Test #2 "The final Muthafuka" Flashcards

1
Q

Fetal Growth and Development:• Understand how to evaluate fetal growth

A
•Establish GA as early as possible
–Using hx, LMP, early US
•Monitor weight gain
•Measure fundal height at each visit
•Serial US as needed
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2
Q

Describe the risk factors, causes, morbidity and mortality for macrosomia

A
Large Gestational age (LGA)
•Birth weight >95th percentile, usually over 4000g (8lbs 13oz)
•Risk factors
–large mother
–GDM
–Postdates
–H/o large babies
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3
Q

LGA Complications

A
Cephalopelvic disproportion
–Labor dystocia/prolonged labor
–Shoulder dystocia
–Maternal soft tissue damage
–Increased c/s
•Postpartum hemorrhage
•Stillbirth
•Neonatal complications
–Low Apgar
–Hypoglycemia
Hematologic abnormalities
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4
Q

• Describe the risk factors for intrauterine growth restriction (IUGR)

A
•Risk factors
–Poor nutrition/weight gain
–Vascular disease/HTN
–Renal disease
–Infection
–Genetic abnormality
–Multiple gestation
–Placental problems
–Pregestational diabetic (type I)
–Drug use/
	smoking/etoh
–Hypoxemia/anemia
–Late onset prenatal care
–Low socioeconomic status
–Prothromibc disorders
-ART
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5
Q

Describe the causes, morbidity and mortality for intrauterine growth restriction (IUGR)

A

IUGR
•Impaired or restricted intrauterine growth
•Significant because there is an inverse relationship between fetal/neonatal weight percentile and perinatal mortality
•Not to be confused with Small-for-gestational age (SGA)
–neonatal diagnosis of size below the 10th percentile
•Usually genetic or due to inadequate nutrition

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6
Q

• IUGR Classifications=Describe the difference between concentric and head-sparing IUGR and complications; Understand preferential perfusion in the fetus

A

•Symmetrical=70%, nutrition based
–Compromised growth in length, head circumference and weight
•Asymmetrical= other factors cause this
– Decreased length and weight, but normal head circumference aka head-sparing
•Complications
–Increased risk fetal distress
–Meconium staining
–Increased perinatal morbidity and mortality

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7
Q

When to be suspicious of IUGR and management

A
Watch for “progressive” growth
•<2cm in 4 wks is suspicious
•If possible, single, consistent examiner
–2 sonos 4 wks apart to confirm
• esp head and abdominal circumference
•AFI check to r/o oligohydramnios
-MANAGEMENT-
limit activity/bedrest
nutrition
cessation of smoking
fetal surveillance= repeat sonos q4-6wks
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8
Q

• Discuss commonly used substances including cigarettes, and understand the basic pathophysiology of how these substances affect both mother and fetus

A
  • Smoking and Pregnancy
  • •The most important modifiable risk factor associated with adverse outcomes
  • •Adverse effects of tobacco
  • –Infertility (maternal)
  • –Low birth weight (LBW)
  • –Miscarriage
  • –Stillbirth
  • –Preterm premature rupture of membranes
  • –Placental abruption/previa
  • –Preterm delivery
  • –Congenital malformations
  • –Postnatal morbidity
  • –Preeclampsia

• –Impaired fetal oxygen delivery
• •Placentas of smokers show structural changes that may contribute to abnormal gas exchange
• –Carbon monoxide exposure
• •Carboxyhemoglobin clears slowly from fetal circulation and diminishes tissue oxygenation
• –Direct damage to fetal genetic material
• –Directly impair lung development
• –Sympathetic activation leading to accelerated heart rate and reduction in fetal breathing movement
• –genetics
higher insidence of SIDS.

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9
Q

• Discuss commonly used substances including alcohol and understand the basic pathophysiology of how these substances affect both mother and fetus

A
  • Alcohol= affect CNS development(3rd trimester)
  • Crosses the BBB. Physical changes small head circumference, small eye opening, thin upperlip, vent septal defect.
  • •Fetal alcohol spectrum disorder (FASD) describes the broad range of adverse sequelae
  • –No effect, normal
  • –Fetal alcohol effects (FAE)
  • –Alcohol related birth defects (ARBD)
  • Fetal alcohol syndrome (FAS)
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10
Q

• Discuss commonly used substances including opiates and understand the basic pathophysiology of how these substances affect both mother and fetus

A

Opiates= •S/sx of high-risk chemical abuse
–Late to prenatal care
–Multiple missed appts
–Impaired school/work performance
–Past OB h/o sab, IUGR, premature birth, placental abruption, stillbirth, precipitous delivery
–Children w/ neuro-developmental problems
–H/o drug/etoh problems

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11
Q

• Discuss commonly used substances including cocaine understand the basic pathophysiology of how these substances affect both mother and fetus

A

Cocaine
–Less women than men use the drug but numbers are growing
•Especially with crack cocaine use
–Effects related to dose and stage of pregnancy
•Decreased birth weight, length and head circumference
•Increased risk prematurity, placental abruption, sab, fetal death
•Readily crosses placenta
–Major mechanism of fetal and placental damage is vasoconstriction
–Maternal cocaine use tests positive in neonatal urine within 2 days of delivery and is excreted within 12-24 hrs
•Meconium stays positive for 3 days and hair for months

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12
Q

• Discuss commonly used substances including methamphetamines, and marijuana, and understand the basic pathophysiology of how these substances affect both mother and fetus

A

Marijuana
–Most commonly used illicit substance taken during pregnancy
–Impact unknown
•Not significantly related to any growth measures at birth, prematurity or congenital anomalies
•Children of heavy uses had smaller head circumferences at all ages
–Associated with etoh and cigarette use

•Methamphetamine
–A neurotoxic agent that damages ending of brain cells containing dopamine
3.5 times more likely to be SGA

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13
Q

Discuss the management of abusive substances while preg

A

Management
•Screen all pregnant women for etoh and substance use
•Counsel regarding risks of specific substance used
•Use behavioral therapy and/or pharmacotherapy to treat addiction
•Test for STDs and treat
•Schedule frequent visits to monitor maternal and fetal status
•Obtain early US to confirm GA and establish accurate baseline for growth
•Begin antepartum fetal surveillance if there is evidence of pregnancy complications

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14
Q

Identify patients at increased risk of complications before pregnancy

A

Age: >35 at increased risk
•Diet: folic acid, MVI; avoid EtOH, tobacco/drugs, caffeine, medications(Warfarin, aspirin are bad)
•Vaccinations: Varicella, Rubella, Hep B(live vaccines are bad)
•Medical history: DM, mental health, STD, etc
•Weight: under or overweight discussed

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15
Q

When does all of the important stuff for the fetus develop?

