Abnormal OB

7/27/2019 Abnormal OB

http://slidepdf.com/reader/full/abnormal-ob 1/34

1.Cord prolapse: Management: With fetal bradycardia, do digital examination of the vaginato assess for umbilical cord; proceed to immediate C/S.

Improve maternal oxygenation: Patient should enter Trendelenburg position and physiciankeeps hand in the vagina to elevate the presenting part to keep pressure off the cord. Moveuterus off of the great vessels (place pt on her side), IV fluid bolus, 100% O2 by face mask,stopping oxytocin if it is given.

2.Cord prolapse: Presentation: During labor, fetal bradycardia, artificial rupture of membranes, fetal head is unengaged (prolapse more likely). Fetal bradycardia associatedwith misoprostol (more so than other prostaglandin agents) cervical ripening is typicallyassociated w/ uterine hyperstimulation (>5 ctx's in a 10 min window).

3.Ectopic pregnancy: Diagnosis: hCG level (if >1500 mIU/mL, pregnancy should be present),transvaginal U/S (assess presence of IUP). Presence of free fluid in the peritoneal cavity or acomplex adnexal mass would make extrauterine pregnancy more likely. Progesterone level>25 ng/mL almost always correlates with normal IUP.

4.Ectopic pregnancy: Presentation: [Triad] Amenorrhea, vaginal spotting, abdominal pain.PE may be normal. Majority occur (97%) in the fallopian tube. 2% of pregnancies areextrauterine. If ectopic ruptures, pain becomes acutely worse, may lead to syncope,

shoulder pain (blood irritating the diaphragm). Hypotension, tachycardia. Uterus may benormal or enlarged. Chance of coexisting intrauterine/extra pregnancies are low (1 in10,000).

5.Ectopic pregnancy: Risk factors: Salpingitis

Tubal adhesive disease

Infertility

Progesterone-secreting IUD

Tubal surgery

Prior ectopic pregnancy

Ovulation induction

Congenital abnormalities of the tube

6.Ectopic pregnancy: Treatment: Salpingectomy: For gestations too large, when roccurred, or future fertility not wanted.

Methotrexate: If ectopic is <4 cm in diameter.

7.HSV complications: Neonatal infection (encephalitis, CNS compromise, eyes, skiexposure occurs through contact in the genital tract

8.HSV DDx:Chancroid (H ducreyi): painful genital lesions, bartholin glands may enlpainless abcesses.

Syphilis (1st stage): Small, round, painless chancre in the area of the body exposed tospirochete.

9.HSV in labor: Sx: Vesicles (cervix, vagina, vulva), tingling itching burning (esp in

region).

10.HSV treatment: Acyclovir (or valacyclovir, famciclovir), C/S. If no signs or sx ogenital tract, can opt for vaginal delivery.

11. Placenta Abruption: Complications: Coagulopathy (can cause fetal demise) is to hypofibrinogenemia, and clinically evident bleeding is usually not encountered unfibrinogen level is below 100 to 150 mg/dL

12.Placenta Abruption: Diagnosis: Clinical picture (see ddx, also preterm labor, stand/or fetal heart rate abnormalities); U/S is not helpful (freshly developed blood clobehind the placenta has the same sonographic texture as the placenta itself). Also lookserial hemoglobin levels, follow the fundal height and assessment of the fetal heart rapattern.



13.Placenta Abruption: Risk factors: HTN, cocaine abuse, short umbilical cord, trauma,uteroplacental insufficiency, submucous leiomyomata, sudden uterine decompression(hydramnios), cigarette smoking, PPROM

14.Placenta accreta: Definition: Placenta is very adherent to the uterus. Histology showsdefect of the decidua basalis layer. No cleavage plane is found on attempt to manuallyremove. Antepartum bleeding may occur.

15.Placenta Accreta: Risk factors: Previous uterine incisions (disturbed endometrium layer).Low-lying placentation or placenta previa, prior C/S or uterine curretage or priormyomectomy. Fetal down syndrome.

16.Placenta Accreta: Treatment: Tx with hysterectomy (attempt to remove placenta maylead to hemorrhage). If childbearing is still strongly desired, may consider methotrexate (riskcoagulopathy, infection).

17.Placenta Increta: Definition: Placenta penetrates into the myometrium

18.Placenta percreta: Definition: Placenta penetrates entirely through the myometrium tothe serosa, often invades the bladder.

19.Placenta Previa: DDx: Placenta abruption: (premature separation of the placenta) usuallyis associated with painful uterine contractions or excess uterine tone

20.Placenta Previa: Definition: Placenta overlying the internal os of the cervix

Low-lying placenta: The edge of the placenta is within 2 to 3 cm of the internal cervical os(low lying or marginal usually resolve if found mid second trimester).

Vasa previa: Umbilical cord vessels that insert into the membranes with the vesselsoverlying the internal cervical os, thus being vulnerable to fetal exsanguination uponrupture of membranes.

21.Placenta Previa: Diagnosis: Ultrasound examination is performed before a vagiexamination because vaginal manipulation (even a speculum examination) may inducbleeding.

22.Placenta Previa: Presentation: Painless bleeding (esp postcoital), usually aftersecond trimester.

23.Placenta Previa: Risk factors: Grand multiparity, prior C/S, prior uterine curettaprevious placenta previa, multiple gestation.

24.Placenta Previa: Treatment: Expectant management, delivery by C/S.

25.Preeclampsia: Complications: Placenta abruption, eclampsia (w/ possible i ntrahemorrhage), coagulopathies, renal failure, hepatic subcapsular hematoma, hepaticrupture, uteroplacental insufficiency

26.Preeclampsia: Definition/presentation: HTN (>140/90, two elevated BPs meapart) with proteinuria (>300 mg over 24 hr) at gestational age >20 wks, caused byvasospasm. Nondependent edema is usually present (hand and face)

Severe: BP >160/110, 24 hr urine >5g protein (or +3 o r +4 dipstick). Maternal end orthreatened, may have vision changes (scotoma), RUQ pain, headache, SOB (pulmonaedema). Must deliver

Superimposed: Development of preeclampsia in a patient with CHTN.

