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Pathophys > Preg and lactation > Flashcards

Preg and lactation Flashcards

1
Q

what is the Zona Pellucida

A

the oocyte membrane which the sperm passes through during fertilization

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2
Q

what hormone is involved in transport of the ovum? when does it occur?

A

Isthmus of the tube remains contracted for first 3 days after ovulation. Progesterone relaxes the smooth muscle allowing entry into the uterus

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3
Q

why is it important that the fallopian tubes remain contracted for the first 3 days after ovulation

A

it allows for several stages of cell division forming the blastocyte

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4
Q

what does the blastocyst use for nutrition as it travels to implantation

A

uterine milk

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5
Q

how long is the blastocyst in the uterus before implantation

A

1-3days

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6
Q

what is the role of the cytotrophoblasts

A

the inner layer of the trophoblast that attaches the blastocyst to the endmetrium

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7
Q

what is the role of the syncytiotrophoblast

A

the outertrophoblast layer that makes the nutrient connection to the endometrium

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8
Q

how does the progesterone (released from the corpus luteum) affect the endometrial cells

A

it causes the endometrial cells to become swollen and filled with glycogen, proteins, and lipids

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9
Q

After implantation Progesterone causes endometrial cells to swell further forming what?

A

DECIDUAL CELLS (decidua) (allow for nutrition)

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10
Q

what is the chorion

A

the layer bt placenta and mother formed by tropoblasts

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11
Q

for how long does the embryo obtain nutrient from the decidua by trophoblastic nutrition? where is the nutritional source after this?

A

up to 8 wks. Then placental diffusion takes over

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12
Q

what do the umbilical arteries do?

A

carry deoxygenated blood from fetus to placenta

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13
Q

what do the umbilical veins do?

A

carry oxygenated blood from placenta to fetus

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14
Q

when is blood pumped by the fetal heart

A

21 days post fertilization

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15
Q

what ratio can be used to assess fetal development

A

fetal placental weight ratio (1g placenta feeds 7g fetal tissue)

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16
Q

what are the typical vascular contents in the umbilical cord

A

2 umbilical arteries, 1 umbilical vein

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17
Q

what 4 factors contribute to the oxygen gradient in the placenta

A

Maternal 50mmHg: fetal 30mmHg
Fetal hemoglobin= inc affinity
Hemoglobin concentration= 50% greater in fetus
Double Bohr Effect- fetal blood alkaline, moms is acidic

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18
Q

how does glu pass through the placenta

A

facilitated diffusion in the placenta

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19
Q

how do fatty acids pass through the placenta

A

diffusion

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20
Q

what secretes hCG

A

tropoblasts

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21
Q

when is hCG detectable in the blood? when does it peak?

A

in blood 8-9 days post ovulation (just after implantation), peaks 10-12 wks

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22
Q

inc hCG effect?

A

Maintains corpus luteum beyond normal lifespan

Stimulates production of progesterone and E2: (keeps FSH low to prevent menstruation)

Endometrium forms decidua-like cells.

hCG receptors in endometrium and myometrium and can inhibit contractions produced by oxytocin

Immunosuppressant

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23
Q

when will the corpus luteum degrade if it is stimulated by hCG

A

Corpus luteum involutes after 13th to 17th week when placenta takes over hormone production.

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24
Q

where is estradiol initially produced (first 5-6wks following implantation)? where is it produced after?

A

Initially produced by corpus luteum (first 5-6 wks) stimulated by hCG
Then from placenta syncytial trophoblast cells (from DHEA-S from adrenals of fetus and maternal)

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25
Q

what is the maternal/ fetal requirement to properly make estrogen and maintain the uterus

A

need healthy adrenal glands in both the mother and the fetus

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26
Q

what is the function of estradiol is preg

A 
Proliferative function
Enlargement of:
-Uterus
-Breast tissue and ducts
-External genitalia
Relax pelvis ligaments (along with relaxin)
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27
Q

how does estradiol affect Sacroiliac joints and

Symphysis pubis

A

Sacroiliac joints: limber

Symphysis pubis: elastic

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28
Q

what does urine estiol indicate

A

index of fetal well-being (fetal and maternal adrenals working)

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29
Q

where is progesterone produced in pregnancy

A

Corpus Luteum followed by placenta production

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30
Q

what do the fetal/maternal adrenal glands use progesterone for

A

it is the major substrate for cortisol and aldosterone

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31
Q

what is the backbone of estrogen and progesterone

A

cholesterol

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32
Q

what is progesterones effect in preg

A

Decreases contractility of uterus: inhibits prostaglandin production and dec sens to oxytocin