A

: In the 1st trimester is when all of the important stuff happens.

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16
Q

Discuss the importance of B-Hcg levels and Progesterone

A

Serum HCG levels are the gold standard
–Quantitative B-HCG radioisotope test used for serial testing
•Level doubles every 48 hrs the first 3-4 wks
•Level peaks at 60-70 days then level off
•Level should be 50 to 250 mIU/mL at the time of the first missed period
–Qualitative results are read as pos or neg
(good to just see if there is pregnancy)

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17
Q

Discuss the importance of Progesterone levels

A

Progesterone Levels
-Remain constant through first 9-10 weeks
-Non viable pregnancies have lower levels
-Highly predictive of pregnancy outcomes
-Performed if frequent SAB
-If level < 20, Progesterone vaginal suppository
(Prometrium 100-200 mg inserted vaginally)

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18
Q

Diagnosis of Pregnancy, like GA?

A

Gestational sac appears at about
4 weeks gestational age
-Grows at 1 mm a day through the
9th week of pregnancy

-Gestational sac seen at the
4th – 5th week of gestation
-Serum hCG levels 1000-1500 mIU

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19
Q

Risk factors for Ectopic.

A

Prior tubal pregnancy
•Tubal reversal surgery
•Endometriosis
•Intrauterine device
–decreases the risk of ectopic because it decreases the risk of pregnancy; if pregnant, more likely ectopic
•Once IUP seen on sono, patient can be reassured

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20
Q

Preg Category C

A

tell patients that the benefits out weight the risks

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21
Q

What is evaluated at each visit concerning pregnancy?

A

Weight gain
–Evaluate fetal growth
–Nutritional intake
•BP: screen for pregnancy induced hypertension (PIH)
•Fundal Height : evaluate fetal growth
•Leopold’s Maneuver : determine fetal position
•Fetal heart tones (FHR): evaluate fetal well being
•Edema: screen for PIH
•Urinalysis: glucose and protein
Symptoms: identify problems, discomforts

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22
Q

whats involved with a Standard OB panel:

A
–Blood type, Rh and antibody screen
–Hgb & Hct
–Pap smear and Chlamydia screening
–Rubella immunity, Hep B sAg
–Urine culture
–RPR, HIV
–Thyroid function
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23
Q

What are the Milestone Visits (timing of prenatal visits)

A

6-12 wks: confirm pregnancy, discuss CVS, initial labs, complete Hx and PE
•10-12 wks: determine fetal age by ultrasound; CVS
•11-14 wks: 1st trimester screen
•15-20 wks: Quad screen, Ultrasound, Amnio if high risk
•24-28 wks: GTT for GDM, Antibody screen if Rh-, Hgb/Hct
35-37 wks: GBS screen

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24
Q

Hegar’s sign?

A

softening of the cervix, 4-6wks after conception)

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25
Q

Chadwicks sign

A

blue vagina
is a bluish discoloration of the cervix, vagina, and labia caused by the hormone estrogen which results in venous congestion. It can be observed as early as 6-8 weeks after conception[1], and its presence is an early sign of pregnancy.

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26
Q

OB physical exam?

A
Complete physical examination
•Explanation of what to expect
•Baseline vital signs: BP, weight 
•Breast exam
•Abdominal exam
–Note surgical scars
–Fundal height in cm(not until 20wks)
–Fetal Heart Rate(not done till later)
•Pap Smear
•Chlamydia
Gonorrhea 
Uterine size by bimanual exam
•Adnexal tenderness or enlargement 
•Fetal heart Tones (FHT) 
–120-160 beats per minute
–Heard at 10-12 weeks with Doppler
•Fetal movement after 18-20 weeks
•Fetal position after 28 weeks
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27
Q

assessing fetal growth

•Positive signs

A

–Fetal heart
•Fetoscope auscultation 17-20 weeks
•US 5-8 weeks for cardiac activity
–Movement
•Palpation of active fetal motion (quickening) at 18-20 weeks
•Crown Rump Length (CRL) up to ~14 weeks: ± 5-7 days accuracy

Visualization of the fetus
•US – fetal pole seen 5-6 weeks
(Different slide)
•10-12 WK: fundus at symphysis pubis
•16 WK: fundus midway btw symphysis pubis and umbilicus
•20-22 WK: fundus at umbilicus
•Measure from symphysis pubis to top of fundus
•Measurement in cm: weeks gestation +/- 3cm, most accurate btw 22-34 weeks

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28
Q

Symptoms of Pregnancy

A
  • •Nausea and Vomiting
  • •Breast Tenderness
  • •Abdominal pain or cramping
  • •Vaginal discharge or bleeding
  • •Urinary frequency
  • •Headache
  • •Nosebleeds, gums bleed • •Heartburn
  • •Back Pain
  • •Quickening(baby moving)
  • •Skin changes
  • •Ptyalism
  • •Absence of menses
  • •Constipation
  • Fatigue
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29
Q

why N & V Common in first trimester

A

. Unknown etiology. Maybe related to high HCG levels.
Frequent, consistent vomiting: dehydration, weight loss, electrolyte imbalance, poor appetitie or food intake, ketonuria may indicate hyperemesis gravidum

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30
Q

Most common problem assoc. With pregnancy

A

Abd. Pain and cramping - associated with round ligament pain. Check for signs of SAB or ectopic pregnancy.
Bleeding can be normal. May indicate infection.
Heavy bleeding is abnormal. Get HcG. Spotting can be implantation of blastocyte resulting from invasive chorionic villi activity in the uterine lining. Usually occurs at time of expected menses if not pregnant.
Ptyalism = excessive secretion of saliva

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31
Q

• Explain antepartum patient education including hydration, wt gain, food faddism

A

•Prenatal Vitamins
•Lab tests
•Exercise(walking, prenatal yoga)(stop if palpitation SOB dizziness, abd. pain bleeding numbess, tingling no FM
avoid standing or sitting for long periods).

