pregnancy Flashcards
1 zygote splits into 2
monozygotic twins (identical)
2 eggs fertilized by 2 sperm
dizygotic (fraternal)
thin inner fetal membrane
amnion
thick outer fetal membrane
chorion
pregnancy located outside uterine cavity
ectopic pregnancy
98%: fallopian tube (ampulla most commonly) → tubal rupture → intrabdominal hemorrhage → death
ovaries
abdomen
risk factors of ectopic pregnancy
prior ectopic pregnancy hx of tubal ligation history of PID smoking (impair tubal motility) infertility IUD in place (↓ overall rate of pregnancy, but if get pregnant more likely to be ectopic pregnancy)
classic triad: amenorrhea vaginal bleeding ab pain physical exam: lower ab tendeness adnexal mass
ectopic pregnancy
severe ab pain, referred pain to shoulder, urge to defecate (blood pooling in pouch of douglas), dizziness/LOC
physical exam: rebound tenderness/guarding (peritoneal, like appendicitis)
ruptured ectopic pregnancy: intraabdominal hemorrhage
labs for ectopic pregnancy
serum bHCG level (confirm pregnant, lower than normal pregnancy since not healthy pregnancy)
US
treatment for ectopic pregnancy
surgery
MTX: folic acid antagonist
“grape-like clusters”
swollen chorionic villi of hydatidiform mole
“snowstorm appearance” on US
swollen chorionic villi of hydatidiform mole
treatment of hydatidiform mole
D&C
follow hCG levels to zero
invasive mole
more common in complete mole
invade locally through uterine wall (can cause uterine rupture + hemorrhage)
metastatic/malignant form of gestational trophoblastic disease
↑↑↑bHCG
chroriocarcinoma
most common cause of placental chroriocarcinoma
50%: complete molar miscarriage normal pregnancy ectopic pregnancy spontaneous
mets of choriocarcinoma goes to
LUNG
perisistent bloody, brown vaginal discharge lasting mos after pregnancy (not typical 4-6 wks) +/-
dyspnea
↑↑↑bHCG
choriocarcinoma
treatment of choriocarcinoma
chemotherapy (MTX, good response to chemo, excellent prognosis)
+/- surgery to reduce size of tumor
follow hCG level to zero
contents of umbilical cord
2 umbilical arteries 1 umbilical vein (O2 rich blood from mom) in Wharton jelly (connective tissue) urachus vitelline duct
urachus
derived from proximal part of allantois
runs between fetal bladder and umbilicus
involutes after birth → median umbilical ligament
persistent median umbilical ligament can cause
vesicourachal diverticulum (outpouching from bladder): remnant where urachus meets bladder or urachal cyst: urachus obliterates at bladder and umbilicus but not midline or patent urachus: urachus doesn't obliterate at all (persistently wet umbilicus)
vitelline duct (omphalomesenteric duct)
connects yolk sac to lumen of midgut
normally disappears in wk 6 of development
patent vitelline duct
vitelline fistula: connects terminal ileum to umbilicus (meconium from umbilicus)
persistently wet umbilicus
patent urachus: urachus doesn’t obliterate at all
meconium from umbilicus
vitelline fistulla (failed involution)
small remnant of vitelline duct at terminal ileum can cause
meckel diverticulum (outpouching of intestine) can contain gastric tissue and cause lower GI bleed
lower GI bleed
meckel diverticulum from remnant of vitelline duct at terminal ileum (contain gastric tissue)
amniotic fluid roles
contained in amniotic sac
room for movement and grow
swallow fluid → GI development
breath fluid → lung development
common causes of oligohydramnios (too little amniotic fluid)
2nd half of pregnancy: fetal urine is most important source of AF
causes of decreased UO:
placental insufficiency: ↓ blood flow to fetus → fetus shunts blood away from kidneys
bilateral renal agenesis (can cause Potter sequence)
obstruction of urine flow (posterior urethral valves in males)
oligohydramnios
pulmonary hypoplasia
limb + facial abnormality
Potter sequence
common causes of polyhydramnios (too much amniotic fluid)
prevent fetus from swallowing: esophageal or duodenal atresia anencephaly too much UO: multiple gestations uncontrolled maternal diabetes (glycosuria and polyuria in fetus) congenital infections: Parvovirus B19 fetal anemia due to Rh alloimmunization
type of antibody that can cross placenta
IgG
prenatal testing
type and screen: determine if mom is Rh (D) - (at risk for Rh alloimmunization)
maternal serum screen in 2nd tri (15-20 wks): triple or quad screen looking for AFP, estriol, hCG, inhibin (quad - inhibin improves sensitivity of test)
causes of ↑ AFP (detected by triple or quad screen)
abdominal wall defects: gastroschisis, omphalocele neural tube defects multiple gestations incorrect dating (big reason)
amniocentesis
karyotype fetal cells to test for genetic diseases or aneuploidy
neural tube defects
chorionic villus sampling (CVS)
can be done earlier: 10-13 wks
karyotype fetal cells for genetic diseases
free fetal DNA testing
baby’s blood cells/DNA are in mom’s blood
ovarian cyst associated with molar pregnancy
theca-lutein cyst: occurs due to ↑bHCG (when can come from chroriocarcinoma)
risk factors for placenta previa
history of C section (biggest risk factor)
↑maternal age
↑ multiparity
PAINLESS vaginal bleeding
in 2nd half of pregnancy
placenta previa
placenta detaches as uterus grows
diagnosis of placenta previa
US BEFORE DIGITAL EXAM!!!
