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OBGYN Clerkship- Amboss Study Plan > Pregnancy Associated Disorders > Flashcards

Pregnancy Associated Disorders Flashcards

1
Q

Intrauterine growth restriction (IUGR)

A

lower than normal fetal growth characterized by an estimated fetal weight below the 10th percentile for a given gestational age.

two types of IUGR: asymmetrical and symmetrical

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2
Q

asymmetrical IUGR

A
  • caused by extrinsic factors which affect the fetus in the later stages of gestation (i.e. 3rd)
  • most common manifestation of IUGR (∼ 70%), has a late onset,
  • usually due to maternal systemic disease (e.g., hypertension) that results in placental insufficiency
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3
Q

symemetrical IUGR

A
  • Caused by intrinsic factors which affect the fetus in the early stages of gestation.
  • less common (∼ 30%)
  • usually due to a genetic disorder (e.g., aneuploidy), congenital heart disease, or early intrauterine TORCH infection that affects the fetus early in gestation.
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4
Q

Maternal Etiologies of IUGR

A
  • Substance use (e.g., alcohol, cigarettes, cocaine, heroin)
  • Teratogenic drugs: ACE inhibitors, carbamazepine, phenytoin, warfarin
  • Systemic diseases resulting in placental insufficiency
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5
Q

Uteroplacental causes of IUGR

A
  1. Placental insufficiency
  2. Placenta Previa
  3. Multiple Gestations
  4. placental abruption
  5. Umbilical artery thrombosis/ extensive infarction
  6. Uterine malformations (fibroids)
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6
Q

Placental insufficiency

A

A disorder of the fetomaternal circulation that causes inadequate blood flow to the placenta and impaired substance exchange (e.g., oxygen) between the mother and fetus, leading to metabolic compromise of the fetus.

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7
Q

Risk factors for placental insufficiency

A

smoking; diabetes mellitus; chronic hypertension; anemia; SLE;

Pregnancy-related conditions (preeclampsia, Rh incompatibility)

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8
Q

Fetal factors for IUGR

A
  • Genetic abnormalities in the fetus (e.g., aneuploidy)
  • Cyanotic congenital heart defects
  • Early intrauterine infections (TORCH)
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9
Q

Pathophysiology of asymmetric IUGR

A
  • insufficient transplacental delivery of oxygen and nutrients to the fetus and impaired return of carbon dioxide and fetal metabolic waste products from the fetus to the mother’s circulation
  • Fetal hypoxia and hypoglycemia → shunting of blood flow to vital fetal organs (brain, heart, and adrenal glands) bypassing other organs (e.g., liver, muscle, fat tissue)
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10
Q

Fetal signs of IGUR

A
  • Small for gestational age (or with a birth weight below 10th percentile)
  • Decreased or absent fetal movements
  • Asymmetrical IUGR: disproportionate growth restriction
    • head are normal while the body and limbs are thin and small
  • Symmetrical IUGR: global growth restriction
    • circumference of the head is proportional
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11
Q

IGUR Diagnostics

A
  1. Serial ultrasonography
    • Decreased fetal growth; fetal weight below the 10th percentile
    • Oligohydramnios
  2. Doppler velocimetry of umbilical artery: reduced or reversed diastolic flow
  3. Nonstress test: late decelerations of the fetal heartbeat
  4. Biophysical profile
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12
Q

Biophysical Profile in IUGR

A
  • Oligohydramnios; AFI < 5 (N=8-18)
  • Absent fetal breathing movements
  • Decreased fetal movement and tone
  • A score ≤ 4 indicates fetal hypoxia and/or placental insufficiency.; labor should be induced.
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13
Q

Tx IGUR

A
  • Treatment of the underlying condition
  • Close monitoring; (NST, CST, BPP)
  • If the infant is close to term, administer steroids and induce labor after 48 hours.
  • If there are signs of nonreassuring fetal status; induce labor or perform immediate cesarean delivery.
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14
Q

IUGR Complications

A
  • stillbirth
  • preterm labor
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15
Q

Hypertensive Preganancy Disorders

A
  1. Gestational hypertension (most common, least severe)
  2. Chronic Hypertension
  3. Preeclampia
    • Superimposed preeclampsia
    • HELLP syndrome
  4. Eclampsia
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16
Q

Gestational hypertension

A
  • pregnancy-induced hypertension with onset after 20 weeks gestation
  • Defined as a systolic blood pressure ≥ 140 mmHg or diastolic blood pressure ≥ 90 mmHg on 2 separate measurements at least 4 hours apart
  • can only be diagnosed if the patient was normotensive prior to 20 weeks gestation
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17
Q

Chronic hypertension

A

hypertension diagnosed < 20 wks gestation or before pregnancy

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18
Q

Preeclampsia

A
  • gestational hypertension with proteinuria, renal insufficiency, thrombocytopenia, evidence or liver damage, pulmonary edema, and or cerebral edemas
  • Superimposed: preeclamsia that occurs in a patient with chronic hypertension
  • HELLP syndrome: a life threatening form of preeclampsia
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19
Q