•Nutrition(not eating for 2 if fetus is size of a gram)
•Sex
•Outline of care
•Handouts, books
•Grooming, dental hygiene(very important), travel(no travelling after 36wks, 28wks O.K)
•Drink plenty of water/fluids
•Get plenty of rest
•Exercise
•Nutrition: Assess Risk Factors
–Encourage appropriate weight gain 25-30 lbs
–Pre-pregnant weight less than 90% (of ideal body wt)or greater than 135%
–Adolescent(eat shitty diets) less than 15
–Two or more pregnancies during 2 years
–Breast feeding
–Multiple gestation
–Food faddism, smoking, drugs, or alcoholism
–Therapeutic diet for chronic systemic disease

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32
Q

What are the specifics for the idetary needs of the pregnant woman.

A
Diet 
•2000-3000 calories per day 
•Vegetarian may be deficient in essential amino acids, iron, complex lipids
•Food allergies
•Calcium intake 1000-1500 mg/day 4 servings (Lactose intolerance?)
	Diet
•Folic acid 800 mcg start preconception
–Prevention of neural tube defects
–Neural tube closes 18-26 days post conception
•Iron 15 mg/day over RDA 30 mg/day 
•Vitamin A  > 10,000 IU/ day Teratogenic
•Vitamin C rich foods 3 servings
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33
Q

Warning Signs During Pregnancy

A
Vaginal bleeding 
–Miscarriage, SAB, Ectopic
•Fluid leaking from vagina 
–PROM
•Persistent headache, dizziness, edema, RUQ pain, HELLP syn, 
–PIH
•Decreased Fetal movement 
–Fetal compromise
•Fever, chills 
–Infection
•Recurrent Vomiting 
–Hyperemis gravidum
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34
Q

ABO Incompatibility

A

40-50% of ABO incompatibility occurs in first pregnancies

•Majority occurs in Type O mothers carrying type A or B fetus

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35
Q

Ehat are the risks for a Rh- mom?

A

•Pt produces IgG antibodies in response to Rh+ fetal RBC in maternal circulation
Sensitization through previous pregnancy
•IgG crosses placenta
Rh+ mom has antigens same as Rh+baby
(Coated erythrocytes destroyed in reticuloendothelial system causing fetal hemolytic anemia)

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36
Q

1st and 2nd Trimester Screening

A

All women should be offered screening for Down syndrome and other genetic abnormalities,
Nuchal Translucency
•An ultrasonic examination to measure the amount of fluid accumulation behind the baby’s neck(•Identify increased risk for Down syndrome)
Amniocentesis
Detects most chromosomal disorders with high degree of accuracy: Down syndrome, Tay-Sachs disease, Neural tube defects, spina bifida, and more

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37
Q

What happens in the 1st trimester (Patho for GDM)

A

1st trimester
•Early in pregnancy maternal estrogens and progesterone increase and promote beta cell hyperplasia and increased insulin release.
• Increase in peripheral glucose utilization and glycogen storage with reduction in hepatic glucose production results in lower fasting glucose levels.

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38
Q

what happens in the 2nd/ 3rd trimester as far as patho for GDM

A

2nd/ 3rd trimester
•Placental steroids and peptide hormones (ie. human chorionic sommatomammotropin, cortisol, prolactin, progesterone and estrogen) rise linearly throughout second and third trimesters.
•These hormones increase tissue insulin resistance and so the demand for insulin increases.
This becomes apparent between 24th-28th week
•The pancreas releases 1 ½ - 2 ½ times more insulin to respond to the increase in insulin resistance.
•Patients with normal pancreatic function are able to meet these demands.
•Borderline pancreatic function leads to inadequate insulin secretion in the presence of increasing insulin resistance.

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39
Q

Meticulous glucose control during pregnancy ?

A

has been shown to reduce the risk of macrosomia=Big gestational babies.

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40
Q

what do you doe for Detection?

A
Detection?
•Risk assessment should be done at the first prenatal visit.  
•Women with clinical characteristics consistent with high risk should undergo testing ASAP:
–advanced maternal age
–morbid obesity
–history of GDM
– glycosuria
–	strong family history of DM
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41
Q

what about low risk pts?

A

Low risk requires no glucose testing but must meet all the following criteria:
•Age <25yrs
•Weight normal before pregnancy
•Member of an ethnic group with a low prevalence of GDM
•No known diabetes in a first degree relative
•No history of abnormal glucose tolerance
•No history of poor obstetric outcome or macrosomic infant

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42
Q

how do you make a GDM Dx?

A

Perform a diagnostic 3hr oral glucose tolerance test (OGTT) without prior plasma or serum glucose screening.
•Two-step approach for women at average risk at 24-28wks:
–Screen by measuring the plasma glucose concentration 1 hr after a 50g oral glucose load.
–If >140mg/dl then schedule a 3 hour OGTT (this identifies 80% of patients with GDM)
–If criteria of >130mg/dl is used this identifies 90% of patients with GDM).
The 3 hr OGTT does not need to be performed on patients with a 1hr 50g glucose screen >185mg/dl or a fasting >126mg/dl.
The 100g, 3 hour OGTT: Must be done after 3 days of an unrestricted carbohydrate diet and while the patient is fasting. Venous plasma glucose is measured at 1, 2 and 3 hours after a 100g glucose load. A positive test requires that 2 values be met or exceeded. One abnormal value should be followed with a repeat test one month later.