Increases secretions of fallopian tubes and uterus

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33
Q

what is the function of Human Chorionic Somatomammotropin (hPL)

A

Development of breast tissue
Similar to action of growth hormone
-formation of protein tissues
-dec insulin sens in mother

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34
Q

when/where is hPL produced

A

Secreted by placenta by 5th week of pregnancy

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35
Q

what happens to resting BS levels during preg

A

they typically inc to allow inc use by the fetus

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36
Q

what are the CO changes during preg

A

Increase in cardiac output: 30-40% by 27th week then slightly above normal at parturition (less active in 3rd trimester= dec need)

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37
Q

what are the blood volume changes during preg

A

inc at least 30%

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38
Q

what needs to be monitored in a hypothyroid pt during preg

A

they may not be able to adapt to the inc in maternal metabolism (need to inc synthroid)

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39
Q

what is the BP changes during preg

A

BP only slightly increases but they dec close to term bc vasodilation causes dec TPR

40
Q

why does respiration inc during preg

A

Progesterone increases respiratory center’s sensitivity to CO2

41
Q

what is the kidney function change during preg

A

Estrogen causes vasodilation of afferent aa.= Increase GFR and Increase RBF

There is also inc Na absorption to allow for inc volume

42
Q

what is the definition of spontaneous abortion

A

pregnancy loss before 20 weeks of gestation

43
Q

when do most spontaneous abortions occur by

A

12wks

44
Q

what % of clinically recognized preg are spontaneously aborted

A

10-15%

45
Q

what is aneuploidy

A

abn # of chromosomes

46
Q

what is polyploidy

A

more than the 2 paired sets of chromosomes

47
Q

what are maternal causes of spontaneous abortions

A 
Luteal-phase defect
Poorly controlled diabetes 
Other uncorrected endocrine disorders
Physical defects of the uterus : 
Systemic disorders affecting maternal vasculature
Bacterial
48
Q

how can lupus cause spontaneous abortions

A

can cause antiphospholipid antibody syndrome= hypercoag state

49
Q

which trimester is ascending infections more common to cause spontaneous abortions

A

2nd

50
Q

what is the definition of ectopic pregnancy

A

Implantation of the fetus in any site other than a normal intrauterine location

51
Q

where is the most common sites of ectopic preg

A 
Fallopian tubes (∼90%)
Ovary
Abdominal cavity
Intrauterine portion of the fallopian tube (cornual pregnancy)
52
Q

what inc risk for ectopic preg

A
  • Prior pelvic inflammatory disease resulting in fallopian tube scarring (chronic follicular salpingitis)
  • Appendicitis
  • Endometriosis
  • Previous surgery
  • Intrauterine contraceptive devices:
53
Q

what is the most common cause of hematosalpinx

A

hematosalpinx(blood-filled fallopian tube) is most commonly caused by tubal pregnancy

54
Q

when does severe abd pain occur with ectopic preg? what other Sx occur?

A

6wks from previous normal menstral period. hemorrhagic shock with signs of an acute abdomen

55
Q

ectopic preg dx

A

Diagnosis : Chorionic gonadotropin assays, ultrasound studies, and laparoscopy

56
Q

when can US imply monozygotic twins

A

only with monoamnionic monochorionic placentas

57
Q

what occurs when division of monozygotic embryo at day 1-3 p fert

A

dichorion-diamnion

58
Q

what occurs when division of monozygotic embryo at day 4-6 p fert

A

monochorion-diamnion

59
Q

what occurs when division of monozygotic embryo at day 7-9 p fert

A

monochorion-monoamnion

60
Q

what is placenta accreta

A

Partial or complete absence of decidua with adherence of the placental villous tissue directly to the myometrium and failure of placental separation

61
Q

what are pridisposing factors for placenta accreta

A 
Placenta previa (60% of cases) 
History of previous cesarean section
62
Q

how do accreta, increta, and percreta differ

A

Accreta: Invasion of myometrium-does not penetrate entire thickness
Increta: Extends into myometrium-penetrating the muscle
Percreta: Penetrates entire myometrium to serosa

63
Q

how does preeclampsia differ from gestational hypertension

A

proteinuria with preeclampsia

64
Q

how does preeclampsia differ from gestational eclampsia

A

convulsions with eclampsia

65
Q

what is HELLP syndrome

A

hemolysis, elevated liver enzymes, low platelets

66
Q

what plays a role in the pathogenesis of preeclampsia/eclampsia

A

The exact mechanisms : still being investigated
Placenta plays a central role in the pathogenesis
Symptoms disappear after delivery of the placenta

