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Life Cycles > Week 6 > Flashcards

Week 6 Flashcards

1
Q

Pregnant woman with aortic stenosis

A

Mother with aortic stenosis can cause issues in pregnancy (regurgitant lesions are better tolerated during pregnancy)

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2
Q

Plasma volume and RBC mass during pregnancy

A

Both increased

Plasma volume increased to greater extent though, leading to dilutional anemiai

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3
Q

CO in pregnancy

A

Increased CO by 40% (increase in HR and SV)

  • Mostly distributed to Breasts, skin, uterus, and kidneys
  • NO change in brain or liver
  • Physiologic sinus tachycardia can occur
  • Systolic murmurs can be physiologic, and S3 is common
  • Can get more frequent arrhythmias
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4
Q

Vascular resistance in pregnancy

A

Decreased vascular resistance (via progesterone)→ decreased BP, decrease in afterload

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5
Q

Preload and pregnancy

A

Increased preload (increased venous return) = increased EDV

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6
Q

Cardiac compliance and myocardial contractility in pregnancy

A

Increased cardiac compliance and myocardial contractility

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7
Q

Specific cardiac physiologic responses that happen during labor

A

Further increase in CO during contraction via sympathetic stimulation and pushing of blood from placenta to systemic circulation (during contraction)

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8
Q

Specific cardiac physiologic responses that occur postpartum

A

Acute increase in CO in first hour

Return to prepregnant baseline over weeks to months

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9
Q

Pathology of cardiovascular adaptations in pregnancy

A

1) Pre-eclampsia = new HTN, proteinuria, edema

2) Preexisting HTN:
- Intrauterine growth retardation
- Pre-eclampsia superimposed on chronic HTN

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10
Q

Respiratory rate in pregnancy

A

unchanged

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11
Q

PaCO2 and PaO2 in pregnancy

A

PaCO2 DECREASES, oxygen consumption and PaO2 INCREASES

pH increases, serum HCO3- decreases - *Pregnancy is a state of primary respiratory alkalosis with a compensatory metabolic acidosis

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12
Q

FEV1 and FEV1/FVC in pregnancy

A

unchanged

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13
Q

Vital capacity in pregnancy

A

unchanged

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14
Q

Tidal volume in pregnancy

A

INCREASES - due to increased chest AP diameter and chest circumference

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15
Q

Inspiratory capacity in pregnancy

A

increased

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16
Q

Inspiratory reserve volume in pregnancy

A

Unchanged

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17
Q

FRC, ERV, RV, and TLC in pregnancy

A

all decreased

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18
Q

GI Tract Physiology in pregnancy:

  • Calori intake
  • saliva production
  • gastric emptying, motility
  • risk of peptic ulcer disease
  • risk of GERD
  • frequency of constipation
  • cholestasis and cholesterol
A
  • Increased caloric intake required (around 200 kcal/day)
  • Increased saliva production (Ptyalism)
  • Decreased gastric emptying, reduced intestinal motility
  • Decreased risk of peptic ulcer disease
  • Increased risk of GERD (decreased LES tone due to progesterone)
  • Increased frequency of constipation
  • Increased cholestasis and cholesterol hypersecretion
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19
Q

Liver and pregnancy

A
  • Increased alkaline phosphatase
  • Decreased serum albumin and total protein (hemodilution)
  • Spider angioma, palmar erythema
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20
Q

Total body water in pregnancy

A

Increase in TBQ from 6.5 → 8.5 L

Chronic volume overload with active sodium and water retention → hemodilution, weight gain, anemia, elevated CO

Impaired volume expansion →
Increased risk for preeclampsia
Impaired fetal growth / fetal growth restriction

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21
Q

Osmoregulation in pregnancy

A

Increased water retention > sodium retention

Increase in all components of RAAS

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22
Q

ANP and BNP in pregnancy

A

increase

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23
Q

Kidneys in preg

A

enlarge

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24
Q

Bladder in pregnancy

A

Bladder capacity decreases (due to enlarging uterus) but increased urine volume

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25
Q

GFR and RPF in pregnancy

A

Increased GFR, increased RPF even more → filtration fraction (GFR/RPF) decreased

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26
Q

2 pathological changes to kidney in pregnancy

A

Relative hydronephrosis of pregnancy

Increased risk of pyelonephritis due to urinary stasis and asymptomatic bacteriuria

