Pregnancy Complications Flashcards

Question

Diabetes Pregnancy Complications

Answer 1

* _Maternal_ * Diabetic complications may worsen: * Retinopathy * Renal, cardiac disease * ↑ Incidence of DKA * **Spontaneous abortion** * **Preeclampsia** * _Fetal_ * **Congenital anomalies** * Cardiac, CNS * **IUFD** (stillbirth) * **Macrosomia and birth injury** * Big babies indicative of GDM * **Growth restriction** * Small babies indicative of pre-gestational DM * **Neonatal cardiomyopathy** * Mostly hypertropic * **Respiratory distress syndrome** * **Neonatal hypoglycemia** * **↑ Risk of childhood obesity**

Answer 2

* **DM treatment** _Achieving glycemic control is the most important factor_ * **Diet and exercise** (A1) * BS goal: fasting \< 95, 2 hrs PP \< 120 * Measure BS 4 times daily * _If BGL remains elevated_ ⇒ **initiate medication therapy** * **Glyburide or metformin** (PO) * **Insulin** (IV) * Many regimens available * Insulin requirements ↑ through pregnancy * ⅔ and ⅓ rule: ⅔ in the AM, ⅓ in the PM * **Imaging:** many ultrasounds * _1^st trimester_ * Early to date and assess viability (high miscarriage rate) * _2^nd trimester_ * Level II US to assess for fetal anomalies @ 18-20 wks * Fetal ECHO @ 22 wks * _3^rd trimester_ * Growth scans every 4 wks until delivery * **Antenatal testing** * NST/AFI or BPP twice weekly * **Timing and mode of delivery** * Glycemic control * Fetal size * Amniocentesis * **Postpartum testing** * Screen at 6 wks to assess for non-gestational DM * ↑ Maternal risk of developing DM later in life

Answer 3

* **~10-15%** of _recognized pregnancies_ end in **spontaneous abortion** * Many more pregnancies end before mother aware she is pregnant * Mechanisms leading to early loss of pregnancy unclear * _Fetal factors_ * **Genetic or acquired anomaly** ⇒ defective implantation * Can’t support fetal development * \> 50% of spontaneous abortions show **chromosomal abnormalities** * _Maternal factors_ * **Inflammatory diseases**, both _localized to the placenta and systemic_ * Includes infections such as **Toxoplasma, Mycoplasma, Listeria** * **Uterine abnormalities** * **Trauma** (very rare cause of spontaneous abortion)

Answer 4

* _Tissue from spontaneous abortion shows:_ * **Focal areas of decidual necrosis** * **Intense neutrophilic infiltration** * **Thrombi within decidual blood vessels** * **Old and recent hemorrhage** * _If a fetus is seen_, can examine it and look for **anomalies** * _Do chromosomal studies if:_ * Pt has had \> 1 early spontaneous loss * Fetus is malformed

Answer 5

* **Delivery prior to 37 completed wks of gestation** * 12% of births in the US * _Consequences:_ * **Death** * **Respiratory distress syndrome** * **Intraventricular hemorrhage** * **Necrotizing enterocolitis** * **Cerebral palsy** * **Visual and hearing impairment**

Answer 6

* **Uterine contractions causing dilation of the cervix** * Unclear etiology * _Management_ * **Tocolysis**: stop contractions * **Steroids**: fetal lung maturity, minimize risks of PTD * **Magnesium sulfate**: neuroprotection, ↓ risk of CP * _Prevention_ * **17 alpha hydroxyprogesterone acetate** (IM injection) * ↓ Risk of recurrent preterm birth

Answer 7

* **Rupture of amniotic sac prior to labor in a preterm gestation** * Etiology is unclear * _Management_ * **Abx**: prolongs the latency to delivery * **Steroids**: fetal lung maturity, minimize risks of PTD * **Magnesium sulfate**: neuroprotection, ↓ risk of CP * _Prevention_: * **17 alpha hydroxyprogesterone acetate**

