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EndoRepro > Week 4 > Flashcards

Week 4 Flashcards

1
Q

explain: Blastocyst Implantation

Apposition

A
  • Apposition: Initial adhesion of the blastocyst to the uterine wall
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2
Q

Explain: Blastocyst Implantation

Adhesion

A
  • Adhesion: Increased physical contact between blastocyst and uterine epithelium
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3
Q

Explain: Blastocyst Implantation

Invasion

what happens to the trophoblasts at this point

A
  • Invasion: Penetration and invasion of trophoblast into the endometrium → inner third of the myometrium and uterine vasculature
    • The trophectoderm gives rise to the first layer of trophoblast cells that surround the blastocyst
    • Trophoblast (8th day after fertilization) differentiates into inner (cytotrophoblast) and an outer layer (syncytiotrophoblast).
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4
Q

Syncytiotrophoblast versus cytotrophoblast

A
  • Syncytiotrophoblast – consists non-individualized cells with amorphous cytoplasm that help facilitate transport; stimulates corpus luteum to secrete progesterone
  • Cytotrophoblast – mononuclear cells that at Day 13-20 form villi
    • *
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5
Q

subtypes cytotrophoblast

A

Villous trophoblast (primary transport oxygen and nutrients)

Extravillous trophoblast (migrates into the decidua and myometrium and penetrates maternal vasculature)

  • Spiral arteries in endometrium are remodeled by extravillous trophoblast cells and NK cells → penetration of myometrium → allows for adequate blood flow/exchange for normal pregnancy
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6
Q

function of placenta

A
  • Basic functions: respiratory exchange, metabolite exchange, hormone synthesis, and hormone regulation
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7
Q

layers of placenta

A
  • Outer layers of placenta: amnion (inner layer) and chorion (outer layer) → eventually fuse laterally
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8
Q

what is the functional unit of the placenta

what is comprised of

A
  • Functional unit of placenta: villus
    • Comprised of a vast surface area filled with fetal capillaries that allow for exchange of nutrients, metabolites, hormones, and oxygen → blood travels through umbilical cord → fetus
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9
Q

what are some characterisitics of circulation of the placenta

A
  • Umbilical vein: O2 rich/Umbilical artery: O2 poor
  • Circulation is hemochorial – no direct connection between spiral arteries and fetal circulation
    • Endometrial arteries/veins: derived from spiral arteries allow for exchange between mother and fetus
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10
Q

Describe changes in the cross-section of placenta villi

A
  • First-trimester placenta: Syncytiotrophoblasts and cytotrophoblasts line the full membrane with no gaps
  • Term placenta: Syncytiotrophoblasts start to form aggregations and few cytotrophoblasts persist (more chaotic state)
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11
Q

what is Morbidly adherent

A
  • Morbidly adherent: when placenta villi invade serosa of uterus (pathological state)
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12
Q

what is the function of hCG

A
  • hCG: glycoprotein very similar to LH/TSH/FSH (same alpha unit) produced almost exclusively in the placenta
    • High carbohydrate content protects the hormone from degradation
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13
Q

what is the function of hPL

A
  • hPL (Human Placental Lactogen): hormone made by early trophoblasts that is analogous to growth hormone (similar to prolactin)
    • Functions: maternal lipolysis (increased circulating fatty acids), diabetogenic (increases maternal insulin level), angiogenic (forms fetal vasculature)
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14
Q

what are the

Hypothalamic-like releasing hormones

A
  • GnRH (gonadotropin releasing hormone), CRH (releases cortisol), GHRH (growth hormone releasing hormone)
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15
Q

what are the functions of the following Placental peptide hormones

Leptin, neuropeptide Y, inhibin & activan

A
  • Leptin: anti-obesity hormone normally secreted by adipocytes → decreased food intake
  • Neuropeptide Y: secreted from cytotrophoblasts → increase in CRH release
  • Inhibin and Activin:
    • Inhibin: secreted by ovarian granulosa cells → ceases possibility of ovulation
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16
Q

Function of

Progesterone and estrogen

A
  • Progesterone: placenta produces a large amount of progesterone from maternal cholesterol → maintains uterine lining through pregnancy
  • Estrogen: derived from fetal androgens
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17
Q

Adrenal gland hormones

what are thoossssssseeeee?

A
  • Fetal zone produces androgens (DHEAS) that are used to synthesize placental estrogens
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18
Q

Describe the anatomical and functional changes in…

CV system

A
  • Anatomic changes: larger cardiac silhouette – mild LV hypertrophy → S3 gallop
  • Function changes:
    • ↑ cardiac output – ↑ HR, SV → tachycardia
    • ↑ blood volume – peaks at week 32
    • Progesterone → ↓ SVR → state of hypotension → fatigue, syncope, ↓ exercise tolerance
    • ↑ venous pressure/ IVC obstruction by growing uterus → edema, distended veins
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19
Q

How does CO an BP change in labor and post-partum

A

↑ CO, BP

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20
Q

Describe the anatomical and functional changes in…

Respiratory

A
  • Anatomic changes: progesterone → chest expands & diaphragm rises (allows uterus to expand) → ↓ TLC, RV, FRC
    • Estrogen → nasal mucosa swollen and edematous
  • Functional changes:
    • ↑ inspiratory capacity, tidal volume, minute ventilation and O2 consumption
    • Vital capacity and RR stays the same
    • Hyperventilation → ↓ PaCO2 → chronic respiratory alkalosis (help transfer O2 from mother to fetus)→ ↑ renal bicarbonate excretion
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21
Q