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27
Q

Pregnant patients with chronic renal insufficiency

A

can have increased risk of complications and worsen their renal diseas

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28
Q

Hematocrit and platelets in pregnancy

A

Hematocrit: Blood volume increases, RBC mass only increases slightly → Hemodilution and physiologic anemia

Platelets: hemodilution, thrombocytopenia

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29
Q

Immune system in pregnancy

A

Increased peripheral WBCs - upper limit of normal is 12,000
During labor can get WBC count up to 20,000-30,000
Want to develop immune tolerance to developing fetus

Successful pregnancy dependent on evasion of immune surveillance or suppression of maternal adaptive response

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30
Q

Coagulation factors in pregnancy

A

Want to decrease risk of hemorrhage → increase total clotting factors, decrease in fibrinolytic system
Factor 11 and 13 are the only clotting factors that decrease
Protein C = Constant
Protein S = Sinks (goes down)
No evidence of increased coagulability

Increased risk for DVT/PE (treat with unfractionated or LMW heparin)

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31
Q

Dermatologic changes in pregnancy

A

Hyperpigmentation - melasma, darkening of linea nigra, areolae, nipples, genital skin, axillae
hCG stimulates MSH

Increased blood flow to skin

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32
Q

Hyperemesis gravidarum:

A

refractory vomiting/nausea + weight loss, dehydration, electrolyte imbalance, ketonemia

Associated with increased levels of hCG (multiple gestion)

Treatment: B6 + doxylamine, diet changes

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33
Q

Cholestasis of pregnancy

A

Most common liver disorder in pregnancy

Progesterone → decreased tone and motility, gallbladder hypomotility

Increased frequency of gallstones

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34
Q

Presentation of cholestasis of pregnancy

A

itching on palms and soles + generalized itching WITHOUT rash
Mild jaundice, mild elevations in AST, ALT
Can be associated with still birth

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35
Q

Tx of cholestasis of pregnancy

A

low fat diet and possibly elective cholecystectomy

Surgery considered after 1st trimester

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36
Q

Placenta polypeptide hormone production

A

CRH, GnRH, GHRH, TRH
hCG, hPL, hPGH
Leptin, neuropeptide Y, inhibin, activin, chorionic ACTH, relaxin, PTH-rp

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37
Q

Placenta steroid hormone production:

A

Estrogen
Progesterone
1,25-OH Vit D

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38
Q

Human chorionic gonadotropin (hCG):

A

Glycoprotein
Produced 8 days after ovulation → doubles every 48 hrs for 1st 5-6 weeks
Peaks at 10-12 weeks

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39
Q

Activity of hCG (8)

A
  1. *Maintains corpus luteum in early pregnancy (until 8-10 wks)
  2. Regulate differentiation of cytotrophoblasts → syncytiotrophoblasts
  3. Controls trophoblastic invasion
  4. Induces apoptosis of endometrial T cells → promote immune survival
  5. Stimulate fetal Leydig cells to produce testosterone
  6. Can cause hyperemesis
  7. Stimulates RELAXIN → increases GFR and RBF, and decreases SVR
  8. Has TSH activity → lower TSH levels early on
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40
Q

hCG clinical correlates (5)

A
  1. hCG induced hyperthyroidism
  2. hCG > 1500 → no gestational sac, ectopic
  3. hCG > 9000 → no cardiac activity
  4. Increased hCG → Down’s
  5. Decreased hCG → trisomy 18
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41
Q

Human placental lactogen (hPL):

A

participates in metabolic adjustments that deliver nutrients to developing fetus

  • Similar to GH and PRL
  • Secreted by syncytiotrophoblasts
  • Secretion rate parallels placental weight
  • Detected 5-10 days → peaks at 32 weeks
  • Made in massive quantities (1-2 g/day)
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42
Q

