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review / wrong answers > DIT review - Reproduction 2 > Flashcards

DIT review - Reproduction 2 Flashcards

1
Q

What are the 4 main categories of ovarian tumors?

A

Epithelial, germ cell, stromal-sex cord, metastatic

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2
Q

What are the different types of ovarian epithelial tumors?

A

Serous, Mucinous, Brenner, Endometriod

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3
Q

Type of epithelium in serous cystadenoma of the ovary

A
  • Lined with fallopian tube-like epithelium (ciliated)
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4
Q

What is the most common type of ovarian neoplasm?

A

Serous cystadenoma

Serous cystadenocarcinoma is most common malignant type

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5
Q

HIstological feature of serous cystadenocarcinoma of the ovary

A

Psammoma bodies

Papillary thyroid carcinoma, serous cystadenocarcinoma, meningioma, mesothelioma

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6
Q

Complication of mucinous cystadenocarcinoma

A
  • Can cause pseudomyxoma peritonei
    • Accumulation of mucinous material within the peritoneum
    • Due to ovarian or appendiceal tumor
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7
Q

Risk factor for endometroid tumor

A

Endometriosis

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8
Q

Epithelium of Brenner tumor

A
  • Composed of bladder-like (transitional) epithelium
  • Solid tumor that is pale yellow-tan and appears encapsulated
  • “Coffee bean” nuclei on H&E
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9
Q

What are the 4 germ cell tumors of the ovary?

A

Cystic teratoma

Dysgerminoma

Endodermal sinus tumor

Choriocarcinoma

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10
Q

What is struma ovarii

A

A type of teratoma containing thyroid tissue

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11
Q

Cell type that makes up dysgerminoma

A

Oocytes

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12
Q

Histology of dysgerminoma

A
  • “Fried egg” cells – large cells with clear cytoplasm and central nuclei
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13
Q

Male equivalent of dysgerminoma

A

Seminoma

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14
Q

Tumor marker of dysgerminoma

A

LDH (lactic dehydrogenase)

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15
Q

Tumor marker and histology of endodermal sinus tumor

A
  • Aka Yolk sac tumor
  • Most common germ cell tumor in children
  • Elevated serum AFP
  • Schiller-Duval bodies
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16
Q

Tumor marker of choriocarcinoma

A

Elevated bHCG

  • Tumor of placenta – mimics placental tissue but villi are absent
  • Comprised of cytotrophoblasts and syncitiotrophoblassts
  • Elevated bHCG (produced by syncytiotrophoblasts)
17
Q

Presentation of granulosa-theca cell tumor

A
  • Malignant
  • Produces estrogen/progesterone
  • Presentation:
    • Precocious puberty
    • Menorrhagia/metrorrhagia
    • Postmenopausal bleeding
18
Q

Histology of granulosa-theca cell tumor

A

Call-Exner bodies

  • Granulosa cells arranged haphazardly around collections of eosinophilic fluid, resembling primordial follicles
19
Q

Histology and presentation of Sertoli-Leydig cell tumor

A
  • Characteristic Reinke crystals
  • May produce androgens à hirsutism, virilization
20
Q

What is Meigs syndrome

A
  • Meigs syndrome:
    • Triad of: ovarian fibroma, ascites, pleural effusion
21
Q

What is Krukenberg tumor

A
  • GI carcinoma metastasis to the ovaries
  • Usually bilateral ovaries affected
  • Contains mucin-secreting signet cells
22
Q

Describe the timeframe of twinning

A
  • 0-4 days – dichorionic/diamniotic
  • 4-8 days – monochorionic/diamniotic
  • 8-12 days – monochorionic/monoamniotic
  • >13 days – conjoined twins
23
Q

With what type of twins can twin-twin transfusion syndrome occur?

A
  • Occurs in monochorionic/diamniotic twins
  • Arterio-venous anastamosis leads to shunting of blood
  • Donor – anemic, pale, growth restricted
  • Recipient – polycythemic, plethoric, overloaded, heart failure
24
Q

Presentation of hydatidiform mole

A
  • Abnormal fertilization with swelling of chorionic villi and proliferation of trophoblasts
  • Presentation:
    • Vaginal bleeding
    • Uterus enlargement
    • “Snowstorm” appearance on US
    • b-hCG higher than would be in normal pregnancy
    • Passage of grape-like masses through vaginal canal
25
Q

Complete vs. Partial mole (chr #, fetal tissue presence, risk for choriocarcinoma)

A
  • Partial mole:
    • Normal ovum fertilized by 2 sperm – 69 chromosomes
    • Fetal tissue present
    • Minimal risk for choriocarcinoma
  • Complete mole:
    • Empty ovum fertilized by 2 sperm – 46 chromosomes
    • Fetal tissue absent (only DNA is from dad)
    • Incrreased risk of choriocarcinoma
26
Q

Presentation of placenta abruption

A
  • Placenta abruption:
    • Premature separation of placenta from uterine wall before delivery
    • Presentation:
      • Abrupt, painful bleeding in the 3rd trimester (vs. placenta previa which is painless)
      • Possible DIC, maternal shock, fetal distress
      • Life threatening for mother and fetus
27
Q

Risk factors for placenta abruption

A
  • Smoking, trauma, HTN, cocaine abuse
28
Q

Differentiate between placenta accreta/increta/percreta and describe the general presentation

A
  • Presentation:
    • No separation of placenta after delivery
    • Postpartum bleeding
  • Types:
    • Placenta accreta – placenta attaches to myometrium without penetration
    • Placenta increta – placenta penetrates into myometrium
    • Placenta percreta – placent penetrates and perforates through the myometrium
      • Can attach to rectum or bladder
29
Q

Presentation of placenta previa

A
  • Attachment of placenta to lower uterus over internal cervical os
  • Presentation:
    • Painless third trimester bleeding (vs. placenta abrupta which is painful)
30
Q

What is vasa previa?

A
  • Fetal vessel run over, or in close proximity to, cervical os
  • May result in vessel rupture, exsanguination, fetal death
31
Q

Diagnostic criteria of preeclampsia

A
  • HTN: BP > 140/90 after 20th week of gestation
  • Proteinuria
  • Edema
32
Q

Treatment of eclampsia

A
  • Preeclampsia + seizures
  • Treatment: IV magnesium sulfate, anti-hypertensives, immediate delivery
33
Q

What does HELLP syndrome stand for and what is the reasoning behind the symptoms

A
  • Stands for:
    • H - Hemolysis (anemia)
    • EL - Elevated Liver enzymes (RUQ pain, jaundice)
    • LP - Low Platelets (bruising bleeding)
  • Preeclampsia + thrombotic microangiopathy
    • Hemolysis = thrombi causing schistocytes
    • Liver enzymes = lack of RBCs leads to infarction of liver tissue
    • Platelets = all used up in thrombi
34
Q

Cause of gestational diabetes

A
  • Human placental lactogen (HPL) leads to increased insulin resistance
    • This allows shunting of glucose to baby
  • Seen at 24-28 weeks
  • Risk for baby:
    • Macrosomia
    • Stillbirth
35
Q

Pathogenesis of Potter sequence

A
  • Urinary tract anomaly -> anuria/oliguria in utero -> oligohydramnios ->
    • Pulmonary hypoplasia
    • Flat facies
    • Limb deformities
  • Can be caused by maternal use of ACEI during pregnancy leading to renal dysgenesis

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