27.Preeclampsia: Risk Factors: Nulliparity, chronic HTN (prior to 20 wks or persispostpartum), extremes of age, AA race, personal or family hx, chronic renal disease,antiphospholipid syndrome, diabetes, multifetal gestation.

28.Preeclampsia: Systemic: See chart



29.Preeclampsia: Treatment: Delivery (when term, or immediate if severe), magnesiumsulfate (anticonsulant, renally excreted, SE pulonary edema and hyporeflexia). Follow up in 1to 2 weeks to check BP, proteinuria.

30.Preterm Labor: Definition: Single exam of 2 cm dilation and 80% effacement in anulliparous woman. Cervical change in the midst of regular uterine contractions occuringbetween 20 to 37 weeks.

Prior to exam, swab posterior vaginal fornix for fetal fibronectin (ffn) which if + may indicaterisk for preterm birth. If negative, strongly asociated with no delivery within 1 week.

Transvaginal U/S showing shortened cervix, low uterine segment changes inc risk

31.Preterm labor: Risk factors: PPROM

Multiple gestations

Previous preterm labor or birth

HydramniosUterine anomaly

Hx of cervical cone biopsy

Cocaine abuse

AA race

Abdominal trauma

Pyelonephritis

Abdominal surgery in pregnancy

32.Preterm Labor: Treatment: Tocolysis (CI is intra-amniotic infx or severe preecplacental abruption), IM antenatal steroids (if <34 weeks), IV abx to reduce risk of Gin neonate.

Tocolytics (delay delivery for preterm labor) See chart for drugs.

33.Preterm Labor: Work up: Hx to assess for risk factors, speculum exam to assesruptured membranes, serial digital cervical exams, CBC, urine drug screen, U/A, gon(strongest assoc to preterm labor), vaginal culture GBS, U/S (fetal weight and presen

34.Pulmonary Embolus: Diagnosis: Spiral CT or MRA. Presumptive dx based on presentation, hypoxemia, clear CXR. May need to look at protein S and C, antithromFVLeiden mutation, hyperhomocysteinemia, antiphospholipid syndrome. Also see ch

35.Pulmonary Embolus: Presentation: Severe dyspnea (MC), pleuritic chest paintachycardia and tachypnea, hypoxia. No cough or fever. Pregnancy predisposes due tohypercoagulable state and venous obstruction (mechanical effect of the uterus on the cava).

36.Pulmonary Embolus: Treatment: IV anticoag for 5 to 7 days. Then maintain aPto 2.5 times control for at least 3 months. After, heparin for prophylaxis. Early ambul

after delivery.

37.Sheehan syndrome: DDx: Asherman syndrome: Intrauterine adhesions caused bcurettage which damages the decidua basalis layer, rendering the endometriumunresponsive (amenorrhea). Need to determine whether the anterior pituitary isfunctioning and whether the uterus is responsive to hormonal therapy. Definitive dx ihysterosalpingogram.

MCC of amenorrhea during reproductive years: Pregnancy

PCOS: Chronic anovulation, hyperandrogenism, small ovarian cysts on U/S, unoppoestrogen and estrogen excess. Inc endometrial hyperplasia and risk for cancer.



38.Sheehan Syndrome: Definition: Anterior pituitary hemorrhagic necrosis caused byhypertrophy of the prolactin-secreting cells i n conjunction with a hypotensive episode,usually in the setting of postpartum hemorrhage. The bleeding induces pressure necrosis.Leads to amenorrhea.

Postpartum hemorrhage: Bleeding >500 ml for vaginal, >1000 ml for C/S.

39.Sheehan syndrome: Diagnostic: For pituitary function: No lactation after delivery, lowthyroid hormone levels, FSH, LH, cortisol levels. Also see chart.

40.Shoulder dystocia: Presentation: External rotation of fetal head is difficult, fetal headretracted back towards mother's introitus (turtle sign). May lead to Erb's palsy (brachialplexus injury)

41.Shoulder dystocia: Risk factors: Multiparous, obesity, GDM, post-term (macrosomnia incrisk). Prolonged 2nd stage is a nonspecific indicator.

42.Shoulder dystocia: Treatment: McRoberts: The maternal thighs are s harply flexedagainst the maternal abdomen to straighten the sacrum relative to the lumbar spine and

rotate the symphysis pubis anteriorly toward the maternal head.

Suprapubic Pressure: push on the suprapubic region in a downward or lateral direction in aneffort to push the fetal shoulder into an oblique plane and from behind the symphysis pubis.

Wood's corkscrew (progressively rotating the posterior shoulder in 180° in a corkscrewfashion),

Delivery of the posterior arm

Zavanelli maneuver (cephalic replacement with immediate cesarean section)

**Do not apply fundal pressure! (risk of fetal injury)

43.Spontaneous abortion: Cl assifications: See chart

44.Spontaneous abortion: Presentation: Intense cramping, some bleeding. Sx respassage of tissue through vagina, closed cervical os. Confirm with quantitative HCG,decrease.

45.Spontaneous abortions: DDx: Molar pregnancy: Trophoblastic tissue w/o fetusspotting, absence of fetal heart tones, size greater than dates, markedly elevated HCGlevels, snowstorm ultrasound. Tx w/ D&C

Incompetent cervix: Painless dilation. Tx w/ cervical cerclage (surgical ligature).

46.Threatened abortion: HCG: Will have a logarithmic increase during early pregnlevel is between 1500 to 2000, fetus can be seen on vaginal ultrasound. HCG should rat least 66% over 48 hours.

47.Threatened abortion: Presentation: Vaginal spotting, abdominal pain (considpregnancy). Hypotensive and tachycardic suggests ruptured ectopic.

48.Threatened abortion: Treatment: For asymptomatic, small (<3.5 cm) ectopic umethotrexate.

Nonviable IUP: D&C or vaginal misoprostol.