HELLP

A

H= hemolysis

EL= elevated liver enzymes

LP= low platelets

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20
Q

Eclampsia

A

severe form of preeclampia with convultive seizures and/ or coma

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21
Q

Risk factors for hypertensive preganancy disorders

A
  • Age < 20 or > 40 years
  • African-American race
  • Diabetes mellitus or gestational diabetes
  • Chronic hypertension
  • Chronic renal disease (e.g., SLE)

Pregnancy-related risk factors

  • Nulliparity
  • Previous preeclampsia
  • Multiple gestation (twins)
  • Hydatidiform moles
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22
Q

Clinical Features: Gestational hypertension

A
  • Asymptomatic hypertension
  • Nonspecific symptoms (e.g., morning headaches, fatigue, dizziness)
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23
Q

clinical features: preeclampsia

without severe features

A
  • Usually asymptomatic
  • Nonspecific symptoms may include:
    • Headaches
    • Visual disturbances
    • RUQ or epigastric pain
    • Rapid development of edema
  • Hypertension
  • Proteinuria
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24
Q

clinical features: preeclampia

with severe features

A
  • Severe hypertension (systolic ≥ 160 or diastolic BP ≥ 110)
  • Proteinuria, oliguria
  • Headache
  • Visual disturbances (e.g., blurred vision
  • RUQ or epigastric pain
  • Pulmonary edema
  • altered mental state
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25
Q

Clinical features: HELLP syndrome

A
  • Onset: most commonly > 27 weeks gestation (30% occur postpartum)
  • Preeclampsia
  • RUQ pain (liver capsule pain; liver hematoma)
  • Rapid clinical deterioration (DIC, pulmonary edema, acute renal failure, stroke, abruptio placentae)
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26
Q

Clinical features Eclampsia

A
  • Onset: the majority of cases occur in the intrapartum and postpartum period
  • Eclamptic seizures: generalized tonic-clonic seizures
  • Deterioration with headaches, RUQ pain, hyperreflexia, and visual changes are warning signs of a potential eclamptic seizure
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27
Q

Initial work up for Pregnancy hypertensive disorders

A
  1. blood pressure must be elevated on at least 2 occasions that are at least 4 hours apart
  2. Urine tests to determine proteinuria
    • 24-hour urine collection (gold standard): ≥ 300 mg/24 h
    • Urine dipstick: 1–2 + protein
  3. Laboratory analysis
    • CBC
    • Kidney function tests
  4. HELLP syndrome is suspected:
    1. Peripheral smear (assess for hemolysis)
    2. coagulation studies are indicated if (i.e., thrombocytopenia and/or liver function)
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28
Q

Diagnostic criteria for preeclampsia without severe features

A
  • Hypertension (> 140/90 mmHg)
  • Proteinuria ≥ 300 mg/24 h
  • If proteinuria is absent, at least one of the following must be present:
    • Thrombocytopenia
    • Impaired renal function
    • Impaired liver function
    • Visual or neurologic changes
    • Pulmonary edema
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29
Q

Diagnostic criteris for preeclampsia with severe features

A

one or more

  • Severe hypertension (> 160 mmHg systolic or > 110 mmHg diastolic)
  • Thrombocytopenia < 100,000/μL
  • Impaired renal function (serum creatinine > 1.1 mg/dL or doubling of serum creatinine)
  • Impaired liver function (elevated transaminases)
  • Pulmonary edema
  • Cerebral or visual symptoms
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30
Q

Diagnotic criteria for eclampsia

A

Primarily a clinical diagnosis: patient with preeclampsia presenting with new-onset grand mal seizures

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31
Q

Differential of eclampsia

A
  1. Epilepsy
  2. Encephalitis
  3. Metabolic disorders (e.g., hypoglycemia, hyponatremia)
  4. Hemorrhagic stroke
  5. Ischemic stroke
  6. Withdrawal syndromes
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32
Q

Differntial of HELLP syndorme

A
  1. Throboticmicroangiopathy (TTP, HUS)
  2. Fulminant VIral Hepatitis
  3. Acute Fatty liver of preganancy
  4. itrahepatic cholestatis of pregnancy
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33
Q

Acute Fatty Liver of Pregnancy

A
  • a rare disease most common in the third trimester characterized by extensive fatty infiltration of the liver, which can result in acute liver failure
  • Pathophysiology: dysfunction of fatty acid β-oxidation
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34
Q

Symptoms of acute fatty liver of pregnancy

A
  • Sudden onset of jaundice
  • RUQ pain, nausea, and vomiting
  • Coagulopathy
  • Hypoalbuminemia; ascites
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35
Q

Complications of acute fatty liver of pregnancy

A
  • Acute liver failure
  • Acute renal failure
  • Encephalopathy
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36
Q

acute fatty liver of preganancy

diagnostics

A

Laboratory analysis:

  • ↑ AST, ↑ALT
  • ↑ WBC, ↓ platelets
  • Hypoglycemia
  • Liver synthesis parameters: ↓↓ clotting factors , ↓↓ Cholinesterase

Imaging: rule out other diagnoses

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37
Q

acute fatty liver of pregnancy Tx

A

Therapy: immediate Cesarean (C)-section

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38
Q

intrahepatic cholestatis of preganancy

A

rare disease most common in the third trimester that presents with pruritus, jaundice, and an elevation in serum bile acid concentrations

