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SMP - APP Part 2 > Lectures 9 & 10 - Pregnancy I & II > Flashcards

Lectures 9 & 10 - Pregnancy I & II Flashcards

1
Q

What is the gestational period?

A

From conception to birth: normally 266 days (9 months or 38 weeks) BUT we calculate gestation from the last menstrual period (2 weeks before ovulation/fertilization), it is 40 weeks (9.5 months or 280 days)

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2
Q

What are the 3 trimesters of pregnancy?

A
  1. 1st – First 12-14 weeks
  2. 2nd – Week 12-14 to week 24-28
  3. 3rd – Week 24-28 to week 37-42
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3
Q

3 types of deliveries with regards to timing? When is delivery optimal?

A
  1. Preterm: any delivery before 37 weeks
  2. Term: delivery between 37-42 weeks:
    a. Early term: 37-38 6/7 weeks
    b. ***Full term: 39-40 6/7 weeks
    c. Late term: 41-41 6/7
  3. Postterm: delivery after 42 weeks
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4
Q

What is gravidity?

A

Number of times a woman has been pregnant including current pregnancy, if applicable

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5
Q

What is parity? What to note?

A

Describes the outcomes of those pregnancies: number of term deliveries, number of preterm deliveries, number of abortions (spontaneous or induced), number of living children

NOTE: count twins as just one pregnancy

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6
Q

3 methods of pregnancy detection?

A
  1. Urine or blood ß-hCG (human chorionic gonadotropin)
  2. Ultrasound identification (4-5 wks)
  3. Fetal cardiac activity by doppler (5.5-6 wks)
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7
Q

How should hCG levels fluctuate in early pregnancy?

A

Should double every 48 hours in early pregnancy

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8
Q

Where does hCG come from? Purpose? What to note?

A

Secreted by the placenta and maintains the corpus luteum which produces progesterone essential for maintaining pregnancy

NOTE: During the 2nd and 3rd trimester, the placenta secretes its own estriol and progesterone and the corpus luteum degenerates

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9
Q

What physiological changes does pregnancy cause?

A

Almost every organ system is affected by pregnancy to accommodate the maternal/fetal environment and allow for delivery: cardiovascular, pulmonary, gastrointestinal, renal, hematological, endocrine, and anatomical changes (everything gets squished)

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10
Q

4 cardiovascular changes in pregnancy?

A
  1. Increase in plasma volume by 50% in preparation for blood loss of delivery, causing a systolic murmur in 90-95% of pregnant women
  2. Red blood cell (RBC) volume increases by 20-30%,

1 + 2 => decrease in hematocrit known as physiologic or dilutional anemia of pregnancy (not true anemia) => resulting decreased blood viscosity improves flow through placenta (decreased resistance)

  1. Cardiac output (CO) increases by 30-50% due to increased BV, decreased afterload, and elevated HR in late pregnancy => causes increased uterine blood flow (12% of CO by late pregnancy instead of 1-2%!)
  2. Systemic vascular resistance decreases causing a decrease in systolic (by 5-10 mm Hg) and diastolic (by 10-15 mm Hg) blood pressure in the first two trimesters due to a decreased responsiveness to hormones that constrict vasculature
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11
Q

How to calculate hematocrit?

A

RBC volume/plasma volume

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12
Q

Does BP return to pre-pregnancy levels by term?

A

YUP (by 12 weeks postpartum)

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13
Q

Effect of progesterone on smooth muscle of the uterus and BVs?

A

Relaxation

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14
Q

3 pulmonary changes in pregnancy?

A
  1. Oxygen consumption increases by 15-20%
  2. Tidal volume increases by 30-40% causing an increase in minute ventilation (RR relatively normal) due to the
    respiratory centers being more sensitive to CO2 (decreased in CO2 in pregnancy compensated by kidneys, pH still in normal range)
  3. Total lung capacity decreases by 5% due to elevated diaphragm => 50-70% of women experience dyspnea of pregnancy
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15
Q

3 endocrine changes in pregnancy?