Answer 8

_Pregnancy loss in 3^rd trimester_ prompts a search for evidence of the following: * **Interruption of blood flow** through the umbilical cord * Ex. constricting knots or compression * **Ascending infections** involving chorioamnionic membranes * **Retroplacental hemorrhage** @ interface of placenta and myometrium (abruptio placentae) * **Rupture of the fetal vessels in terminal villi** (intervillous hemorrhage) * **Uteroplacental insufficiency** * Precipitated by abnormal placentation, altered placental development, or maternal vascular thrombosis

Answer 9

**Structural weakness of the cervical tissue that leads to pregnancy loss** * Asymptomatic: cervix opens without feeling contractions * Recurrent * Occurs during **2^nd trimester** * **Congenital** vs **acquired** * D&E, LEEP, ablation procedures on cervix * _If hx in a prior pregnancy:_ * Follow w/ US (cervical length) * **Cervical cerclage**

Answer 10

* **Needs to be done on all placentas (triage)** * _Required observations:_ * Complete or fragmented * Weight (after removal of cord and membranes) * Shape * Discoid/normal * Multilobate * Accessory lobes * % of maternal surface covered by retroplacental hematoma

Answer 11

* **Missing cotyledons** from _maternal surface_ * **Poor vascularization** of _fetal surface_ * **Abnormal placental shape and peripheral cord insertion** * Marginal * Velamentous * **Hemorrhage or stricture** _at cord insertion site_ * **Vessel number** * **Cord accident** (true knots)

Answer 12

* Length * Local abnormalities * Nearest distance to margin of placenta * Vessel number * Knots (true versus false) * Embryonic remnants * Thrombosis

Answer 13

* **Meconium staining** * Caused by in utero passing of meconium * **Gross discoloration** * **Vacuolation** of amniotic epithelium, **cell degeneration**, epithelial **necrosis** w/ finely granular **brown pigment in MΦ** of amnion, chorion and decidua * **Squamous metaplasia** * **Amnion nodusum** * See aggregates of **squames** and **hair** * Related to oligohydramnios * **Early amnion rupture sequence (bands)** * Example of **disruption of normal development**

Answer 14

**Partial or complete absence of endometrial decidua w/ adherence of placenta directly to myometrium.** * Abnormally adherent to uterus ⇒ **fails to** **separate following delivery** * Attempts to separate can lead to **massive hemorrhage** * _Incidence varies depending on obstetric hx_ * Prior cesarean section * Prior D&E * Multiparity * Thought to be caused by **damage to endometrial/decidual layer** * _Diagnosis_ * US, confirmed by MRI antenatally * _Different degrees_ * **Accrete**: attaches to the myometrium * **Increta**: invades the myometrium * **Percreta**: penetrates through the myometrium * _Management_ * Prepare for **massive transfusion** * Plan for **cesarean hysterectomy**

Answer 15

* **Placenta covers the internal cervical os** * Implants in the _lower uterine segment or cervix_ * 1/200 pregnancies * _Clinical manifestations:_ * **Painless** **antepartum bleeding** in _2^nd and 3^rd trimester_ * **Premature labor** * **Labor or digital exam can lead to massive bleeding** * Diagnosis via US * Requires delivery by **cesarean section** * May be indication for **preterm delivery if significant bleeding**

Answer 16

* **Dizygotic twins**: fertilization of two ova * **Monozygotic twins**: division of one fertilized ovum * Occurs via splitting of inner cell mass of blastocyst * _3 basic types of twin placentas:_ 1. **Dichorionic-Diamnionic** * Each fetus has its own amniotic sac and its own chorion * 2 placentas can be separate or fused * May occur w/ either monozygotic or dizygotic twins and is not specific 2. **Monochorionic-Diamnionic** * Each fetus has its own amniotic sac and these are covered by one common chorion * Most common type of monozygotic twinning * Split of fertilized egg on day 3-4 * Need to look for vascular anastomoses 3. **Monochorionic-Monoamnionic** * Both fetuses in one sac * Monozygous gestation * Split of fertilized egg on day 7 or later