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39
Q

intrahepatic cholestatis of pregnansy

symptoms

A

jaundice

pruritis

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40
Q

intrahepatic cholestatis of pregnancy

complications

A

Fetal growth restriction

fetal mortality

Premature labor; preterm birth

Recurrence in following pregnancies

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41
Q

intrahepatic cholestatis of pregnancy

diagnostics

A
  • ↑ Total serum bile acid levels (cholic acid and chenodeoxycholic acid) > 10 micromol/L
  • ↑ ALP
  • ↑ ALT, AST
  • ↑ direct bilirubin
  • Hepatitis serology (to rule out viral hepatitis)
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42
Q

intrahepatic cholestatis of pregnancy

tx and prognosis

A

Therapy

  • First-line medication: ursodeoxycholic acid PO
  • An early therapy with ursodeoxycholic acid reduces the risk of preterm birth and stillbirth.

Prognosis: fully reversible postpartum

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43
Q

gestational hypertension and preeclampsia w/o severe features

treatment

A
  • antepartum evaluation (Ultrasound, NST, BPP)

Hospitalization and deilvery if:

  1. greater than or 37 0/7 wks
  2. suspected placental abption
  3. Labor or rupture of membranes
  4. Fetal weight < 5th percentile
  5. Oligohydramnios
  6. Abnormal maternal or fetal test results

if not outpatient with antihypertensives: labetalol, hydralazine, nifedipine

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44
Q

preeclampsia with severe features

treatment

A

DELIVERY if

  • Pregnancy is ≥ 34 0/7 weeks gestation
  • Pregnancy is < 34 0/7 weeks gestation with maternal or fetal instability
    • Immediate delivery after stabilization (IV magnesium sulfate prophylaxis, antihypertensive drugs, corticosteroids )

If mom is stable:

  • monitor in patient
  • treat severe hypertension
  • magnesium sulfate
  • corticosteroids
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45
Q

eclampsia treatment

A

Stabilization

  • Magnesium sulfate IV (first-line)
    • Antidote: calcium gluconate IV if early signs of magnesium toxicity (decreased deep tendon reflexes)
  • Position patient on left lateral decubitus position → prevent placental hypoperfusion through compression of the inferior vena cava

Delivery: once the mother is stable and seizures have stopped

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46
Q

HELLP syndrome treatment

A

Stabilization

  • Blood transfusions
  • Antihypertensive agents (labetalol, hydralazine)
  • Magnesium sulfate

Delivery: if ≥ 34 weeks gestation or at any gestational age with deteriorating maternal or fetal status

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47
Q

Maternal complications of hypertensive pregnancy disorders

A
  1. Placental abruption
  2. Cerebral hemorrhage, stroke
  3. DIC
  4. Acute respiratory distress syndrome (ARDS)
  5. Maternal death

ARDS and cerebral hemorrhage are the most common causes of death.

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48
Q

fetal complications of hypertensive pregnancy disorders

A
  • Fetal growth restriction
  • Preterm birth
  • Seizure-induced fetal hypoxia
  • Fetal death
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49
Q

Prevention preeclampsia

A

Prophylactic low-dose ASA PO from 12–14 weeks gestation for patients with a high risk

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50
Q

Nausea and comiting of pregancy

A

Risk factors

  • Nulliparity

Clinical features

  • Nausea and/or vomiting
  • Normal vital signs, lab findings, and normal physical examination
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51
Q

nausea and vomiting of pregnancy

Tx

A
  • Rehydration
  • Nonpharmacologic options
    • Adapt diet and avoid triggers.
    • Ginger tea/capsules
  • Antiemetic (add in a stepwise manner)
    1. Pyridoxine (vitamin B6) and/or doxylamine
    2. For refractory symptoms, add one of the following:
      • Diphenhydramine
      • Dimenhydrinate
    3. Last resort; methylprednisolone
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52
Q

Hyperemesis gravidarum

A

severe, persistent nausea and vomiting associated with a > 5% loss of pre-pregnancy weight and ketonuria

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53
Q

hyperemesis gravidum clinical features

A
  • nausea, vomiting,
  • physical signs of dehydration,
  • hypersalivation,
  • orthostatic hypotension,
  • malnourishment
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54
Q

Hyperemesis gravidarum

Tx

A
  • Antiemetic therapy:
    • May require glucocorticoid therapy
  • IV fluid resuscitation/replacement
  • Electrolyte and thiamine repletion
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55
Q

Cervical insufficiency

A
  • painless cervical dilation, in the absence of uterine contractions;
  • second trimester of pregnancy

Clinical features

  • Painless cervical dilation with or without prolapsed membranes
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56
Q

cervical insufficiency

diagnosis

A
  • Clinical diagnosis typically before 24 weeks’ (may be up to 28 weeks’) gestation
  • history of ≥ 2 previous mid-trimester pregnancy losses
  • history ≥ 3 preterm births not explained by any other cause
  • transvaginal ultrasound cervical length < 25 mm before 24 weeks’ gestation
    • A shortened cervical length alone is not sufficient to diagnose must have history.
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57
Q

cervical insufficiency

Tx

A
  • Serial cervical ultrasound monitoring should be commenced in high-risk women (i.e., previous preterm birth) between 16–24 weeks’ gestation.
  • Cervical cerclage
  • Progesterone supplementation (vaginal or intramuscular): indicated for a short cervical length at < 24 weeks’ gestation
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58
Q

cervical cerclage

A
  • Definition: placement of a supportive suture in the cervicovaginal junction to prevent early pregnancy loss or preterm birth
  • Indications: only in singleton pregnancies
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59
Q

Supine hypotensive syndrome

A

Compression of the vena cava and pelvic veins by the uterus may occur during the third trimester of pregnancy as a result of the mother lying in a supine position.