Describe the changes in…

Hematology (Rahul’s fav subject)

No one cares about hematology

A
  • Hypotension → activation of RAAS → salt retention and thirst → ↑ plasma → ↑ circulating volume → dilutional anemia
  • Progesterone + prolactin → ↑ RBCs
    • ↑ iron demand (~100 mg) → anemia
  • Estrogen + cortisol → ↑ WBC (~16000); more during labor
    • Immune tolerance to fetus (NOT deficiency)
      • ↓ cellular immunity: ↑ susceptibility to CMV, varicella, malaria AND improvement in autoimmune disease like RA
      • Enhanced AB-mediated immunity, IgG decreases because it goes to placenta → passive immunity
  • ↑ coagulation factors ( VII, VIII, IX, X) and ↓ Protein C/S → ↑ risk of venous thromboembolism → DVT, PE (Higher risk postpartum)
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22
Q

Describe anatomical and functional changes in…

renal system

A
  • Anatomical changes: enlarged kidneys, dilation of collecting systems (due to progesterone)
    • Compression of bladder by uterus → stress incontinence → ↑ RV → ↑ risk of UTI
  • Functional changes:
    • ↑ renal blood flow → ↑ GFR → ↑ clearance of creatinine (↓ serum creatinine/BUN), glucose, vitamins (not proteins) and ↑ reabsorption of salt
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23
Q

Describe anatomical and functional changes in…

GI

what are other random sx that happen

A
  • Anatomical changes: appendix displaced by uterus
  • Functional changes:
    • ↓ tone/motility → reflux and constipation
    • ↑ venous pressure → hemorrhoids
    • ↓ gallbladder contractility → cholestasis, gallstones
  • Other signs/symptoms: N/V (hyperemesis gravidarum caused by beta-hCG), dietary changes, blunted taste, pica, ptyalism (↑ saliva produced), gingival disease
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24
Q

what are the anatomical and functional changes that happen in..

endocrine system

A
  • Anatomical changes: thyroid enlarges (no change seen in adrenal gland)
  • Functional changes:
    • Thyroid: alpha- hCG binds to thyroid receptors → ↑ T4 secretion → ↓ TSH (mimics hyperthyroidism)
      • ↑ in TBG → serum T4 unchanged → euthyroid
    • Adrenal: ↑ release of cortisol, corticotropin, aldosterone, deoxycorticosterone, DHEAS
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25
Q

what are some changes that happen in..

metabolism of

carbs, lipids, protein

A
  • Carbohydrate: hPL → Reduced tissue response to insulin → hyperinsulinemia/hyperglycemia (fasting hypoglycemia)
  • Lipid (breast feeding reduced lipids)
    • Early: fat storage
    • Late: lipolysis → fasting hypoglycemia
  • Protein: ↑ intake and utilization
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26
Q

what are the functional and atanomical changes that oocur in..

MKS

A
  • Anatomic changes:
    • Change in center of gravity → lordosis → back pain
    • Laxity of ligaments/joint loosening
    • Pubic symphysis separation
  • Functional changes
    • Calcium: ↑ need for fetus → ↑ absorption and ↓ excretion
      • Maternal bone mass maintained b/c ↑ calcitonin
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27
Q

list some changes in

skin, reproductive tract, hair, eyes

A
  • Skin: Spider angiomata, Palmar erythema, Striae gravidarum, Hyperpigmentation, Melasma/Chloasma, Acne, Change in nevi
  • Hair: hirsutism (↑ androgens/cortisol), telogen effluvium (thinning of hair on scalp)
  • Reproductive tract: vulvar varicosities, leukorrhea (white vaginal fluid), ↑ uterine size
  • Eye: ↑ corneal thickness and ↓ intraocular pressure → blurry vision
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28
Q

what are anatomical and functional changes of

breasts

what are sx

A
  • Anatomical changes: enlarged breast, nipple enlarge and mobile, deeply pigmented areolae
  • Functional: estrogen → ductal growth; progesterone → alveolar hypertrophy
  • Signs and symptoms: tingling and tenderness of breast
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29
Q

fun facts bout fetal Hbg

A
  • Fetal Hgb has a higher O2 affinity and O2 saturation than adult Hgb at any given O2 tension
  • Fetal O2 curve shifts to left→ increase oxygen binding affinity
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30
Q

Discuss how to date a pregnancy

mainly what is LMP

A
  • Dating: determine gestational age of pregnancy using time since last menstrual period (LMP – first day of last normal menstrual period)
    • True gestational period = time since LMP – 2 weeks (corrects for period of ovulation – 14 days)
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31
Q

discuss LMP vs. CRL

A
  • Ultrasound dating of fetus: LMP vs CRL
    • CRL: crown rump length is a measurement of the fetus from the crown (head) to the buttocks (rump)
      • CRL can be used if there is a difference > 5 days between CRL and LMP
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32
Q

