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Pathology Post Midterm > Module 3: Genital: Vular Carcinoma, Ectopic, Abortion, Hydatidiform and Chorio > Flashcards

Module 3: Genital: Vular Carcinoma, Ectopic, Abortion, Hydatidiform and Chorio Flashcards

1
Q

First topic of this set is vulvar carcinoma. There are two types of vulvar carcinoma. The first types is classic type. What are some features?

A

HPV 16,18,31,33 mutation

  • -women around 40 years old
  • –smoking/immunosuppressed patients
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2
Q

Leukoplakia is seen in patients with vulvar intraepithelial neoplasia classic types. What are the types of leukoplakia?

A

Lichen sclerous/Kraurosis Vulvae: autoimmune and in post menopausal women
–scaly plaques; thin parchment like with dense collagen
–slight increased risk for carcinoma
Squamous Cell Hyperplasia/Hyperplastic dystrophy: post menopausal women
–localized hyperplastic dermis
–no malignant potential

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3
Q

The next type of vulvar carcinoma is vulvar intraepithelial neoplasia differentiated type. what are some features?

A

More Common

  • -greater than 60 years old
  • -anterior 2/3rd of labia major most common site
  • -squamous cell carcinoma
  • -inguinal and pelvic lymph nodes
  • -greater than 1mm than increased risk of metastasis
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4
Q

If invasion of either type ,what is a symptom?

A

Inguinal lymphadenopathy

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5
Q

Next topic dealing with pregnancy is ectopic pregnancy. what does the gross image look like?

A

Intratubal hematoma of the Ampulla of the Fallopian Tube with a small embryo
–congested and dilated

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6
Q

What is the etiology for an ectopic pregnancy?

A

Interference of passage of the ovum either due to:

  • -chronic PID and scarring (untreated chlamydia from US)
  • -Endometriosis (cause scarring of the tubes from inflammation)
  • -any condition that causes blockage or fibrosis of the fallopian tubes or surrounding areas
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7
Q

What is the pathogenesis for an ectopic pregnancy?

A

Fertilized ovum implanted outside the uterine cavity
–Initially embryo is viable and women have amenorrhea and elevation of b-hCG which produces progesterone — causes hypersecretion in endometrium
After about 2-6 weeks post fertilization: Due to lack of space and blood supply embryo dies – drop in b-hCG–leads to degeneration of corpus luteum — decreased progesterone and estrogen – lower abdominal pain and vaginal bleeding due to the endometrium breaking down

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8
Q

What are common sites for ectopic pregnancy?

A

1% of pregnancies implant ectopically
–90%: Ampulla of fallopian tubes
other sites include cervix, ovaries and abdominal cavity
–in the Ampulla because fertilization happens here

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9
Q

What investigations are done for ectopic pregnancy?

A

Ultrasound most accurate tool
–visualize fetus in the fallopian tube, complete absence of uterine enlargement, expansion of adenxa
Surgical or Methotrexate treatment

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10
Q

What are complications of an Ectopic Pregnancy?

A

Rupture of ectopic pregnancy — sudden onset of intense abdominal pain – hypovolemic shock and death

  • -prompt surgical intervention
  • -Mimics acute appendicitis if on right side
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11
Q

If you do a D and C of the endometrium in patients with ectopic pregnancy what will you see?

A

Hypersecretory glands without chorionic villi

  • -on histology you will see arias stella reaction due to increased progesterone
  • -remember that spontaneous abortion also has hypersecretory glands except that it also has chorionic vili b/c implantation is in the right place.
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12
Q

Moving onto abortion around what time does this happen in the body?

A

Delivery 8-20 weeks due to defective chromosomes

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13
Q

What symptoms do patients get who are undergoing an abortion?

A

Vaginal Bleeding — rapid/severe shock

Lower abdominal pain due to uterine contractions

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14
Q

What is seen on D and C for abortion?

A

Have chorionic vili and hypersecretory glands because implanting in the right place

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15
Q

What are the three different types of placentas in a patient that can lead to an abortion?

A
  1. Placenta Previa: abnormal placental implantation, implants on LUS, internal OS in 3rd trimester
  2. Abruptio Placenta: implants normally but for some unexplained reason there is premature separation of placenta, leading to sudden massive hemorrhage
  3. Absence of plane of separation between vili and myometrium and vili go deep into the myometrium and mother will have retention of the placenta leading to severe hemorrhage.
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16
Q

Next topic of pregnancy relates to Pre-Eclampsia. This happens during the third trimester. What are the general presentation of these women?

A

Gestational Edema with Proteinuria and HTN (GEPH)

  • -different from a hypertensive patient becoming pregnant
  • -induce labor or do a C-section
17
Q

What are the pre-disposing factors?

A 
Primigravida over 35 
multiple pregnancies 
hydramnios 
pre-existing HTN 
Hydatidiform mole
18
Q

What is the pathogenesis for Pre-Eclampsia?

A
  1. Autoimmune reaction to placenta — placental ischemia
  2. Decreased production of PGE2 and NO by placenta — increased sensitivity to renin angiotensin
  3. DIC due to thromboplastic tissue factor and thromboxane released by ischemic placenta
  4. Increased vascular permeability (proteinuria and edema)
19
Q

What is seen in the kidneys and liver in pre-eclampsia?

