1
Q
explain: Blastocyst Implantation
Apposition
A
- Apposition: Initial adhesion of the blastocyst to the uterine wall
2
Q
Explain: Blastocyst Implantation
Adhesion
A
- Adhesion: Increased physical contact between blastocyst and uterine epithelium
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).
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
- *
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
6
Q
function of placenta
A
- Basic functions: respiratory exchange, metabolite exchange, hormone synthesis, and hormone regulation
7
Q
layers of placenta
A
- Outer layers of placenta: amnion (inner layer) and chorion (outer layer) → eventually fuse laterally
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
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
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)
11
Q
what is Morbidly adherent
A
- Morbidly adherent: when placenta villi invade serosa of uterus (pathological state)
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
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)
14
Q
what are the
Hypothalamic-like releasing hormones
A
- GnRH (gonadotropin releasing hormone), CRH (releases cortisol), GHRH (growth hormone releasing hormone)
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
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
17
Q
Adrenal gland hormones
what are thoossssssseeeee?
A
- Fetal zone produces androgens (DHEAS) that are used to synthesize placental estrogens
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
19
Q
How does CO an BP change in labor and post-partum
A
↑ CO, BP
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
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
- Immune tolerance to fetus (NOT deficiency)
- ↑ coagulation factors ( VII, VIII, IX, X) and ↓ Protein C/S → ↑ risk of venous thromboembolism → DVT, PE (Higher risk postpartum)
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
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
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
- Thyroid: alpha- hCG binds to thyroid receptors → ↑ T4 secretion → ↓ TSH (mimics hyperthyroidism)
25
what are some changes that happen in..
metabolism of
carbs, lipids, protein
* 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
26
what are the functional and atanomical changes that oocur in..
MKS
* 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
27
list some changes in
skin, reproductive tract, hair, eyes
* 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
28
what are anatomical and functional changes of
breasts
what are sx
* 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
29
fun facts bout fetal Hbg
* 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
30
Discuss how to date a pregnancy
mainly what is LMP
* 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)
31
discuss LMP vs. CRL
* 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
32
DDx for N/V in early pregnancy
viral gastroenteritis, food poisoning, normal N/V or pregnancy, and hyperemesis gravidarum
33
normal N/V vs. hyperemesis gravidarum
discuss wt change, impact, tx
34
Develop a differential diagnosis for 1st trimester bleeding
how do we diagnosis this
* 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
35
definition and complications of ectopic pregnancy
* 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
36
**Know the gestational ages of different findings during embryological development**
* Gestational sac: 5 weeks
* Yolk sac: 6 weeks
* Embryo: 6 weeks
* Cardiac activity: 7 weeks
37
# define the following
threatened, inevitable, incomplete, complete, missed abortion
how to treat missed abortion
* 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)
38
what are some fun facts bout miscarriage
**_What cruel human being thinks miscarriage is "fun"?_**
* 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)
39
**Define recurrent pregnancy loss, anembryonic gestation, Rho (D) treatment**
* 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
40
discuss the differences between fraternal and the different type of identical twins
in terms of # concepti, age of seperation and chorionicity
41
describe process of implantation
* Implantation: Fertilization → zygote → two-cell stage → four-cell stage → eight-cell stage → morula → blastocysts → implantation
42
what is normal placenta anatomy
* Anatomy: placenta made up of fetal and maternal surface
* Maternal surface contains numerous nodules made up of villi called cotyledons
43
describe normal hiotology of placenta
* 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)
44
* Changes that occur in gestation - histology based
* 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
45
Choriocarcinoma of placenta
descritpion, etiology, epidemiology, tx
* 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)
46
complete hydatidiform mole
pathophys, villi, embryo, villious capillaries, gestational age when mother id symptomatic, hCG titer, malignant potential, karyotype, gross pathology
47
partial hydatidiform mole
pathophys, villi, embryo, villious capillaries, gestational age when mother id symptomatic, hCG titer, malignant potential, karyotype,
48
normal placenta
49
* Syncytiotrophoblast – blurred multi-nucleated cells (2)
* Cytotrophoblasts – mon-nucleated cells (1)
50
* Choriocarcinoma of placenta
51
Complete Hydatidiform Mole
52
partial Hydatidiform Mole
53
what are primoridal germ cells
* 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
describe steps of Spermatogenesis
* 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
describe steps of oogenesis
* 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
explain process of fertilization
* 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
embryo: week 1
what happens in first 72 hrs
* 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
embryo week 1
what happens after day 5
* 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
embryo: week 3
neurulation
what happens?