DDx for N/V in early pregnancy

A

viral gastroenteritis, food poisoning, normal N/V or pregnancy, and hyperemesis gravidarum

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33
Q

normal N/V vs. hyperemesis gravidarum

discuss wt change, impact, tx

A
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34
Q

Develop a differential diagnosis for 1st trimester bleeding

how do we diagnosis this

A
  • DDx for 1st trimester bleeding: threatened/actual abortion, ectopic pregnancy, cervicitis, cervical polyps, molar pregnancy, neoplasia, trauma
  • Diagnosis: Transvaginal US and bHCG levels
    • bHCG levels should normally double every 48 hours for ten weeks
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35
Q

definition and complications of ectopic pregnancy

A
  • Definition: pregnancy that implants outside of the endometrium of the uterus
  • Complications of ectopic pregnancy:
    • Loss of this pregnancy, decreased/lost fertility, damage to non-reproductive organs, maternal hemorrhage, possible need for maternal hospitalization/transfusion/surgery
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36
Q

Know the gestational ages of different findings during embryological development

A
  • Gestational sac: 5 weeks
  • Yolk sac: 6 weeks
  • Embryo: 6 weeks
  • Cardiac activity: 7 weeks
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37
Q

define the following

threatened, inevitable, incomplete, complete, missed abortion

how to treat missed abortion

A
  • Threatened abortion (miscarriage): bleeding in first trimester without loss of fluid or tissue
  • Inevitable abortion (miscarriage): bleeding or rupture of membranes in the presence of cervical dilatation (>2 cm – can put speculum in cervix)
  • Incomplete abortion (miscarriage): documented pregnancy where passage of some blood and some tissue occurs, but some products of conception remain within the uterus
  • Complete abortion (miscarriage): documented pregnancy that ends with the spontaneous passage of all of the products of conception
  • Missed abortion (miscarriage): the retention of a failed intrauterine pregnancy with a gestational age less than 28 weeks, for 8 weeks or more
    • Expectant Tx, Dilation and curettage, and misoprostol (painful)
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38
Q

what are some fun facts bout miscarriage

What cruel human being thinks miscarriage is “fun”?

A
  • Risk of miscarriage is inversely proportional to gestational age
  • 20% of women experience 1st trimester vaginal bleeding
  • Most miscarriages are caused by genetic defects
  • Miscarriage is less frequently caused by hormonal deficiencies, structural abnormalities, or other exposures (infection)
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39
Q

Define recurrent pregnancy loss, anembryonic gestation, Rho (D) treatment

A
  • Recurrent pregnancy loss: three straight miscarriages (no full term pregnancy in between)
  • Anembryonic gestation: no development of yolk sac or fetal pole
  • Rho (D) treatment: patients who are Rh (-) should receive Rho(D) immunoglobulin if undergoing ectopic pregnancy or abortion/miscarriage
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40
Q

discuss the differences between fraternal and the different type of identical twins

in terms of # concepti, age of seperation and chorionicity

A
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41
Q

describe process of implantation

A
  • Implantation: Fertilization → zygote → two-cell stage → four-cell stage → eight-cell stage → morula → blastocysts → implantation
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42
Q

what is normal placenta anatomy

A
  • Anatomy: placenta made up of fetal and maternal surface
    • Maternal surface contains numerous nodules made up of villi called cotyledons
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43
Q

describe normal hiotology of placenta

A
  • Histology: villi and endometrial glands separated by intervillous space (where maternal blood bathes villi for exchange) (pic)
    • Syncytiotrophoblast – blurred multi-nucleated cells (2)
    • Cytotrophoblasts – mon-nucleated cells (1)
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44
Q
  • Changes that occur in gestation - histology based
A
  • Endometrial gland – cell look atypical with clear cytoplasm (confused with cancer) due to high levels of progesterone
  • Myometrium – muscles undergoes early hyperplasia then later hypertrophy to accommodate pregnancy
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45
Q

Choriocarcinoma of placenta

descritpion, etiology, epidemiology, tx

A
  • Description: A rare malignant epithelial tumor (carcinoma) of trophoblast origin that can arise following any type of pregnancy (normal, molar, ectopic, abortion)
  • Etiology: 50% complete mole, 25% Normal, 25% abortions
  • Epidemiology: women of reproductive age
  • Tx: Chemo (Methotrexate)
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46
Q

complete hydatidiform mole

pathophys, villi, embryo, villious capillaries, gestational age when mother id symptomatic, hCG titer, malignant potential, karyotype, gross pathology

A
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47
Q

partial hydatidiform mole

pathophys, villi, embryo, villious capillaries, gestational age when mother id symptomatic, hCG titer, malignant potential, karyotype,

A
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48
Q
A

normal placenta

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49
Q
A
  • Syncytiotrophoblast – blurred multi-nucleated cells (2)
  • Cytotrophoblasts – mon-nucleated cells (1)
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50
Q
A
  • Choriocarcinoma of placenta
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51
Q
A

