
  2. Germ cells (15-20%)
  3. Stromal cells (less than 5%)
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4
Q

What are the common sx of an epithelial ovarian tumor?

A

Vague abdominal pain/fullness

Signs of compression like urinary frequency

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5
Q

What serum maker is effective at monitoring tx response and recurrence of ovarian epithelial tumors?

A

CA-125

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6
Q

Epithelial ovarian tumors come in 2 different flavors that are then divided into 3 sub-flavors. Discuss.

A

Epithelial ovarian tumors are either SEROUS or MUCINOUS.

Within those 2 categories, they can be benign, borderline, or malignant

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7
Q

For serous tumors, tell me:

  1. Bilateral or unilateral?
  2. Gross appearance
  3. Mutations associated with low/high grade
  4. Mostly benign or malignant
  5. Recurrance rate
A
  1. Bilateral
  2. Thin walled cyst with watery, clear fluid
  3. Low-grade:KRAS or BRAF (stromal invasion)
    High-grade:p53 or BRCA1 (frank invasion)
  4. 60% benign
  5. High recurrence
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8
Q

For mucinous tumors tell me:

  1. Bilateral or unilateral
  2. Gross appearance
  3. Mostly benign or malignant
  4. Recurrence rate
A
  1. Unilateral
  2. Multicystic filled with gelatinous mucin
  3. 85% benign/borderline
  4. Low recurrence
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9
Q

What are the histological differences between benign, borderline and high grade ovarian epithelial tumors?

A

Bengin: single layer of columnar epithelium w/abundant cilia
Borderline: more complexity of stromal papillae, stratification of epithelium, nuclear atypia
High grade: more complex growth, branching papillary architecture + atypia, infiltration, PSAMMOMA bodies

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10
Q

Pseudomyxoma peritonei is what? Where does it come from?

A

Mucinous ovarian tumor that produces mucin leading to lots of mucin in the peritoneum and adhesions. It arises from a mucinous tumor of the appendix. “JELLY BELLY!”/ascites results.

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11
Q

A benign cystadenoma has what kind of histology?

A

One cell layer thick, with tall mucin secreting epithelium

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12
Q

A malignant cystadenocarcinoma has what kind of histology?

A

Complex, solid sheets of neoplastic cells with high N/C ratio and mitoses

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13
Q

Endometrioid ovarian tumors arise from what and are usually benign or malignant?

A

They can arise from endometriosis and are usually malignant . Another type of surface epithelial tumor.

*similar to endometrioid carcinoma of the uterus

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14
Q

Would you want to get clear cell adenocarcinoma?

A

NO, it a surface epithelial tumor that doesn’t respond to therapy and has a very poor prognosis.

It is the bad cousin of endometroid adenocarcinoma. Good thing it’s not super common.

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15
Q

A brenner tumor is a surface epithelial tumor that is a_________-like epithelial neoplasm that is usually unilateral/bilateral (pick one)

A
  1. Bladder like
  2. Unilateral

*epithalial nests appear inside ovarian stroma. RARE.

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16
Q

A cystadenofibroma is benign or malignant?

A

Benign. It’s rare.

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17
Q

Germ cell tumors represent what percentage of all ovarian neoplasms and are usually unilateral or bilateral?

A
  1. 15-20%

2. Unilateral

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18
Q

What are teratomas made of and what is the key imaging thing you’ll see. Is it benign or malignant? Is it common or uncommon? Tell me everythingggggg

A
  1. Contain all 3 embryonic layers
  2. Rokitansky tubercle (nodular protuberance) seen on the cyst wall
  3. Bengin
  4. COMMON (most common benign germ cell tumor)
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19
Q

In a dysgerminoma, what do you see on histology?

A

Large, cells with clear cytoplasm with round nuclei

20
Q

Dysgerminoma:

  1. Common or uncommon?
  2. Prognosis?
  3. What’s its testicular brother tumor?
A
  1. Common (most common malignant germ cell tumor)
  2. Good prognosis (responds to therapy)
  3. Seminoma
21
Q

A yolk sac tumor has tons of buzz words. Tell me what you’ll find on labs, histology and who gets this kind of tumor most commonly

A

BASCIALLY, if you see a CHILD with a tumor that secretes AFP and has SCHILLER-DUVAL bodies on histology, you can be like, yup, this kid’s got yolk sac tumor which is very sad because it is malignant.

22
Q

Now would you want to get choriocarcinoma? Why or why not? Support your answer with details on how you would know you have choriocarcinoma (histology, and labs)

A

No you would not because this malignant tumor does not respond well to chemo and has early hematogenous spread.

You would know you have it because the proliferating syncytiotrophoblasts would produces lots of hCG, and on histology you would would see placenta like tissue with no villi and lots of hemorrhage

23
Q

Embryonal carcinoma is made of what kind of cells? Is it a nice little tumor or a mean and deadly tumor?

A

It is made of large primitive cells and it is super mean and aggressive and has early metastasis.

24
Q

Finally we get to the sex-chord stromal tumors which as a whole make up

A
  1. Granulosa cell tumor
  2. Fibromas
  3. Sertoli-Leydig cell tumor
25
Q

In a granulosa cell tumor, what hormone is SUPER high and what kind of symptoms does this cause?

A

The proliferation of granulosa and theca cells in this tumor lead to very high levels of ESTROGEN. This causes precocious puberty and menorrhagia or metrorrhagia. It can lead to post-menopause endometrial hyperplasia and uterine bleeding, but has low risk of mets.