•Criteria of positive 100gm OGTT
•Fasting glucose: 	  95mg/dl
•1 hour glucose:	180mg/dl
2 hour glucose:	155mg/dl
•3 hour glucose:	140mg/dl
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43
Q

Short and longterm risks of GDM

A

Immediate risks:
–Increased incidence of cesarean section (30%)
–Preeclampsia (20-30%)
–Polyhydraminos (20%)
•Long term risks:
–Recurrent GDM and high risk for developing diabetes (8%/yr)
Screening for diabetes should be done at the 6wks post partum visit

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44
Q

Short term risks for the baby

A

Macrosomia due to excessive fetal insulin due to increased delivery of glucose and amino acids to the fetus via maternal circulation.
–Typically defined as birth weight above 90th percentile for gestation age or greater than 4000g (8.8lbs).
Shoulder dystocia due to macrosomia
•Neonatal hypoglycemia
•With extremely poor glucose control increase risk of fetal mortality due to fetal acidemia and hypoxia.(must keep blood sugar levels controlled before delivery!!!)

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45
Q

Treatment options for GDM

A

Dietary therapy is the foundation for the treatment of GDM.
(Cold cereal and milk can cause a huge burden on the pancrease for insulin production)
•Post prandial values have been more strongly associated with the risk of macrosomia
–modest carbohydrate restriction 45% of total calories, may blunt postprandial glucose excursion.
Exercise is an adjuvant therapy in GDM

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46
Q

Treatment options for GDM like medications?

A

No oral diabetes medications are currently approved for use in pregnancy
Glyburide has been shown to not cross the placenta No other oral medications should be used
•Targets
– fasting 60-90mg/dl
–1 hr PPG < 130mg/dl
try to control the bedtime blood sugar rising with a long lasting insulin=
•NPH, Regular, aspart, Lispro and detemir are category B
Exercise is an adjuvant therapy in GDM

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47
Q

Long term risk for baby from mom with GDM?

A

Increased risk of adolescent obesity
•Increased risk of developing Type 2 diabetes
•The goal of management of third trimester pregnancies in women with diabetes are to prevent still birth and asphyxia.

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48
Q

Vaginal Bleeding risk factor

A

Rh+father and Rh- mom=risk for the fetus.

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49
Q

Vaginal Bleeding management

A
Management= Misoprostel (Cytotec) 
Highly effective in missed SAB 
No benefit in incomplete SAB 
Completes first trimester SAB within 2 weeks: 66% 
•Dilatation and Curettage Indications 
•Gestational age 8 to 14 weeks 

•Dilatation and Evacuation (D&E) - 2nd trimester procedure

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50
Q

Threatened Abortion. what is it?

A

Bleeding before 20 weeks’ gestation in the presence of an embryo with cardiac activity and CLOSED cervix

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51
Q

Complete abortion ?

Incomplete abortion ?

A

Complete passage of all products of conception

•Incomplete abortion - Occurs when some, but not all, of the products of conception have passed

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52
Q

Missed abortion= Embryonic demise

A

An embryo larger than 5 mm without cardiac activity
•Retained non-viable conception products up to 4 weeks
•Additional definitions

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53
Q

Septic abortion

A

Incomplete abortion associated with ascending infection of the endometrium, parametrium, adnexae, or peritoneum

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54
Q

Inevitable abortion

A

Bleeding in the presence of a dilated cervix; indicates that passage of the conceptus is unavoidable

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55
Q

Ectopic Pregnancy?

A

Pregnancy outside the uterine cavity (most commonly in the fallopian tube) but may occur in the broad ligament, ovary, cervix, or elsewhere in the abdomen with BLEEDING!!!!

56
Q

Ectopic Pregnancy dx?

A

=•Diagnostic tests for ectopic pregnancy
•Urine pregnancy test (doesn’t confirm IUP!)
•Ultrasonography - diagnostic test of choice
•Serum progesterone level - >25ng/ml can almost always exclude the presence of an extrauterine pregnancy
•B - hcg measurement - ectopic suspected if:
•Transabdominal ultrasonography does not show an intrauterine gestational sac and the patient’s beta-hCG level is greater than 6,500 mIU per mL (6,500 IU per L)
•OR if transvaginal ultrasonography does not show an intrauterine gestational sac and the patient’s beta-hCG level is 1,500 mIU per mL (1,500 IU per L) or greater

57
Q

Ectopic Pregnancy risk factors?

A

Current intrauterine device
•History of ectopic pregnancy
•History of in utero exposure to diethylstilbestrol
•History of genital infection, including PID, chlamydia, or gonorrhea
•History of tubal surgery, including tubal ligation or reanastomosis of the tubes after tubal ligation
•In vitro fertilization
•Infertility
•Smoking

58
Q

Ectopic Pregnancy Expectant Management

A

No evidence of tubal rupture
•Minimal pain or bleeding
•Patient reliable for follow-up
•Starting β-hCG level less than 1,000 mIU per mL (1,000 IU per L) and falling
•Ectopic or adnexal mass less than 3 cm or not detected
•No embryonic heartbeat

59
Q

Ectopic Pregnancy Medical Management

A

Stable vital signs and few symptoms

•No medical contraindication for methotrexate therapy (e.g., normal liver enzymes, CBC/platelet count)

60
Q

Medical Management with Methotrexate

A

Unruptured ectopic pregnancy
•Absence of embryonic cardiac activity
•Ectopic mass of 3.5 cm or less
•Starting β-hCG levels less than 5,000 mIU per mL (5,000 IU per L)

61
Q

Fetal demise. what is it?

A

The delivery of a fetus showing no signs of life as indicated by the absence of breathing, heartbeat, umbilical cord pulsation, or definite movements of voluntary muscles –
•Term stillbirth preferred among parent groups
Suggested requirement - fetal loss after 20 weeks gestational age (EGA), or of fetal weight of > 350 g
•Death occurring prior to 20 weeks gestation usually classified as a spontaneous abortion
(preferenceMom needs to lay down and fell 10 good movements and hr)

62
Q

Fetal demise dx?