Complete Hydatidiform Mole

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52
Q
A

partial Hydatidiform Mole

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53
Q

what are primoridal germ cells

A
  • Definition: cells that form sex cells or gametes
    • Can be identified during the 4-6th week of gestation of developing fetus
    • Spermatogonia (male) and oogonia (female)
54
Q

describe steps of Spermatogenesis

A
  • Spermatogonia remain dormant until puberty in males
  • Genesis: spermatogonia under goes mitosis → primary spermatocyte → 1st meiotic division → haploid secondary spermatocyte → 2nd meiotic division → 4 spermatids → spermiogenesis → 4 mature sperm → sex → capacitation → fertilization
    • Spermiogenesis: nucleus condenses, acrosome forms, cytoplasm is shed, tail forms

Capacitation: occurs in female genital tract by changing the acrosome to allow for penetration of zona pellucida of the ovum; needed for fertilization

55
Q

describe steps of oogenesis

A
  • Oogonia form primary oocytes that remain dormant until puberty
  • Genesis: Oogonia undergoes mitosis → primary oocytes → first meiotic division that ceases at prophase during fetal life → birth → activation during puberty → oocytes enter menstrual cycle → first meiotic division completed → secondary oocyte → second meiotic division that stops at metaphase → fertilization → completion of second meiotic division → mature oocyte
56
Q

explain process of fertilization

A
  • Occurs in ampulla of fallopian tube
  • Process: sperm released hyaluronidase from the acrosome → passes through corona radiata → sperm releases acrosin, esterases, and neuraminidases from the acrosome → penetration/lysis of zona pellucida → fusion of plasma cell membranes of oocyte and sperm → zona pellucida reaction occurs → zona pellucida is permeable to other sperm → formation of male and female pronuclei → pronuclei plasma membranes break down → male and female DNA combine → zygote
    • Plasma membrane and mitochondria sperm stay behind
57
Q

embryo: week 1

what happens in first 72 hrs

A
  • Zygote undergoes the following division as it travels down the fallopian tube
  • First 72 hours: zygote → 2 cell/blastomere stage → 4 cell/blastomere stage → 8 cell/blastomere stage → morula → blastocyst (32 cell stage)
    • After 8 cell stage, compaction of blastomeres occur (process of blastomeres changing shape and increasing cell-to-cell interactions)
      • Inner blastomere mass known as embryoblasts
      • Flattened blastomeres on the outside are known as trophoblasts → secrete hCG
    • As morula enters uterus, uterine fluid passes through the zona pellucida forming the blastocystic cavity
58
Q

embryo week 1

what happens after day 5

A
  • After day 5: Blastocyst hatches from the zona pellucida → implants into the endometrium (day 6) → hypoblasts (cuboidal cells) form dividing the blastocystic cavity from the embryoblasts (day 7)
    • Implantation into the endometrium causes trophoblasts into:
      • Cytotrophoblasts: surrounds the blastocyst
      • Syncytiotrophoblasts: implants into the endometrial tissue
59
Q

embryo: week 3

neurulation

what happens?

A
  • Some mesodermal cells migrate cranially, forming the notochordal process
  • The floor of the notochordal process fuses with endoderm, forming a notochordal plate
    • Infolds → forms the notochord
  • Notochord induces the formation of the neural plate
    • Primordium of the CNS
    • Basis of axial skeleton
  • Neural/notochordal plate invaginates, forming a neural groove and 2 neural folds
  • Neural folds fuse at the median forming a neural tube and canal → induces the proliferation of the intraembryonic mesoderm
    • Paraxial mesoderm, intermediate mesoderm, lateral mesoderm (somatic/splanchnic layers)
  • Neural crest cells migrate from neural folds and are found dorsal to the tube
60
Q

embryo: week 3

grastulation

what happens?

A
  • Bilaminar disc forms intro trilaminar disc
    • Ectoderm (derived from epiblasts), mesoderm, endoderm (derived from hypoblasts)
  • Primitive streak forms (thickened band of epiblasts)
  • Primitive node with a primitive pit forms cranially
  • Primitive groove forms within the streak due to invagination of epiblastic cells
  • Cells from the deep surface of the primitive streak migrate and form mesenchyme → mesoderm
61
Q

embryo: week 2

end of week 2

what happens?

A
  • Proliferation of cytotrophoblasts → formation of primary chorionic villi
  • Extraembryonic mesoderm differentiates into
    • Somatic mesoderm (lines trophoblasts and amnion)
    • Splanchnic mesoderm (surrounds umbilical vesicle)
62
Q

embryo: week 2

day 12: closing of plug

what happens?

A
  • Embryo is completely embedded in the endometrium → closing plug (layer of endometrial epithelium) forms around enclosed embryo
    • Endometrial cells undergo transformation → decidual cells → allow for immunological privilege of the embryo
  • In synctytiotrophoblasts, lacunae fuse to form lacunar networks → intervillous space in placenta
  • Extraembryonic mesoderm proliferates → coelomic spaces fuse → extraembryonic coelom forms → splits primary umbilical vesicle → secondary umbilical vesicle forms
  • Thick connecting stalk allows for the ventral yolk sac to be suspended in the chorionic cavity
63
Q

embryo: week 2

formation of umbiicla vesicle

what happens?

A
  • Exocoelomic cavity + membrane → becomes umbilical vesicle (yolk sac) → yolk sac becomes smaller because formation of extraembryonic membrane and coelomic spaces
  • Lacunae (filled with maternal blood) form within syncytiotrophoblasts
64
Q

embryo: week 2

formation of bilaminar disc

what happens?