49.Threatened abortoin: Diagnosis: HCG level is above U/S threshold and there isonographic evidence of IUP, then risk of ectopic is high (85%).

Spontaneous abortion vs ectopic pregnancy: Uterine curettage will show histologicconfirmation of chorionic villi (miscarriage) or no villi (ectopic)

Pregnancy Induced Hypertension

Study online at quizlet.com/_e8l87

1.Are diuretics used for women with pre-eclampsia?: Yes



2.How would you palpate the uterus to see if the eclamptic woman was havingcontractions?: Place the hand flat on the abdomen over the fundus with the fingers apartand press lightly

3.If pre-eclampsia is mild will the woman be hospitalized?: No, just rest at home

4.In eclamptic client what ominous sign almost always proceeds a seizure?: Severeepigastric pain

5.Multi or prima gravida clients are most likely to get PIH?: Primagravida

6.Name 5 thigns included in seizure precautions?: Suction machine in room, 02 in room,padded railes up x4, must stay on unit, ambulation with supervision only, no more than 1pillow

7.Name the three symptoms of PIH?: Hypertension, weight gain; edema, proteinuria

8.Pre-eclampsia makes the neuromuscular system more or less irritable?: More

9.The urine output of the eclamptic will decrease or increase?: Decrease

10.What age groups are most likely to experience PIH?: Patients under 18 or over 35

11. What are the three major treatment objectives in eclampsia?: Decrease blood pressure,control convulsions, diuresis

12.What is the activity order for a woman with severe pre-eclampsia: Bed rest

13.What is the best position for the client with severe pre-eclampsia?: Left side lying

14.What is the dietary order for the woman with severe pre-eclampsia?: Low salt, highprotein

15.What measurement must the woman pre-eclampsia make every day?: She must weighherself

16.What type of diet is i ndicated for a woman with pre-eclampsia?: Increasednormal salt intake; typically, no restriction

17.What type of precautions will be in effect for a woman with severe pre-eclampsia?: Seizure precautions

18.What vision problem do women with pre-eclampsia have?: Blurred vision

19.When a woman is hospitalized for severe pre-eclampsia the nurse should test the:reflexes, then the urine for protein

20.When does pre-eclampsia usually begin in pregnancy?: After 20 weeks

21.When is pre-eclampsia called eclampsia?: Once convulsions have occurred

22.When pre-eclampsia gets worse the deep tendon reflexes will be hypo or hyperreflexive?: Hyper-reflexia

Gestational DM

.4 cardinal signs of diabetes mellitus: -polyuria- when water is not reabsorbed bytubules because of the osmotic activity of glucose.

-polydipsia- dehydration from polyuria

=polyphagia- caused by tissue loss and a state of starvation from the inability of the cuse blood glucose.

-weight loss-use of fat and muscle tissue for energy.

2.ABO INCOMPATIBILITY:o Commonly affects type A or B fetus of O mom

o Maternal serum antibodies present in serum

o Hemolysis of fetal RBC's



• No antepartal treatment required

• Assess newborn for hyperbilirubinemia- 24 hrs

• O babies never affected because of moms type, because they have no antigenic sites onthe RBCs

3.Abruptio Placentae: -the premature separation of a normally implanted placenta from theuterine wall.

- sudden onset of pain with darker blood, hard board abdomen, increase in size of abdomen,uterine quivering, might not have bleeding

-cause unknown, but more frequent in pregnancies complicated by smoking, prematureROM, multiple gestation,\

advanced maternal age, cocaine use, chrioamnionits and HTN.

4.Abruptio Placentae-Fetal/Neonatal Risks: the worse the separation the higher the rate of mortality, fetal outcome depends on maturity,PTL, anemia, hypoxia-> brain damage or fetaldemise.

5.Abruptio Placentae-Maternal Risks: hemorrhage, hemorrhagic shock, renal failure.

6.Abruptio P lacentae-Nursing: coagulation tests of platelets and fibrinogen (for DIC theseare usually decreased), PT and PTT are normal or prolonged , maintain cardiovascular statusof mom and baby, IV 16-18 g LR, EFM, C-section usually s afest option, type and cross-mathch blood for transfusions (at least 3 units).

7.Abruptio P lacentae-Types: -marginal: part of the placenta becomes dislodged.

-central: detatches in the middle, destructs uterine muscle, frequently necessitateshysterectomy due to

hemorrhage, OB EMERGENCY

-Complete: total separation, massive vaginal bleeding. Triggers development of DIC.

8.Alcohol: crosses the placenta, excreted in breastmilk and may inhibit letdown refleintake is safe.

-Maternal effects: withdrawl seizures (12-48 hrs after cessation), malnutrition (folic athiamine deficiency), bone marrow suppression, increased incidence of infection, livedisease.

-Fetal effects: birth defects can occur in the first 3-8 wks of development. withdrawlsyndrome, and fetal alcohol s yndrome (physical & mental abnormalities).

-Nursing considerations: social service consult, seizure precautions, IV fluid therapyhydration, prepare for an addicted newborn.

9.Amniocentesis: A procedure used for genetic diagnosis. A sterile needle (under uguidance) is inserted into the uterine cavity through the maternal abdomen so a smallamount of amniotic fluid can be removed, and genetic testing is performed.

10.Amniocentesis -Procedure: woman should be placed in a left lateral tilt positioplacing a wedge under her right hip to prevent hypotension during the procedure. Th

abdomen is scanned by ultrasound to locate the placenta, the fetus, and an adequatepocket of fluid. The needle insertion site is of the utmost importance because the fetuplacenta, umbilical cord, bladder, and uterine arteries must all be avoided. The imporof locating the placental cannot be stressed enough, especially in cases of Rhisoimmunization, in which trauma to the placenta increases fetal-maternal transfusionworsens the isoimmunization.

*Rh-negative women are given Rh immune globulin after amniocentesis. Provided thare not already sensitized.

