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PFizz S2015 > Female Repro L1: Pregnancy > Flashcards

Female Repro L1: Pregnancy Flashcards

1
Q

Anatomy of the female genital system

A
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2
Q

Bleeding in early pregnancy

A
  • – Physiologic (Implantation bleeding)
  • – Miscarriage
  • – Ectopic pregnancy
  • – Gestational trophoblastic diseases
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3
Q

Bleeding in late pregnancy

A

– Placenta praevia
– Abruptio placentae
– Vasa praevia

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4
Q

Diagnosis of Spontaneous Abortion

A
  • A period of amenorrhea confirmed to be pregnancy
  • – Intrauterine location of gestational sac determined before or during the abortion process
  • Vaginal bleeding ± pelvic pain
  • Progressive dilatation and effacement of the cervix
  • Rupture of membranes before 20 weeks of gestation
  • Cessation of fetal heart activity (fetal demise) before 20 weeks of gestation
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5
Q

Threatened Abortion

A
  • Affects 20-30% of pregnancies in first trimester
  • Painless, vaginal bleeding
  • Uterine size consistent with gestational age
  • Cervix is long and closed
  • Pathogenesis attributed to marginal separation of the placenta
  • Prognosis is excellent
    • – > 95% of pregnancy will progress normally with normal fetal heart activity
  • Risk of miscarriage decreases with advancing gestation
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6
Q

Inevitable Abortion

A

Period of amenorrhea confirmed to be pregnancy

Increased vaginal bleeding, and cramping abdominal and waist pain

Uterus appropriate for GA

Effacement and dilatation of the cervix

Products of conception visualized or palpable in the cervical canal

Ultrasound scan shows

– Detachment of the placenta from thedecidua,

– Dilatation of the cervix

– Gestational sac in the lower segment of the uterus

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7
Q

Incomplete spontaneous abortion

A
  • Severe vaginal bleeding with passage of fleshy mass
  • Persistence of cramping, lower abdominal pains
  • Uterine size is smaller than GA
  • Cervix is effaced and dilated
  • More products still pluggingthe cervical canal
  • Gestational sac is deflated with irregular, echogenic material
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8
Q

Complete Abortion

A
  • Cessation of bleeding and pain following passage of products
  • Uterus is smaller than GA
  • Cervix is closed
  • Ultrasound findings
  • – Endometrium appears closely apposed
  • – Endometrial lining regains its reflective appearance
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9
Q

Missed Abortion

A
  • No history of vaginal bleeding
  • Regression of symptoms of pregnancy
  • Uterine size may be reduced but cervix is long and closed
  • Ultrasound scan shows an irregular gestational sac and absence of fetal heart motion
  • Fetal death but no effort to expel the products of conception
  • Continued production of normal levels of progesterone
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10
Q

Recurrent/Habitual Abortion

A
  • Three or more consecutive, spontaneous pregnancy losses before 20 weeks of gestation
  • Affect one percent of women
  • Generally accepted etiologies include
  • – Chromosomal abnormalities
  • – Uterine malformations
  • – Antiphospholipid syndrome
  • Prognosis depends on maternal age and abortion karyotype
  • A normal karyotype carries a higher recurrence risk than an abnormal karyotype
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11
Q

Risk factors for Ectopic Pregnancy (Partial)

A
  • In-utero diethylstilbesterol (DES) exposure
  • Progesterone-only contraceptives
  • Cigarette smoking
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12
Q

Pathophysiology of Ectopic Pregnancy

A
  • Damage to ciliated surface of endosalpinx impairs tubular transport of fertilized ovum
  • Implantation begins on the 6th day post- fertilization regardless of the location of the zygote
  • In tubal implantation, trophoblastic invasion and progressive distension lead to rupture.
  • Pregnancy tends to abort into the peritoneal cavity if close to the fimbriae .
  • Gain of alternative blood supply leads to secondary abdominal ectopic pregnancy

Dx

  • Light microscopy of the endometrium reveals changes of pregnancy
  • Cells with hyperchromatic, hypertrophic, irregularly-shaped nuclei, and foamy vacuolated cytoplasm (“Arias-Stella reaction”)
  • Endometrial tissue may be passed out as fragments called decidual casts
    • – Characterized by the presence of superficial secretory endometrium
    • – No trophoblastic cells are seen
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13
Q