A
  • Embryoblasts/inner cell mass → turns into epiblasts → part of epiblasts differentiate into amnioblasts to form amnion → remaining epiblasts forms bilaminar disc with existing hypoblasts → part of hypoblasts differentiate and form the exocoelomic membrane
  • 2 cavities form: amnion cavity and exocoelomic cavity (former blastocystic cavity)
65
Q

embryo: week 2
* Completion of implantation:

what happens?

A
  • Syncytiotrophoblasts continue to embed into the uterine wall via proteolytic enzymes → uterine tissue cells become engulfed for nutrients
  • Site becomes loaded with lipids and glycogens
66
Q

Isoimmunization

description and pathophys

what are events that lead to fetal-maternal bleeding

A
  • Description: formation of maternal ABs to fetal blood group factor (inherited by father)
  • Pathogenesis: Rh D-negative woman pregnant with first baby who inherited Rh D Ag from father → fetal-maternal bleeding → maternal exposure to fetal RBCs → formation of IgG ABs → 2nd pregnancy of Rh D-positive occurs → transplancetal passage of ABs → fetal hemolysis, bilirubin release (kernicterus → brain damage due to jaundice), and anemia
    • Possible events that lead to fetal-maternal bleeding
      • Childbirth, abortion, ectopic pregnancy, placental previa/abruption, amniocentesis, abdominal trauma, external cephalic version
67
Q

what are fetal complications and their mechanisms (3)

also what tx?

A
  • Anemia → increased fetal hematopoiesis → liver production of RBCs → decreased production of other proteins → low oncotic pressure → ascites and hydrops (fetal edema)
  • Anemia → decreased O2 saturation → increased cardiac output (heart working harder to meet O2 demand) → myocardial ischemia/dysfunction
  • Isoimmunization progressively worsens with each subsequent pregnancy due to anamnestic response (enhanced maternal immune response)
  • Tx: Rhogram (Ig-Rho) – stops antibodies from forming in first pregnancy
68
Q

what are two types of twins

describe them

A
  • Dizygotic (fraternal: 2 ova/2 sperm) – increased chance of dizygotic twins with increasing maternal age
    • Results in 2 separate amniotic sacs and 2 separate placentas (chorions)
  • Monozygotic (identical: zygote divides after conception) – rarer form
    • The timing of cleavage determines chorionicity (number of chorions) and amnioncity (number of amnions) → later cleavage results in decreased chorionicity
69
Q

what are risks of multifetal gestation

A
  • Preterm labor/delivery, intrauterine growth restriction (IUGR), polyhydramnios, preeclampsia, congenital anomalies, postpartum hemorrhage, placental abruption, umbilical cord accidents, single umbilical artery (look for renal agenesis), and intrauterine fetal demise
70
Q
  • Twin-twin transfusion syndrome

what is it? pathophys? symptoms(donor versus recipient twin)?

A
  • Description: complication specific to monochorionic gestations
  • Pathophysiology: vascular anastomoses between fetuses resulting in net flow from one twin to another
  • Symptoms
    • Donor twin: impaired growth, anemia, hypovolemia, oligohydramnios
    • Recipient twin: hypervolemia, hypertension, polycythemia, congestive heart failure (volume overload), polyhydramnios
71
Q

macrosomia

what is it? etiology? pathophys?

A
  • Terminology: Fetal macrosomia (fetal weight > 9lbs 15oz), Large for gestational age (birth weight > 90th percentile)
  • Etiology
    • Maternal factors: gestational diabetes, Hx of macrosmia, multifetal gestation
    • Fetal factors: male, Beckwith-Wiedemann
  • Pathophys: maternal diabetes → glucose crosses placenta → fetal pancreas increases insulin production → insulin is a growth factor → macrosomia
    • Post-delivery complication: hypoglycemia due to high levels of insulin
72
Q

IUGR

what is it? pathophys? etiology?

A
  • Terminology: IUGR (fetal weight <10%), small for gestational age (birth weight <10%), low birth weight (<2500g)
  • Pathophysiology:
    • If in early pregnancy: dysfunctional cellular hyperplasia/division → irreversible reduction in size and function of organs
    • If in late pregnancy: dysfunctional cellular hypertrophy → reversible reduction in cell size
  • Etiology
    • Maternal: Viral infections (TORCH – rubella, varicella, CMV), substance abuse, medication use (teratogenic meds), <16 y/o, >35 y/o, maternal disease
    • Fetal: Inherent growth potential, chromosomal abnormalities, multifetal pregnancies, gastroschisis, renal agenesis
    • Placental: early and rapid placental growth, placental abnormalities
73
Q

PTB

what is it? types? patho?

A
  • Definition: delivery that occurs before 37 completed weeks
    • Most common cause of perinatal mortality/morbidity: respiratory distress syndrome (RDS)
  • Types:
    • Spontaneous PTB: occurs without intervention – possibly due to rupture of membranes of the amniotic sac
    • Indicated PTB: occurs with intervention (induced or C-section)
  • Pathogenesis
    • Abnormal activation of HPA axis (stress), inflammation (infection), decidual hemorrhage (abruption), AND/OR pathologic uterine distension (polyhydramnios) →
      • Activation of proteases → rupture of amniotic sac → PTD
      • Activation of uretonins → uterine contractions → PTD
74
Q

PTB

risk factors? tx?