11. Amniocentesis-risks/SE: minor complications are infrequent and may include trvaginal spotting, cramping, or amniotic fluid leakage in 1% to 2% of cases performe



12.ANTEPARTAL CLINICAL THERAPY- Mild preeclampsia: • Home care- BP < equal to150/100, proteinuria < 1 g?24hrs or 3+ dipstick, platelet count greater than 120,000, andnormal fetal growth, must be able to recognize s/s of worsening preeclampsia, mustaccurately count fetal movements, and know when to call Dr.. she's not restricted to bedrest, but encouraged to rest frequently especially in L lateral position. Monitor her own BP,weight, and urine protein daily. Weight gain of 3lbs in 24 hrs or 4 lbs in a 3 day period arecauses of concern. NST daily to biweekly.

• Hospital care- on bed rest, in L lateral position. Na intake <6g/day. Fetal well being by:NST, fetal kick count, ultrasound, biophysical profile, amniocentesis, Doppler... Mom well-being: BP 4xdaily, daily weight gain, daily urine dipstick, periodic assessment of Labs

13.ANTEPARTAL CLINICAL THERAPY-Eclampsia:• Signs & symptoms- scotomata (dark spotsor flashing lights), blurred vision, epigastric pain, vomiting, persistent headache, neurogenichyperactivity, pulmonary edema and cyanosis

• DURING SEIZURE- assess time of onset, progress of seizure, body involvement, duration,incontinence, fetus status, and signs of placental abruption. Airway maintained, administerO2, positioned on her side, suction to keep airway clear, side r ails up

• Management- Mg SO bolus of 6g IV over 20-30 minutes followed by 2-3g/hr IV infusion. If 2nd seizure administer 2g of Mg SO IV over 5-10 min. if convulsions continue, sodiumamobarbitol IV. Antihypertensive- hydralazine hydrochloride Q15min to a max of 20mg IVbolus, then 20-80mg Q10min until 300mg. ausculate lung sounds for pulmonary edema.Furosemide (Lasix) may be given in low doses

• Mg SO s/e loading dose: flushing, a f eeling of warmth, headache, nystagmus, nausea, drymouth, and dizziness. Fetal s/e: hypotonia, lethargy for 1-2 days, hypoglycemia, andhypokalemia.

14.ANTEPARTAL CLINICAL THERAPY-Severe preeclampsia: NPO because she can aspirateher food, there is a genetic link. Bed rest, diet ( high protein, moderate Na),

• IV Fluids & electrolytes- goal is to achieve a balance between correcting hypovolempreventing circulatory overload. May be started to KVO in case drug therapy needed.

• Anticonvulsants-Mg SO

• Corticosteroids- betamethasone or dexamethasone to promote fetal lung maturation

• Antihypertensives- major indication is prevention of stroke, given for 160/110 or >diastolic btwn 90-100. Labetolol (avoided in women wasthma or CHF) and hydralazinifedipine IV acts fast and fewer s/e, sodium nitroprusside fo r acute emergency.

15.Assessment tip for substance abuse and t herapy: -screen all pregnant pts

-if suspected, start with less threatening direct questions, then build up to most threatndrugs.

-the more nonjudgemental and matter-of-fact the nurse is, the more likely the pt willanswer honestly.

-cold turkey is not adviseable

-urine screen done regularly

-screening strategies should include maternal informed consent.

follow up!!

16.Battery During Pregnancy: o Results in psychologic distress, loss of pregnancylabor, LBW infant, maternal/fetal injury/ fetal death

o Indications- chronic psychosomatic symptoms, nonspecific/ vague complaints, assescars, bruises, dec ey contact, silence when partner is in r oom, and hx of nervousnessinsomnia, drug overdose, or alcohol problems.

o Complications- poor maternal weight gain, infection, anemia, and 2nd and 3rd trim

bleeding.



o Woman who are battered may experience more sex abuse and inc risk for STD.

o Treatment goals

• Identify a problem and help mom come up w a safety plan

• Increase decision making abilities to dec the potential for further abuse

• Provide safe environment

17.Biophysical profile: (3rd trimester)

-Includes the assessment of 5 fetal biophysical variables:

FHR acceleration

Fetal breathing

Fetal movements

Fetal tone

Amniotic fluid volume

-FHR acceleration is assessed with the NST. The other variables are assessed by ultrasoundscanning.

18.Bleeding During Pregnancy: o Major causes of bleeding

o First and second trimesters

• Abortion- pregnancy termination prior to 20wks gestation, natural/ induced,medical/surgical interruption.

• spontaneous abortion - miscarriage

• Ectopic pregnancy

• Gestational trophoblastic disease

o Third trimester

• Placenta previa- type and hold for blood, fluids, NPO anticipate for C section, ultraand nonreassuring FHR

• Abruptio placentae- painful, hard abdomen, may/may not have bl eeding, immediateof fetal distress, tender, darker

19.Bleeding During Pregnancy: Nursing: o Regardless of cause of bleeding (such exercise as a result of trauma to the highly vascular cervix, cervical/vaginal lesions,implantation of the pregnancy, or impending miscarriage).

o NO VAGINAL EXAMS

o Monitor signs of shock & vital signs- pallor, clammy skin, perspiration, dyspnea, orestlessness

o Administer oxygen if needed

o Count & weigh pads

o Save tissue/clots expelled

o If beyond 12 weeks, assess FHTs w doppler

o Initiate IVF

o Prepare supplies for exam: speculum

o Type & cross match if significant bl eeding



o Assess coping mechanisms, support systems & family's response. Most important preparemom for fetal loss

20.BPP: indications & uses: -BPP helps to identify the compromised fetus and confirm thehealthy fetus.

-Indications for the BPP include those situations in which the NST and CST would be done.

-Most useful in the evaluation of women who experience decreased fetal movement(nonreactive NST) and in the management of IUGR, preterm labor, gestational diabetes,postterm pregnancies, and PROM.

21.Cardiac Disease and Pregnancy: -The higher the class, the more the risk of complications.

-As pregnancy progresses it is important to minimize workload and promote tissueprofussion.