A

Dx: •Reported decreased fetal movement
•Inability to obtain fetal heart tones not diagnostic
•Must be confirmed by ultrasonographic examination
•Diagnosed by visualization of fetal heart and absence of cardiac activity

63
Q

Fetal demise Risk Factors=Maternal causes

A
Obesity 
•BMI >30 - 5.5/1000 ; BMI >40 - 11/1000
•Independent risk factor after controlling for smoking, gestational diabetes and preeclampsia
•Smoking
•Drugs/ETOH
•Low educational attainment
•Diabetes
•Preconception care and optimal glycemic control can lower risk of perinatal death
•Hypertension - Chronic HTN and PIH
•Preeclampsia/Eclampsia
64
Q

Fetal demise, Fetal Causes

A

•Multiple gestations
•Twin - twin transfusion
•Intrauterine growth restrictions (uterine abnormalities)
•Congenital abnormality
•Abnormal karyotype in approximately 8-13% of fetal deaths
•Most common are monosomy X, trisomy 21, trisomy 18 and trisomy 13
•Infection
•e.g. parvovirus, cytomegalovirus, Listeria monocytogenes and syphillis
•Hydrops fetalis(severe edema)
immune or non-immune

65
Q

Fetal demise Management

A

Method and timing of delivery after fetal death depends on gestational age, maternal hx and maternal preference
•Timing not critical - most pts. desire prompt delivery
•Dilation and evacuation may be offered in 2nd trimester
•Experienced provider
•May limit efficacy of autopsy
•Labor induction
•Later gestational ages
•If D&E unavailable

66
Q

Placental Causes of fetal demise

A
Cord accident
•Dx should be made with caution
•cord abnormalities found in approx. 30% of normal births, and may be incidental
•should be evidence of obstruction or circulatory compromise and other causes excluded
•Abruption
•Premature rupture of membranes
•Vasa previa/velamentous insertion
•Fetomaternal hemorrhage
Placental insufficiency
67
Q

Pregnancy Induced Hypertension.

Def chronic, mild, severe

A
  • Chronic hypertension (HTN) defined hypertension present before 20th week of pregnancy or hypertension present before pregnancy
  • Mild hypertension – systolic of > 140-180 mmHg or diastolic > 90-100 mmHg or both
  • Severe hypertension - systolic of > 180 mmHg or diastolic > 100 mmHg
  • Major risk factor with chronic HTN is development of preeclampsia or eclampsia later in pregnancy
68
Q

Pregnancy Induced Hypertension Management

A

Management =(Don’t give Ace Inhibitors)•antihypertensive medications for women with chronic hypertension generally not given unless systolic pressure is 150 - 160 mm Hg or diastolic pressure 100 - 110 mm Hg
•purpose of medication is to reduce likelihood of maternal stroke
•methyldopa, combined alpha - and beta - blocker (i.e. labetalol) and calcium channel blockers (i.e. nifedipine)

69
Q

what is The biophysical profile (BPP) has 5 components?

A

: 4 ultrasound (US) assessments and a nonstress test(NST). The nonstress test (NST) evaluates fetal heart rate and response to fetal movement. The five discrete biophysical variables:

  1. Fetal movement
  2. Fetal tone
  3. Fetal breathing
  4. Amniotic fluid volume
  5. Fetal Heart Rate
70
Q

what is Preeclampsia

A

Development of hypertension with proteinuria and edema after 20 weeks gestation
•Blood pressure of > 140mm Hg systolic or > 90 mmHg diastolic (two occasions, >6hrs but 1+ protein on UA dipstick
Edema and hyperreflexia no longer diagnostic criteria

71
Q

Preeclampsia signs and sx’s

A

Signs/symptoms: visual disturbances, severe/persistant HA, RUQ pain, Hx of LOC/seizures, dizziness
•BP - Proper position important/cuff size
•BP tends to decline in 2nd trimester
•Weight - rapid weight gain (2 lbs/week)
•Edema - unresponsive to rest in supine position especially in upper extremities, sacral region and face
•DTRs - hyperreflexia or clonus at ankle worrisome

72
Q

Preeclampsia LABS

A

CBC, Platelet count, (PT,PTT) Liver func, serum creatinine, uric acid, 24hr urine, creatinine clearance, total urinary protein, ULS, BPP(look left)

73
Q

Preeclampsia patho

A

Pathophysiology =•Predominant pathophysiological finding is maternal vasospasm - several potential causes:

74
Q

Preeclampsia vascular changes, hemostatic changes

A

Vascular changes - theorized that a shallowly implanted placenta becomes hypoxic => upregulates placental inflammatory mediators => acts on vascular endothelium
–Hemostatic changes=•Increased platelet activation with increased consumption in microvasculature
•Endothelial fibronectin levels are increased and anti-thrombin III and a2 - antiplasmin levels are decreased (reflects endothelial damage)
Management =•2x weekly nonstress tests, biophysical profiles or both
•U/S q 3 weeks for fetal growth and amniotic fluid assessment
•Daily kick counts

75
Q

parameters for Severe Preeclampsia

A

Blood pressure of > 160mm Hg systolic or > 110 mmHg diastolic
•Marked proteinuria - > 5 g per 24-hour urine or 3+ on two dipstick of random urine samples collected at least 4 hours apart
•Oliguria - < 500 mL in 24 hours
Cerebral or visual disturbances (headache •and scotomata)
•Pulmonary edema or cyanosis
•Epigastric or RUQ pain
•Evidence of hepatic dysfunction
•Thrombocytopenia

76
Q

Severe Preeclampsia Management

A

=•Best managed in a tertiary - care setting
•Antihypertensive therapy if indicated
•If repeated systolic BP > 160 mmHg or diastolic > 105 - 110 mmHg
•Usually Hydralazine given in 5 - 10 mg increments until acceptable blood pressure response
•10 - 15 min response time is usual
Goal of therapy is to reduce diastolic pressure to 90 - 100 mmHg range
•Stabilization with magnesium sulfate
•Delivery by either induction or cesarean section

77
Q

whats Eclampsia

A

Presence of convulsions (grand mal seizures) in a woman with preeclampsia not explained by neurological disorder

Most cases occur within 24 hours of delivery but approximately 3% of cases diagnosed between 2 and 10 days postpartum
HELLP With or without proteinuria

78
Q

Eclampsia Management

A

Eclamptic seizure is life-threatening for both mother and fetus
•Tx directed to initiation of magnesium sulfate to prevent further seizures
•If pt already receiving magnesium sulfate, additional 2g can be given (slowly) and blood level obtained
•Foley catheter should be placed to monitor urinary output
•Central venous catheter or continuous EKG may be appropriate
•if BP to high, urinary output low, or evidence of cardiac disturbance

79
Q

whats Premature Rupture of Membranes

A

PROM is the rupture of chorioamniotic membranes before the onset of labor

  • Term PROM: PROM occurring > 37 weeks gestation
  • Preterm PROM (PPROM): PROM that occurs before 37 weeks gestation
80
Q

Premature Rupture of Membranes
Polyhydramnios?
Oligohydramnios?