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60
Q

peripheral edema in pregnancy

A
  • Very common, benign finding

Management

  • Rule out DVT and preeclampsia
  • Monitoring; usually no treatment necessary
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61
Q

MSK pain in pregnancy

A
  1. Lower back pain: increased lumbar lordosis caused by relaxation of the ligaments supporting the joints of the pelvic girdle in preparation for childbirth
  2. Carpal tunnel syndrome (caused by peripheral edema; usually resolves after delivery)
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62
Q

Pregnancy loss definitions

A
  • Spontaneous abortion/miscarriage: loss of pregnancy before 20 weeks’ gestation
  • Stillbirth: loss of pregnancy after 20 weeks’ gestation
  • Recurrent pregnancy loss: two or more miscarriages occurring before 20 weeks’ gestation
63
Q

Maternal Etiologies for spontaneus abortion

A

Abnormalities of the reproductive organs

  • Septate uterus
  • Uterine leiomyomas
  • Uterine adhesions
  • Cervical incompetence

Systemic diseases

  • diabetes mellitus,
  • hyperthyroidism,
  • hypothyroidism,
  • genetic disorders,
  • infections,
  • hypercoagulability (e.g., antiphospholipid syndrome
64
Q

non maternal etiologies for spontaneus abortion

A

Fetoplacental

  • Chromosomal abnormalities account for up to half of all spontaneous abortions
  • Congenital anomalies

Miscellaneous

  • Trauma
  • Iatrogenic
  • Environmental
65
Q

Fetoplacental etiologies for still birth

A
  1. Intrauterine growth restriction
  2. Placental abnormalities
  3. Infection
  4. Chromosomal abnormalities
  5. Congenital malformations
  6. Umbilical cord complications (nuchal cord or knot)
  7. Fetal hydrops
66
Q

maternal etiologies for stillbirth

A
  1. Fetal-maternal hemorrhage
  2. Diabetes mellitus
  3. Hypertensive pregnancy disorders
  4. Uterine rupture
  5. Advanced age
  6. Heavy smoking
67
Q

Threatened abortion clinical features

A
  • vaginal bleeding
  • fetal activity
  • cervical os closed
68
Q

inevitable abortion clinical features

A
  • vaginal bleeding
  • visible/ palable products of conception
  • fetal activity may be present
  • cervical os dialated
69
Q

missed abortion clinical features

A
  • No bleeding
  • No expulsion of the products of conception
  • No fetal activity
  • cervical os closed
70
Q

incomplete abortion clinical features

A
  • Vaginal bleeding;
  • products of conception within the cervical canal or uterus
  • Usually occurs > 12 weeks’ gestation
  • cervical os dialated
71
Q

complete abortion clinical features

A
  • Vaginal bleeding;
  • products of conception completely outside of the uterus
  • Usually occurs < 12 weeks’ gestation
  • cervical os closed
72
Q

Stillbirth clincal features

A
  • absence of fetal movements and cardiac activity
  • cervical os variable
73
Q

Spontaneous abortion diagnostics

A
  • Absence of fetal cardiac activity
  • Pelvic examination should be performed; visualization of the cervix is necessary to confirm that the source of bleeding is uterine.
  • Transvaginal ultrasound is the best imaging test:
    • Absence of fetal cardiac motion
  • A downtrending β -hCG is consistent with a failed pregnancy
74
Q

stillbirth diagnostics

A
  • Ultrasound examination is the best diagnostic modality to confirm loss of fetal heart activity
  • Fetal autopsy
75
Q

Threatened abortion Tx

A
  1. Expectant management
  2. Avoid strenuous physical activity
  3. Weekly pelvic ultrasound
  4. Rule out treatable causes of vaginal bleeding
  5. Rh(D)-negative women should receive Rh(D)-immune globulin
76
Q

inevitable, incomlete or missed abortion Tx

A
  • Expectant management (option for women < 14 weeks gestation);
  • Medical evacuation
    • Misoprostol is used to induce cervical ripening and expulsion of the products of conception.
    • Pretreatment with mifepristone 24 hours prior is recommended.
  • Surgical evacuation is usually recommended if evacuation does not occur after 4 weeks
    • Preferred method in septic abortion or if there is heavy bleeding
77
Q

Medical Abortion

A
  • Definition: method for terminating unwanted pregnancy in an early stage
  • Treatment: combination of a progesterone antagonist (mifepristone) and a prostaglandin analog (e.g., misoprostol)
78
Q

Stillbirth Tx

A
  1. Spontaneous labor usually begins within 2 weeks of intrauterine fetal death.
  2. Labor may be induced with oxytocin if maternal disease develops or if the patient prefers induction.
  3. Vaginal delivery is safer than cesarean section
  4. Express empathy and acknowledge patient grief; provide privacy and emotional support.
  5. Patients should be offered a fetal autopsy to determine the cause of death.
79
Q

complications of preganancy loss

A
  1. Septic abortion: retained products of conception become infected
    • Broad-spectrum antibiotics, D&C
  2. Retained products of conception → release of thromboplastin into systemic circulation → DIC (disseminated intravascular coagulation)
  3. Endometritis
80
Q