-spontaenous natura labor with adequate pain relief in recomended for patients in class 1 &2. Class 3 & 4 may need to be hospitalized before the onset of labor for cardiovasculatstabilization. Vaginal birth with low dose regional epidural with the use of forceps o r

vacuum if necessary to limit maternal pushing.22.Cardiac Disease and Pregnancy- Nursing: -Monitor vital signs (danger signs: HR >100, RR> 24 indicate cardiac decompensation, especially if accompanied with dyspnea and rales.

Auscultate lungs, Maintain semi-Fowler's position with lateral tilt or side-lying withhead/shoulders elevated (place women left side, oxygen, fluid bolus)Apply oxygen &medications as indicated, Keep patient/family informed of labor progress ContinuousEFM,Push with open glottis, Major concern is physical adaptation to increased cardiacoutput & blood volume, Monitor vital signs & signs of cardiac decompensation, Monitor forsigns of postpartum complications, Maintain position, Administer stool softeners,Promoteattachment,

Breastfeeding unless contraindicated by medication therapy, Contraceptive counseling.

23.Cardiac Disease and P regnancy-Assess...: stress of pregnancy on functional caheart, Identify infection, anemia, anxiety, lack of support systems, and household/cardemands, Frequent visits,Recognize potential complications.

24.Cardiac Disease and P regnancy-Patient teaching:: Diet: high iron, protein annutrients, but low sodium. Activity & rest: resistrict activity to preserve cardiac functsleep 8-10 hrs and rest periods throughout the day. During firs t half of pregnancy woseen biweekly, then weekly in the second half. Visits are most important during 28-30as blood volume peaks.

-Recognize and reduce amount of physical exertion & fatigue

25.Cervical Insufficency-Contributory factors: -congenital: may be found in womto DES (diethystilbesterol) or with a bicornuate uterus.

-aquired: related to inflammation, infection, s ubclinical uterine activity,cervical traumcone biopsy, late Second trimester elective abortions, or increased volume (twins).

-environmental (hormonal): relaxin may be an endocrine cause of C.I.

26.Cervical Insufficency-Nursing: -transvaginal US between 16-24wks "funneling"

effacement.-warning signs of impending birth: lower back pain, pelvic pressure, changes in vagidischarge.

27.Cervical Insufficency-Risk factors: multiple gestations, repetitive 2nd trimester previous premature babies, progressively earlier

births with each subsequent pregnancy, short labors, previous elective abortions or cemanipulation, DES exposure, or other uterine anomaly.

28.Cervical Insufficency-Treatment: -medical: bed rest, frequent ultrasounds, antiprogesterone supplement, anti-inflammatory drugs



-surgical: cerclage- a surgical procedure in which a stitch is placed in the cervix to prevent aspontaneous

abortion or premature birth. Tocolytics, broad spectrum abx, anti-inflammatories. Cerclagemust be cut before birth is permitted.

29.Cervical Insufficiency: -painless dilation of cervix without uterine contractions due tostructural or functional defect of cervix.

-whitish discharge, most common in 2nd trimester.

-advanced effacement and dilation, bulging membranes.

30.CHARACTERISTICS OF PREECLAMPSIA:o Maternal vasospasm- narrowing of thevasculature

o Can occur postpartum

o Decreased perfusion to all organs- including placenta

o Decreased plasma volume

o Increased viscosity of blood

o Activation of coagulation cascade

o Dec renal perfusion- dec in GFR, serum levels of creatinine, BUN and uric acid begin to risefrom normal preg levels, dec urine output

o Decreased GFR

o Hyperreflexia

o Headache

o Edema (often)- sudden onset of severe edema

31.Chronic HTN: o BP ≥ 140/90 before 20 weeks or persists 42 days postpartum

o Nutrition- low Na,

o Bed rest

o Medication- antiHTN= mathyldope/ aldamet,

o Prenatal visits- q 2 wks, then q. wk

o BP monitoring

o Fetal surveillance- NST= nonreactive, then co ntraction stress test

meds= Methyldopa and Labetolol 1st choice. Ace-inhibitors contraindicated in 2nd atri. due to fetal risk and renal failure. with superimposed preeclampsia- onset of proteafter 20wks gestation and worsening HTN, rise in serum uric acid in 2nd trimester

32.Cocaine/Crack: - crosses placenta and into breastmilk. onset occurs rapidly, euphlasts for 30min. Irritability, depression, pessimism, fatigue, and desire for more followeuphoria.

-Maternal effects:causes vasoconstriction, tachycardia, and HTN. Metabolitesmay bepresent in urine 4-7 days following use. seizures, hallucinations, pulmonary edema, rfailure, cardiac problems. spontaneous first timester abortion, abruptio placentae, IUGpreterm birth weight, still birth. mothers are less engaged in infant bonding.

-Fetal effects: vasoconstriction decreases blood flow to the fetus, decrease birth weighead circumference. irritability, jitteriness, tremors, high-pitched cry, excessive suck.difficult feeders. CocaineBreast fed infants: extreme irritibility, N/V/D, dilated pupils

-Nursing considerations: help mom with feeding cues, and mother-infant bonding, doencourage breastfeeding in on cocaine.





40.CVS Risks/Benefits: - Spontaneous abortion risk of 0.3% in cases

-Other risks include failure to obtain tissue, rupture of membranes, leakage of amnioticfluid, vaginal spotting or bleeding, chorioamnionitis, intrauterine infection, maternal tissuecontamination of the specimen, oromandibular defects, and Rh isoimmunization. Rh-negative women are given Rh immune globulin to cover the risk of immunization from theprocedure.

41.CVS: Chorionic Villus Sampling: -A procedure (as invasive as the amniocentesis) that isused to detect genetic, metabolic, and DNA abnormalities. CVS involves obtaining a smallsample (5 to 40 mg) of chorionic villi from the edge of the developing placenta. CVS isperformed in some medical centers for first trimester diagnosis after 9 completed weeks.Villi in the chorion frondosum, present from 8 to 12 weeks gestation, are believed to reflectfetal chromosome, enzyme, and DNA content, thereby permitting earlier diagnosis than canbe obtained amniocentesis. CVS cannot detect neural tube defects, however, and theMSAFP test should still be performed at 16 weeks.