26
Q

What is the super high yield syndrome Fibromas are associated with?

A

This tumor of fibroblasts is associated with MEIGS syndrome, which is a combination of pleural effusions + ascites. When you take out the tumor, Meigs goes away.

27
Q

When I say Sertoli-Leydig Cell tumor, you say __________ crystals!

A

REINKE

28
Q

What sx will you see in a Sertoli-Leydig Cell tumor?

A

Excess androgens leading to hirsutism and virilization.

29
Q

Metastatic gastric carcinoma can cause __________ tumor

A

Krukenberg, a bilateral mucinous ovarian tumor

30
Q

In a spontaneous abortion, what symptoms will you see?

A

This person will come in with vaginal bleeding and crampy pain because of the passage of fetal tissue. In order for you to call this a miscarriage is has to occur before 20 wks.

31
Q

What are the common causes of spontaneous abortions

A
  1. Chromosomal anomalies (trisomy 16)
  2. Antiphospholipid snydrome (hypercoaguable state)
  3. Congenital infection
  4. Teratogens (esp in 1st 2 weeks of embryogenesis)
32
Q

A woman walks into the ER with acute abdominal pain and vaginal bleeding. You measure her hCG and it’s elevated. What is the top dx on your differential and what risk factors does she probably have that led to this dx?

A

Ectopic pregnancy

Risk factors for this include SCARRING, which can be secondary to:

  1. PID
  2. Endometriosis
  3. Chronic salpingitis
  4. Previous ectopic
  5. Tubal ligation
  6. permutable adhesions
  7. Reconstructive surgery
33
Q

On histology, what you likely to see with an ectopic pregnancy?

A

Hemorrhage, blood clots and chorionic villi in the fallopian tube lumen (or where ever the ectopic is). Chronic presentation will include plasma cells and lymphocytes.

34
Q

What is the difference between placenta previa and placental abruption?

A

In placenta previa, the placenta implants in the lower uterine segment so that it overlies the cervical os. It presents with 3rd trimester bleeding and the fetus will be delivered via C-section.

On the other hand, in placental abruption there is separation of the placenta from the decidua before the fetus is delivered, which means you’ll still have 3rd trimester bleeding but also have fetal insufficiency since nutrient/O2 transport to the baby is compromised. This will commonly lead to a still birth.

35
Q

If your patient has a difficult delivery of the placenta and then has postpartum bleeding, what dx should you think of? What is the treatment?

A

Think of a placenta accrete, which is when the placenta implants into the myometrium (not where its supposed to be obviously) leaving little or no intervening decidua.

The treatment for this is hysterectomy.

36
Q

What 3 criteria make you think “Oh, this person probably has preeclampsia!”

A
  1. HTN (>140/90)
  2. Proteinuria (>300mg/24hr)
  3. Edema
37
Q

What is the cause of preeclampsia and when does it usually present?

A

Remember, it is caused by an abnormality of the vascular interface of the placenta, and it usually presents in the 3rd trimester of pregnancy.

38
Q

How is eclampsia different from preeclampsia and how might you prevent/treat it?

A

Eclampsia is preeclampsia with seizures. In a woman with preeclampsia you may give MgSO4 prophylactically or for treatment

39
Q

HELP, What is HELLP??

A

H: Hemolysis
EL: Elevated Liver enzymes
LP: Low Platelets

Basically this is preeclampsia with a super bad liver disorder (liver thrombotic microangiopathy) added as an extra bonus.

40
Q

Your patient comes in with hCG way higher than is appropriate for her gestational age and a gigantic uterus. What do you think she has? What is she possibly at risk for?

A

Molar pregnancy.
Can be either complete or partial.

If she has a complete molar pregnancy, then she is at increased risk for choriocarcinoma.

41
Q

How do you tell the different between complete and partial molar pregnancies based on genotype?

A

Complete: A nonviable egg (one that has lost its DNA) is fertilized by a sperm that duplicates itself or by 2 sperm, and then it implants into the uterus. You get a genotype of 46XX or 46XY.

Partial: An egg is fertilized by a sperm that duplicates itself or by 2 sperm and implants into the uterus. You get a genotype of 69XXY or 92XXXY.

42
Q

How will you tell the difference between complete and molar pregnancies based on histology?

A

Complete: There is no fetal tissue, you have edematous, hydropic villi, and there is diffuse proliferation of trophoblasts around the hydropic villi

Partial: There is fetal tissue, and you have mostly normal villi with some hydropic villi. There is only focal proliferation of trophoblasts around the hydropic villi.

43
Q

Can the mole go through the uterine wall? If so, where can it go/what can it cause?

A

YES it can. This is called an invasive mole. It can embolize to the lung or brain or cause hemorrhage due to uterine rupture.

44
Q

What type of cells is a gestational choriocarcinoma made of? Does it have a good prognosis?

A

This rapidly invasive malignancy is made of syncytiotrophoblasts and cytotrophoblasts (cells that make up the placenta) but there are no chorionic villi.

It has a good prognosis despite the fact that it is prone to hematogenous spread

45
Q

Placental Site Trophoblastic Tumor is made of a specific type of trophoblastic cell. What are they, and what’s the general prognosis of this tumor?

A

Intermediate trophoblastic cells (arise from cytotrophoblastic cells)

This tumor is confined to the uterine cavity so has an excellent prognosis. Tx is surgery.

Female Repro Physiology (21 decks)

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