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NM 706 Adv Midwifery Care-Perinatal & Neonatal > Module 1 Study Guide > Flashcards

Module 1 Study Guide Flashcards

1
Q

What is the definition of placental abruption?

A

Antenatal decidual hemorrhage leads to the premature separation of the placenta. AKA, the placenta detaches from the uterus before the baby is delivered. It can fully or partially separate. This is often caused by sculpture of maternal vessels in the decidua basalis, the bleeding is almost always of maternal origin.

Note: concealed abruption occurs when the separation is in the midsection, and the edges remain attached.

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2
Q

What are the risk factors for placental abruption?

A

Hx of Abruption
Increasing Parity
PPROM
Short interpregnancy interval
Cocaine use in third-trimester
Hx C/S or Leiomyoma (aka fibroids)
Rapid uterine decompression (Mulitple grestation or Polyhydramnios)
Maternal Hx: Thrombophylia, hypothyroidism, asthma, HTN (sig. Increases risk), AMA, smoker, ETOH use
**Blunt trauma
Unexplained elevated maternal serum AFP (protein produced by fetal liver)

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3
Q

What are the signs and symptoms of placental abruption?

A

Early stages: may have no clinically evident signs
Concealed abruption: cramping, contractions, uterine tenderness, back pain
“Classic Signs”: vaginal bleeding with abdominal pain, hypotonic uterus, and tenderness, maternal tachycardia, abnormal FHR. For a posterior placenta, there may be back pain as well.

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4
Q

What testing or imaging is available to diagnose placental abruption?

A

Ultrasound (fresh blood can look like the placenta and may be difficult), symptom-based diagnosis, or diagnosed retrospectively

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5
Q

How should placental abruption be managed?

A

Delivery if >34-36 weeks and or unstable
If bleeding is minor and both the pregnant person and baby are stable and/or preterm may lead to antepartum admission and monitoring.

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6
Q

What is the definition of placenta previa?

A

Abnormally located placenta, near the internal os. If the embryo implants by the cervical os, the placenta will grow there. If it is diagnosed early in the pregnancy, as the uterus grows, it can self-resolve.

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7
Q

What are the risk factors for placenta previa?

A

Hx of placenta previa, multiple gestations (because of more placentas being present), uterine surgery

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8
Q

What are the signs and symptoms of placenta previa?

A

Painless vaginal bleeding

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9
Q

What testing or imaging is available to diagnose placenta previa?

A

Ultrasound to assess the location of the placenta

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10
Q

How should placenta previa be managed?

A

***DO NOT perform cervical exams
If stable: Pelvic rest! Limited physical activity/bed rest. C/S at 34 weeks
If unstable (hemorrhaging/unstable BPs): Urgent/Emergent C/S, blood transfusions as needed

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11
Q

What is the definition of vasa previa?

A

The umbilical cord lies across the cervical os. Often is seen with a velamentous cord insertion.

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12
Q

How is vasa previa diagnosed?

A

Typically diagnosed by routine ultrasound.

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13
Q

How should vasa previa be managed?

A

Antenatal steroids at 30-32 weeks and delivery by C/S at 33-34 weeks

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14
Q

What are the signs and symptoms of retained placenta?

A

When the third stage of labor (i.e. delivery of the placenta) lasts longer than 30 minutes.

Incidence of PPH increases after 17 minutes

If a placenta is retained for >60 minutes, it should be assumed to be invasive (i.e. accreta, increta, percreta)

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15
Q

How does retained placenta cause postpartum hemorrhage?

A

When the placenta is still attached, the blood vessels where it is attached continue to bleed. The uterus is also unable to contract appropriately to stop the blood flow.

Contractions are ineffective when the placenta is retained.

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16
Q

What is uterine atony?

A

Uterine atony refers to the inadequate contraction of the corpus uteri myometrial cells in response to endogenous oxytocin release.