A
  • Risk factors: prior PTB, multifetal gestation, PROM (premature rupture of membranes), UTI, vaginal bleeding
  • Treatment
    • Indicated in high risk women with Hx of prior PTD:
      • Weekly IM progesterone caproate from 16-20 wks through 36 weeks
  • Improvement of outcomes: corticosteroids (fixes respiratory distress syndrome - RDS/intraventricular hemorrhage - IVH), magnesium (fixes cerebral palsy), tocolytic therapy
    • Tocolytic therapy: CCB, NSAIDS, beta agonists, magnesium sulfate
75
Q

Discuss differential diagnosis of third trimester bleeding

A
  • DDx for 3rd trimester bleeding: friable cervix, hemorrhoids, placenta previa, placental abruption, PTB
76
Q

placenta previa versus abruption

description and presentation

A
  • Placenta previa
    • Description: implantation of the placenta in the lower uterine segment
    • Presentation: third trimester bleeding, requires C-section
  • Placenta abruption
    • Description: separation of placenta from the decidua prior to the delivery
    • Presentation: third trimester bleeding, stillbirth
      • Maternal: severe abdominal pain
      • Fetal: irregular heart rates
    • Risk factors: DIC, cocaine use, maternal HTN, multiple gestations
77
Q

PROM vs. PPROM

definition, etiology, complications

A
  • PROM (premature rupture of membranes)
    • Definition: rupture prior to onset of labor at full term
    • Etiology: infection (inflammation weakens amniotic sac)
    • Complications: intrauterine infection, prolapsed cord, placental abruption
  • PPROM (preterm premature rupture of membrane)
    • Definition: rupture prior to onset of labor and occurring before 37 weeks
    • Etiology: infection (inflammation weakens amniotic sac)
    • Complications: leading cause of neonatal morbidity/mortality (i.e. RDS, IVH, infection)
78
Q
  • Post-term pregnancy

definition, etiology, complications

A
  • Definition: pregnancy lasting > 42 weeks
  • Etiology: inaccurate dating, anencephaly, fetal adrenal hyperplasia, placental sulfatase insufficiency
  • Complications: macrosomia, meconium aspiration → RDS, dysmaturity syndrome, oligohydramnios → umbilical cord compression
79
Q

what are the FDA drug classifications

A
80
Q

FAS

patho? abnormalities?

A
  • Pathogenesis: failure of cell migration during gestation
  • Congenital abnormalities: growth restriction, facial abnormalities (shortened palpebral tissues, low-set ears, midfacial hypoplasia, smooth philtrum, and thin upper lip) and CNS dysfunction (microcephaly, mental retardation, and ADD)
81
Q

Leading cause of low birth weight, pre-term labor, placental problems, IUGR, SIDS

A

Nicotine (vasoconstriction) and CO (impaired O2 delivery)

82
Q

Associated with low birth weight, pre-term birth, IUGR, and placental abruption

A

Cocaine (vasoconstriction)

83
Q

Most common teratogen that causes birth defects, intellectual disability, fetal alcohol syndrome (FAS)***

A

Alcohol

84
Q
  • Exposure to less than 5 rads is not associated with fetal anomalies

If exposed to more leads to microcephaly and intellectual disability

A

Radiation

85
Q

Associated with irreversible arthroapthies and cartilage erosion

A

Aminoglycosides

86
Q

Associated with yellow-brown discoloration of teeth and inhibited bone growth

A

Tetracycline

87
Q

Ototoxicity

A

Aminoglycosides

88
Q

Avoid near delivery as they are associated with hyperbilirubinemia

A

Sulfa drugs

89
Q

Often used in pregnancy, but is associated with hemolytic anemia in G6PD deficiency

A

Nitrofurantoin

90
Q

Avoid near delivery as they are associated with thrombocytopenia, bleeding, and electrolyte disturbances

A

Thiazide diuretics

91
Q

Associated with fetal growth restriction, neonatal hypoglycemia, possible transient hypotension

A

Beta blockers

92
Q

Renal damage → polyhydramnios (growth restriction, limb contractures, abnormal skull/calvarium development)

A

ACEi/ARBs

93
Q

Only SSRI with an increased risk of ventral/atrial septal cardiac defects

A

Paroxetine (SSRI)

94
Q

Avoid use late in pregnancy as it is associated with neonatal behavioral syndrome (increased muscle tone, irritability, jitteriness, & respiratory distress)

A

SSRIs

95
Q

Associated with Ebstein anomaly (apical displacement of the tricuspid valve → atrialization of the RV)

A

Lithium (depression med)

96
Q

Associated with spina bifida/neural tube defects with exposure during embryogenesis → Tx: folate supplements before sex

A

Valproic acid and carbamazepine

97
Q

Associated with abnormal facies, cleft lip/palate, microcephaly, growth deficiency, and hypoplasia of nails/DIPs