Answer 17

* Seen in **monochorionic placentas** * **Vascular anastamoses** create _abnormal sharing of fetal circulations_ through shunting * Can get **marked disparity in fetal blood volumes** w/ **possible death of one or both fetuses**

Answer 18

* **Acardiac twin** (“Twin reversed arterial perfusion sequence or TRAPS”) * Rare complication of monochorionic twin pregnancies * Severe variant of twin-to-twin transfusion syndrome (TTTS) * The “acardiac twin” is severely malformed * **Fetus papyraceous** * Intrauterine fetal demise of a twin occurs early in pregnancy * Retention of the fetus for min. of 10 wks * Results in mechanical compression of the small fetus and loss of fluid ⇒ resembles parchment paper

Answer 19

* _Can see inflammation in:_ * Placental cotyledons (**villitis**) * Membranes (**chorioamnionitis**) * Umbilical cord (**funisitis**/**vasculitis**) * _Organisms can reach placenta by 2 pathways:_ * **Ascending infection through birth canal** * Most common route * Usually **bacterial** * Can lead to premature rupture of membranes (PROM) ⇒ organisms ascend further * See **cloudy amniotic fluid** and **PMNs in membranes** (**chorioamnionitis**) * Can also see fetal response w/ **PMNs in the umbilical cord** (**funisitis)** * **Hematogenous (transplacental) infection** * Less common * Usually results in **villitis** * May be due to infection w/ organism in the **TORCH group**

Answer 20

**Preeclampsia** and **Eclampsia** A _pregnancy specific syndrome_ of **↓ end-organ perfusion** secondary to **vasospasm** and **endothelial activation.** Incidence in US **~ 5%** * **Preeclampsia** * **HTN**, **proteinuria**, and **edema** * Usually in the **3^rd trimester** * More commonly in **primiparas** * Pts can develop **DIC** w/ lesions in the _liver, kidneys, heart, placenta, and brain_ * No absolute correlation b/t severity of eclampsia and magnitude of anatomic changes * **Eclampsia** * **Seizures** in _women w/ preeclampsia_ not attributable to other causes * **HELLP Syndrome** * **H**emolysis, **E**levated **L**iver Enzymes, and **L**ow **P**latelets in women w/ preeclampsia * Seen in ~10% of women w/ severe pre-eclampsia

Answer 21

* Appears to begin w/ **abnormal placentation** that leads to **placental ischemia** * Insufficient trophoblast invasion * Decidual vasculopathy * Possible trophoblast/cytotrophoblast abnormalities * **↓** **Uteroplacental perfusion** ⇒↑ release of **vasoconstrictor** substances * **Vasospasm** and **endothelial activation** ⇒ DIC, HTN, and organ damage * **Thrombosis of arterioles and capillaries** ⇒ lesions in the _liver, kidneys, brain, pituitary and placenta_ * **HTN** of toxemia may be d/t defects in **RAAS** and **prostaglandin** systems

Answer 22

Classification dependent on the severity of signs and sx: * **_Non-Severe_** * **BP 140/90** * **Proteinuria** * \> 300 mg in 24-hr collection or persistent 1+ on dipstick * Asymptomatic * Outcomes are similar to nl pregnancy * **_Severe_** * **BP \> 160/110** on 2 occasions or while on bedrest * Proteinuria * ≥ 5 g in 24-hr collection or persistent 3+ on dipstick * _Or any of the follow manifestations:_ * **Renal insufficiency** * Serum creatinine \> 1.1 * Oliguria \< 500ml in 24 hrs * **Cerebral or visual disturbances** * **Pulmonary edema or cyanosis** * **Evidence of hepatic dysfunction** * ↑ LFTs * Epigastric or RUQ pain * **Thrombocytopenia** (\< 100k/μL) * **↑ risks compared to nl pregnancies**

Answer 23

* **Chronic HTN** plus **new-onset proteinuria** or * **Onset of CNS sx** or **evidence of HELLP syndrome** * Sudden ↑ in BP or proteinuria from baseline * Complicates **25%** of those w/ chronic HTN

