pregnancy Flashcards

1
Q

1 zygote splits into 2

A

monozygotic twins (identical)

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2
Q

2 eggs fertilized by 2 sperm

A

dizygotic (fraternal)

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3
Q

thin inner fetal membrane

A

amnion

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4
Q

thick outer fetal membrane

A

chorion

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5
Q

pregnancy located outside uterine cavity

A

ectopic pregnancy
98%: fallopian tube (ampulla most commonly) → tubal rupture → intrabdominal hemorrhage → death
ovaries
abdomen

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6
Q

risk factors of ectopic pregnancy

A
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)
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7
Q
classic triad:
amenorrhea
vaginal bleeding
ab pain 
physical exam:
lower ab tendeness
adnexal mass
A

ectopic pregnancy

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8
Q

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)

A

ruptured ectopic pregnancy: intraabdominal hemorrhage

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9
Q

labs for ectopic pregnancy

A

serum bHCG level (confirm pregnant, lower than normal pregnancy since not healthy pregnancy)
US

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10
Q

treatment for ectopic pregnancy

A

surgery

MTX: folic acid antagonist

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11
Q

“grape-like clusters”

A

swollen chorionic villi of hydatidiform mole

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12
Q

“snowstorm appearance” on US

A

swollen chorionic villi of hydatidiform mole

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13
Q

treatment of hydatidiform mole

A

D&C

follow hCG levels to zero

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14
Q

invasive mole

A

more common in complete mole

invade locally through uterine wall (can cause uterine rupture + hemorrhage)

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15
Q

metastatic/malignant form of gestational trophoblastic disease
↑↑↑bHCG

A

chroriocarcinoma

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16
Q

most common cause of placental chroriocarcinoma

A
50%: complete molar
miscarriage
normal pregnancy
ectopic pregnancy
spontaneous
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17
Q

mets of choriocarcinoma goes to

A

LUNG

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18
Q

perisistent bloody, brown vaginal discharge lasting mos after pregnancy (not typical 4-6 wks) +/-
dyspnea
↑↑↑bHCG

A

choriocarcinoma

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19
Q

treatment of choriocarcinoma

A

chemotherapy (MTX, good response to chemo, excellent prognosis)
+/- surgery to reduce size of tumor
follow hCG level to zero

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20
Q

contents of umbilical cord

A
2 umbilical arteries
1 umbilical vein (O2 rich blood from mom)
in Wharton jelly (connective tissue)
urachus
vitelline duct
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21
Q

urachus

A

derived from proximal part of allantois
runs between fetal bladder and umbilicus
involutes after birth → median umbilical ligament

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22
Q

persistent median umbilical ligament can cause

A
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)
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23
Q

vitelline duct (omphalomesenteric duct)

A

connects yolk sac to lumen of midgut

normally disappears in wk 6 of development

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24
Q

patent vitelline duct

A

vitelline fistula: connects terminal ileum to umbilicus (meconium from umbilicus)

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25
Q

persistently wet umbilicus

A

patent urachus: urachus doesn’t obliterate at all

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26
Q

meconium from umbilicus

A

vitelline fistulla (failed involution)

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27
Q

small remnant of vitelline duct at terminal ileum can cause

A
meckel diverticulum (outpouching of intestine)
can contain gastric tissue and cause lower GI bleed
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28
Q

lower GI bleed

A

meckel diverticulum from remnant of vitelline duct at terminal ileum (contain gastric tissue)

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29
Q

amniotic fluid roles

A

contained in amniotic sac
room for movement and grow
swallow fluid → GI development
breath fluid → lung development

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30
Q

common causes of oligohydramnios (too little amniotic fluid)

A

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)

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31
Q

oligohydramnios
pulmonary hypoplasia
limb + facial abnormality

A

Potter sequence

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32
Q

common causes of polyhydramnios (too much amniotic fluid)

A
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
33
Q

type of antibody that can cross placenta

A

IgG

34
Q

prenatal testing

A

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)

35
Q

causes of ↑ AFP (detected by triple or quad screen)

A
abdominal wall defects: gastroschisis, omphalocele
neural tube defects
multiple gestations
incorrect dating (big reason)
36
Q

amniocentesis

A

karyotype fetal cells to test for genetic diseases or aneuploidy
neural tube defects

37
Q

chorionic villus sampling (CVS)

A

can be done earlier: 10-13 wks

karyotype fetal cells for genetic diseases

38
Q

free fetal DNA testing

A

baby’s blood cells/DNA are in mom’s blood

39
Q

ovarian cyst associated with molar pregnancy

A

theca-lutein cyst: occurs due to ↑bHCG (when can come from chroriocarcinoma)