42.CVS: Results and Preparation: -A normal CVS result indicating normal chromosomalconfiguration in the first trimester does not ensure a healthy infant. Routine prenatal careand appropriate follow-up are needed.

-Before the CVS, an ultrasound is done to determine placental location, uterine position,and presence of intervening structures.

43.CYTOMEGALOVIRUS:o Most common cause of intrauterine infection!!!

o Belongs to the herpes simplex virus group and causes both congenital and acquireddisorders.

o Found in urine, saliva, cervical mucus, semen and breast milk... passed by kissing,breastfeeding, and sex intercourse.

o Virus is innocuous in adults and children, it may be fatal to the fetus.

o Diagnosis- identification of the virus in amniotic fluid by PCR or culture is the mossensitive and specific way of diagnosing congenital infection. Best documented byseroconversion.

o Fetal/neonatal risks- fetus can acquire from placenta or if comes in contact, babies tare born w this you just wait and see what happens. Mental retardation, auditory deficintellectual disability. For fetus, i nfection can result in extensive intrauterine tissue dathat leads to fetal death; it can result in fetal survival but with microcephaly, hydrocepcerebral palsy, or intellectual disability; or it can result in fetal survival w no damageNewborn is often SGA. Principal tissues affected are blood, brain, and liver. Hemolyto anemia and hyperbilirubinemia.

o Treatment- NONE, or no effect w tx

o CMV- don't feel well low grade fever, its most common cause of intellectual disabil

o Woman may have perpetual fetal loss because of CMV

o Can be detected but there's no tx

44.Deep Tendon Reflex Scale: o 4+ hyperactive, very brisk, jerky, or clonic responabnormal

o 3+ brisker than avg. may not be abnormal

o 2+ average response

o 1+ diminished response, low normal

o 0 no response, abnormal

45.Doppler flow analysis: (3rd trimester)

-Looks at placental functioning through the umbilical artery

-Measures blood flow velocity using systolic to diastolic ratio (S/D ratio)



-The S/D ratio is considered abnormal if it is elevated above the 95th percentile forgestational age or reversed after 18 to 20 weeks of gestation.

-Most commonly used when they suspect IUGR

-The

-2nd line measure of flow of blood through the placenta

-Advances in ultrasound technology have made it possible to study NONINVASIVELY theblood flow changes that occur in maternal and fetal circulations in order to assess placentalfunction.

-An ultrasound beam, like that provided by the pocket Doppler (handheld ultrasounddevice) is directed at the umbilical artery.

46.Eclampsia: seizures, can lead to stroke

47.Eclampsia Clinical Manifestations: s/s= seizure or coma, can occur 40hrs after delivery,sometimes they give them another antiseizure med= valium. If she's in labor we have tomonitor cervix, if fetus starts decompensating you need to move to C-section

o APRESSALINE= antihypertensive, shown to be safe for mom and baby, has been gi ven fordecades... if you drop maternal blood pressure too low to quickly= rebound HTN/ placentalabruption

48.Ectopic Pregnancy: o Implantation of fertilized ovum in a site other than the endometriallining of the uterus.

o MOST COMMON LOCATION FOR IMPLANTATION IS IN THE AMPULLA OF TUBE

49.Ectopic Pregnancy- Diagnosis: LMP, pelvic exam, LABS, ultrasound, inch CG values ( 53%in 2 days), laparoscopy (for diagnosis and tx)

50.Ectopic Pregnancy- Risks Factors: tubal damage cause by PID, previous pelvic/surgery, endometriosis previous ectopic pregnancy, presence of IUD, >levels of progesterone (alters motility of egg in fallopian tube), use of ovulation-inducing dr ugprimary infertility, smoking, and advanced maternal age.

51.Ectopic Pregnancy-Management: • Medical- methotrexate, given IM in singlemultiple dose.

• Surgical- if future childbearing is desired- laparoscopic linear salpingostomy to genevacuate the ectopic pregnancy and preserve the tube. If future preg not an is sue-salpingectomy (removal of tube). If woman in shock and unstable - abdominal incisiobe made. Most potential risk during surgery is hemorrhage.

52.Ectopic Pregnancy-Nursing: assess amount and appearance of bleeding, monitoand P for s/s of developing shock), emotional/educational needs, analgesics for pain

53.Ectopic Pregnancy-S/S: amenorrhea, breast tenderness and nausea. Adenexaltenderness. LABS= low H/H level, and inc leukocyte level.

54.Folic Acid Deficiency Anemia: -megaloblastic: larger than normal RBCs

-Folate deficiency is most common cause of megaloblastic anemia, more in twinpregnancies.

- folic acid is needed for DNA and RNA synthesis and cell duplication.

55.Folic Acid Deficiency Anemia-Clinical therapy: -Inadequate folic acid intake iwith neural tube defects.

usually detected in late pregnancy or during puerperium. Women with true folic aciddeficency present with n/v and anorexia. hgb levels may be as low as 3-5.

Prevented with a 0.4mg supplement of F.A. also needs iron supplements.

56.Folic Acid Deficiency Anemia-Nursing: teach about F.A. rich foods, best source

green veggies, O.J., citrus fruits and juices, red meats, poultry, and l egumes.



57.GBS Indications and Treatment: o Treatment indications

• Previous infant with GBS disease

• GBS bacteriuria during current pregnancy

• Positive GBS screen during current pregnancy (unless C/S before labor or ROM)

• Unknown GBS status

• Gestation less than 37 weeks

• ROM 18 hours or more before delivery

• Maternal temperature of 38.0°C (100.4°F) or more

o Treatment- Ampicillin, penicillin g, if allergy then on clindamycin or Zosyn

58.GBS Transmisson: can occur from vertical transmission from the mother as the fetuspassess through the birth canal, resulting in early onset o f GBS. Horizontal transmissionfrom colonized nursery personnel or infants will result in l ate onset of GBS.