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17
Q

What are risk factors for uterine atony?

A

Uterine overdistention secondary to hydramnios, multiple gestation, use of oxytocin, fetal macrosomia, high parity, rapid or prolonged labor, intra-amniotic infection and use of uterine-relaxing agents.

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18
Q

What are the signs of uterine atony?

A

Excessive bleeding, fundus may be boggy/high/deviated and does not resolve with a massage.

If significant bleeding has occurred, pt may become hypotensive, tachycardic, pale, or dizzy

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19
Q

How does uterine atony cause postpartum hemorrhage?

A

This is the primary cause of PPH. The uterus is not contracting and stopping the blood flow like it should, leading to hemorrhage.

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20
Q

What is a uterine inversion?

A

When the fundus collapses into the endometrial cavity, turning the uterus partially or entirely inside out.
I
ncomplete: Fundus within endometrial cavity
Complete: fundus protrudes through the cervical os
Prolapsed: fundus protrudes to or beyond the vaginal introitus
Total: Both the Uterus and vagina are inverted

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21
Q

How does uterine inversion cause postpartum hemorrhage?

A

It is associated with disseminated intravascular coagulation (DIC). The uterus cannot contract appropriately because it is “inside out”

Note: Most common symptom is maternal shock

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22
Q

What is the management for an inverted uterus?

A

Immediately attempt to reposition the uterus as this is more successful if done before the lower uterine segment and cervix contract. If the placenta is attached, DO NOT remove it. The provider will use their hand to “push” the uterus back into place and then hold it in place with their first while waiting for a physician. Request blood to be prepared or initiate the PPH protocol.

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23
Q

How do vaginal and cervical lacerations cause postpartum hemorrhage?

A

Significant tearing can cause increased bleeding. To stop the bleeding, the tear must be repaired.

Cervical lacerations may not be quickly identified and can be difficult to repair. They may need to be repaired in the operating room for the best visualization.

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24
Q

What is the difference between early and late postpartum hemorrhage?

A

Early PPH occurs within 24 hours of delivery, a late PPH occurs after 24 hours, and up to 12 weeks postpartum. A late PPH is most often the result of subinvolution but could also be due to retained placenta or products of conception.

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25
Q

How should an early postpartum hemorrhage be managed?

A

Varies on cause of hemorrhage. You should immediately start to assess the cause and stop the bleeding.
Causes: TTTT-Tone, Trauma, Tissue, Thrombin

Medications:
Pitocin-first line 10-40 U in 500-1000 cc IV at 250 cc/hr or 10 U IM
Methergine-2nd line* 0.2 mg IM q2-4h (Note: avoid in HTN due to increased BP, can repeat PO TID-QID for up to 1 week
Hemabate-2nd line 0.25 IM or intramyometrium q15m x8 (Note: avoid in asthma, causes severe diarrhea)
Cytotec 600-800 mcg SL/PO or 800-1000 mcg PR (Note: causes fever and shivering)
TXA: to be used in conjunction with other meds. Give within 3 hours of birth (Note: is NOT a uterotonic)
PRB-type and cross for 2 units

Monitor vital signs: tachycardia and hypotension are signs of significant blood loss
Fundal massage/Bimanual massage to remove clots
Empty bladder
Call for MD backup
2nd IV
MD should assume care if PPH is stage 3

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26
Q

What is a hematoma?

A

A pool of mostly clotted blood as a result of damage to blood vessels. They are most common at the vulva, vagina, or retroperitoneum.

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27
Q

What are the signs and symptoms of a hematoma?

A

Significantly worse pain than expected from delivery/type of tear.

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28
Q

How are hematomas diagnosed?

A

Can be diagnosed by a physical exam. Some may not be visible and would require a gentle internal digital exam.

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29
Q

How are hematomas managed?

A

Frequent assessment, Ice packs, pain management, side-lying, IV placement in case of need for volume resuscitation, foley catheter placement, CBC to establish baseline.