Activity of hPL

A

Stimulates insulin secretion (also has some anti-insulin effects)
Mobilization and utilization of FFAs for energy by increasing lipolysis
Weak GH activity → promotes growth of mammary tissue

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43
Q

Human placental growth hormone (hPGH):

A

contributes to insulin resistance of pregnancy

Secreted by syncytiotrophoblasts

Differs from GH only by 13 aa - NOT regulated by

GHRH, but binds same receptor

Secreted tonically, REPLACES pituitary GH later in pregnancy

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44
Q

Activity of hPGh

A

Anti-insulin effects → maternal insulin resistance necessary to shunt glucose and aa to fetus to ensure adequate growth
Pre-existing insulin resistance → gestational diabetes

Growth hormone effects

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45
Q

Progesterone in pregnancy

A

Critical to maintain pregnancy

Corpus luteum produces it prior to 8-11 weeks → then made by placenta

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46
Q

Biosynthesis of progesterone in pregnancy

A

dependent on LDL receptors on trophoblast plasma membrane

Maternal cholesterol → pregnenolone (placental) → progesterone

Progesterone → fetal adrenal gland → DHEAS

DHEAS → placenta for conversion to estriol and estrone

DHEAS → fetal liver → 16-OH DHEAS → estriol (in placenta)

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47
Q

Activity of progesterone (8)

A
  1. Promotes decidua formation
  2. Substrate for synthesis of cortisol and aldosterone in fetal adrenal cortex
  3. Inhibits uterine contractions
  4. Modulates immune system (promotes Th2 and suppress Th1)
    * *Can improve Grave’s in third trimester
  5. Stimulates minute ventilation
  6. Smooth muscle relaxant (GI, uterus, GU)
  7. Promotes lobular development in breast → inhibit milk secretion
  8. Contributes to decreased SVR
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48
Q

Estrogen in pregnancy

A

Levels may increase 100x
High levels of placental aromatase
DHEAS → estrogens by placenta
90% of estradiol secreted into maternal circulation

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49
Q

10 activities of estrogen

A
  1. Stimulates growth of myometrium
  2. Induces hypercoagulable state → thrombosis
    Leading cause of maternal mortality
    **Causes proliferative retinopathy to worsen
  3. **Increases Thyroid Binding Globulin
  4. Induces lactotrophs (increases PRL)
  5. Peripheral vasodilation
  6. Increases CO, increases HR
  7. Increases uterine blood flow and decreases resistance
  8. Increases blood volume, renal perfusion and GFR
  9. Increases TG synthesis → Pancreatitis
  10. Increases pituitary size and vasculature → Sheehan’s syndrome
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50
Q

Trophoblastic cell type responsible for hormone production

A

Syncytiotrophoblasts

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51
Q

Hemochorial endothelial placentation

A

MOST placental hormones secreted exclusively into maternal circulation
Bathed directly by maternal blood within intervillous space, separated from fetal blood by several layers of tissue
Net transfer of steroids and polypeptide hormones to maternal blood is&raquo_space; fetus

52
Q

Cytotrophoblasts and hormone production

A

can synthesize some peptide hormones, but no steroid hormones

53
Q

Placental transfer of hormones

A

More permeable to lipid soluble molecules

Hormones actively metabolized by placenta (T4 → T3, and cortisol → cortisone

54
Q

Changes in carbohydrate and fat metabolism in pregnancy:

LATER ON:

A

CATABOLIC
Insulin resistance: NORMAL in pregnancy (later on)
- Physiologic adaptation to ensure adequate nutrients to fetus
- Human placental growth hormone is main anti-insulin hormone
- Must increase insulin secretion by 2-3x in pregnancy to maintain euglycemia

Catabolic state with increased lipolysis, glycogen store depletion
→ shift from carb to fat metabolism and conserve glucose for fetal-placental unit resulting in increased ketones
Prolonged fasting → starvation ketosis → high risk of DKA in pregnancy