otherwise bleeding previa → hemorrhage →Csection
risk factors for:
placenta accreta
placenta increta
placenta percreta
history of placenta previa
history of C section
abnormal attachment of placenta to myometrium
placenta Accreta = Attaches
invasion of placenta into myometrium
placenta Increta = Invasion
placenta peforates through uterus
placenta Percreta = Perforate
diagnosis of placenta accreta/increta/percreta
US
sometimes won’t know until trying to deliver placenta and won’t come out + bleeding during delivery → massive, life-threatening hemorrhage
treatment of placenta accreta/increta/percreta
Csection
hysterectomy
premature separation of placenta from uterus before delivery
maternal hemorrhage or DIC possible
baby deprived of O2
placental abruption
risk factors
history of prior placental abruption HTN (included preeclampsia) trauma (MVA) smoking cocaine use
complication of pregnancy with cocaine use
placenta abruption
sudden onset
PAINFUL vaginal bleeding in 2nd half of pregnancy
ctx
fetal distress on HR monitor
placental abruption
painful due to irritation of uterus → ctx → fast labor
treatment of placental abruption
emergency C section
causes of postpartum hemorrhage
uterine atony - spiral arteries of uterus are still open, myometrium not contracting down to constrict vessels (most common)
retained placental tissue - prevents myometrium from contracting down
genital lacerations
abnormal placentation (placenta accreta/increta/percreta)
uterine rupture
coagulation defects
enlarged, soft, boggy uterus
bleeding minutes after delivery (can occur up to a couple days after)
postpartum hemorrhage
risk factor of PPH
overdistended uterus (large fetus, multifetal gestation) induced or augmented labor prolonged labor - overworked uterus
patient had HTN before pregnancy
chronic HTN
antihypertensive that is a teratogen
ACEi (renal abnormalties)
antihypertensives safe during pregnancy (for chronic HTN)
methyldopa: α2 agonist
labetalol: α + ß blocker
new-onset HTN >140/90 after 20 wks GA pregnancy and resolves postpartum
no proteinuria
gestational HTN
treatment of gestational HTN
no treatment - doesn’t help outcomes
close monitoring to watch for any progression of disease
new-onset HTN >140/90 after 20 wks GA pregnancy + proteinuria (equal or greater than 300 mg in 24hrs) or end-organ dysfunction (thrombocytopenia, renal insufficiency, ↑LFTs, pulmonary edema, cerebral or visual sx: headache, visual disturbance, seizure)
preeclampsia
considered severe if: end-organ dysfunction or bp >160/110
potential pathophysiology of preclampsia
may be due to abnormal development of placental blood vessels → placental ischemia → inflammatory response
or mom’s immune system reacts to paternally derived antigens in placenta
widspread endothelial dysfunction → leaky vessels → vasospasm → HTN + proteinuria or end-organ dysfunction during pregnancy
preeclampsia
risk factors of preeclampsia
history of preeclampsia extremes of age: 40 yo nulliparity chronic HTN diabetes multifetal gestation hyatidiform mole
HELLP syndrome: variant of severe preeclampsia
Hemolysis
Elevated Liver enzymes
Low Platelets
preeclampsia + seizure
eclampsia
anticonvulsant for seizures in eclampsia
magnesium sulfate to prevent or terminate a seizure (eclampsia)
antihypertensive for preeclampsia, HELLP, eclampsia
rapid acting antihypertensive if >160/110 (prevent stroke, placenta abruption): hydralazine labetalol nifedipine definitive treatment: delivery
placenta secretes hormone: human placental lactogen (HPL)
↓ insulin sensitivity in mom to allow glucose to go to baby instead of mom
exaggerated HPL response
diabetes develops during pregnancy
resolves postpartum
gestational diabetes
screen for gestational diabetes
oral glucose tolerance test: 24-28 wks GA
treatment of gestational diabetes
diet +/- insulin
complication of gestational diabetes
macrosomia
hypoglycemia of infant: ↑ fetal exposure to glucose → fetal ßcells in pancreas undergo hyperplasia to produce more insulin → once delivery (no glucose source) → hypoglycemic
have type 1 or type 2 DM before pregnancy
pregestational diabetes
treatment of pregestational diabetes
insulin
complications of pregestational diabetes
macrosomia
hypoglycemia
congenital anomalies (CV defects, caudal regression syndrome (sacral dysgenesis - lower part of body doesn’t form properly), stillbirth)
bp drops in supine position
compression of IVC by uterus (lie on L or R decubitus)
↓preload →↓SV