A

Almost every hormone is affected:

  1. Hyperestrogenic state produced mainly by the placenta and necessary for fetal well being => increased risk of blood clots (DVT, PE) due to hypercoagulable state (and sometimes forced immobility)
  2. Diabetogenic state due to increased blood sugar due to increased insulin resistance
  3. Progesterone causes smooth muscle relaxation, which is necessary to relax the uterus
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16
Q

What happens during delivery aka parturition?

A
  1. Fetal hormone secretion stimulates placenta to release large amounts of estrogen => prepares myometrium for oxytocin (posterior pituitary) and prostaglandins (uterine) by upregulating receptors
  2. Oxytocin from fetus initiates cervical dilation and uterine prostaglandin secretion
  3. Cervical dilation stimulates release of maternal oxytocin (Ferguson reflex) => uterine contractions and positive feedback
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17
Q

What are the 3 stages of labor? Timing for each?

A
  1. First stage: dilation of the cervix to 10 cm and effacement (thinning of the cervix) => longest stage: 6-12 hours
  2. Second stage: time from full dilation to delivery of the fetus => bout an hour
  3. Third stage: delivery of the placenta (about 30 min after birth)
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18
Q

During what labor stage is there a bleeding risk? Why?

A

Third stage because of placental delivery causing the break of many blood vessels

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19
Q

List reasons for Cesarean deliveries in order of prevalence.

A
  1. Labor arrest
  2. Malpresentation
  3. Non-reassuring fetal tracing
  4. Multiple gestation
  5. Maternal-fetal complications
  6. Other obstetric indications
  7. Macrosomia
  8. Preeclampsia
  9. Maternal request
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20
Q

Rate of C-section in the US?

A

30% (10-15% is the goal)

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21
Q

2 early gestation pathologies?

A
  1. Miscarriage

2. Ectopic pregnancy

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22
Q

3 late gestation pathologies?

A
  1. HT problems
  2. Gestational diabetes
  3. Placental abnormalities
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23
Q

What is a miscarriage?

A

Spontaneous abortion with pregnancy loss before 20 weeks gestation

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24
Q

When are miscarriages most common?

A

1st trimester spontaneous abortions are extremely common, 2nd trimester rare

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25
Q

4 possible causes of miscarriages?

A
  1. Fetal chromosomal anomalies, anembryonic implantation (blighted ovum)
  2. Teratogen exposure
  3. Endocrine abnormalities (low progesterone, hypothyroidism)
  4. Space in uterus: leiomyomas (fibroids), uterine malformation etc.
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26
Q

4 risk factors for miscarriages?

A
  1. Advanced maternal age
  2. Previous miscarriage (especially consecutive)
  3. Maternal smoking
  4. Intrauterine trauma (previous medical procedures)
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27
Q

Clinical presentation of miscarriage?

A
  1. Vaginal bleeding
  2. Pelvic pain
  3. Open cervical os
  4. Expulsion of fetal content
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28
Q

Is vaginal bleeding normal during pregnancy?

A

YUP

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29
Q

2 types of miscarriages?

A
  1. Complete abortion: all fetal material expelled, usually in early pregnancy
  2. Incomplete abortion: retention of products of conception with increased infection (endometritis) risk if untreated
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30
Q

What is a threatened abortion? Treatment?

A

Vaginal bleeding with closed cervical os

No treatment other than observation but may be nothing because vaginal bleeding is normal during pregnancy

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31
Q

How to clinically manage miscarriages? What to note?

A
  1. Ultrasonography helpful to monitor fetal cardiac activity, gestational sac, yolk sac
  2. Examination of expelled contents, but difficult to distinguish complete from incomplete abortions
  3. Removal of retained tissue:
    - Dilatation and curettage (D&C) = dilate cervix and scrape uterus (definitive treatment)
    - Medical treatment with misoprostol: cervix dilation, uterine contractions (but D&C might still be needed)
    - Expectant management: wait and look out for symptoms of endometritis

NOTE: #3 is the same for induced abortions

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32
Q

Incidence of ectopic pregnancies? Why is it rising?

