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OB/PEDs: Final > Complications of Pregnancy: > Flashcards

Complications of Pregnancy: Flashcards

1
Q

Abortion/Miscarriage

A
  • Less than 20 weeks gestation
  • May be induced or spontaneous
  • 15%-20% of all pregnancies end in miscarriage with most in the first trimester
  • Incidence increases with age.
  • Causes: Chromosomal abnormalities-60%
    — Infection, endocrine abnormalities and anatomic defects of uterus, fallopian tube, cervix.
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2
Q

Ectopic Pregnancy: most common site

A

the fallopian tube

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3
Q

Ectopic Pregnancy: s/s

A

severe sudden pain on one side
- Tube rupture: internal hemorrhage signs

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4
Q

Ectopic Pregnancy: treatment

A

Chemo drug: Methotrexate
- Folic acid inhibitor
— Cells need folic acid to replicate; this drug stops the replication
— Dont give foods high in folic acid:
— Leafy green veggies
— Spinach/ Kale/ beans/ lagoons/ cereal or bread fortified with folic acid

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5
Q

Ectopic Pregnancy: causes

A
  • previous sexually transmitted infection/ scarring
  • Multiple partner; inflamation
  • IUD; scarring
  • Previous miscarriages
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6
Q

Hydatidiform Mole-Gestational Trophoblastic Disease: MOLAR Pregnancy

A

Abnormal development of the placenta.
*Brown to redish bleeding
*Uterine enlargement greater than gestational age or smaller than expected. (dependent on type)
Hcg levels high
Treatment- D&C : dilation and curettage
*Monitor for uterine cancer

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7
Q

Placenta Previa

A
  • Placenta is improperly implanted in the wrong area (lower uterine segment)
  • seen on ultrasound
  • Schedule c-section
  • Cause hemorrhage
  • Sudden onset of painless uterine bleeding in the later half of the pregnancy or during labor
  • No Vaginal exam
  • No pitocin to augment labor
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8
Q

Abruptio Placentae

A
  • Is the premature separation of a normally implanted placenta from the uterine wall
  • Cause hemorrhage
  • May not see bleeding; blood pools behind placenta
    — Look for internal hemorrhage signs
  • Board like abdomen with tenderness, painful bleeding either visible or concealed.
  • Vasoconstriction can cause this:
    — Vasoconstriction drugs
    — Cocaine
    — Cigarettes
    — Preeclampsia/ hypertensive disease
  • Precipitous labor
  • Short umbilical cord
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9
Q

Hyperemesis Gravidarum: Definition

A
  • Excessive vomiting during pregnancy
  • More frequently under age 25
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10
Q

Hyperemesis Gravidarum: Diagnostic criteria

A
  • Hx of intractable vomiting in 1st half of pregnancy
  • Dehydration
  • Ketonuria
  • Weight loss of 5% of prepregnancy weight
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11
Q

Hyperemesis Gravidarum: Treatment

A
  • Control vomiting with antiemetics
    — Zofran (ondansetron)
  • Correct dehydration: IV fluids/ (TPN/ Lipids)
  • Restore electrolyte balance
  • Maintain adequate nutrition
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12
Q

Hypertensive Disorders:

Preeclampsia

A

indicates that this is a progressive disease unless there is intervention to control it

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13
Q

Hypertensive Disorders:

Eclampsia

A

means “convulsion.”
- If a woman has a convulsion, she is considered “eclamptic”

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14
Q

Hypertensive Disorders

*Preeclampsia

A

– characterized by development of hypertension, proteinuria, and *sudden onset of edema
- Increase in systolic blood pressure of 30 mm hg “or” an increase of diastolic pressure of 15 mm hg over baseline after 20 weeks gestation
- On at least two occasions 6 hours or more apart
- In the absence of baseline values, a blood pressure of 140/90 has been accepted as hypertensive

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15
Q

Pathophysiology of PIH: pregnancy induced hypertension

A
  • Etiology is still unclear
  • Abnormal development of placental spiral arteries
  • It is a multi-systemic disorder characterized by vasoconstriction which reduces perfusion to maternal organs
  • Response linked to the ratio between Prostaglandins:
    — Decreased Prostacyclin (vasodilator)
    — Increased Thromboxane (vasoconstrictor)
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16
Q

Mild Preeclampsia

A
  • Blood pressure findings:
    — Rise in systolic blood pressure of 30 mm hg or more or a rise in diastolic blood pressure of 15 mm hg or more above the baseline
    — 2 occasions at least 6 hours apart
  • Generalized edema
  • Wt gain more than 1.5kg/month 3 rd trimester
  • Proteinuria 1+ to 2+
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17
Q

Severe Preeclampsia

A
  • BP 160/110 or higher on 2 occasions at least 6 hours apart while the woman is on bed rest
  • Proteinuria > or = 5 g/l in 24 hours or 3+ or greater on 2 random urine samples collected at least 4 hrs apart
  • Oliguria: urine output < or = 500 ml in 24 hours
  • Cerebral or visual disturbances
  • Pulmonary edema or cyanosis
  • Epigastric or RUQ pain
  • Impaired liver function
  • Thrombocytopenia: PLT aggregation at sites of vessel tears: less circulation PLTs
  • Fetal growth restriction
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18
Q