Note: the midwife SHOULD NOT incise the hematoma without additional aid

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30
Q

What is subinvolution?

A

Subinvolution is delayed return of the enlarged uterus to normal size and function. By 2 weeks PP, the uterus can no longer be palpated abdominally though involution is not complete until 6 weeks PP. When this does not occur in the expected time frame, subinvolution has occurred.

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31
Q

What are potential causes subinvolution?

A

Retained placental fragments or products of conception, infection, leiomyomas (fibroids), exessive maternal activity

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32
Q

What are the signs and symptoms of subinvolution?

A

Prolonged lochial discharge.
Irregular or excessive bleeding.
Larger than normal uterus.
Boggy uterus (occasionally)

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33
Q

How is subinvolution treated?

A

Depends on severity and cause
D&C can be performed
Medications: the same meds used for an early PPH
Treatment of infection

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34
Q

What is Rh-D isoimmunization?

A

Rh factor is a protein on red blood cells. Rh incompatibility is when a mother has Rh-negative blood and her baby has Rh-positive blood. Rh isoimmunization is when the blood from the baby makes the mother’s body create antibodies that can harm the baby’s blood cells.

35
Q

What affect does Rh-D isoimmunization have on the fetus?

A

If the mother is Rh- and the baby is Rh+ then the mother’s body could “attack” those proteins. This can happen anytime where this is mixing blood due to trauma, bleeding, delivery, etc. In the current pregnancy, it can cause hydrops fetalis and a severe hemolytic disease. It will also affect a future pregnancy if the baby is also Rh+ and can cause IUFD and loss of pregnancy.

36
Q

How can Rh-D isoimmunization be prevented?

A

300 mcg of Anti-D immunoglobulin (RhoGAM), a human plasma-derived product, is given at 28 weeks gestation and within 72 hours of delivery.

In case of trauma, KB stain can be done and 10 mcg/ml of additional RhoGAM given

37
Q

What is the difference in how Rh-D isoimmunization affects the first pregnancy versus subsequent pregnancies?

A

In the first pregnancy, there tends to be little mixing and, therefore low risk of problems; significant problems are more likely to occur in subsequent pregnancies because those antibodies remain in the maternal immune system and may later cross the placenta.

38
Q

What is ABO incompatibility?

A

ABO incompatibilities exist between the mother and fetus when the mother is blood type O and the fetus has a different blood type (Type A, B, or AB). The Anti-A and Anti-B antibodies in the mother’s serum can cross the placenta and potentially hemolyze fetal RBCs. Most often, ABO incompatibility is less severe than Rh incompatibility.

39
Q

What blood type most commonly has an ABO incompatibility?

A

Maternal O blood type and fetal A

40
Q

What affect does ABO incompatibility have on the fetus?

A

This is the most common cause of hemolytic anemia in newborns and is usually mild.

41
Q

How can an ABO incompatibility be managed?

A

There is no prenatal treatment, only neonatal monitoring and observation for hyperbilirubinemia.

42
Q

What is Kell sensitization?

A

The third most potent cause of hemolytic disease of the newborn. The disease results when anti-Kell antibodies from the mother cross the placenta to the fetus. The antibodies can cause a more rapid and severe fetal anemia than Rh incompatibility. The antibodies stop the development of red blood cells and lyse blood cells (hemolysis) that are already present.

43
Q

What affect does Kell sensitization have on the fetus?

A

Can cause hemolytic disease and severe anemia because it suppresses RBC production

44
Q

How should the nurse-midwife manage Kell sensitization when it is recognized?

A

Any positive antibody warrants: Antibody identification, titer and consult with MD

45
Q

What lab values enable the nurse-midwife to diagnose iron deficiency anemia?