* 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
embryo: week 3
grastulation
what happens?
* 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
embryo: week 2
end of week 2
what happens?
* Proliferation of cytotrophoblasts → formation of primary chorionic villi
* Extraembryonic mesoderm differentiates into
* Somatic mesoderm (lines trophoblasts and amnion)
* Splanchnic mesoderm (surrounds umbilical vesicle)
62
embryo: week 2
day 12: closing of plug
what happens?
* 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
embryo: week 2
formation of umbiicla vesicle
what happens?
* 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
embryo: week 2
formation of bilaminar disc
what happens?
* 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
embryo: week 2
* Completion of implantation:
what happens?
* 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
Isoimmunization
description and pathophys
what are events that lead to fetal-maternal bleeding
* 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
what are fetal complications and their mechanisms (3)
also what tx?
* 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
what are two types of twins
describe them
* 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
what are risks of multifetal gestation
* 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
* Twin-twin transfusion syndrome
what is it? pathophys? symptoms(donor versus recipient twin)?
* 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
macrosomia
what is it? etiology? pathophys?
* 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
IUGR
what is it? pathophys? etiology?
* 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
PTB
what is it? types? patho?
* 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
PTB
risk factors? tx?
* 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
**Discuss differential diagnosis of third trimester bleeding**
* DDx for 3rd trimester bleeding: friable cervix, hemorrhoids, placenta previa, placental abruption, PTB
76
placenta previa versus abruption
description and presentation
* 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
PROM vs. PPROM
definition, etiology, complications
* 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
* Post-term pregnancy
definition, etiology, complications
* 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
what are the FDA drug classifications
80
FAS
patho? abnormalities?
* 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
Leading cause of low birth weight, pre-term labor, placental problems, IUGR, SIDS
Nicotine (vasoconstriction) and CO (impaired O2 delivery)
82
Associated with low birth weight, pre-term birth, IUGR, and placental abruption
Cocaine (vasoconstriction)
83
Most common teratogen that causes birth defects, intellectual disability, fetal alcohol syndrome (FAS)\*\*\*
Alcohol
84
* Exposure to less than 5 rads is not associated with fetal anomalies
If exposed to more leads to microcephaly and intellectual disability
Radiation
85
Associated with irreversible arthroapthies and cartilage erosion
Aminoglycosides
86
Associated with yellow-brown discoloration of teeth and inhibited bone growth
Tetracycline
87
Ototoxicity
Aminoglycosides
88
Avoid near delivery as they are associated with hyperbilirubinemia
Sulfa drugs
89
Often used in pregnancy, but is associated with hemolytic anemia in G6PD deficiency
Nitrofurantoin
90
Avoid near delivery as they are associated with thrombocytopenia, bleeding, and electrolyte disturbances
Thiazide diuretics
91
Associated with fetal growth restriction, neonatal hypoglycemia, possible transient hypotension
Beta blockers
92
Renal damage → polyhydramnios (growth restriction, limb contractures, abnormal skull/calvarium development)
ACEi/ARBs
93
Only SSRI with an increased risk of ventral/atrial septal cardiac defects
Paroxetine (SSRI)
94
Avoid use late in pregnancy as it is associated with neonatal behavioral syndrome (increased muscle tone, irritability, jitteriness, & respiratory distress)
SSRIs
95
Associated with Ebstein anomaly (apical displacement of the tricuspid valve → atrialization of the RV)
Lithium (depression med)
96
Associated with spina bifida/neural tube defects with exposure during embryogenesis → Tx: folate supplements before sex
Valproic acid and carbamazepine
97
Associated with abnormal facies, cleft lip/palate, microcephaly, growth deficiency, and hypoplasia of nails/DIPs
Phenytoin
98
Severe fetal malformation → contraception is mandatory with use
Isotretinoin (acne med) /VitA
99
* Methotrexate is used in ectopic pregnancy
Contraindicated in normal pregnancy due to neural tube defects
Methotrexate/ Trimethoprim (folate antagonists)
100
* Easily crosses the placenta
Contraindicated in first trimester as it is associated with bone deformities, fetal abnormalities, abortion, ophthalmologic abnormalities
Warfarin
101
Long-term use usually avoided as it can be associated with ductus arteriosus constriction → pulmonary HTN