A

1-2 in 100 pregnancies

Because incidence of pelvic inflammatory disease (risk factor) is rising

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33
Q

List 7 locations for ectopic pregnancies in order of prevalence.

A
  1. Ampulla
  2. Isthmus
  3. Fimbriae
  4. Ovarian
  5. Abdominal
  6. Interstitial
  7. Cervical
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34
Q

What are the risk factors for ectopic pregnancy?

A

Factors that disrupt the fallopian tube and causes scaring or decreased peristalsis:

  1. Pelvic inflammatory disease: causes scarring in reproductive tract
  2. Prior tubal surgeries: ligation
  3. Endometriosis
  4. Intrauterine device: creates harsh intrauterine environment
  5. Smoking: interferes with motility
  6. In vitro fertilization
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35
Q

Symptoms of ectopic pregnancy?

A
  1. Abdominal or pelvic pain
  2. Missed menses (or known pregnancy)
  3. Vaginal bleeding
  4. If ruptured and bleeding, patient may show signs of hemodynamic instability (tachycardia, hypotension etc.) => emergency!
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36
Q

Clinical presentation of ectopic presentation during exam?

A
  1. Abdominal/pelvic tenderness
  2. Palpable adnexal mass
  3. Or no abnormality at all
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37
Q

How to diagnose ectopic pregnancies? Why?

A
  1. Any female of reproductive age complaining of acute onset abdominal pain needs a pregnancy test because this is a difficult diagnosis to make => if qualitative β-hCG is positive and does not increase appropriately over time (quantitative serum β-hCG serum test), then abnormal pregnancy is likely (including ectopic)
  2. Transvaginal ultrasound: looking for intrauterine pregnancy or adnexal mass; needs to be done at threshold β-hCG level of 1,500 IU/L:
    - Above threshold levels: if pregnancy not in uterus, then likely ectopic
    - Below threshold: lack of visualization inconclusive, repeat hCG and u/s in 2-3 days
38
Q

What is a heterotopic pregnancy? What to note?

A

One pregnancy in uterus and one in the Fallopian tube (very rare)

NOTE: only considered with IVF pregnancies

39
Q

How to manage an ectopic pregnancy once confirmed?

A
  1. If hemodynamically unstable, rupture likely so immediate surgery and resuscitative care
  2. If stable => medical or surgical treatment:
    - Surgical: laparoscopic salpingectomy (for severe tubal damage, repeated ectopics, no future pregnancies planned or only IVF) or salpingostomy and tissue removal (but may increase risk for future ectopic due to scarring)
    - Medical: methotrexate
40
Q

How does methotrexate work? What to note?

A

Folic acid antagonist that inhibits DNA synthesis and targets rapidly dividing cells

Low dose given and can be given in combination with other therapies and either as single or multi-dose regimen depending on decline of hCG levels (must follow hCG decline post-treatment) down to 0

NOTE: many contraindications, need to be healthy to be able to take it and hCG levels need to be < 5,000 IU/L without any fetal cardiac activity (would have higher treatment failure rate) + patient must be willing to comply with follow up or NOT a candidate for medical management

41
Q

What is methotrexate also used for (other than for ectopic pregnancies)?

A

Also used for cancer and some autoimmune diseases

42
Q

What is gestational hypertension? What to note?

A

BP > 140/90 mmHg or significantly elevated above pre-pregnancy levels after 20 weeks gestation

NOTE: classically problems arise during the 3rd trimester

43
Q

Prevalence of gestational HT?

A

5-10% of pregnancies

44
Q

Risk factor for gestational HT?

A

Increased risk with multiple gestations

45
Q

Clinical management of gestational HT?

A

Monitor patient and access for preeclampsia, worsening disease, fetal wellbeing etc.

46
Q

How does BP fluctuate during pregnancy?