59.GBS- Fetal Risk Factors: o Prematurity

o Maternal intrapartum fever

o Membranes ruptured for longer than 18 hours

o A previously infected infant with GBS disease

o GBS bacteriuria in the current pregnancy

o Young maternal age

o African American or Hispanic race.

o GBS- causes severe, invasive disease in affected infants. In newborns, the majorityoccur within the first week of life and are thus designated as early-onset disease.

60.GBS-Contraindicated for prophylactic use.: o previous pregnancy with a positscreening culture( unless a culture was also positive during the current pregnancy)

o planned cesarean birth performed in the absence of labor or membranerupture(regardless of maternal GBS culture status)

o Negative vaginal and rectal GBS screening culture in late gestation during the currepregnancy, regardless of intrapartum risk factors.

61.GBS-Indicated for prophylactic use: o Previous infant with invasive GBS disea

o GBS bacteriuria during current pregnancy

o Positive GBS screening culture during current pregnancy(unless a planned cesareanin the absence of labor or amniotic membrane rupture, is performed)

o Unknown GBS status (culture not done, incomplete, or results unknown) and any ofollowing

o Birth at less than 37 weeks gestation

o Amniotic membrane rupture longer than or equal to 18 hrs*

o Intrapartum temperature greater than or equal to 100.4F (less than or equal to 38C)

62.GBS-Maternal Risk factors: African American colonize twice as faster as Cauca

63.Gestational Diabetes: -definition: carbohydrate intolerance of variable severity onset or first recognition during pregnancy.



-Screening: all pregnant women should have their risk of diabetes assessed. women at highrisk should be screened asap: prior hx of GDM, LGA infant, marked obesity, diagnosis of PCOS, glucosuria, strong family hx of T2DM

-Diagnosis: HA1c greater than or equal to 6.5% would be consiered diagnostic or fastingplasma glucose greater than or equal to 126mg/dL. OGTT : Fasting 92, 1hr 180, 2hr, 153. if 1hr OGTT incicated GDM, OGTT is administered again and if 2 or more of the following aremet then GDM is confirmed: fasting 95, 1hr 180, 2hr 1 55, 3hr 140.

64.Gestational hypertension: BP 140/90 after 20wk, NO protein in urine. Inc BP after midpregnancy w/out proteinurea or other signs of preeclampsia. If BP returns to normal by12wks = diagnosis.

65.GESTATIONAL TROPHOBLASTIC DISEASE (GTD):o Trophoblast is outermost layer of embryonic cells and gives rise to the chorion.

o Includes:

• Hydatiform mole (molar pregnancy) - result in formation of placenta characterized byhydropic (fluid-filled) grapelike clusters. Two types: complete and partial.

§ Complete- develops from an anuclear ovum that contains no maternal genetic material(an "empty egg"). No embryonic or fetal tissue or membranes are found.

§ Partial- usually has triploid karyotype-69 chromosomes. Most often, a normal ovum w 23chromosomes is fertilized by 2 sprem. Partial moles are recognized only after spontaneousabortion, or they go unnoticed. Identifiable fetal parts may be present

• Invasive mole (chorioadenoma destruens)- similar to a complete mole but involves uterinemyometrium.

• Choriocarcinoma- invasive form of cancer from trophoblastic tissue

66.GESTATIONAL TROPHOBLASTIC DISEASE ( GTD)- Follow Up:• Continuing high/rising hCGsuggests metastases; chemotherapy is needed

• Rh immune globulin if not sensitized

67.GESTATIONAL TROPHOBLASTIC DISEASE (GTD)- Symptoms:-vaginal bleedi4th wk or as late as 2nd trimester. Anemia (cuz LOB), hydropic vesicles may be passits diagnostic), uterine enlargement (greater than expected for gestational age, classicfor complete moles), absence of fetal heart sounds , elevated serum hCG (cuz continusecretion by proliferating trophoblastic tissue), very low levels of maternal serumfetoprotien, hyperemesis gravidarum (cuz of high levels of hCG), preeclampsia,hyperthyroidism (rarely)

68.GESTATIONAL TROPHOBLASTIC DISEASE (GTD)-DIAGNOSIS:ultrasound afte(when the vesicular enlargement of the villi can be identified)

69.GESTATIONAL TROPHOBLASTIC DISEASE ( GTD)-Treatment:suction evacuatmolar pregnancy and curettage of the uterus to remove all fragments of the placenta. earlier the better. Hysterectomy if woman is ol der or if excess bleeding. AVOID UTECONTRACTIONS, to prevent embolization of trophoblastic tissue to the lungs. Admimmune globulin after evacuation of uterus

70.Group Beta streptococcus: bacterial infection found in the lower GI or urologicMaybe transmitted in utero or during transition.

-All pregnant women screened for both vaginal and rectal GBS colonization at 35-37gestation.

71.HELLP SYNDROME:o Hemolysis- termed microangiopathic hemolytic anemia

o Elevated liver enzymes

o Low platelets

o JUST AN FYI:

• RBCs are distorted during passage through small/damaged blood vessels. Vascular because of vasospasm and platelets aggregate at sites of damage resulting in low plat



count. Elevated liver enzymes occur from blood flow that is obstructed because of fibrindeposits. Deposits of fibrin-like material found in the hepatic sinusoids cause obstructionand hepatocellular injury.

o Signs- N/V, malaise, flulike symptoms, epigastric pain

o Treatment- assess moms condition and stabilize, assess fetus using NST and biophysicalprofile. Mom should give birth, sometimes better to deliver premie than for baby to die in

utero

72.HELLP Syndrome: - not always elevated BP, hemolysis=destruction of RBC, H and H willdec., elevated liver (AST/ALT), low platelets..., sometimes better to deliver premie than forbaby to die in utero

73.Herpes Simplex Virus: o Fetal/neonatal risks

• If primary outbreak in 1st trimester: spontaneous abortion

• If primary outbreak in 2-3 trimesters: PTL, IUGR, neonatal infection

• Delivery considerations- C section recommended, symptoms include fever (hypothermia), jaundice, seizures, and poor feeding.