A

H/H 1st: <11/<33, 2nd: <10.5/<32, 3rd: <11/<33. Diagnostic tests=CBC with indices and serum ferritin (Ferritin <12 is likely IDA)

46
Q

What lab values enable the nurse-midwife to diagnose megaloblastic anemia?

A

Megaloblastic Anemia (Previously pernicious anemia): Serum B12 and folate levels [One of both def=B12 def and/or Folate Def. If borderline, measure MMA and homocysteine [both increased=B12 Def, only homocysteine increased=Folate Def.)

47
Q

In a patient with anemia, what differential diagnoses can be listed?

A

Iron Deficiency Anemia
Beta/Alpha Thalassaemia
Blood Loss
Folate Deficiency
B12 Deficiency
Sickle Cell
Megaloblastic Anemia

48
Q

What are the risks of iron deficiency anemia?

A

Preterm delivery, cesarean section, low fetal birth weight, lower fetal mental and psychomotor performance.

49
Q

What are the risks of megaloblastic anemia?

A

Pregnancy loss, neural tube defects, cardiac defects, preterm birth, pre-eclampsia, placental abruption, smaller fetal brain size, fetal cognitive defects and behavioral problems, and autism.

50
Q

What are the various approaches to prescribing iron supplementation in pregnancy?

A

PNV with 30-60 mg/d
If Hgb<11 and Ferritin <30: 60-120 mg/d or every other day 2-3x/week.
Oral Iron: 40-80 mg/d (Ferrous sulfate/gluconate/fumarate)
Injectable
Iron transfusions if severe

51
Q

What is the best dietary counseling to give a pregnant patient with anemia?

A

Heme Iron (Animal sources) is absorbed better than Non-Heme (plant-based and supplements)
Sources: Red meat, chicken breasts, lentils, edamame, chickpeas, fortified oatmeal, black beans, chocolate.
Megaloblastic Anemia: Green leafy vegetables, lentils, beans, and fortified foods.

52
Q

What populations are most affected by sickle cell trait (Hemoglobin AS) and sickle cell anemia (Hemoglobin SS)?

A

Hgb AS & SS: People of African descent. 1/12 AA people have sickle cell trait. 1/300 AA has a form of sickle cell disease. 1/600 AA has sickle cell anemia. It is also found in high frequency in Greek, Italian (Sicilian), Turks, Arabs, Southern Iranians, and Asian Indians.

53
Q

What populations are most affected by alpha and beta thalassemia?

A

Alpha: Southeast Asian, African.
Beta Thalassemia: Mediterranean, Middle Eastern, African, and SE Asian ethnicities

54
Q

What is the genetic inheritance pattern (i.e. autosomal recessive, autosomal dominant, etc.) for sickle cell trait/anemia, alpha thalassemia, and beta thalassemia?

A

Sickle cell trait/anemia: Autosomal recessive
Alpha Thalassemia: Autosomal recessive genetic disorder
on chromosome 16 [1-4 alpha gene deletion(s)]
Beta Thalassemia: Autosomal recessive genetic disorder on chromosome 11 [Point mutation or gene deletion (rare)]

55
Q

What is the difference between alpha thalassemia minor and major?

A

Minor: MCH=25-27. Alpha Thalassemia minor is often unrecognized and causes no major maternal problems and very little problem for the fetus as well. Mild anemia may occur.

Major (Aka Hb Bart Disease): MCH=<25. This is when all four abnormal gene globins are inherited. Oxygen is transported poorly, and these babies are stillborn or are born with hydrops fetalis and die soon after birth.

56
Q

What is the difference between beta thalassemia minor and major?

A

Minor: Presentation ranges from absence of anemia to mild/moderate anemia characterized by hypochromia and microcytosis. It can cause mild anemia in pregnancy due to ineffective erythropoiesis. It is associated with fetal growth restriction.