Gestational Diabetes mellitus

A

Impaired glucose tolerance diagnosed during pregnancy; associated with an increased risk of maternal and fetal morbidity

81
Q

gestational DM pathophysiology

A
  1. In the first trimester, insulin sensitivity increases and there is a tendency towards hypoglycemia.
  2. In the second and third trimesters, hormonal changes trigger progressive insulin resistance that results in hyperglycemia,
82
Q

Gestational DM

risk factors

A
  • Gestational diabetes in prior pregnancy
  • Recurrent pregnancy loss
  • At least one birth of a child diagnosed with fetal macrosomia
83
Q

Gestational DM

Clinical Features

A
  • Mothers are usually asymptomatic
  • May present with edema;
  • warning signs include polyhydramnios or large-for-gestational age infants (> 90th percentile)
84
Q

Gestational DM

Screening and diagnostis

A

First and second trimester:

  • confirmed with two independent measurements ≥ 126 mg/dL and 92–125 mg/dL respectively

Third trimester (at 24–28 weeks)

  • Initial screening: 50-g, one-hour oral glucose challenge test
    • blood glucose level should be < 135 mg/dl
  • Confirmation test: 100-g, three-hour oral glucose tolerance test(oGTT)
    • blood glucose level should be < 140 mg/dl
85
Q

Gestational DM

Tx

A
  • Glycemic control
    • Dietary modifications and regular exercise (walking)
    • Strict blood glucose monitoring (4x daily)
    • Insulin therapy if insufficient with dietary modifications
  • Regular ultrasound to evaluate fetal development
  • Consider inducing delivery at week 39–40 if glycemic control is poor or if complications occur
86
Q

Gestational DM

Complications

A

Maternal

  • Gestational hypertension
  • Preeclampsia, eclampsia, and HELLP syndrome
  • Urinary tract infection

Fetal:

  • Diabetic fetopathy
87
Q

Diabetic fetopathy

A

A constellation of features that can develop due to fetal hyperinsulinemia during gestation which include:

  • macrosomia,
  • postnatal
  • hypoglycemia,
  • polycythemia .
88
Q

Gestational Dm

Prognosis

A
  1. In most cases, gestational diabetes resolves after pregnancy.
  2. Increased risk of gestational diabetes recurring in subsequent pregnancies (∼ 50%)
  3. Increased risk of developing type 2 diabetes mellitus (up to 50% over 10 years)→ screen for DM 6–12 weeks postpartum (75 g 2-hourGTT); repeat every 3 years
89
Q

pregestational DM

A

Diabetes mellitus (type 1 or type 2) that is present prior to pregnancy, which is associated with a significantly increased risk for maternal complications during pregnancy and delivery, and congenital malformations

90
Q

complications of pregestational DM

A

Maternal

  1. Diabetic ketoacidosis (in type 1), hyperosmolar hyperglycemic nonketotic coma (in type 2)
  2. hypertensive disorder
  3. Urinary tract infection
  4. Increased risk of premature birth
  5. Spontaneous abortions
  6. Postpartum hemorrhage

Fetal

  1. Diabetic embryopathy (first trimester)
  2. Diabetic fetopathy (second and third trimester)
91
Q

Diabetic embryopathy

A
  • transposition of the great vessels; ventricular septal defect; truncus arteriosus
  • Neural tube defects
  • Caudal regression syndrome
    • aplasia or hypoplasia of the sacrum or lumbosacral spine

Clinical features

  • paralysis; bladder incontinence
  • Anorectal malformations and sacral agenesis
  • Lower limb or foot deformities
92
Q

Gestational Trohoblastic disease

A
  • include hydatidiform moles (both complete and partial), invasive moles, and choriocarcinoma.
  • arise from the abnormal fertilization of the ovum
93
Q

Hydatidform Mole

A
  • Benign trophoblastic disease
  • complete or partial moles
  • May develop malignant traits and become an invasive mole
94
Q

Invasive mole

A
  1. No histologic signs of malignancy in the primary tumor
  2. Trophoblasts infiltrate the myometrium and gain access to the vascular system.
  3. Hematogenic dissemination leads to metastatic growth in different organs (brain, lungs, liver).
95
Q

Risk factors for Hydatidiform mole

A
  • Prior molar pregnancy
  • History of miscarriage
  • Patients ≤ 15 and ≥ 35 years
96
Q

Complete Vs Partial

embryonic parts

A

Complete

does NOT contain any fetal or embryonic parts

Partial

contains fetal or embryonic parts in addition to trophoblastic tissue

97
Q

complete vs partail

causation

A

Complete:

  • fertilizationof an empty egg that does not carry any chromosomes. The physiological haploid chromosome set contributed by the sprem is subsequently duplicated.
  • result of paternal disomy

Partial:

  • Fertilization of an egg containing a haploid set of chromosomes with two sperms
  • result of triploidy
98
Q

complete vs partial

karyotype

A

Complete:

46XX (90%)

46XY (10%)

Partial:

69(xx,xxy,xyy)

99
Q

Hydatidform

Pathophysiology

A

Hydropic degeneration of chorionic villi with concomitant proliferation of cytotrophoblasts and syncytiotrophoblasts → death of embryo

100
Q

Invasive Mole

Pathophysiology

A
  • trophoblasts invade the myometrium → increased risk of bleeding and hematogenous spread
  • Metastases without histological signs of malignancy
101
Q

Hydatidiform Complete Mole

Clinical features

A
  • Vaginal bleeding during the first trimester
  • Uterus size greater than normal for gestational age
  • Pelvic pressure or pain
  • Passage of vesicles
  • Endocrine symptoms (due to ↑ β-hCG level)
    • Preeclampsia (before the 20th week of gestation)
    • Hyperemesis gravidarum
    • Ovarian theca lutein cysts: bilateral, large, cystic, adnexal masses that are tender to the touch
    • Hyperthyroidism
102
Q

Hydatidiform Partial MOle

clinical features

A
  • Less severe symptoms than in complete mole
  • Vaginal bleeding
  • Pelvic tenderness
103
Q

Hydatidiform Mole

Labs

A
  • β-hCG level measurement (initial test of choice)
  • Markedly elevated (higher than expected for the gestational age)
  • Higher in complete mole compared to partial mole.
104
Q

Hydatidiform Complete mole

Ultrasound

A
  1. Theca lutein cysts
  2. Echogenic mass interspersed with many hypoechogenic cystic spaces that represent hydropic villi (referred to as “swiss cheese”, “honeycomb”, “bunch of grapes”, or “snowstorm”)
  3. No amniotic fluid
  4. No fetal parts
  5. Lack of fetal heart tones
105
Q

Hydatidiform Partial Mole

Ultrasound

A
  1. Fetal parts
  2. Fetal heart tones may be detectable
  3. Amniotic fluid is present.
  4. Increased placental thickness
106
Q

Hydatidiform Mole

Tx

A
  1. Uterine evacuation by dilation and suction curettage
  2. Monitor β-HCG levels
  3. Chemotherapy (usually methotrexate) if unresolved, as indicated by any of the following:
    • β-HCG values do not decrease.
    • Histological features of malignant GTD are present.
    • Metastases are present on chest x-ray.
107
Q

Hydatidiform Partial Mole

Histopathology

A
  • Microscopy: partial occurrence of hydropic villi, minimal trophoblastic proliferation
  • Immunohistochemical staining: p57 positive
108
Q

Choriocarcinoma

A
  • Highly aggressive, malignant tumor consisting of trophoblastic tissue
  • tendency to metastasize early
    *
109
Q

Choriocarcinoma

Eitiology

A
  • develops after fertilization and implantation of the egg
  • Most cases of choriocarcinoma are preceded by
    • Hydatidiform mole (50%)
    • Normal pregnancy (25%)
    • Miscarriages or ectopic pregnancy (25%)
110
Q

Choriocarcinoma

Pathophysiology

A

Destructive growth into myometrium without chorionic villi →risk of hemorrahage and early metastasis( lung, vagina, brain, liver)

111
Q

Choriocarcinoma

Clinical features

A
  • postpartum vaginal bleeding and inadequate uterine regression after delivery
  • multiple theca lutin cysts
  • addisionat symptoms depend on the size of the metastasis:
    • seizures from metastases in the brain
    • dyspnea/ hemoptysis from metastases in the lungs
112
Q

Choriocarcinoma

Diagnostics

A
  • Labs: very high HCG
  • Ultrasound
    • mass of varying apperance
    • hypercascular on color doppler
  • Uterine D&C
    • ​diagnostic and therapeutic
113
Q

Choriocarcinoma

Staging

A

chest Xray: cannonball metastases (heme spread → multiple nodules in the lung)

114
Q

Choriocarcinoma

Tx

A
  • methotrexate
  • Surgical treatment (e.g., hysterectomy): may be indicated to stop bleeding from cancerous lesions or to excise distant metastases
  • Monitor β-HCG levels for at least 12 months.
115
Q

Antepartum Hemorrahage

A
  • serious complication of pregnancy occurring within the third trimester. It is associated with significant maternal and fetal morbidity and mortality
  • cases of severe hemorrhage, patients may present with signs of hypovolemic shock.
  • Common Causes:
    • bloody showassociated with labor,
    • placental previa,
    • placental abruption.
  • Rare Causes:
    • vasa previa
    • uterine rupture
116
Q

Placental Abruption

A
  • Partial or complete separation of the placeta from theuterus prior to delivery
  • hemorrahge from both maternal and fetal vessels
  • occures most oftern in the thrid trimester
    *
117
Q

Placental Abruption

Predisposing factors

A
  • Vascular changes
    • Hypertension (most common cause)
    • Preeclampsia/eclampsia
  • (Abdominal) trauma; car accidents
  • Previous abruption
  • > 35 years
  • Alcohol and cigarette consumption, cocaine use
118
Q

Placental Abruption

Clinical Features

A

Following placental separation of more than 30%, sudden onset:

  • Continuous, dark, vaginal bleeding
  • Retroplacental hemorrhage (20%); vaginal bleeding does not occur (signs of hypovolemic shock)
  • Abdominal pain or back pain , uterine tenderness
  • Hypertonic contractions (rigid uterus), premature labor
  • Fetal distress (60% of cases)
    • Decelerations seen on fetal heart monitor
119
Q

Placental Abruption

Diagnostics

A
  • Clinical DIagnosis! Rapid treatment vital for survival.
  • Vaginal exam contraindicated: may worsen bleeding!
  • Ultrasound
    • possible retroplacental hematoma
    • montoring vital signs of the fetus (distress)
  • Labs:
    • CBC
    • Coag Factors
120
Q

Placental Abruption

Tx in normal fetal findings and heme stable mom

A

General approach

  • Hemodynamic control: monitor vital signs, maintain airways, volume resuscitation, type and crossmatch blood
  • RhD prophylaxis in RhD negative mothers

Up to the 34th week of pregnancy

  • Fetal lung maturity induction with corticosteroids (e.g., betamethasone)
  • If necessary, tocolysis (e.g., nifedipine, β2-adrenergic agonist)
  • Aim for a normal delivery

34th to 36th week

  • Active uterine contractions present: vaginal delivery
  • No contractions + no signs of fetal distress + bleeding has stopped: expectant management

All pregnancies are delivered if acute abruption occurs after 36th weeks.

121
Q

PLacental abruption

Tx in acute symptoms

A

Live Fetus:

  • Emergency Cesarean sections independent of gestational age unless vaginval delivery is impanding.

Intrauterine fetal death

  • induction of vaginal delivery through pharmacologic uterine contraction inducers and opening of the amniotic sac
  • Emergency C-section if maternal risk
122
Q

Placental Abruption

Complications

A
  • Intrauterine fetal death (12%)
  • Maternal DIC and hypovolemic shock
  • Couvelaire uterus
123
Q

Couvelaire uterus

A

Definition: widespread extravasation of blood into the uterine musculature and beneath the serosa, especially at the cornua.

  • may extend through the uterus into the peritoneum.
  • The myometrium is weakened: uterine rupture during contractions
124
Q

Placenta Previa

A
  • Presence of the placenta in lower uterine segment, either over or very near the internal cervical os;
  • Leads to partial or full obstruction of the neck of the uterus with high risk of hemorrhage (rupture of placental vessels) and birth complications
  • the placenta goes before the fetus into the birth canal
125
Q

Placeta Previa risk factors

A
  • Maternal age > 35 years,
  • multiparity, short intervals between pregnancies
  • Previous curettage or cesarean section
  • Previous placenta previa
126
Q

Placenta Previa Classification:

A
  • Low-lying placenta: placenta lies less than 2 cm from the internal cervical os
  • Marginal previa: placenta reaches the internal cervical os
  • Partial previa: placenta partially covers the internal cervical os
  • Complete previa (total previa): placenta completely covers the internal cervical os
127
Q

Placenta Previa

Clincal Features

A
  • Sudden, painless, bright red vaginal bleeding
  • Usually occurs during the 3rd trimester (before rupture of the membranes), stops spontaneously after 1–2 hours, and recurs during birth
  • Soft, nontender uterus
  • Usually no fetal distress
128
Q

PLacenta Previa.

Diagnostics

A
  • Transvaginal ultrasound to assess the position of the placenta
  • Digital vaginal examinations are CONTRAINDICATED in cases of hemorrhage of unknown cause
129
Q

Placenta Previa

Treatment

A

Gestational age < 37 weeks

  • No active bleeding AND no evidence of fetal distress: expectant management
  • Severe, active bleeding OR evidence of fetal distress: stabilization and emergency cesarian section

Gestational age > 37 weeks: immediate delivery

Expectant management

  • If gestational age is < 34 weeks: fetal lung maturity induction with corticosteroids
  • If gestational age is between 34 and 37 weeks and delivery is likely within 7 days: fetal lung maturity induction with corticosteroids
  • If mild uterine contractions are present: tocolysis with magnesium sulfate
130
Q

PLacenta previa

Route of delivery

A
  • Lower segment cesarean section; ideally scheduled at 36–37 weeks gestation
  • Vaginal delivery may be performed if placenta lies > 2 cm away from the internal os on ultrasonography
  • Vaginal delivery should never be attempted outside the operating room in a patient with placenta previa
131
Q

Vasa Previa

A
  • The fetal vessels are located in the membranes near the internal os of the cervix
  • can be torn with cervical dilatation or membrane rupture, and laceration can lead to rapid fetal exsanguination.
  • vessels can also be compressed by a presenting fetal part.
132
Q

Vasa Previa

Risk Factors

A
  • Placental anomalies (e.g., bilobate or succenturiate placenta, velamentous umbilical cord insertion)
  • Placenta previa
  • Multiparity
133
Q

Vasa Previa

Clinical Features

A
  • Painless vaginal bleeding (fetal blood) that occurs suddenly after rupture of membranes
  • Fetal distress
    • fetal bradycardia;
    • decelerations or sinusoidal pattern on fetal heart tracings
134
Q

Vasa Previa

Diagnostics

A

Transabdominal or transvaginal ultrasound with color Doppler shows fetal vessels overlying the internal os and decreased blood flow within fetal vessels

