Diseases Of Pregnancy Flashcards
2 pathways of infections reaching the placenta (chrioamnionitis)
1) ascension through the birth canal
- far more common
- usually bacterial and tied with premature rupture of the fetal membranes
- most common is mycoplasma candida and urea plasma urealyticum
- can also be GBS and gardnerella vaginalis
2) hematogenous spread
- rare but usually due to TORCH infections
Both result in chorioamnionits (infection of amniotic fluid and placenta)
- shows fever, tachycardia, uterine tenderness and pelvic pain with Purulent vaginal discharge and amniotic fluid on amniocentesis in mother
- shows fetal tachycardia (>160 bmp)
- treatment = IV ampicillin + gentamicin
Ectopic pregnancy
Implantation of a fertilized ovum in any site other than the uterus
- 90% = Fallopian tubes
- 10% = any other site
**is a medical emergency since it risks rupture of the Fallopian tubes
50% of ectopic pregnancy is caused by chronic inflammation and scarring of the oviduct
- other 50% = no evident cause
If tubal pregnancy = causes intratubal hematoma and/or intraperitioneal hemorrhage due to placenta eroding the Fallopian tube
Symptoms:
- acute severe abdominal pain (4-6 weeks after their last menstrual period)
- cervical motion tenderness with enlarged uterus and Fallopian tubes (if applicable)
- may or may not present with vaginal bleeding
Diagnosis
- Transvaginal ultrasound as imaging
- increased B-hCG on lab values
- biopsy (not needed but will show decides without chorionic villi or implantation site)
Gestational trophoblastic disease (GTDs)
Abnormal proliferation of fetal trophoblast cells
WHO divides these diseases into two catagories
1) molar lesions
2) nonpolar lesions (choriocarcinoma and other malignancies)
all GTDs produce excessive hCG at higher levels than those found in pregnancy
- are used to both diagnosis and monitor treatment efficacy
Hydatidiform mole
Voluminous mass of swollen chorionic villi that appear as “grapelike” structures.
- is a molar GTD
Two subtypes
1) complete = NOT comparable with embryogenesis and the chorionic villi are diploid always
- only contains paternal chromosomes
- 1:2000 pregnancies
- more common <20 and >40 yrs old
2) partial = is compatible with early embryo formation (may contain fetal parts) but not with life. Also always Triploid (69, XXY/XYY)
- contains two paternal chromosome and 1 maternal chromsome
Both subtypes result with excess paternal genetic material from abnormal fertilization
Both show elevation of hCG and absence of fetal heart sounds
80-90% are cured with curettage but 10% of complete moles are invasive
- only 2% chance of choriocaricnoma though
Invasive moles
Complete moles that are locally invasive but lack metastatic potential of choriocarcinoma
These moles retain the hydropic villi but can cause rupture of the uterus and sometimes life treating hemorrhages
Always appear with black necrotic foci
- *while they dont metastasis, surgery is difficult since the hydropic villi can embolization to distant organs such as lungs or Brain**
- however these embolism vili dont act like Mets and can regress spontaneously
Treatment = curratage initially, but if hCG levels dont decline then need to do chemotherapy
- If embolized vili present = chemotherapy regardless of hCG levels
Gestational choriocarcinoma
Very aggressive malignant tumor from gestational chorionic epithelium or totipotential cells within the gonads
Rare in western world but common in African and Asian countries
- western = 1:30,000
- Asian and African = 1:2000
50% arise from complete hydatidiform moles
25% arise after abortions
25% arise after a normal pregnancy
There are NO chorionic villi**
Symptoms:
- blood /brown discharge accompanied by a rising titer of B-hCG in blood and urine (MUCH higher than what is seen in a general hydatidiform mole
- postpartum vaginalis bleeding and hypertrophic uterus after pregnancy
- metastatic symptoms (most are diagnosed with metastasis present (most common site = lungs and vagina))
- physical exam or imaging may show multiple theca lutein cysts
Treatment = chemotherapy for placental choriocaricnoma (extremely sensitive and nearly 100% are cured even with Mets by chemo as long as it’s caught early enough)
- gonadal choriocarcinoma = poor prognosis even with chemotherapy
Preeclampsia
Development of HTN (>140/90) and proteinuria w/ edema (>300mg/24hrs of protien in urine) in the 3rd trimester of pregnancy (usually weeks 24-25)
Occurs in 5-10% of pregnancies and is more common in 2st pregnancies in women older than 35 yrs old
becomes true eclampsia if new onset grand mal seizures occur due to untreated preeclampsia
While not fully understood, it is believed that insufficient maternal blood flow to the placenta via inadequate remodeling of the spiral arteries is the pathogenesis behind this disorder
- the musculoelastic walls of the spiral arteries dont dilate and remain narrow
- this results in placental hypoxia, increased sFLt1 and soluble endogenous (sEng), and decreased VEGF = decreased angiogenesis and increased risk for end-organ microangiopathy
Treatment:
- preeclampsia only = induce iratogenic pregnancy only if > 37 +0 and give hydralazine and labetalol to drop HTN (can also use Methyldopa and nifedipine if needed)
- eclampsia = magnesium sulfate or calcium gluconate (magnesium is first line always though). Also need iratogenic pregnancy immediately once stable as long as > 34 +0
- HELLP syndrome = blood transfusions, magnesium sulfate, hydralazine and labetalol and iratogenic pregnancy once stable if > 34 +0
HELLP syndrome
Occurs in 10% of patients with severe preeclampsia
- HTN >160/110 usually is needed
Shows hemolysis, elevated liver enzymes and low platlets (<100,000)
This occurs to DIC occurring in the body
Placenta abruption
Tearing of the placenta of the uterine wall usually due to trauma or uncontrolled HTN (most common)
- produces life threatening hemorrhages and presents with PAINFUL vaginal bleeding (abrupt abdominal pain with uterine tenderness)
Placenta previa and vasa previa
Placenta previa = presence of the palcenta in the internal os which can partially or fully obstruct the neck of the uterus
- high risk for hemorrhage and birth complications and ALWAYS presents with sudden painless bright red vaignal bleeding
- usually 3rd trimester
- ** ALWAYS before rupture of membranes
- **no fetal distress usually
- requires C-section
Vasa previa = fetal vessels are located near the internal os of the cervix
- high risk for hemorrhage and birth complications and ALWAYS presents with sudden painless bright red vaignal bleeding
- ** ALWAYS after rupture of membranes occurs
- fetal distress is common (usually bradycardia)
- requires C-section
Placenta accreta/increta/percreta
Accreta = Chorionic villi attach to the myometium but DONT invade the myometrium
Increta = chorionic villi attach to the myometrium and invade it
Percreta = chorionic vili attach to the myometrium, invade it and penetrate the serosa layer
all three result in a placenta that does not remove easily at birth and causes risk of life threatening hemorrhages
All three increase rates with:
- advanced maternal age
- multiparity
- prior C-sections
- history of uterine surgery of any kind
- placenta previa currently or in the past
Symptoms for all
- abnormal uterine bleeding
- postpartum hemorrhages at time of placenta separation
Treatment = all requires a C-section
(Dont try to save the placenta or do natural vaignal birth since this will just cause hemorrhaging)_