67
Q

what are the critical abnormalities in preeclampsia

A

Diffuse endothelial dysfunction
Vasoconstriction (leading to hypertension)
Increased vascular permeability (proteinuria and edema)

68
Q

what are the characteristic findings of the placenta in eclampsia

A

Thrombosis, lack of normal physiologic conversion, fibrinoid necrosis, or intraintimal lipid deposition (acute atherosis)

69
Q

how is the liver affected from eclampsia

A

irregular, focal, subcapsular, and intraparenchymal hemorrhages lesions

70
Q

how are the kidneys affected from eclampsia

A

Glomerular lesions : diffuse, marked swelling of endothelial cells, the deposition of fibrinogen-derived amorphous dense deposits on the endothelial side of the basement membrane, and mesangial cell hyperplasia
Bilateral renal cortical necrosis : in severe cases

71
Q

what other organs can have thromboses/hemorrhage from eclampsia

A

liver, kidney, Brain, heart and the anterior pituitary

72
Q

what causes the proliferation of placental tissue(either villous or trophoblastic) seen in gestational trophoblastic diseases

A

Amplification and overexpression of oncogene products: erbB-2 & EGFR
Downregulation of tumor suppressor genes: p53, Rb

73
Q

what lesions are included in gestational trophoblastic diseases

A

Hydatidiform mole (complete and partial)
Invasive mole
Choriocarcinoma
Placental-site trophoblastic tumor

74
Q

what are hydatidiform moles characterized histologically by

A

cystic swelling of the chorionic villi

variable trophoblastic proliferation

75
Q

what do hydatidiform moles inc risk for

A

Associated with an increased risk of persistent trophoblastic disease (invasive mole) or choriocarcinoma

76
Q

what causes complete moles

A

Results from fertilization of an egg that has lost its chromosomes, and the genetic material is completely paternally derived

77
Q

what causes partial moles to form

A

Partial moles arise from two sperm fertilizing a single ovum

Karyotype is triploid (e.g., 69,XXY) or occasionally tetraploid (92,XXXY)

78
Q

what type of mole has a risk of causing choriocarcinoma

A

only complete

79
Q

why is hCG extremely elevated with hydatidiform moles?

A

trophoblasts produce hCG

80
Q

what is the classic gross appearance of hydatidiform mole morphology

A

delicate, friable mass of thin-walled, translucent, cystic, grapelike structures

81
Q

how do partial and complete moles differ histologically

A

Partial mole :
Fetal parts are more commonly present
Some villi are edematous
Trophoblastic proliferation is focal and less marked
Complete mole :
All or most of the villi are enlarged and edematous
Diffuse trophoblast hyperplasia

82
Q

what is used to differentiate partial from complete moles

A

p57- which is maternally transcribed but paternally imprinted

83
Q

what is seen with US with hydatidiform mole

A

diffuse villous enlargement

84
Q

how are hydatidiform moles monitored to determine if they become persistent/invasive or choriocarcinomas

A

serum HCG levels are usually followed until they fall to and remain at zero for 6 months to a year

85
Q

what is a invasive mole

A

A mole that penetrates or even perforates the uterine wall

Invasion of the myometrium by hydropic chorionic villi, accompanied by proliferation

86
Q

what are clinical features of invasive moles

A

Vaginal bleeding and irregular uterine enlargement

Persistently elevated serum HCG

Varying degrees of luteinization of the ovaries

May result in uterine rupture

87
Q

how are invasive moles//choriocarcinomas treated

A

both respond well to chemotherapy

88
Q

what is necessary if a invasive mole results in uterine rupture

A

hysterectomy

89
Q

what are choriocarcinomas

A

A malignant neoplasm of trophoblastic cells derived from a previously normal or abnormal pregnancy, which can even include extrauterine ectopic pregnancy

90
Q

choriocarcinoma have a overexpression of what

A

EGFR

91
Q

what is the gross morphology of choriocarcinomas

A

Classically a soft, fleshy, yellow-white tumor

Large pale areas of ischemic necrosis, foci of cystic softening, and extensive hemorrhage

92
Q

what is the histological morphology of choriocarcinomas

A

Does not produce chorionic villi
Consists entirely of a mixed proliferation of syncytiotrophoblasts and cytotrophoblasts
Mitoses are abundant

93
Q

where are choriocarcinoma metastases found

A

Metastases are found in the lungs, brain, bone marrow, liver, and other organs

94
Q

what are placental-site trophoblastic tumors (PSTT)

A

Neoplastic proliferation of extravillous trophoblast

95
Q

what are the clinical features of PSTT

A

Uterine mass with

  • Abnormal uterine bleeding
  • Amenorrhea
  • Moderate elevation of β-HCG

Pathophys (15 decks)

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