Ectopic Pregnancy: Clinical Features

A

SYMPTOMS

  • Pain(100%)
  • Bleeding
  • Amenorrhea
  • Syncope–dizzyspell, light headedness

SIGNS

  • Hemodynamic instability
  • Abdominal tenderness
  • Adnexal and cervical
  • motion tenderness
  • Adnexal mass
  • Uterine changes of pregnancy
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14
Q

GESTATIONAL TROPHOBLASTIC DISEASES (GTD)

A
  • A proliferative disorder of trophoblastic cells
  • Result from aberrant fertilization and are fetal in origin
  • The success story of gynecological oncology

– Highly susceptible to chemotherapy (>90%) even with widespread metastasis

– A unique and characteristic tumor marker, human chorionic gonadotrophin (hCG)

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15
Q

GTDs: Spectrum

A
  • Include a tumor spectrum of
  • Hydatidiform mole
    • – Complete
    • – Partial
  • Persistent/Invasive mole
  • Choriocarcinoma
  • Placental-site trophoblastic tumor (PSTT)
  • Malignant end of the spectrum – Choriocarcinoma and PSTT
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16
Q

Risk factors for GTD

A
  • Extremes of maternal age (<20 and >35 years)
  • Assisted reproduction technology
  • History of previous GTD
  • Others
    • – Nulliparity
    • – Low socioeconomic status
    • – Diet deficient in vitamin A
    • – Current smoking (>15 cigarettes per day)
    • – Maternal blood type AB, A or B
17
Q

Cytogenetics of Hydatidiform Mole

A

Abnormal fertilization with excess of paternal chromosomes

Fertilization of an empty ovum (absent or inactivated maternal chromosomes) by a haploid sperm that then duplicates or by two sperm (Complete mole).

– Resultant karyotype is 46,XX or 46, XY.

– 46,YY is not seen (lethal karyotype)
– “A pure paternal allograft”

Fertilization of an ovum with an active set of chromosomes by a duplicated sperm or by two haploid sperm (Partial mole). A triploidy with

– 69,XXY (70%)

– 69,XXX (27%)

– 69,XYY (3%)

18
Q

Pathophysiology of H. Mole

A
  • Paternal genes control placental growth while maternal genes control fetal growth
  • Excess paternal genes result in excessive trophoblastic proliferation
  • Amplification and over expression of various oncogene products (c-
  • erbB-2; c-myc; c-fms; mdm-2) associated with behavior of the mole
    • – Higher proliferation index
    • – More aggressive behavior
    • – Development of malignancy
  • Epidermal growth factor receptor (EGFR) is highly expressed in complete mole and choriocarcinoma
  • Down regulation of tumor suppressor genes, such as p53, p21 and Rb
19
Q

H. mole: Diagnosis

A
  • Vaginal bleeding
  • Uterine size larger than anticipated by date
  • Pelvic pressure and pain
  • Anemia
  • Hyperemesis gravidarum
  • Hyperthyroidism: alpha-HCG share sequence similarity with TSH
  • Onset of preeclampsia before 20 weeks of gestation
  • Passage of hydropic vesicles
20
Q

Diagnosis of Choriocarcinoma

A

Irregular uterine bleeding

– Related to early vascular invasion

– Late postpartum bleeding

– Primary or secondary postpartum hemorrhage

– Antecedent pregnancy can be up to one year or more

Symptoms related to metastatic site

– Lungs: cough, chest pain, hemoptysis

– Vagina: bleeding from deposits

– Gastrointestinal tract: melena, rectal bleeding

– Urologic: hematuria

– Brain: Intracerebral hemorrhage, coma

– Liver: Right upper quadrant abdominal pain

Pelvic features

– Enlarged uterus

– Bilateral ovarian cysts

– Metastasis to the vaginal wall

21
Q

ABRUPTIO PLACENTAE

A
  • Premature separation of the placenta before delivery of the fetus
  • Incidence: 1 in 77 -89 deliveries
  • Severe if it results in fetal death
  • Same mechanism as placental sinus bleed
Concealed form (20%)
– Hemorrhage is concealed within uterine cavity

– Placental detachment may be complete
– Complications are often severe
– May be associated with significant coagulopathy

External (Revealed) form (80%)
– Hemorrhage is obvious
– Placental detachment more likely incomplete