55
Q

Changes in carbohydrate and fat metabolism in pregnancy:

Early ON:

A

ANABOLIC → storage of fat
Insulin sensitive 1st trimester: can get INCREASED sensitivity to insulin → severe nocturnal hypoglycemia in 1st trimester

56
Q

Gestational diabetes

A

glucose intolerance recognized for the first time during pregnancy
Prevalence has doubled in 10 years due to obesity epidemic

57
Q

Risk factors gestational diabetes

A
  • Obesity/Overweight
  • Insulin resistant
  • Thin GDM women often GAD ab positive → risk for autoimmune DM (type 1)
58
Q

Pathogenesis of gestational diabetes

A
  • Marked decrease in insulin mediated glucose disposal
  • Impaired glucose transport into skeletal muscle and adipose tissue
  • B-cell cannot compensate for insulin resistance despite hyperinsulinemia → hyperglycemia
  • BOTH first and second phase insulin secretion impaired
  • Hepatic overproduction of glucose
59
Q

Fetal response to gestational diabetes (6)

A
  1. Macrosomia (LGA = large for gestational age) - Fetal overgrowth
    - Pancreatic hyperplasia, cardiac hypertrophy
  2. Shoulder dystocia
  3. Increased mortality because they overgrow their blood supply
  4. Infant respiratory distress syndrome
  5. Neonatal hypoglycemia, from hyperinsulinemia
  6. Hyperbilirubinemia and polycythemia
60
Q

Complications with gestational diabetes

A

Most never return to normal insulin sensitivity → HIGHER risk of T2DM later on

Higher risk of infection, C-section, Preeclampsia

61
Q

Thyroid function and pregnancy:

A

Increase in TBG → increased TOTAL T4
Free T4 and T3 normal
TSH normal or slightly low in 1st and 2nd trimester (due to hCG)

62
Q

Fetal thyroid function:

A

Fetal brain dependent on mom’s T4

T4 transporters in fetal brain, no T3 → do NOT use T3 in pregnancy

63
Q

B-hCG and TSH:

A

hCG has same a-subunit as LH, FSH, and TSH

64
Q

Iodine deficiency

A

Leading preventable cause of mental retardation
Cretinism: due to both maternal and fetal iodine deficiency
Baby needs iodine to make thyroid hormone

65
Q

Maternal Hypothyroidism:

A

Typically due to Hashimoto’s

Must increase thyroid hormone dosage because of increased TBG and T4 crossing placenta

66
Q

Maternal Hyperthyroidism:

A

**hCG can induce hyperthyroidism

Grave’s Disease → can cause fetal problems because thyroid hormone AND antibodies cross placenta to stimulate fetal thyroid hormone production → fetal tachycardia, IUGR, premature

67
Q

When hCG levels are… what stage is the pregnancy in?

1,500 IU/mL hCG→

4,000 IU/mL hCG→

A

1,500 IU/mL hCG→ + Intrauterine pregnancy seen by transvaginal US (around 5-6 weeks gestational age)

4,000 IU/mL hCG→ + IUP by transabdominal US (around 7 weeks gestational age)

68
Q

Ectopic pregnancy

A

hCG LOWER than expected

1/150 pregnancies

Typically implantation in fallopian tube

Can cause hematosalpinx

35% with prior PID

Diagnosis: clinical symptoms, B-hCG, ultrasound

69
Q

Gestational trophoblastic disease

A

abnormal growth of cells that would normally develop into the placenta

Can be benign or malignant

Some due to abnormal conception/pregnancy

Some true neoplasms → uncontrolled tumor-forming proliferation of malignant trophoblast

**Massively elevated hCG around 5-6 weeks

Complete or partial mole

70
Q

Need both maternal and paternal DNA for normal development

what does mom’s DNA develop? what about dad’s?

what happens when you have too much paternal DNA?

A

Mom → embryonic tissue
Dad → Placental tissue

Too much of Dad’s DNA → overgrowth of placental type cells

71
Q

Complete Mole

chromosome number?
mechanism?