NSAIDS
102
Associated with aplasia cutis congenita (absence of skin à hole in head)
Methimazole (hyperthyroidism med)
103
Associated with flipper limb defects
Thalidomide
104
Can result in caudal regression syndrome, congenital heart defects, macrosomia, and neonatal hypoglycemia
Diabetes
105
Associated with absence of digits and other anomalies
Alkylating agents (cancer drug)
106
Associated with vaginal clear cell carcinoma and congenital Müllerian anomalies
Diethylstilbestrol (DES)
107
Associated with congenital goiter or hypothyroidism (causes cretinism: stunted physical/mental growth)
Iodine (lack/excess)
108
Found in swordfish, shark, tilefish, king mackerel → neurotoxicity
Fish is safe when less than 12oz/week
Methylmercury
109
**Compare and contrast the clinical presentations of true and false labor**
**tx for flase?**
* 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
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* Stages of Labor
explain in detail
* 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)
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* Cardinal movements of labor (7)
explain in detail
* 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
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* Phases of uterine activity
explain in detail ... aka what hormome is responsible for each phase
* 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)
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explain the following drugs
oxytocin, misoprostol, mehtylergonovine, prostaglandin F2/E2
MOA? SE? and contraindiactions
114
what are indications for antepartum tests
* Indications for antepartum tests: diseases during pregnancy (diabetes, HTN, twins, polyhydramnios, advanced maternal age)
115
explain the following
fetal kick counts, non-stress test, biophysical profile
* * 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
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**Describe the physiologic changes that occur with transition from fetus to neonate**
* 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)
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What are the chromosomal (sex-linked and autosomal) factors that determine sex?
* 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)
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What determines gonadal sex?
* Gonadal sex
* Urogenital ridge turns to either testes or ovaries depending on SRY
*
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How do hormones determine sex?
* Hormonal sex
* Male: Leydig produces testosterone and Sertoli cells produce anti-Mullerian hormone (AMH)
* Female: no testosterone is produced
120
What determines the female phenotypic sex (external and male)? Be sure to identify what parts of the female are internal and external.
* 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
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What is the pathogenesis and preentation of Klinefelters?
* 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)
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What is the pathogenesis and presentation of Turner's syndrome?
* Turner syndrome (45, Xnull)
* Pathogenesis: decreased estrogen → increased LH, FSH
* Presentation: menopause before menarche (amenorrhea), short stature, ovarian dysgenesis, CVD, lymphatic defects, horseshoe kidney
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What is the presentation of double y males?
* Double Y males (XYY)
* Presentation: look normal possibly tall, normal fertility, may be associated with severe acne, learning disability
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What is ovotesticular disorder?
* Ovotesticular disorder (46XY or XX) aka true hermaphroditism: both ovarian and testicular tissue present
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What are disorders of 46, XX DSD? ther are 3. Explain what occurs in each!
* 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
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What are disorders of 46, XY DSD? ther are 2. Explain what occurs in each and how to diagnose each!
* 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
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What is the pathogenesis and presentation of Kallmann syndrome?
**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
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How do you diagnose DSD?
* Dx: Chromosomal analysis, CAH panel, pelvis US, biochemical panel (hormones)
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Define sex assignement and sex rearing.
**Sex development issues**
* Sex assignment – gender assigned at birth
* Sex of rearing – how a child is raised
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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
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EndoRepro
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