Risks from Preeclampsia
Maternal:

A
  • Impacts most organ systems
  • Central nervous systems changes include hyperreflexia, headache, and eclamptic seizure
  • Thrombocytopenia complicates severe preeclampsia in about 10% of women
  • Can be treated with mag-sulfate
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19
Q

Risks from Preeclampsia
Fetal-Neonatal:

A
  • SGA
  • Premature
  • Hypermagnesemia: if mom is treated with mag- sulfate
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20
Q

Severe Preeclampsia: Treatment

A
  • Bed rest
  • Diet- high-protein, moderate-sodium diet
  • Anticonvulsants - Magnesium sulfate is the treatment of choice for convulsions; antidote calcium gluconate
  • Corticosteriods - controversial; can affect surfactant production
  • Fluid and electrolyte replacement
  • Sedatives
  • Antihypertensives: calcium channel blocker= Nifedipine
    — Could lower BP too low
    — Headache: Tylenol or ibuprophen
    — Placental abruptio???
21
Q

PIH: Nursing Assessment & Diagnosis

A
  • T,P,R,BP every1-4 hrs
  • Fetal heart rate
  • Urinary output
  • Urine protein
  • Urine specific gravity
  • Edema
  • Weight - daily
  • Strict I & O
  • ## Bed pan
  • Pulmonary edema
  • Deep tendon reflexes
  • Placental separation
  • Headache.
  • Visual disturbance.
  • Epigastric pain.
22
Q

Deep tendon reflex rating scale:

A
  • 4+: hyperactive; very brisk, jerky, or clonic response; abnormal
  • 3+: brisker than average; may not be abnormal
  • 2+: average response; normal
  • 1+: diminished response; low normal
  • 0: no response; abnormal
23
Q

Eclampsia

A
  • Characterized by convulsion or coma
  • Occurring before the onset of labor, during labor, or early in the postpartal period
  • The only known cure for PIH and eclampsia is birth of the infant
24
Q

Severe eclampsia: HELLP

A
  • Hemolysis: lycing of RBC as they pass through narrowed placental arteries
  • Elevated Liver function tests: ALT/AST
  • Low Platelet count
    Symptoms may include
  • nausea, vomiting, malaise, flu like symptoms, or epigastric pain
  • Perinatal morbidity and mortality with HELLP syndrome are high
  • Platelet transfusions are indicated for platelet counts below 20,000/mm
25
Q

ABO Incompatibility

A
  • Type A or B has an antigen. Type O does not.
  • Usually occurs with Type O mother and Type A or B infant.
    — Babies blood lyces mothers blood and causes excess bilirubin= jaundice/ hyperbilirubinemia
    — Combs test can be done
26
Q

Rh factor

A
  • Rh is a protien on the surface of erythrocytes, either you have it or you don’t have it
  • If you have it you’re RH+
  • If you dont have it you’re RH-
  • If an RH neg. person is exposed to Rh pos. blood, an antigen-antibody response occurs, antibodies are formed and the person becomes sensitized.
  • During pregnancy there is very little blood exchange between mother and fetus if any at all; mostly occurs during delivery
    — Sensitization happens if a mom is Rh neg. And fetus is RH+
    — Moms body creates antibodies against the baby’s blood (bc baby’s blood has an antigen)
    — After her first birth her body will recognize the antigen and create antibodies towards it; no issue for fetus bc antibodies aren’t abundant enough to cause harm
    — But during second pregnancy the moms blood has antibodies that could attack the fetus
    — when antibodies attack fetus it is called erythroblastosis fetalis
    — Causes agglutination and hemolysis of RBCs
    —— Leads to bilirubin increase in the brain= causes Kernicterus= retardation or death
27
Q

when antibodies attack fetus it is called

A

erythroblastosis fetalis
— Causes agglutination and hemolysis of RBCs
— Leads to bilirubin increase in the brain= causes Kernicterus= retardation or death

28
Q

Rh testing/ Diagnosis: Antepartal

A
  • At 28 weeks- Rh neg mother= titer drawn: to see if she has antibodies formed yet
  • No antibody (means she’s not sensitized yet)= give RhoGam (prevents her body from developing antibodies)
  • not sensitized and father is Rh positive or unknown=RhoGam
  • Also give post abortion/ miscarriage
  • After amniocentesis= RhoGam
29
Q

Rh testing/ Diagnosis: Postpartal

A
  • Indirect Coombs- done on mother to determine the number of Rh positive antibodies
  • Direct Coombs- done on infant to detect antibody coated Rh positive
  • If both negative=no sensitization-give RhoGam within 72 hrs
  • If both positive= monitor infant for hemolytic disease
  • If Mom negative and infant positive- give RhoGam
30
Q

Rh Postpartal Management

A
  • RhoGam prevents antibodies from being formed which prevents problems in subsequent pregnancies
  • This protocol reduces the incidence of antenatal sensitization by 93%
  • If not treated- leads to severe hemolysis of the infant which could lead to erythroblastosis fetalis, mental retardation or death.
31
Q