A

Kidney: Glomerular Endothelial Swelling, Mesangial proliferation, fibrin thrombi and cortical necrosis
Liver: periportal hemorrhage

20
Q

What is seen on histology for patients with Pre-Eclampsia

A

Degenerated/ischemic Placenta= hyaline, calcification, congestion, infarcts, thrombosed spinal arteries, hemorrhages
-spinal arteries fail to dilate and thin out like a normal pregnancy due to lack of a smooth muscle coat
Acute Atherosis: foamy macrophages in necrotic vessel wall

21
Q

Before moving on to the next topic, what is a chorionic Villi?

A

Mother’s blood surrounds the villi (intervillous space)
Vili lined by inner cytotrophoblast (closer to stroma) and outer synctiotrophoblast (closer to mother)
–synctio is multinucleated, cyto is not
–synctio produces beta HCG
Baby’s blood in stroma of villi

22
Q

Now moving on to Hydatidiform Mole, what is this disease?

A

Gestational Trophoblast Disease (produces beta HCG)

  • -low end of spectrum of GTD
  • -complete and partial moles
  • -increase b HCG as the mole progresses
23
Q

What is the presentation for Hydatidiform Mole?

A

Age and Race are the two big Predisposing factors
Asian Women (far eastern)
–less than 20 and over 40 y/o
–high b HCG – morning sickness and amenorrhea (patients think they are prego)
—At 3 months, pass grape -like vesicles (increased b-HCG) – withdrawal bleeding (endometrium sloughs off)

24
Q

What do the various investigations for Hydatidiform Mole show?

A
  1. Pelvic Exam: uterus to large for date and grape like vesicles in the uterus
  2. Ultrasound: snowstorm appearance: fluid filled vesicles and no fetal heart sounds
  3. Presence of fetal parts: partial mole
25
Q

The definitive diagnosis is suction cutterage. What does this show?

A

Loose and hydropic stroma in the villi

  • -complete mole: all villi are abnormal
  • -partial mole: some villi are abnormal
26
Q

What does histology for patients with hydatidiform mole show? slide 11a and 11b

A

Edematous villi with proliferation of trophoblasts

27
Q

What are complications of hydatidiform mole?

A

High degree of recurrence
–dont attempt pregnancy for the next year: this allows serial monitoring of beta-HCG levels
Complete mole: gestational choriocarcinoma or invasive mole
Partial will not become invasive or choriocarcinoma
Bilateral theca luteal cysts in all beta-HCG elevated conditions (elevated progesterone)

28
Q

What are features of partial mole?

A
  1. Normal ovum + 2 sperm
  2. 69 chromosomes (69,XXY): triploid
  3. Fetal Tissue Present
  4. Some villi are hydropic
  5. Focal trophoblast proliferation
  6. Complications: recurrence and bilateral theca lutein cysts
  7. No risk of malignancy
29
Q

What are features of complete mole?

A
  1. Empty ovum+ 2 sperm (loss of all maternal chromosomes)
  2. 46 Chromosomes (46, XX) or (46, XY)
  3. Fetal Tissue Absent (or parts)
  4. Most villi are hydropic
  5. Diffuse trophoblast proliferation
  6. Complication: invasion
    - -bilateral theca lutein cysts in ovaries due to the beta HCG
    - -invasion of the myometrium
    - -gestational cohriocarcinoma (goes into endometrial cavity)
  7. Uterus is significantly enlarged
  8. Genotype is purely paternal
  9. 2% chance of choriocarcinoma
30
Q

What does invasive mole mean?

A

Invades the myometrium

–histology shows abnormal chorionic villi among normal smooth muscle

31
Q

Now moving on to gestational choriocarcinoma. what is the etiology?

A 
Complete Mole (most common) 
Spontaneous Abortion 
Ectopic or Normal Pregnancy 
Can develop de novo 
Highest level of beta HCG
32
Q

What is the presentation for a patient with gestational choriocarcinoma?

A 
Amenorrhea 
Exaggerated morning sickness
Brownish vaginal discharge and  bright red blood
--hemorrhagic tumor, new and old blood 
Pregnancy test positive
33
Q

What is the histology for gestational choriocarcinoma? slide 12

A

Malignant cytotrophoblasts and syncytiotrophoblasts
–no chorionic villi
Well differentiated (malignant cyto and syncytio)
Poorly differentiated : anaplasia

34
Q

Gestational Choriocarcinoma does not go through the lymph, what is the travel?

A

Travels via blood: vagina, liver, lung (cannonball opacities), brain, bone, kidney (hemoptysis and hematuria)

35
Q

What is the most accurate diagnostic test?

A

Scope

36
Q

Gestational Choriocarcinoma is chemotherapy sensitive why?

A

Beta-HCG tumor marker
Has paternal antigens
–reason it responds to chemo
–non- gestational (ovarian) is not chemo sensitive because no paternal antigens

37
Q

Patients with mole are told to not get pregnant for a year why?

A

So serial beta HCG can be done

Pathology Post Midterm (50 decks)

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