A

diandric DIPLOID (46, XX or XY)

One sperm fertilizes anucleate egg and divides (85%) OR two sperm fertilize anucleate egg (15%)

ALL genetic material is paternally derived

72
Q

Complete Mole

Classic appearance on US (4)

A

1) “cluster of grapes”
2) “snowstorm” appearance
3) cystically dilated spaces WITHOUT fetal parts (NO mom DNA)
4) placental overgrowth

73
Q

Complete Mole

Appearance (5)

A

1) “Grape-like vesicles”
2) Abnormal placental tissue with NO fetal development
3) Circumferential trophoblastic hyperplasia **
4) ABSENT staining of villous stromal cells
5) **HYDROPIC Vili (edemetous, watery)

74
Q

Complete Mole

Presentation (5)

A

1) Typically present in second trimester
2) Vaginal bleeding, anemia
3) Vaginal passage of “grape-cluster” hydropic molar vesicles
4) Uterine size larger than would be expected
5) EXTREMELY elevated B-hCG (>100,000)→ hyperemesis gravidarum, early pre-eclampsia, hyperthyroidism, theca-lutein ovarian cysts

75
Q

Complete Mole - what are the risks? (2)

A

1) 20% of complete moles develop persistent GTD (PREMALIGNANT CONDITION)
2) Most common precursor of CHORIOCARCINOMA (1-2% progress)

76
Q

Choriocarcinoma

Presentation

A

-most common precursor is hydatidiform mole

Can be widely metastatic at discovery, but highly chemosensitive

Frequently metastasizes hematogenously (rather than lymphatically) –> Lung > vagina&raquo_space;> brain, liver, kidney

77
Q

Choriocarcinoma

Appearance (5)

A

1) single/multiple hemorrhagic, well-circumscribed nodules in uterus
2) soft yellow-white tumor with large areas of ischemic NECROSIS and HEMORRHAGE
3) **Biphasic pattern (cytotrophoblasts = MONOnuclear, syncytiotrophoblasts = MULTInuclear)
4) Marked nuclear atypia and mitoses
5) No chorionic villi*

78
Q

Treatment for complete mole (3)

A

1) D&C (dilation and suction Curettage)
2) MUST administer Rh Ig (Rhogam) at time of D&C because Rh(D) expressed on trophoblastic cells
3) Monitor hCG levels for signs of invasive mole/choriocarcinoma –> MTX if present

79
Q

Partial Mole

chromosomes?
mechanism?

A

diandric TRIPLOID (69, XXY)

Two sperms fertilize one egg

80
Q

Partial Mole

US appearance (2)

A

large cystic spaces +/- fetal tissue - subtle

81
Q

Partial Mole

Histology (4)

A

1) admixture of hydropic and fibrotic villi
2) “Lacy” trophoblast hyperplasia
3) Villous inclusions
4) Association with fetal syndactyly (fusion of digits)

82
Q

Partial Mole

Complications?

A

Virtually no partial moles recur/progress (unlike complete hydatidiform mole)

83
Q

Placental Site Trophoblastic Tumor (PSTT)

A

neoplastic proliferation of EXTRAvillous trophoblast (VERY rare)

5-8% develop after molar pregnancy

Hysterectomy usually curative

84
Q

Placental Site Trophoblastic Tumor (PSTT)

Appearance

A

Infiltrative mass + sheets and cords or trophoblasts growing between muscle fibers

Invasion into myometrium NOT in presence of pregnancy

85
Q

Maternal surface of placenta

A

maternal surface of the placenta appears bumpy due to cotyledons (separations of the decidua basalis composing an individual chorionic villus).

86
Q

Fetal surface of placenta

A

fetal surface of the placenta appears smooth and pink or blue, with visible chorionic blood vessels that join to form the umbilical cord.