40
Q

risk factors for placenta previa

A

history of C section (biggest risk factor)
↑maternal age
↑ multiparity

41
Q

PAINLESS vaginal bleeding

in 2nd half of pregnancy

A

placenta previa

placenta detaches as uterus grows

42
Q

diagnosis of placenta previa

A

US BEFORE DIGITAL EXAM!!!

otherwise bleeding previa → hemorrhage →Csection

43
Q

risk factors for:
placenta accreta
placenta increta
placenta percreta

A

history of placenta previa

history of C section

44
Q

abnormal attachment of placenta to myometrium

A

placenta Accreta = Attaches

45
Q

invasion of placenta into myometrium

A

placenta Increta = Invasion

46
Q

placenta peforates through uterus

A

placenta Percreta = Perforate

47
Q

diagnosis of placenta accreta/increta/percreta

A

US
sometimes won’t know until trying to deliver placenta and won’t come out + bleeding during delivery → massive, life-threatening hemorrhage

48
Q

treatment of placenta accreta/increta/percreta

A

Csection

hysterectomy

49
Q

premature separation of placenta from uterus before delivery
maternal hemorrhage or DIC possible
baby deprived of O2

A

placental abruption

50
Q

risk factors

A
history of prior placental abruption
HTN (included preeclampsia)
trauma (MVA)
smoking 
cocaine use
51
Q

complication of pregnancy with cocaine use

A

placenta abruption

52
Q

sudden onset
PAINFUL vaginal bleeding in 2nd half of pregnancy
ctx
fetal distress on HR monitor

A

placental abruption

painful due to irritation of uterus → ctx → fast labor

53
Q

treatment of placental abruption

A

emergency C section

54
Q

causes of postpartum hemorrhage

A

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

55
Q

enlarged, soft, boggy uterus

bleeding minutes after delivery (can occur up to a couple days after)

A

postpartum hemorrhage

56
Q

risk factor of PPH

A
overdistended uterus (large fetus, multifetal gestation)
induced or augmented labor
prolonged labor - overworked uterus
57
Q

patient had HTN before pregnancy

A

chronic HTN

58
Q

antihypertensive that is a teratogen

A

ACEi (renal abnormalties)

59
Q

antihypertensives safe during pregnancy (for chronic HTN)

A

methyldopa: α2 agonist
labetalol: α + ß blocker

60
Q

new-onset HTN >140/90 after 20 wks GA pregnancy and resolves postpartum
no proteinuria

A

gestational HTN

61
Q

treatment of gestational HTN

A

no treatment - doesn’t help outcomes

close monitoring to watch for any progression of disease

62
Q

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)

A

preeclampsia

considered severe if: end-organ dysfunction or bp >160/110

63
Q

potential pathophysiology of preclampsia

A

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

64
Q

widspread endothelial dysfunction → leaky vessels → vasospasm → HTN + proteinuria or end-organ dysfunction during pregnancy

A

preeclampsia

65
Q

risk factors of preeclampsia

A
history of preeclampsia
extremes of age: 40 yo
nulliparity
chronic HTN 
diabetes
multifetal gestation
hyatidiform mole
66
Q

HELLP syndrome: variant of severe preeclampsia

A

Hemolysis
Elevated Liver enzymes
Low Platelets

67
Q

preeclampsia + seizure

A

eclampsia

68
Q

anticonvulsant for seizures in eclampsia

A

magnesium sulfate to prevent or terminate a seizure (eclampsia)

69
Q

antihypertensive for preeclampsia, HELLP, eclampsia

A
rapid acting antihypertensive if >160/110 (prevent stroke, placenta abruption): 
hydralazine
labetalol
nifedipine
definitive treatment: delivery
70
Q

placenta secretes hormone: human placental lactogen (HPL)

A

↓ insulin sensitivity in mom to allow glucose to go to baby instead of mom

71
Q

exaggerated HPL response
diabetes develops during pregnancy
resolves postpartum

A

gestational diabetes

72
Q

screen for gestational diabetes

A

oral glucose tolerance test: 24-28 wks GA

73
Q

treatment of gestational diabetes

A

diet +/- insulin

74
Q

complication of gestational diabetes

A

macrosomia
hypoglycemia of infant: ↑ fetal exposure to glucose → fetal ßcells in pancreas undergo hyperplasia to produce more insulin → once delivery (no glucose source) → hypoglycemic

75
Q

have type 1 or type 2 DM before pregnancy

A

pregestational diabetes

76
Q

treatment of pregestational diabetes

A

insulin

77
Q

complications of pregestational diabetes

A

macrosomia
hypoglycemia
congenital anomalies (CV defects, caudal regression syndrome (sacral dysgenesis - lower part of body doesn’t form properly), stillbirth)

78
Q

bp drops in supine position

A

compression of IVC by uterus (lie on L or R decubitus)

↓preload →↓SV