A

Polyhydramnios AFI >20cm – assoc. with Down’s/Edwards, GDM,
Oligohydramnios AFI <5cm – urinary tract abnormalities (bilat. renal agenesis - Potter’s syndrome), maternal dehydration

81
Q

Premature Rupture of Membranes risk factors?

A
Risk Factors=Sexually transmitted diseases 
•women who smoke during pregnancy 
•prior PROM
•short cervical length 
•prior preterm delivery
•polyhydraminos
•multiple gestations
•bleeding in early pregnancy (threatened abortion)
82
Q

PROM Dx

A

Dx=•Fluid passing though the vagina must be presumed to be amniotic fluid UNTIL proven otherwise
•Pt will usually describe a “gush” of fluid or give history of steady leakage of small amounts of fluid
•Evaluation - don’t forget vitals, abdominal exam
•AVOID DIGITAL EXAMINATION - or at least keep to a minimum due to risk of infection
•Sterile Speculum examination
•obtain cervical or vaginal cultures for N. gonorrhoeae, B-hemolytic strep, chlamydia trachomatis
•cervix visualized for degree of dilation and free flowing amniotic fluid

83
Q

fern test

A

Fern test
•named for pattern of arborization occurs when amniotic fluid is placed on slide and allowed to dry in room air
•cervical mucus usually does not fern but when it does it is a thick pattern with less branching

84
Q

nitrazine test

A

Nitrazine test

•uses pH to distinguish amniotic fluid from urine & vaginal secretions

85
Q

PROM and ULS?

A

ULS=•Can be helpful in evaluating the possibility of rupture of membranes
•Looking for less than expected amount of fluid around fetus, then ddx of oligohydraminos is considered

86
Q

PROM Managment

A

Management - PROM =•Term PROM
•90% of pts will experience spontaneous labor within 24 hours
•Induction of labor at any time after PROM also considered appropriate
•oxytocin administration associated with decreased risk of chorioamnionitis and endometritis

87
Q

HELLP syndrome

A

no proteinuria, no HTN, appears as a viral sx’s, •nausea and vomiting, viral - like syndrome
•90 % of patients present with generalized malaise
65 % with epigastric pain, 30 % with nausea and vomiting, and 31 % with headache
•Hemolytic anemia
•Elevated Liver enzymes
Low Platelet count

88
Q

HELLP syndrome tx

A

Treatment – Prompt delivery of the baby!
•Magnesium sulfate - decrease risk of seizures
•Blood transfusions - anemia
•DIC - Fresh frozen plasma
•Antihypertensives (labetalol, hydralazine, nefedipine)

89
Q

PPROM

A

Latency period inversely related to gestational age

90
Q

Management – PPROM before 20 - 22 weeks

A

Risks of prematurity and infection
•Additional risks secondary to prolonged oligohydraminos:
•pulmonary hypoplasia
•skeletal malformations
•may be permanent deformities
•These pts should be counseled regarding impact of immediate delivery and potential risks and benefits of expectant management

91
Q

PPROM=•Less than 24 weeks

A

Patient counseling regarding outcomes
•Expectant management or induction of labor
•Group B strep prophylaxis not recommended

92
Q

Preterm (24 weeks to 31 completed weeks)

A

Expectant management
•Group B strep prophylaxis recommended
•Single - course corticosteroid use recommended

93
Q

Preterm (32 weeks to 33 completed weeks)

A

Expectant management, unless fetal pulmonary maturity is documented
•Group B strep prophylaxis recommended
•corticosteroids - no consensus, but some experts recommend
•antibiotics recommended to prolong latency, if no contradictions

94
Q

what is TORCH?

A
Toxoplasmosis
•“Other” 
–Syphilis
–HIV
–Hepatitis B 
–Rubella
•CMV 
•Herpes
95
Q

Toxoplasmosis screening?

A

Routine screening in pregnancy NOT recommended except in presence of maternal HIV infection
•Diagnosis depends on demonstration of seroconversion
•Positive IgG titer – indicates infection at some point and time
•Negative IgM – rules out recent infection
–Positive IgM may persist for long periods – not reliable is assessing duration of disease

96
Q

Toxoplasmosis other test?

A

Polymerase chain reaction on body fluids, including CSF, amniotic fluid, BAL fluid, and blood, may be useful in the diagnosis
•Skin tests that show delayed skin hypersensitivity to T gondii antigens may be useful as a screening test.
•Antibody levels in aqueous humor or CSF may reflect local antibody production and infection at these sites.
•Perform amniocentesis at 20-24 weeks’ gestation if congenital disease is suggested

97
Q

Toxoplasmosis during pregnancy

A

If mom acquires the infection in 1st trimester and goes untreated, risk of infection to the fetus approximately 14-17%, sequelae in infant is usually severe.
•If the mom infected in the 3rd trimester and goes untreated, risk of fetal infection approximately 59-65%, and involvement is mild or not apparent at birth.
Approximately 67% of patients have no signs or symptoms of infection

Intracranial calcifications develop in about 10%.
•Infected newborns have anemia, thrombocytopenia, and jaundice at birth.
•Microcephaly has been reported.
•Affected survivors may have mental retardation, seizures, visual defects, spasticity, or other severe neurologic sequelae.

98
Q

Toxoplasmosis tx?