87
Q

Fetal:Placental Weight Ratio

A

reflects balance between fetal and placental growth → Increases with gestational age

88
Q

What structures are in the umbilical cord? (4)

A

R and L umbilical umbilical arteries

Left umbilical vein

Wharton’s Jelly (mucous connective tissue)

Allantoic duct

89
Q

What conditions are associated with single umbilical artery? (5)

A

Congenital cardiovascular abnormalities

Restricted intrauterine growth

Prematurity

Genitourinary malformations

Chromosomal anomalies

90
Q

Function of umbilical arteries and vein?

A

TWO umbilical arteries carry DEOXYGENATED blood from the fetus to the placenta

SINGLE left umbilical vein carries OXYGENATED blood from the placenta to the fetus.

91
Q

What happens if the umbilical cord is too long or too short?

A

Longer cord (> 75 cm)→ fetal entanglement (possible hyperactivity later in life)

Shorter cord (< 30 cm) → decreased fetal movement and neurodevelopmental problems

92
Q

Chorionic plate vs. decidua basalis - what is the space in between called?

A

Maternal space (INTERvillous) -between chorionic plate/decidua basalis

Chorionic plate = fetal side

Decidua basalis = derived from endometrium - maternal side, containing maternal blood in lacunae

93
Q

Function of placental membranes?

A

1) turnover of amniotic fluid (produced by amniotic cells and mainly derived from maternal blood)
2) enzymatic activity during initiation of labor.

94
Q

Layers of placental membrane

A

Amnion (outer surface) → chorion → extravillous trophoblast → decidua capsularis

95
Q

Amnion

A

single layer of flat, cuboidal or columnar epithelial cells derived from fetal ectoderm. Passively attached to chorion by amniotic fluid pressure.

96
Q

Chorion

A

tough fibrous layer that carries fetal blood vessels, often with atrophied villous remains (chorion frondosum).

97
Q

Fetal parenchyma:
-Fetal compartment is ________

-Maternal compartment is _______

A

Fetal compartment = INTRAvillous

Maternal compartment= INTERvillous

98
Q

Fetal parenchyma can be infected with what bacteria?

A

**Listeria infection - cause of acute inflammation and abscess within placenta parenchyma

99
Q

Gravida/Para nomenclature

A 
G = NUMBER
P = OUTCOME

→ TPAL = Term delivery, Preterm delivery, Abortion (< 20 weeks), Living children

100
Q

Acute Chorioamnionitis

A

secondary to intra-amniotic infection with neutrophils in fetal membranes

occurs in 25% of live births, 67% preterm deliveries (> 20 weeks)

Poor correlation with clinical chorioamnionitis (Fever, leukocytosis, uterine tenderness, tachycardia) with histological chorioamnionitis

Typically due to group B strep

Can get fetal acute inflammation in response to maternal infection

101
Q

Acute Chorioamnionitis

2 possible routes of infection

A

1) Ascending: bacterial from cervico-vaginal flora → maternal neutrophils in membranes

2) Transplacental (hematogenous) → chronic villitis
- TORCHES = Toxoplasma, Rubella, CMV, HIV/HSV, Syphilis

102
Q

Bugs that can cause infectious villitis? (4)

A

1) Syphilis → perivascular fibrous proliferation
2) Toxoplasmosis → granulomatous with cysts
3) Herpes → multinucleated cells with inclusions
4) Listeria → acute inflammation destroying villi

103
Q

Villitis of unknown etiology

A

Maternal infiltrate of lymphocytes that attack and destroy the villi

10-15% recur → ⅔ get IUFD

104
Q

Meconium

A

NEVER normal before 36 weeks GA

Due to fetal stress vs. fetal maturity

→ toxic to baby, placenta, and vascular smooth muscle

Can result in aspiration pneumonia and myonecrosis

105
Q

feto-maternal hemorrhage (FMH)

A

Represents a massive amount of fetal blood in maternal circulation (> 20%)

Can test for this with Kleihauer-Betke Test (tests for HbF)

106
Q

Placental Infarct

A

acute cessation of maternal flow to live fetus

→ central more significant than peripheral

107
Q

Placenta Accreta

A

placenta attaches to myometrium WITHOUT penetrating it

Most common time

Trophoblasts invade abnormally deeply → chorionic villi adhere to myometrium → postpartum hemorrhage

Risk with prior C-section, endometrial ablation, and multiple D&Cs

108
Q

Placenta Increta

A

placenta villi INVADE into myometrium

109
Q

Placenta Percreta

A

placenta villi PENETRATE through serosa (myometrium)

110
Q

Placenta Previa

what is it?
how does it present?