A

Initially drops in first trimester and then rises but should not exceed normal BP

47
Q

What is gestational HT a risk for?

A
  1. Risk factor for HT and CVD later in life

2. Risk of progression to preeclampsia

48
Q

Describe mild preeclampsia.

A

BP changes of gestational hypertension with proteinuria (>300 mg/24hrs, >1+ dipstick) and sometimes non-dependent edema (aka not dependent on gravity, but in hands and face)

49
Q

Descrive severe preeclampssia.

A
  1. BP >160/110 mmHg
  2. Severe proteinuria (>5g/day)
  3. Edema
  4. End organ damage: neurological symptoms (severe headache, visual change), renal failure, liver dysfunction, pulmonary edema
  5. HELLP syndrome = hemolysis elevated liver enzymes and low platelets: associated with hypertensive states
50
Q

Describe eclampsia.

A

Severe preeclampsia + SEIZURES

51
Q

Prevalence of HELLP syndrome in patients with severe preeclampsia?

A

10% of patients with severe preeclampsia

52
Q

Describe HELLP syndrome.

A
  1. Hemolysis: elevated bilirubin and LDH, peripheral smear with burr cells, schistocytes, or other abnormal RBC forms
  2. Thrombocytopenia: low platelet count
  3. Elevated liver enzymes: high AST/ALt and LDH
53
Q

Pathophysiology of preeclampsia?

A
  1. Placental pathophysiology: generalized arteriolar constriction and vascular damage (placental ischemia), shallow placental implantation, and inadequate placental perfusion in late gestation =>
    placenta releases chemicals that lead to maternal systemic vasoconstriction and endothelial dysfunction: brain, kidneys, liver etc.
  2. Immune system component: anti-angiotensin II AT-1 receptor ab stimulates receptor activation in blood vessel cells, antiangiogenesis
  3. Imbalance in angiogenic/anti-angiogenic factors
  4. Endothelial dysfunction: dysregulation of vascular tone
    with HTN, increased vascular permeability with edema and proteinurea, and the endothelium expresses factors for normal coagulation causing coagulopathies
54
Q

What exactly is the problem with the placental perfusion in preeclampsia? Why does this occur?

A

Failure of cytotrophoblast invasion into maternal spiral arteries in myometrium for remodeling of arteries to increase blood flow (supposed to occur by 20 weeks gestation) => narrow vessels => placental hypoperfusion

POSSIBLE REASONS:

  1. Trophoblast cell failure to express adhesion molecules necessary for invasion
  2. Disorders of vascularity associated with preeclampsia
  3. Immune system rejection of paternal antigen
55
Q

2 possible reasons to explain the imbalance in angiogenic/anti-angiogenic factors seen in preeclampsia?

A
  1. Genetic

2. Placental mediated

56
Q

3 risk factors for preeclampsia?

A
  1. Genetic: previous personal and/or family history
  2. Immunogenic: increased paternal antigen exposure may be protective:
    - Primiparity (first pregnancy) is a risk factor
    - New partner with short co-habitation and barrier contraception use
    - Preeclampsia in pregnancy with one partner, no preeclampsia in pregnancy with different partner
  3. History of diseases involving vascular dysfunction: systemic lupus erythematosus, HT, renal disease, DM, clotting disorders
57
Q

Clinical management of preeclampsia?

A
  1. Ultimate treatment is delivery, which depends on mother’s condition and fetal gestational age => need to weigh risks and benefits of early delivery vs. worsening disease
  2. Mild/stable disease: monitoring for symptoms and BP, CBC, Cr, platelets, AST
  3. Severe disease with underdeveloped fetus: inpatient monitoring, magnesium sulfate for seizure prophylaxis, anti-hypertensives to reduce risk of MI/stroke, and corticosteroids for fetal lung development
58
Q

When is urine protein measurement useful in preeclampsia?

A

Only useful for initial diagnosis

59
Q

Side effects of magnesium sulfate given to mothers with preeclampsia?