A

Phenytoin

98
Q

Severe fetal malformation → contraception is mandatory with use

A

Isotretinoin (acne med) /VitA

99
Q
  • Methotrexate is used in ectopic pregnancy

Contraindicated in normal pregnancy due to neural tube defects

A

Methotrexate/ Trimethoprim (folate antagonists)

100
Q
  • Easily crosses the placenta

Contraindicated in first trimester as it is associated with bone deformities, fetal abnormalities, abortion, ophthalmologic abnormalities

A

Warfarin

101
Q

Long-term use usually avoided as it can be associated with ductus arteriosus constriction → pulmonary HTN

A

NSAIDS

102
Q

Associated with aplasia cutis congenita (absence of skin à hole in head)

A

Methimazole (hyperthyroidism med)

103
Q

Associated with flipper limb defects

A

Thalidomide

104
Q

Can result in caudal regression syndrome, congenital heart defects, macrosomia, and neonatal hypoglycemia

A

Diabetes

105
Q

Associated with absence of digits and other anomalies

A

Alkylating agents (cancer drug)

106
Q

Associated with vaginal clear cell carcinoma and congenital Müllerian anomalies

A

Diethylstilbestrol (DES)

107
Q

Associated with congenital goiter or hypothyroidism (causes cretinism: stunted physical/mental growth)

A

Iodine (lack/excess)

108
Q

Found in swordfish, shark, tilefish, king mackerel → neurotoxicity

Fish is safe when less than 12oz/week

A

Methylmercury

109
Q

Compare and contrast the clinical presentations of true and false labor

tx for flase?

A
  • True labor (normal labor) – regular painful contractions resulting in cervical dilation (10 cm) with a frequency of contractions every 5 minutes and duration of 60 seconds
  • False labor – contractions (duration < 60s) not associated with cervical dilation
    • Suggestive of cervical insufficiency in the second trimester
    • Tx: rest and hydration
110
Q
  • Stages of Labor

explain in detail

A
  • First: Interval between onset of contractions and complete cervical dilation
    • Latent: effacement of cervix and early dilation (0-6 cm)
    • Active: rapid cervical dilation (6-10 cm @ 1 cm/hr)
  • Second: Interval between complete cervical dilation and delivery of infant
    • Requires maternal effort (pushing) – delivery takes 1-3 hours (longer for first pregnancy)
    • Delivery → restitution of fetal head → palpate for nuchal cord (umbilical cord wrapped around neck of fetus) → delivery of shoulders + rest of infant → cord clamping
  • Third: Interval between delivery of infant and delivery of placenta
    • Normally occurs within 30 minutes
    • If placenta fails to deliver, manual extraction is performed
    • Important to examine placenta following delivery to ensure there is no remaining placenta in the uterus because it can lead to postpartum hemorrhage
    • Signs of placenta delivery: lengthening of cord, gush of blood, uterus rises in abdomen
  • Fourth: 1-2 hours after delivery of placenta
    • Involves assessing mother, administering oxytocin, and inspect for perineal lacerations (laceration involving rectal area are more severe)
111
Q
  • Cardinal movements of labor (7)

explain in detail

A
  • Engagement: baby moving into pelvis below ischial spine
  • Descent: continued descent through the pelvis prior to labor
  • Flexion: flexion of chin to chest due to resistance of pelvis
  • Internal rotation: occiput (back of head) rotates to face the pubis symphysis → baby facing downwards
  • Extension: vectors of force direct the tip of head through the introitus past pubic symphysis
  • External rotation (restitution): re-aligning of head with shoulders
  • Expulsion: delivery of shoulders and remainder of infant
112
Q
  • Phases of uterine activity

explain in detail … aka what hormome is responsible for each phase

A
  • Phase 0: inhibition (inhibition of uterine activity due to progesterone)
    • Progesterone
      • Stimulated uterine relaxation and inhibits uterine contractions
  • Phase 1: Myometrial activation (tissue is activated to respond to uterotropins in preparation for labor via normal muscle activation pathways)
    • Characterized by increased expression of contraction associated proteins (receptors for prostaglandins and oxytocin)
    • Estrogen (made by the placenta)
      • Inhibits uterine relaxation and activates uterine contractions
  • Phase 2: Stimulation (uterine contractions)
    • Prostaglandins (E and F)
      • Produced by decidua and fetal membranes → contractions → labor
    • Oxytocin (peptide hormone synthesized in hypothalamus → released by posterior pituitary)
      • Most potent uterotonic agent and can be released by nipple stimulation
      • Concentration of oxytocin remains the same, but receptor concentration increases 200 fold throughout pregnancy (peaking at labor)
  • Phase 3: Involution (returning of uterus to pre-pregnant state ~ 6 weeks)
    • Oxytocin (see above)
113
Q

explain the following drugs

oxytocin, misoprostol, mehtylergonovine, prostaglandin F2/E2

MOA? SE? and contraindiactions

A
114
Q

what are indications for antepartum tests

A
  • Indications for antepartum tests: diseases during pregnancy (diabetes, HTN, twins, polyhydramnios, advanced maternal age)
115
Q

explain the following

fetal kick counts, non-stress test, biophysical profile

A
    • Fetal kick counts: look for 5 fetal movemements per hour
      • Non-stress test: 2 or more fetal HR accelerations in a 20 minute period
      • Biophysical profile (via US): 2 points per component (reactive NST, ≥1 episode of fetal breath movements lasting more than 30s, 3 limb movements, 1 episode of extremity extension/flexion, vertical AF pocket >2cm); 8/10 is normal
116
Q