A

Spiramycin (Rovamycine)
–DOC for maternal or fetal toxoplasmosis. Alternative therapy in other patient populations when unable to use pyrimethamine and sulfadiazine.
–Does not prevent sequelae in fetus if infection has occurred
–Only available through FDA
•If fetal infection has occurred, pyrimethamine and sulfadiazine therapy may decrease risk of congenital infection and severity of manifestations

99
Q

Syphilis and the fetus

A

Generally considered to cross placenta to fetus after 16 weeks gestation
•Trasmission can occur at any stage of maternal infection; documented as early as 6 weeks gestation
•Neonatal infection more likely in primary or secondary rather than latent syphilis
•Newborns with congenital syphilis may be asymptomatic or have classic signs of syndrome

100
Q

Syphilis and the fetus sx’s

A
Infants usually develop evidence of disease for 10 – 14 days after delivery
•Early evidence of disease include:
–Maculopapular rash
–“Snuffles”
–Mucous patches on the oropharynx
–Hepatosplenomegaly 
–Jaundice 
–Lymphadenopathy
Chorioretinitis 
Later signs include:
•Hutchinson’s teeth
•Mulberry molars
•Saddle nose
•Saber shins
101
Q

Syphilis labs?

A

All pregnant women should be screened serologically as early as possible and again at delivery
•Serologic testing is mainstay of diagnosis
•Nontreponemal testing
–VDRL (Venereal disease Research laboratory)
–RPR (Rapid Plasma Reagin)
–Both sometimes falsely positive
•Treponemal – specific tests
–FTA-ABS (flourescent treponemal antibody absorbed)
–TP-PA (T. pallidum particle agglutination)
–Positive treponemal test result indicates either active disease or previous exposure
–Regardless of treatment, test remains positive for life in most individual

102
Q

Syphilis tx?

A

No proven alternative therapies to penicillin for treating syphilis in pregnancy
•Patients with penicillin sensitivity require skin testing followed by de-sensitization for those with true allergy
•Jarisch – Herxheimer reaction occurs most often among patients with early syphilis
–In pregnancy, this reaction may precipitate preterm labor or cause fetal distress; recommend close observation

103
Q

Syphilis tx monitoring what?

A

Post treatment titers (RPR or VDRL) should be followed for at least one year
•Adequate treatement = 4 fold decrease in titers by six months
•Fourfold increase or persistent or recurrent signs or symptoms may indicate inadequate treatment or reinfection

104
Q

Hepatitis B clinical pres?

A

HBV transmitted by parenteral route and through sexual contact
•most asymtomatic
–may develop jaundice, joint pain, fatigue, nausea, decrease in appetite

105
Q

Hepatitis B testing?

A

Testing for hepatitis B surface antigen (HBsAg) during pregnancy is routine

106
Q

Hepatitis B and the fetus?

A

Vertical transmission is related to presence of absence of maternal HBeAg
–if patient positive for “e” antigen - indicated high viral load and active viral replication
–fetus has 70% to 90% risk of becoming infected and most of those will become chronic carriers

107
Q

Hepatitis B tx?

A

Treatment
–Treated as soon as possible with hepatitis B immune globulin (HBIG) and begin vaccination against Hepatitis B
•initial injection given between 2 days and 2 months of delivery
–Infants of mothers who are HBsAg positive should receive vaccine and HBIG within 12 hours of birth
–Breastfeeding is not contraindicated in women who are chronic carriers if infant has received both vaccination and HBIG withing 12 hours of delivery

108
Q

Rubella is the biggest risk when?

A

Risk of congenital disease related to gestational age at time of infection
–highest in first month of pregnancy decreases with increasing gestational age
–Defects rare when infection occurs after 20th week of gestation

109
Q

Rubella fetal presentation

A
Birth - 50-70% normal
–In Utero 
•SAB / Stillborn 
•Microcephaly 
•IUGR
–Congenital 
•Deafness 
•Cataracts/Glaucoma 
•Neurologic: Meningoencephalitis / MR 
•Cardiac: PDA /PA stenosis
–Early Childhood 
•Radiolucent bone disease 
•Blueberry muffin rash
•Thrombocytopenia/HSM 
–Late Childhood
•Thyroid abnormalities    
•Panencephalitis		     
•Pnuemonitis/DM
(Hemorrhagic lesions of the skin = blueberry muffin rash
Cataracts acquired in the 3rd month of pregnancy)
110
Q

Rubella screening and testing

A

Serologic testing for IgM and IgG antibodies for Primary infection
Prenatal screening for IgG rubella antibodies is routine
•Vaccination postpartum at time of hospital discharge is recommended
•Breastfeeding NOT contraindicated
•If rubella diagnosed during pregnancy, patient should be advised of risk of fetal infection and counseled regarding option for continuing pregnancy
•Immune globulin may be given to an infected woman but does not prevent fetal infection

111
Q

HSV (1 and 2)

Primary out break?

A
HSV - 1 (herpes labialis, gingivostomatitis and keratoconjucnctivitis) 
•HSV- 2 (genital)
•Primary=this is the 1st ever out break
–no evidence of prior HSV infection
–poses greatest risk to fetus
112
Q

HSV= how is fetus affected?

A

Fetus/neonate infected from ascending infection secondary to spontaneous rupture of membranes or passage through infected lower genital tract
•Primary infection at time delivery
–risk of neonatal infection approx 50%

113
Q

HSV= how the baby is affected with localized HSV infection compared to a disseminated infection?