A
  1. Hot flashes
  2. Sweating
  3. Nausea
  4. Toxicity (rare): loss of tendon reflexes, respiratory/cardiac failure
60
Q

What are 4 other complications of preeclampsia? Clinical management for each?

A
  1. Possibility of seizures post delivery => need to continue Mg sulfate 48+ hours post delivery
  2. Recurrence rate with subsequent pregnancy high, especially with severe disease => need to initiate counseling and early monitoring, and low dose aspirin has been shown to slightly reduce risk of preeclampsia in women with high risk given starting at the end of the first trimester
  3. Fetal growth restriction, pre-term labor, placental abruption, fetal death
  4. Maternal risk for long term CVD, renal disease
61
Q

What is gestational diabetes? When does it manifest?

A

Impairment of carbohydrate metabolism that manifests during pregnancy and does not include patients who have pregestational diabetes

Manifests in 3rd trimester when insulin resistance is highest

62
Q

Populations at higher risk of gestational diabetes?

A

Populations with higher DM type 2 risk: Hispanic, Native American and African American women

63
Q

Pathophysiology of gestational diabetes?

A

Pregnancy hormones like human placental lactogen increase insulin resistance and blood sugar levels (so the baby can grab it up) => stress on the mother’s carbohydrate metabolism and some have inadequate pancreatic insulin secretion to cover insulin resistance

64
Q

Risk caused by gestational diabetes? Why?

A

4-10 fold increased risk of developing diabetes mellitus during their life time

Because GDM is a preview of how mother’s body can deal with carbohydrate stress

65
Q

6 risk factors for gestational diabetes?

A
  1. Previous GDM, family history of DMII, or impaired glucose tolerance
  2. Obesity and metabolic syndrome
  3. PCOS
  4. History of previous fetal loss or LGA baby (large for gestational age)
  5. Ethnicity
  6. Age > 25
66
Q

How to make a gestational diabetes diagnosis?

A

Screen for GDM at the end of the 2nd trimester (24-28 weeks) in all women with:

  1. Glucose screening test: one-hour GTT with 50g glucose load (>130/140mg/dl is abnormal)
  2. Glucose Tolerance Test (GTT): 100g glucose load, glucose checked at fasting and hourly interval, 2 elevations above normal = positive test (diagnostic if screen is positive)
67
Q

How to clinically manage gestational diabetes?

A
  1. Prepregnancy: counseling on weight loss, exercise, and appropriate pregnancy weight gain
  2. At diagnosis: diet to prevent excess weight gain, glucose monitoring, and insulin therapy if glucose is persistently high (fasting >95 mg/dl, 1 hr post prandial >130-140mg/dl)
68
Q

3 maternal complications of GDM?

A
  1. Preeclampsia
  2. C-section delivery
  3. Future T2 DM
69
Q

5 infant complications of GDM?

A
  1. Macrosomia: birth weight > 10 lbs => can cause birth injury
  2. Neonatal hypoglycemia (due to high fetal insulin to compensate for maternal hyperglycemia)
  3. Respiratory distress
  4. Fetal/neonatal demise
  5. Future obesity and DMII
70
Q

3 types of abnormal placental conditions?

A
  1. Placenta previa
  2. Placental abruption
  3. Abnormal placental attachment
71
Q

What is placenta previa?

A

Abnormal location of the placenta over or near the cervical os causing painless bleeding after 20 weeks gestation due to slight detachment of tissue at lower uterine segment

72
Q

What is placental abruption?

A

Premature separation of the placenta from the uterus after 20 weeks gestation causing painful bleeding and abdominal pain with contractions

73
Q

2 possible causes of placenta previa?

A
  1. Interference with normal placental migration

2. Abnormal endometrium in upper uterine cavity from surgery or prior pregnancy

74
Q

7 risk factors for placenta previa?