Describe the physiologic changes that occur with transition from fetus to neonate

A
  • Umbilical cord is clamped
  • Alveolar fluid clearance (due to change of lungs being filled with amniotic fluid)
  • Lung expansion
  • Conversion from fetal to newborn circulation
  • Increased pulmonary arterial blood flow (lungs were not used during pregnancy)
  • Increased systemic pressure
  • Closure of the right-to-left shunts (foramen ovale and ductus arteriosus)
117
Q

What are the chromosomal (sex-linked and autosomal) factors that determine sex?

A
  • Chromosomal/Genetic sex
    • Sex-linked gene
      • Male: 46XY positive SRY
      • Female: 46XX negative SRY
    • Autosomal
      • WT1 (Denys-Drash), SF1 (Adrenal failure), SOX9 (Campomelic dysplasia and sex reversal), DAX1 (adrenal hypoplasia and hypogonadism)
118
Q

What determines gonadal sex?

A
  • Gonadal sex
    • Urogenital ridge turns to either testes or ovaries depending on SRY
      *
119
Q

How do hormones determine sex?

A
  • Hormonal sex
    • Male: Leydig produces testosterone and Sertoli cells produce anti-Mullerian hormone (AMH)
    • Female: no testosterone is produced
120
Q

What determines the female phenotypic sex (external and male)? Be sure to identify what parts of the female are internal and external.

A
  • Female:
    • External (clitoris, labia majora/minora and vagina): absence of testosterone or nonfunctional androgen receptors will develop female genitalia
    • Internal (Fallopian tubes, uterus, upper third of vagina): absence of testosterone and AMH will cause regression of Wolffian ducts and persistence of Mullerian ducts
121
Q

What is the pathogenesis and preentation of Klinefelters?

A
  • Klinefelters syndrome (47, XXY) – presence of X chromosome Barr body
    • Pathogenesis
      • Dysgenesis of seminiferous tubules → decreasing inhibin B → increasing FSH
      • Abnormal Leydig cell function → decreased testosterone → increased LH → increasing estrogen
    • Presentation: testicular atrophy, tall with long extremities, gynecomastia, female hair distribution, breast and wide hips, primary hypogonadism (infertility)
122
Q

What is the pathogenesis and presentation of Turner’s syndrome?

A
  • Turner syndrome (45, Xnull)
    • Pathogenesis: decreased estrogen → increased LH, FSH
    • Presentation: menopause before menarche (amenorrhea), short stature, ovarian dysgenesis, CVD, lymphatic defects, horseshoe kidney
123
Q

What is the presentation of double y males?

A
  • Double Y males (XYY)
    • Presentation: look normal possibly tall, normal fertility, may be associated with severe acne, learning disability
124
Q

What is ovotesticular disorder?

A
  • Ovotesticular disorder (46XY or XX) aka true hermaphroditism: both ovarian and testicular tissue present
125
Q

What are disorders of 46, XX DSD? ther are 3. Explain what occurs in each!

A
  • 46, XX DSD – ovaries present but external genitalia are masculine/ambiguous
    • Excess androgen (testosterone tumor or exogenous administration)
      • Dx: increased testosterone and decreased LH
    • Congenital adrenal hyperplasia (CAH) – 21-hydroxylase deficiency → unable to produce cortisol → increased ACTH → excess androgens
    • Placental aromatase deficiency – can’t convert androgens to estrogen → excess androgens
126
Q

What are disorders of 46, XY DSD? ther are 2. Explain what occurs in each and how to diagnose each!

A
  • 46, XY DSD – testes present but external genitalia are female/ambiguous
    • Androgen insensitivity syndrome – defective androgen receptors → female external genitalia
      • Dx: increased levels of testosterone, LH, estrogen
    • 5alpha-reductase deficiency – autosomal recessive disorder with decreased amounts of 5alpha reductase → no conversion of testosterone to DHT → ambiguous genitalia until puberty
      • After puberty increasing levels of testosterone → masculinization of external genitalia
      • Dx: testosterone/estrogen levels normal, LH is normal or increased
127
Q

What is the pathogenesis and presentation of Kallmann syndrome?

A

Kallmann Syndrome

  • Pathogenesis: defective migration of GnRH-releasing neurons → decreased synthesis of GnRH in hypothalamus → decreased LH, FSH, testosterone
  • Presentation: infertility (low sperm count or amenorrhea), cryptorchidism, anosmia (can’t smell), secondary hypogonadism
128
Q

How do you diagnose DSD?

A
  • Dx: Chromosomal analysis, CAH panel, pelvis US, biochemical panel (hormones)
129
Q

Define sex assignement and sex rearing.

A

Sex development issues

  • Sex assignment – gender assigned at birth
  • Sex of rearing – how a child is raised
130
Q

Diagnose the following trends:

  • LH, testosterone both go up
  • T goes up, LH goes down
  • T goes down, LH goes up
  • LH and TH both go down
A
131
Q
A

EndoRepro (8 decks)

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