Gestational Diabetes

A
  • Gestational Diabetes occurs in 6.8%-16.3% of pregnancies
  • 50% will develop Type 2 diabetes later in life
32
Q

Influences of pregnancy on Diabetes:

A
  • Disease may be more difficult to control
  • Increased energy needs
  • The renal threshold for glucose decreases (120-130: spills into urine)
  • Increased risk of ketoacidosis
  • Vascular disease may progress
  • Nephropathy & retinopathy
33
Q

Detection and Diagnosis of Gestational Diabetes:
Two Screening Tests

A
  • Urine testing
  • 50 g oral glucose tolerance test
34
Q

Detection and Diagnosis of Gestational Diabetes:
Diagnostic Tests

A

3 hour glucose tolerance test

35
Q

Maternal Risks: Gestational Diabetes

A
  • Hydramnios (increased amniotic fluid; bc fetus urinates more)
  • Pregnancy-induced hypertension (PIH)
  • Preeclampsia
  • Ketoacidosis
  • Dystocia - difficult labor: baby tends to be larger in a pt with diabetes
  • monilial vaginitis: yeast infections
  • Urinary tract infections
  • Retinopathy
36
Q

Fetal Risks: Gestational Diabetes

A
  • Congenital anomalies 5% to 10% and are the major cause of death for infants of diabetic mothers
  • Anomalies often involve the heart, central nervous system, and skeletal system
  • Large for gestational age (LGA) = Birth trauma
    — Shoulder dystocia
    — Clavicle fracture
37
Q

Newborn Risks: Gestational Diabetes

A
  • Hypoglycemia
  • Lethargic/ tired
  • Poor feeding
  • Sweating
  • Intrauterine growth restriction (IUGR)
  • Respiratory distress syndrome
  • Polycythemia: produce more RBC
  • Hypocalcemia
  • Hyperbilirubinemia
38
Q

Insulin Needs

A
  • *First trimester- decreased due to low placental hormones which are antagonistic to insulin, N/V
  • *Second and Third Trimester- Increase due to resistance to insulin, increased metabolic demand
  • *Labor- Maintain tight level of 80-110 mg/dl
  • *Postpartum- decreases significantly- may not need at all.
39
Q

Care of the Woman with Heart Disease

A
  • Most common cause of maternal death
  • Maintain cardiac output, heart rate and blood volume.
  • Decrease overexertion
    — Bed rest/ bed pan
    — No labor
    — Planned C-section
40
Q

TORCH: common infections during pregnancy

A
  • T toxoplasmosis
  • O other infections
  • R rubella
  • C cytomegalovirus
  • H herpes
41
Q

Toxoplasmosis

A
  • Caused by the protozoan, Toxoplasma gondii
  • 40% to 50% of adults have antibodies to this organism
  • The highest rate of fetal infection (65%) occurs when the mother contracts the infection in the third trimester
  • Contracted from eating undercooked meat, drinking unpasteurized milk, contact of cat feces.
42
Q

GBS- group B strep

A
  • Leading cause of neonatal sepsis
  • 20%-30% of woman are carriers
43
Q

GBS treatment

A
  • All women are screened at 35-37 weeks
  • For vaginal births, if GBS positive, will receive IV antibiotic prior at the onset of birth.
44
Q

Rubella (German measles)

A
  • Are no more severe for pregnant women, nor are there greater complications in pregnant women
  • Greatest teratogenic effects of rubella on the fetus is during the first trimester
  • Early in the second trimester, the resultant fetal effect is most often permanent hearing impairment, microcephaly, or psychomotor retardation
45
Q

Cytomegalovirus (CMV)

A
  • Herpes simplex virus group and causes both congenital and acquired disorders
  • Most frequent agent of viral infection in the human fetus
  • Can result in extensive intrauterine tissue damage that leads to fetal death
  • SGA, tissues and organs affected are the blood, brain, and liver, mental retardation, learning disabilities, hearing loss.
46
Q

Herpes Simplex Virus

A
  • Estimated that more than 30 million people are infected with genital herpes and that more than 500,000 new cases are diagnosed in the united states each year
  • Herpes simplex virus (HSV-I or HSV-II) infection can cause painful lesions in the genital area
  • if no outbreak= can be delivered vaginally.
47
Q

Incompetent Cervix

A
  • Premature dilation of the cervix.
  • Cerclage- suture to hold cervix closed.
  • Usually placed on bedrest.
48
Q

Substance Abuse

A
  • Alcohol- No amount is safe. Increased risk of miscarriage, preterm labor, FAS.
  • Tobacco/Nicotine- vasoconstrictive
  • Marijuana- cognitive, emotional, behavioral deficits in child
  • Cocaine- vasoconstrictive- miscarriage, preterm birth, abruptio placentae
  • Amphetamines- NAS- poor feeding, jittery, irritable, high pitched cry
  • Opiates- placental abruption, IUGR, preterm labor and fetal death. NAS, seizures, birth defects, mental retardation.

OB/PEDs: Final (18 decks)

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