A

Factors affecting placental migration:

  1. Prior C-section
  2. Prior privia
  3. Uterine surgery
  4. Multiple gestations
  5. Multiparity
  6. Smoking
  7. Advanced age
75
Q

How to diagnose placenta previa? What to note?

A

Placental location can be identified by transabdominal ultrasound

NOTE: vaginal exam contraindicated

76
Q

Clinical management of placenta previa?

A
  1. If mother and baby are stable, “pelvic rest” and support and preparation for (possible preterm) delivery => must deliver via C-section at 36-37 weeks, even if asymptomatic due to hemorrhage risk
  2. Emergency delivery for fetal distress, severe maternal bleeding, labor
77
Q

What is placental abruption linked to?

A

Linked to early placental disease

78
Q

7 risk factors for placental abruption?

A
  1. Hypertension, preeclampsia, etc.
  2. Cocaine use
  3. Trauma
  4. Previous abruption
  5. Advanced maternal age
  6. Multiple gestation
  7. Smoking
79
Q

What can placental abruption lead to?

A

Uteroplacental insufficiency => 12% fetal mortality rate

80
Q

How to diagnose placental abruption?

A

Difficult to detect by ultrasound, so need to make clinical diagnosis by excluding other conditions

Sometimes retroplacental hematoma may be observed

81
Q

How to clinically manage placental abruption?

A
  1. Maternal/fetal monitoring
  2. Support and preparation for (possible preterm) delivery via vaginal delivery if stable
  3. Immediate delivery if mother or baby are unstable: risk of severe maternal blood loss which will compromise fetal blood supply => fetal distress, risk of fetal demise due to asphyxia
  4. Delivery if >36 wks gestation
82
Q

3 types of abnormal placental attachments? Describe each. Most common one?

A
  1. ***Placenta accreta: placenta attaches through the endometrium to the myometrium
  2. Placenta increta: placenta attached into the myometrium of the uterus
  3. Placenta percreta: placenta attaches through the myometrium into uterine serosa and may even invade nearby organs
83
Q

What 2 factors increasing incidence of placenta accreta? Why?

A
  1. Placenta previa
  2. Prior uterine surgery (e.g. C-section)

Weakened uterine wall from scarring => deep placental implantation

84
Q

Diagnosis of abnormal placental attachments?

A

Ultrasound

85
Q

Clinical management of abnormal placental attachments?

A
  1. C-section and placental resection (possible hysterectomy)
  2. Prepare for maternal hemorrhage during delivery when placenta attempts to separate
86
Q

Target rate of C-sections by WHO?

A

10-15%

87
Q

5 disadvantages of C-section vs vaginal delivery?

A
  1. Longer short-term recovery period and hospital stay
  2. Maternal morbidity: higher risk of cardiac event, blood clot, hysterectomy, wound healing
  3. Future risk of asthma in child
  4. Fetal respiratory distress, increased fetal mortality (especially <39 weeks)
  5. Future pregnancy: greatly increased risk of placenta previa and accreta, uterine rupture especially with repeat C-section
88
Q

Is sexual function affected by C-section vs vaginal delivery? What about incontinence?

A
  • Sexual function equally unaffected > 3 months postpartum

- Incontinence rates equal 2 months postpartum

89
Q

What is erythroblastosis fetalis? What to note? Treatment?

A

Caused by Rh incompatibility between mother and fetus => antibodies cross the placenta and attack the fetal RBCs => hemolysis => death

NOTE: happens in subsequent pregnancies: during first delivery there is mixing of the bloods => antibodies formed

90
Q

Is most of the population Rh + or -?

A

Positive

91
Q

Anatomical abnormalities in erythroblastosis fetalis? Explain.

A
  1. Hepatomegaly due to increased hepatic

2. Kernicterus = yellowing of brain regions due to hyperbilirubinemia

92
Q

Treatment for erythroblastosis fetalis? How does it work?

A

Rhogam at 28 weeks and at birth: anti Rh antibody that binds to Rh antigen so that the maternal immune system does not get involved

SMP - APP Part 2 (7 decks)

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