A

Infants with localized herpes usually do well, those with disseminated disease do very poorly

114
Q

HSV= Congenital HSV infection presentation

A

microcephaly,
–hydrocephalus,
–chorioretinitis
–vesicular skin lesions.
–Three subtypes acquired infection have been identified:
1.Disease localized to the skin, eye or mouth;
•Virutally no mortality
2.Encephalitis, with or without skin, eye or mouth involvement
•Mortality approx 15%
3.Disseminated infection that involves multiple sites, including the central nervous system, lung, liver, adrenals, skin, eye or mouth
•Mortality approx 57% even with antiviral therapy
–Long-term morbidity is common in infants who survive with encephalitis or disseminated disease, and may include seizures, psychomotor retardation, spasticity, blindness or learning disabilities

115
Q

HSV testing

A

Clinical examination
–Confirmation with viral culture
–PCR testing (more sensitive than culture)
–Serologic testing for HSV-1 and HSV-2 immunoglobulin, type specific
(•Routine screening for HSV NOT currently recommended)

116
Q

HSV management

A

Management
–Acyclovir safe in pregnancy
–IV acyclovir indicated for severe maternal infection (i.e. encephalitis, pneumonitis, hepatitis)
–Cesarean section recommended if herpes lesions are identified

117
Q

HIV=does it affect pregnancy outcome

A

HIV infection does not seem to have direct affect on pregnancy course or outcome and pregnancy does not seem to affect course of HIV

118
Q

HIV= when does transmission occur

A

Transmission can occur antepartum, intrapartum or postpartum with breastfeeding
•66-75% occur during or close to intrapartum period

Breastfeeding avoided
•estimated to have accounted for up to 50% of newly infected children worldwide

119
Q

HIV SCREENING AND TESTING

A

–Initial screening with enzyme-linked immunosorbent assay (ELISA)
•99% of cases antibodies become detectable by 3 months after infection
–If ELISA positive confirm with a Western blot test
–3rd trimester repeat screening recommended for at-risk populations

120
Q

HIV management

A

Management
–antiretroviral therapy

Breastfeeding avoided
•estimated to have accounted for up to 50% of newly infected children worldwide

121
Q

CMV: transmitted how?

A

Most common congenital viral infection
•Transmitted in saliva, semen, cervical secretions, breast milk, blood or urine
•May cause short febrile illness, usually asymptomatic

122
Q

CMV: presentation

A
May present with: 
–petechiae 
–hepatosplenomegaly
–jaundice 
–thrombocytopenia 
–microcephaly
–Chorioretinitis
–nonimmune hydrops fetalis
•Long term sequelae - severe neurologic impairment and hearing loss
123
Q

CMV:screened?

A

Routine screening NOT recommended

124
Q

Varicella-Zoster virus screening?

A

Routine screening

125
Q

Varicella-Zoster virus during pregnancy?

A

If chickenpox diagnosed during pregnancy, antiviral therapy should be considered
–not shown to decrease the rate or severity of fetal infection
–Fetal infection during first half of pregnancy may result in varicella embryopathy
–Limb atrophy
–Scarring of skin on extremities
–Central nervous system involvement
–Ocular manifestations
Any infants with this type of exposure should receive VariZIG

126
Q

Group B strep sx’s of fetus

A
Clinical Manifestations in Newborn
–Early – onset infection 
The most common cause of neonatal sepsis
Babies have respiratory symptoms that resemble in RDS
•First week of life
•Respiratory distress
•Septicemia or Septic shock
•Pneumonia
•Meningitis 
(May be associated with still birth)
127
Q

Group B strep screening?

A

Universal screening for GBS between 35-37 weeks

128
Q

Group B strep with pregnant women

A

All women who are GBs positive by rectovaginal culture should receive antiobiotic prophylaxis in labor or with rupture of membranes

129
Q

Bact Vaginosis presentation and tx in pregnant?

A
Presentation
–c/o ‘fishy” odor , most pronounced after intercourse
–Gray-white or yellow discharge
–Mild vulvar irritation 
-clue cells

Treatment
–Oral or topical metronidazole
–Oral or topical clindamycin
–Neither drug shown to have teratogenic effects

130
Q

Candidiasis presentation and tx in pregnancy

A

Presentation
–Itching most common complaint – up to 20% asymptomatic
–Burning, external dysuria and dyspareunia common
–Vulva and vaginal tissue – bright red in color
cottage cheese” discharge, odorless

Treatment
–Topical application synthetic imidazoles
•Miconazole, clotrimazole, butoconazole, or terconazole
•Pregnant women should be treated with topical agents due to risk of birth defects associated with high doses of fluconazole

131
Q

Trichomonas presentation and tx in pregnancy

A
Presentation
–Vulvar itching or burnging
–Copious discharge with rancid odor - “frothy”, thin and yellow-green to gray color
–Dysuria 
–Dyspareunia
–Edema or erythema of vulva
–Petechiae or “strawberry patches” upper vagina or cervix 
Treatment 
–Oral metronidazole or tinidazole
132
Q

• Discuss intrapartum fetal monitoring, including meconium staining,

A

Amniotic fluid =•Check color, odor, presence of blood
–Term or postterm fetus are developmentally able to move their bowels and may do so spontaneously causing meconium stained fluid
–Stressed/hypoxic baby will also pass meconium
•If light meconium, expectant management
•Thick or dark meconium requires peds notification

133
Q

• Discuss intrapartum fetal monitoring, including including fetal heart rate monitoring

A

Electronic Fetal Monitoring (EFM)
Fetal monitor noted q 15-30 min in active labor, q 5-10 second stage
•Monitors fetal well being, tolerance of labor, occurrence of uterine contractions
-•Accels - a reassuring indicator of fetal well-being
-•Decels - periodic FHR changes associated with UCs

134
Q

• Understand the indications for biometric evaluation of fetal well-being, and discuss the implications of an abnormal nonstress test

A

Nonstress test (NST)
–Most commonly used 3rd tri measure of fetal well being
•Reactive meets or exceeds criteria
•Nonreactive is nonreassuring finding

135
Q

• Discuss intrapartum fetal monitoring, including contraction stress test

A

Contraction stress test (CST)
–Most accurate predictor of uteroplacental insufficiency
–More expensive, takes more time, high false positives
–Can be used from 26 wks on
–Used to f/u nonreactive NST
–Can cause labor
•Uses oxytocin (pitocin) or nipple stimulation to create uterine contractions
•Criteria: 3 UCs/10 min, felt or not
•Negative (good): FHR stable, no late decels
•Positive (bad): repetitive late decels with each UC

136
Q

• • Discuss isoimmunization in the maternal-fetal circulation and postpartum period

A

Rh Isoimmunization
•Red cells of the fetus or newborn are destroyed by maternally-derived alloantibodies
•Complications
–Alloimmune hemolytic disease of the newborn (HDN)
–aka erythroblastis fetalis (when it is of the fetus)
–Subsequent anemia and risk for neuro defects, heart failure, edema and ascites