Answer 24

* _Histological changes:_ * **↑** **Villous ischemia** * Formation of prominent **syncytial knots** * **Thickening of trophoblastic BM** * **Villous hypovascularity** * **Fibrinoid necrosis** and **intramural lipid deposition** (acute atherosis) in walls of uterine vessels * _Gross changes:_ * **Placental** **infarcts**, occur in nl full-term placentas, are **larger and more numerous** * Seen in many conditions, including pre-eclampsia * Evolution from **red** to **white infarcts** w/ time * Early infarct: **congested, hemorrhagic villi w/ villous crowding** * Late infarct: **necrosis w/ ghost villi** * ↑ Frequency of **retroplacental hematomas**

Answer 25

* _Liver:_ * **Irregular, focal, subcapsular, and intraparenchymal hemorrhage** * **Fibrin thrombi** in _portal capillaries_ w/ foci of characteristic **peripheral hemorrhagic necrosis** * _Kidney__:_ * **Fibrin thrombi** in _glomeruli and capillaries of the cortex_ * **±** **Bilateral renal cortical necrosis** * _Brain__:_ * Gross or microscopic **foci of hemorrhage** along w/ **small-vessel thromboses**

Answer 26

* _Pre-eclampsia_ * Usually starts **insidiously** after **32nd week** of pregnancy w/ **HTN** and **edema** * **proteinuria** follows within several days * **Headaches** and **visual disturbances** are common * _Eclampsia_ = CNS involvement ⇒ **convulsions** and eventual **coma**

Answer 27

* _Non-severe preeclampsia_ * **Expectant management to term** * Controlled by bed rest, a balanced diet, and antihypertensive agents * _Severe preeclampsia_ * **If \> 34 wks** ⇒ deliver * **Expectant management to 34 wks** if _mother and fetus stable_ * With admin of steroids ⇒ deliver * _If mother and/or fetus not stable_ ⇒ **deliver** * **Induction of delivery** is the only definitive tx of established preeclampsia and eclampsia

Answer 28

**Premature separation of normally implanted placenta** **from the uterus** **prior to the birth of the fetus.** * 1 in 120 births * Pathophysiology: **hemorrhage into decidua basalis** * _Clinical presentation:_ * **Bleeding w/ painful uterine contractions** * Bleeding can be concealed ⇒ occurs _b/t uterine decidua and placenta_ * Vaginal bleeding (80-90% of cases) * Uterine tenderness/abd pain * Uterine hypertonus * _Management:_ * **Close monitoring of mother and fetus** * Mom: VS, CBC, coags * Fetus: HR monitoring * **May require transfusion of blood products** * **Timing of delivery** * Can wait if preterm and bleeding is limited * If massive, delivery regardless of gestational age * **Mode of delivery** * Can attempt vaginal delivery if bleeding is minimal * May require cesarean section

Answer 29

* HTN * Maternal trauma * Cocaine * Cigarette use * Previous abruption * Sudden decompression of uterus * Prelabor Rupture of Membranes (PROM)

Answer 30

* _First trimester:_ * **Large villi w/ few vessels** * _Second trimester:_ * **Smaller villi w/ moderately cellular collagenized stroma** * Percentage of villi w/ inner layer of cytotrophoblast cells falls * MΦ less numerous * **Capillaries located centrally and peripherally** * _Third trimester:_ * Smaller villi due to **predominance of terminal villi**, w/ **syncytiotrophoblastic knots** in 30% of villi * **↑** **Formation of vasculosyncytial membranes**

Answer 31

* Group of disorders w/ **proliferation of pregnancy-associated trophoblastic tissue** * **Can have malignant potential** * _Types:_ * **Hydatidiform mole** * Complete * Incomplete (partial) * **Invasive Hydatidiform Mole** * **Choriocarcinoma** * **Placental site trophoblastic tumor**