Major (aka Cooley Anemia): Serious and frequently fatal. Hemolysis is intense and leads to severe anemia. Many patients are transfusion dependent. Pregnancy is safe if the maternal cardiac function is normal. The patient will need transfusions throughout to pregnancy to maintain Hgb of 10 g/dl. Prior to blood transfusion and iron chelation, pregnancy with cooley anemia was rare.

57
Q

What lab test(s) are used to diagnose hemoglobinopathies?

A

Hemoglobin Electrophoresis. DNA testing must be done to diagnose Alpha Thalassemia.

58
Q

What hemoglobin is present in sickle cell anemia? in alpha thalassemia? in beta-thalassemia?

A

Sickle Cell Anemia Hb SS
Alpha Thalassemia: ABA1 and HBA2 (Rarely Hb H or Hb Bart)
Beta Thalassemia: Absence of Hb A. Electrophoresis HbA1 is low, HbA2 is high and HbF is high

59
Q

What are the associated risks of sickle cell anemia?

A

SAB, Stillbirth, Preterm labor, PPROM, antepartum hospitalization, postpartum infection, IUGR, low birth weight, preterm delivery. Sickle cell crisis, acute chest syndrome, infection, severe anemia, cholecystitis, hypersplenism.

60
Q

What level of interprofessional management is warranted in the care of a patient with sickle cell anemia? thalassemia minor? thalassemia major?

A

Sickle Cell Anemia: Should be comanaged with perinatology due to risk for complications
Thalassemia Minor: Comanage with a physician. Does not typically affect pregnancy beyond anemia.
Thalassemia Major: Should be referred for care with perinatology/specialist

61
Q

What is the difference between gestational thrombocytopenia and ITP?

A

Gestational Thrombocytopenia: Defined as a platelet count below 150,000 in pregnancy
ITP: Acquired Autoimmune disorder-IgG antibodies prematurely destroying platelets

62
Q

How does the clinical presentation of ITP differ from gestational thrombocytopenia?

A

Gestational Thrombocytopenia: More likely to occur in the late 2nd to 3rd trimester and normalizes spontaneously 1-2 months PP. The patient will have no history of low platelets or abnormal bleeding. Typically asymptomatic if over 75,000
ITP: If noted in the first trimester, more likely to be ITP. The majority of cases are pre-existing before pregnancy. May have a history of easy bruising, gums bleeding etc.

63
Q

What labs test/values diagnose gestational thrombocytopenia? What labs test/values diagnose ITP?

A

Diagnosis of exclusion-there are no specific diagnostic tests. GT is a presumptive diagnosis, official diagnosis can be made after platelets normalize PP.
Labs: CBC, Peripheral blood smear, retic count, LFTs, Viral screening (HIV, HCV, HBV)

64
Q

What are the associated risks of gestational thrombocytopenia and ITP?

A

GT: Generally none. May not have epidural if platelets <80
ITP: Serious problems are rare. Small increased risk of bleeding, PP venous thromboembolism, may not be able to get an epidural.

65
Q

How can gestational thrombocytopenia and ITP be managed by the nurse-midwife?

A

Both should be comanaged with an OB/hematology

66
Q

What population(s) is/are most affected by G6PD deficiency?

A

Mediterranean and African descent

67
Q

What is the genetic inheritance pattern (i.e. autosomal recessive, autosomal dominant, etc.) for G6PD?

A

X-linked

68
Q

What are the signs/symptoms of G6PD?

A

Ranges from asymptomatic to severe acute/chronic hemolytic anemia.
Jaundice. When your skin turns yellow.
Amber Urine
Fatigue.
Paleness
Tachycardia
Shortness of Breath
Enlarged spleen.

69
Q

What risk does G6PD pose to the pregnancy? to the fetus?

A

ITU, pre-eclampsia, neonatal jaundice, hydrops fetalis, stillbirth

70
Q

How should the nurse-midwife manage a patient with G6PD?

A

Surgery can cause an episode of hemolysis, therefore any MD that may care for the patient must know about it.
Note: Can also be triggered by the following: infection, sulfa, macrobid, NSAIDs, methylene blue, fava beans, and certain legumes.