135
Q

Vasa Previa

Tx

A

Emergency C-section if there are signs of fetal distress

136
Q

Chorioamnionitis

A

intrauterine infection of the fetal membranes and amniotic fluid caused by bacteria ascending from the vagina

137
Q

Chorioamnionitis

Etiology

A
  • Infection of the amniotic fluid, fetal membranes , and placenta
  • Causal Organisms
    • Ureaplasma urealyticum( 50%)
    • Mycoplasma hominis( 30%)
    • bacteroides;
    • group B Streptococcus;
    • E. coli
138
Q

Chorioamnionitis

Risk Factors

A
  • Prolonged labor or premature rupture of membranes (PROM)
  • Pathological bacterial colonization of vaginal tract
  • multiple digital vaginal exams, invasive procedures
139
Q

Chorioamnionitis

Symptoms

A

Maternal

  • Fever (> 38 °C)
  • Tachycardia > 120/min
  • Uterine tenderness
  • Malodorous and purulent amniotic fluid, vaginal discharge

Fetal tachycardia > 160/min

140
Q

Chorioamnionitis

Diagnosis

A

clinical diagnosis (fever plus ≥ 1 additional symptom)

  • Maternal blood tests
    • Leukocytosis > 15,000 cells/μL
  • Bacterial cultures
    • Urogenital secretions
    • Amniotic fluid
  • Group B Streptococcus screening: cervicovaginal and rectal swabs
141
Q

Chorioamnionitis

Tx

A

Maternal antibiotic therapy

  • Vaginal delivery: IV ampicillin plus gentamicin
  • Cesarean delivery: IV ampicillin and gentamicin, plus clindamycin

Delivery

  • Swift delivery is generally indicated to minimize both maternal and fetal complications.
  • Cesarean delivery is not generally indicated, but is often necessary because of obstetrical complications
142
Q

Chorioamninitis

Complications

A

Maternal

  • endometritis
  • Septic shock, DIC

Fetal/neonatal

  • premature birth
  • Asphyxia, intraventricular hemorrhage
  • Neonatal infection
143
Q

Neonatal Infection Etiology

Early Onset

A
  • ≤ 72 hours
  • chorioamnionitis, bacterial colonization
  • Common pathogens:
    • group B Streptococcus (GBS, Streptococcus agalactiae);
    • E. coli;
    • Listeria monocytogenes
  • Streptococcus agalactiae and Escherichia coli are the most common causes of both early- and late-onsetneonatal sepsis!
144
Q

Neonatal Infection Etiology

Late Onset

A
  • > 72 hours
  • nosocomial infection
  • Common pathogens:
    • group B Streptococcus
    • coagulase-negative Staphylococcus
  • Streptococcus agalactiae and Escherichia coli are the most common causes of both early- and late-onsetneonatal sepsis!
145
Q

Neonatal Infection Risk Factors

A

Maternal

  • PROM (premature rumpture of membranes)
  • premature labor
  • Infections

Fetal

  • Premature birth,
  • low birth weight,
  • low Apgar score
  • Difficult delivery
146
Q

Neonatal Infection Symptoms

A
  1. Irritability, lethargy, poor feeding
  2. Temperature changes (fever and hypothermia both possible)
  3. Tachycardia, hypotension
  4. Tachypnea, dyspnea; expiratory grunting
  5. Skin tone: jaundiced and/or bluish-gray (indicates poor perfusion)
147
Q

Neonatal Infection

Meningitis Symptoms

A
  • Often no signs of meningism
  • Early phase: general symptoms and vomiting
  • Late phase: bulging fontanelles, shrill crying, seizures, stupor
148
Q

Neonatal Infection

Pneumonia symptoms

A
  1. Tachypnea with intercostal/sternal retractions and nasal flaring
  2. Reduced oxygen saturation with cyanosis
149
Q

Neonatal Infection Diagnosis

A
  1. Blood tests
    • Leukocytopenia or leukocytosis, thrombocytopenia
    • ↑ CRP
  2. Lumbar puncture: test cerebrospinal fluid for meningitis
  3. Chest x-ray: signs of pneumonia
150
Q

Neonatal Infection

Tx

A

Broad-spectrum antibiotics: IV ampicillin and gentamicin

151
Q

Neonatal Infection

Prophylaxix for GBS

A

Indication

  • Anytime GBS bacteriuria occurs during pregnancy or if a previous newborn had a GBS infection

Medication

  • Intrapartum IV penicillin G or ampicillin
152
Q

Omphalitis

A
  • Bacterial infection of the umbilical stump occurring 3–9 days after delivery
  • Pathogens:
    • Staphylococcus aureus, group A Streptococcus, E. coli, Klebsiella pneumoniae
    • Clostridium tetani: developing countries
153
Q

Omphalitis

Symptoms

A
  1. Periumbilical redness, tenderness, swelling, and hardening
  2. Purulent discharge
  3. Signs of systemic infection
154
Q

Omphalitis

Tx

A
  • Broad-spectrum IV antibiotics
    • Antistaphylococcal penicillin (e.g., ampicillin) plus
    • Aminoglycosides (e.g., gentamicin)
  • Surgery:
    • complete debridement if complications arise

OBGYN Clerkship- Amboss Study Plan (9 decks)

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