– Complications fewer and less severe

Etiology

  • PREDISPOSING FACTORS
    • Previous placental abruption
    • Hypertensive state of pregnancy (2.5-17.9%)
    • Advanced maternal age
    • Multiparity
    • Uterine over distension(multiple gestation, polyhydramnios)
    • Vascular disease (DM, SLE)
    • Chronic renal failure
    • Thrombophilias
    • Cigarette smoking
    • Alcohol consumption
    • Cocaine use
  • PRECIPITATING FACTORS
    • Trauma (abdominal trauma , fetal manipulation)
    • Sudden reduction in uterine volume
    • Abnormally short cord
    • Increased venous pressure

Pathophysiology

  • Important mechanisms include
    • – Local vascular injury
    • – Abrupt rise in uterine venous pressure
    • – Mechanical factors
    • – Initiation of the coagulation cascade
  • Tissue disruption by bleeding
  • Infiltration of blood into the myometrium provokes uterine tetany
  • Extensive intramyometrial bleed leads to Couvelaire uterus
  • Secondary hemorrhagic diasthesis
  • Fibrin deposition in small capillaries results in potentially lethal complications such as
    • – cor pulmonale
    • – renal cortical necrosis
    • – anterior pituitary infarction (Sheehan’s syndrome)
  • Fetal hypoxia and death result from amount and duration of placental separation, and severity of fetal hemorrhage

Sx

  • The degree of placental separation determines clinical presentation
  • Asymptomatic; identified postpartum on inspection of the placenta
  • Abdominal/back pain and uterine irritability
  • High frequency uterine contractions
  • Vaginal bleeding
  • – Revealed or concealed
  • Symptoms in severe cases
    • – Fetal distress, fetal death
    • – Uterine tetany
    • – Disseminated intravascular coagulopathy (DIC)
    • – Hypovolemic shock

Labs

  • Severity of anemia considerably more than expected for amount of blood loss
  • Peripheral blood smear
    • – A reduced platelet count
    • – Evidence of intravascular coagulation: presence of schistocytes
  • Coagulation profile: PT, PTT, platelet count, fibrinogen and FSP
  • Ultrasound findings often inconclusive

Complications

  • DIC
  • Renal cortical necrosis
  • Fetal death
  • Maternal death
22
Q

PLACENTA PRAEVIA

A

Attachment of the placenta in the lower uterine segment

– Zone of effacement and dilatation of the cervix

A significant cause of maternal and fetal morbidity and mortality

Incidence: 1 in 200 births (0.5%)

**Classification: **Type does not determine the presentation

  • Complete (30%)
  • Partial
  • Marginal
  • Low-lying placenta

Etiology

  • Multiparity
  • Advancing maternal age
  • Previous caesarean delivery
  • Multiple gestation
  • Smoking
  • Maternal syphilis
  • Succenturiate lobe of placenta

Pathophysiology

  • Placenta proliferates towards well vascularized areas of the endometrium
  • Mechanisms include:
  • Scarred or poorly vascularized endometrium in the fundus
    • – Multiparity and previous C/S or repeat elective termination of pregnancies
  • Compensatory increase in placental mass
    • – Multiple pregnancy
    • – Chronic hypoxic conditions (smoking and residence in high altitude)
  • Abnormal form of placentation (succenturiate lobe of the placenta)
  • Mechanism of bleeding in placenta praevia
    • Mechanical separation of the placenta from implantation site
    • Rupture of engorged, poorly supported, venous channels

Sx

  • Sudden, painless, profuse vaginal bleeding
    • – After 20 weeks of pregnancy (warning bleed) – 70%
    • – Subsequent bleed is usually heavier than the first
  • Intrapartum bleed (10-20%)
    • – Uterine contractions
    • – Following membrane rupture
  • Asymptomatic, detected by ultrasound <10%
  • Uterus usually soft, relaxed and non-tender
  • Abnormal fetal lie or presentation common
  • Fetal heart abnormalities unlikely

Dx

  • Typical presentation
  • Incidentalfinding
    • – 30% in mid second trimester
    • – 3% at term
  • Ultrasonography: Transabdominal ultrasound definitive in 95% of cases
  • MRI: Better image

Complications

  • Morbid placental adherence
  • Malpresentation
  • Vasa previa and velamentous umbilical cord
  • Amniotic fluid embolism
  • Preterm premature rupture of membranes
  • Intrauterine growth restriction
  • Congenital anomalies
  • Prematurity
  • Fetal death

PFizz S2015 (35 decks)

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