A

placenta covers internal cervical os or lower uterine segment

Increased risk for abruption, postpartum hemorrhage, C-section

Associated with PAINLESS third trimester bleeding

111
Q

How will placenta ccreta, increta, and percreta present?

A

Often detected on US prior to delivery

No separation of placenta after delivery –> postpartum bleeding –> can cause sheehan syndrome

112
Q

Abruptio Placentae

what is it?
risk factors for it?

A

premature separation (partial or complete) of placenta from uterine wall before delivery of infant

SX: vaginal bleeding, abdominal/back pain, rapid uterine contractions
Can be chronic or acute
Causes fetal deprivation of oxygen and nutrients

113
Q

Preeclampsia

A

HTN + proteinuria after 20 weeks gestational age

May proceed to eclampsia (+ seizures) and/or HELLP syndrome

Incidence increased in patients with preexisting HTN, diabetes, chronic renal disease, or autoimmune disorders

114
Q

Presentation of placental abruption?

A

ABRUPT, PAINFUL bleeding (concealed or apparent) in third trimester

Possible DIC, maternal shock, fetal distress

Life threatening for mother and fetus

115
Q

What causes preeclampsia?

A

Caused by abnormal placental spiral arteries (muscular, thick maternal endothelial cells NOT replaced by trophoblasts)

–> endothelial dysfunction, vasconstriction, ischemia

116
Q

Spontaneous abortion:

causes in first, second and third trimesters?

A

First trimester - chromosomal (vast majority)

Second trimester - structural defects, placental, infectious

Third trimester - placental, structural defects

117
Q

Intrauterine Growth Restriction (UGR)

if growth restircition is symmetric then…

If it is asymmetric, then…

A

Symmetric → genetic etiology

Asymmetric → relative macrocephaly, placental or maternal etiology, often oligohydramnios

118
Q

Intrauterine fetal demise (IUFD) - what happens to hCG

A

hCG initially normal and then reduces when baby dies

119
Q

Trisomy 21

A 
47 (XX or XY)
Small for gestational age
Round/flat face with slanting palpebral fissures
TRansverse palmar crease
Heart (typically ASD) and GI anomalies
Pancreatic or bone marrow fibrosis
Increased risk of ALL and Alzheimer’s
120
Q

Trisomy 13

A 
Patau’s Syndrome, 47 XX or XY
Small for gestational age
Polydactyly and facial defects
Cutis aplasia
Heart (VSD) and brain defects (holoprosencephaly)
Pancreatico-splenic fusion
NORMAL quad screen early in gestation
121
Q

Trisomy 18

A 
Edward’s Syndrome, 47 XX or XY
Small for gestational age
Hand deformities, micrognathia
Rocker bottom feet
Heart anomalies, renal fusion
Omphalocele
122
Q

Triploidy

A

69XXX or 69XXy
Incompatible with life
Severe IUGR
Syndactyly (fusion of digits)

123
Q

Fetal hydrops

A

abnormal fluid collection (edema) under skin, within abdomen or chest cavity - often polyhydramnios

124
Q

Fetal hydrops

Immune vs. non-immune causes?

A

Immune: maternal ab against fetal RBCs cross placenta → hemolyzed in fetal spleen → severe anemia
Usually Rh antigens

Non-immune: infectious, cardiac, or other congenital anomalies

125
Q

Acardiac twin

A

“Parasitic twin” fails to develop head, arms, and heart → gets blood from host twin → Host twin gets CHF because it is doing double work to perfuse both

126
Q

Teratomas

where is the most common site in a newborn?

A

Sacrococcygeal: most common neoplasm of newborn

Life Cycles (8 decks)

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