Answer 32

Complete and Partial **Cystic swelling of chorionic villi** **±** **trophoblastic proliferation** * 1 in 1-2k pregnancies in the US * Much more common in the Far East * Highest risk for women in **teens** **or b/t age 40-50** * May precede **choriocarcinoma** * Most pts present in **4^th or 5^th month of pregnancy** * _Clinical manifestations:_ * **Vaginal bleeding** * **Uterus that is larger than expected for duration of pregnancy** * **↑ Serum β-HCG**

Answer 33

* **All villi are affected** (edematous, hydropic) * **Grape-like swellings** * See **central cisterns** in **avascular villi** * Can see **trophoblastic proliferation** * Karyotype is usually **46,XX** * **No fetal parts are seen** * **Small probability of development of choriocarcinoma (~2%)**

Answer 34

* **Not all villi are affected** * **Less trophoblastic proliferation** * May see **fetal parts** * Karyotype is usually **triploid (69, XXY)** * **Lower risk of development of choriocarcinoma** compared to complete mole

Answer 35

* **Treated by currettage to remove tissue** * _If complete mole:_ * ↑ Beta HCG for length of gestation * After removing tissue, **need to monitor pt’s level of HCG to be sure it falls to non-pregnancy level** * 2.5% chance of evolving into **choriocarcinoma** * 10% chance of developing into an **invasive mole**

Answer 36

* **Locally destructive mole** * Can **perforate uterine wall** * Hydropic villi **can** **embolize to distant sites** * Pt experiences **vaginal bleeding, uterine enlargement,** ↑ **beta-HCG** * Risk of **uterine rupture** * **Responds well to chemotherapy**

Answer 37

* **Rapidly invasive, widely metastasizing malignant neoplasm** * Precursor lesions can be **hydatidiform moles** * Responds very well to **chemotherapy** * **Can invade the myometrium, penetrate blood vessels and lymphatics, and extend through uterus** * _Metastasizes to:_ * **Lungs** (50%) and **vagina** (30% to 40%) * Followed in descending order of frequency by the **brain, liver, and kidney** * See ↑ **beta-HCG** * _Gross_: * **Soft, fleshy**, yellow-white tumor w/ **ischemic necrosis, cystic softening, and extensive hemorrhage** * _Microscopic_: * **No villi** * **Anaplastic cells**, lots of **mitoses** * **Proliferation of cytotrophoblast and syncytiotrophoblast**

Answer 38

* **Intermediate trophoblasts** can remain @ _residual placental implantation site_ (**implantation site nodule**) following pregnancy * May give rise to **placental site trophoblastic tumors (PSTTs)** * Rare: \< 2% of gestational trophoblastic neoplasms * **Neoplastic polygonal cells** infiltrate the _endomyometrium_ * Can follow a **normal pregnancy** (½), **spontaneous abortion** (⅙), or **hydatidiform mole** (⅕) * Pts whose tumor is dx **\< 2 yrs after the prior pregnancy or w/ localized tumors** usually do well * **Later dx or more widespread tumor** implies a poor prognosis

Answer 39

* **Implantation of the fetus in any site other than a normal uterine location** * Fertilized ovum undergoes usual development * Formation of placental tissue, amniotic sac, and fetus * Host implantation site develops decidual changes * **1/150 pregnancies** * Unusual locations can **very rarely have live birth** * _Common sites:_ 1. **Within the fallopian tubes (~ 90%)** 2. **Ovary** (Ovarian pregnancy) * Fertilization and trapping of ovum within the follicle @ time of rupture 3. **Abdominal cavity (**Abdominal pregnancies) * Fertilized ovum falls from fimbriated end of the tube 4. **Intrauterine portion of fallopian tube** (cornual pregnancy) * _Risk factors:_ * **PID w/ chronic salpingitis** (35-50%) * **Peritubal adhesions** due to appendicitis, endometriosis, leiomyomas, and previous surgery * 50% of occur in nl appearing tubes * _Clinical manifestations:_ * **Severe abd pain ~6 wks after LNM** * Pain d/t **rupture of the fallopian tube** w/ resulting **pelvic hemorrhage** * Can be a **life-threatening condition** for the mother