71
Q

What is indirect bilirubin (unconjugated bilirubin)? How is it excreted from the newborn?

A

​​Indirect bilirubin is formed by the breakdown of hemoglobin in the red blood cells. Indirect bilirubin is bound to albumin in the blood. The liver converts this bilirubin into direct bilirubin, which can then be released into the intestine by the gallbladder for elimination. It is excreted in stool or urine.

72
Q

What are the causes of elevated indirect bilirubin in the newborn?

A

Physiologic jaundice: immature liver, short lifespan on RBCs in newborns. Usually occurs on day 2-4 PP and resolves in 2 weeks.
Pathologic jaundice: Occurs in the first 24 hours of life.
Breastfeeding jaundice: occurs in the first week of life due to inadequate feeding/dehydration. There is decreased intestinal motility and decreased elimination of bilirubin.
Breast milk jaundice: occurs late in the first week and resolves by week 12 and is less common than breastfeeding jaundice. Higher levels of free fatty acids result in increased enterohepatic circulation.

73
Q

What is pathologic hyperbilirubinemia? How does pathologic hyperbilirubinemia differ from physiologic jaundice?

A

Pathologic: the most serious type of jaundice. It occurs within 24 hours after birth, and is characterized by a rapid rise in a baby’s bilirubin level. The most likely cause is blood incompatibility or liver disease.

Pathologic jaundice presents in the first 24 hours and physiologic presents later and is a normal result of the short lifespan of RBCs in newborns and immature liver.

74
Q

What laboratory testing is available to evaluate newborn bilirubin levels?

A

Total bilirubin levels

75
Q

At what level(s) is/are total serum bilirubin (TSB) levels considered abnormal?

A

As total serum bilirubin levels increase, jaundice progresses cephalocaudally from the face (5 mg/dL) to the trunk (upper chest 10 mg/dL, abdomen 12/mg/dL) and extremities, eventually including the palms and soles (>15 mg/dL) (Porter & Dennis, 2002) (progresses below the nipple line).

76
Q

What is Bhutani’s nomogram?

A

The Bhutani Nomogram is used to determine the level of risk based on the Infant’s hours of age and serum bilirubin result.

77
Q

How does acute bilirubin encephalopathy differ from kernicterus?

A

Bilirubin encephalopathy: refers to cerebral symptoms associated with hyperbilirubinemia such as irritability, high-pitched cry, hypertonia or hypotonia, seizures, and possibly death if left untreated.

Kernicterus: used to describe the chronic and permanent sequelae of ABE in infants who sustain permanent cerebral damage as the result of hyperbilirubinemia.

78
Q

What are early signs of acute bilirubin encephalopathy?

A

Extreme jaundice, absent startle reflex, poor feeding/sucking, lethargy/low muscle tone

79
Q

What are risk factors for newborn anemia?

A

Alloimmunization, infection (parvovirus), genetic disorders (G6PD def.), fetomaternal hemorrhage.

80
Q

What is polycythemia?

A

Increased circulating red blood cell mass. Polycythemia in the newborn is a central venous Hct over 65% or a Hgb above 22.

81
Q

What are the associated risks of polycythemia?

A

Maternal DM, inherited, intrapartum hypoxia, Twin to twin tr

82
Q

What are the signs and symptoms of polycythemia?

A

Lethargy, irritability, jitteriness, tremors, seizures, cerebrovascular accidents, oliguria and/or hematuria, respiratory distress, cyanosis, and apnea.

83
Q

What are the potential complications of polycythemia?

A

Thrombosis, ischemia of end organs, hypoperfusion to lungs and renal system by decreasing blood flow. Hypoperfusion to the brain due to a change in oxygen content.

NM 706 Adv Midwifery Care-Perinatal & Neonatal (11 decks)

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