• Approximately one half of infected infants develop the characteristics vesicular lesions.

o Treatment- acyclovir, famciclovir, and valacyclovir- have an advantage of betterabsorption and a longer half-life than acyclovir.

74.HIV/AIDS and Pregnancy: -Transmission:HIV is found in blood, semen, vaginal fluid, andbreast milk.

-Factors leading to reduced transmission: Enhanced prenatal HIV counseling and testing,Highly active antiretroviral therapy (HAART), Increase in elective CS delivery for women withHIV RNA levels > 1000 c/mL.

75.HIV/AIDS and Pregnancy-Clinical Tx of mom: HIV screening early on. the carwho chose to continue their pregnancy should focus on stabilizing the disease, preveopportunistic infections and transmisson of the virus and providing psychosocial andeducational support. Antiretroviral therapy should be recommended, it is best to startprophylaxis after the 1st trimester and no later then 28wks . also treat other STDs andvaccinate for flu, pneumonia, and hepatitis. routine labs: platelets, CBC & differentiaPostpartal hemorrhage, infection, poor wound healing,and GU infections are increase

76.HIV/AIDS and Pregnancy-Clinical Tx of neonate: prophylactic ART of mom, section at 38wks before ROM, and avoid breastfeeding. NST is begun at 32 wks and ultrasounds for IUGR detection. NO INVASIVE PROCEDURES unless risk outweigHIV exposed infants should complete 6wk regimen of oral zidovudine prophylacticalfollow up with HIV tests.

77.HIV/AIDS and Pregnancy-Fetal-neonatal risks: transmission via breaskmilk mbut the majority of all infections occur during labor and birth. moms who have not betreated have a 25% chance to transmit to newborn.

78.HIV/AIDS and Pregnancy-Maternal risks: For women who have not yet had acART or who are non-comliapnt, AIDS definging symptoms that are more common inthan in men include wasting syndrome, esophageal candidiasis, and herpes simplex v

disease.

79.HTN DISORDERS OF PREGNANCY:o Preeclampsia- most common HTN disordpregnancy. Defined as an inc in BP after 20 wks gestation accompanied by proteinuripreviously normotensive woman.

• Mild

• Severe

o Eclampsia

o Chronic hypertension



o Chronic hypertension with superimposed preeclampsia

o Gestational hypertension

o PIH= PREGNANCY INFUSED HTN

80.HYPEREMESIS GRAVIDARUM:Severe N/V affecting hydration & nutritional status

81.HYPEREMESIS GRAVIDARUM- Diagnostic Criteria: hx of intractable vomiting in the 1sthalf of preg, dehydration, ketonuria, and a weight loss of 5% of prepregnancy weight.

82.HYPEREMESIS GRAVIDARUM-Nursing:o Control vomiting, correct dehydration, replaceelectrolytes, and maintain adequate nutrition.

o Complementary & alternative therapies- ginger to relief N/V, acupuncture/acupressure,hypnosis

o Begin slowly with food if the pt is feeling ok- frequent small meals of high carb, low-fatcontent

o If pt hospitalized- ultrasound, IV fluids to correct dehydration, K chloride is added toinfusion, replacement of thiamine (vit B1) & pyroxidine (vit B6) to prevent peripheralneuropathy. Desired urine output is minimum of 1000mL/ 24hrs.

83.HYPEREMESIS GRAVIDARUM-Treatment: antiemeitc Zofran, corticosteroids, F&Ereplacement. Pyridoxine (vit B6) for N/V, sometimes given w doxylamine succinate(antihistamine that improves efficacy). Promethazine (Phenergan), metoclopramide(Reglan), and odansetron (Zofran).

84.HYPERTENSIVE EFFECTS ON FETUS:o Placental infarcts

o Fetal growth restriction- SGA because of IUGR

o Chronic hypoxia

o Prematurity

o Perinatal mortality

o At birth, may be over sedated because of meds given to mom. Also, may havehypermagnesemia.

o If vasospasm and hypovolemia- Fetal hypoxia and malnutrition

o If placental abruption 2ndary to HTN- fetal hypoxia or even death

85.HYPETENSIVE DISORDERS: MATERNAL RISKS:o If severe preeclampsia is not can lead to these:

• Intercerebral hemorrhage= MOST COMMON CAUSE OF DEATH IN WOMEN WPRE/ECLAMPSIA, if they survive they may suffer permanent disability. PreeclampsCNS (hyperreflexia, headache, and eclamptic seizure)

• Retinal detachment-because of inc intraocular pressure

• Acute tubular necrosis- from underperfusion of the kidneys (this is associated whypovolemia and renal vasoconstriction),

• Thrombocytopenia- r/t endothelial damage and activation of thrombin. The release procoagulants, such as thromboplastin, can result in acute disseminated intravascularcoagulation (DIC)

• Subscapular hematoma of the liver- rupture is a life-threatening event. Woman maycomplain of R shoulder pain or severe epigastric pain persisting for several hrs beforcirculatory collapse is evident. This is a surgi cal emergency!

• Pulmonary edema- due to inc capillary permeability

• Vaginal birth is preferable to cesarean birth in women w preelampsia or HELLP syn



86. Influence of GDM of baby: Complications: in presence of maternal DKA the risk of fetaldemise increases., macrosomia, Respiratory distress syndrome, hyperbilirubinemia,congential abnormalities often ivolving the heart, CNS, skeletal system. Septal defects,coarction of the aorta, and transposition of the great vessles. most common heartcomplications. CNS abnormalities: hydrocephalus, mengomyelocele, anacephaly. SACRALAGENESIS appears only in infants of mothers with diabetes.

87. Influence of GDM on Mother: Complications include: hydraminos,

preeclampsia/eclampsia, hyperglycemia may lead to DKA, difficult labor or dystocia,recurrent monilial vagnintits and UTIs, pregnancy worsens retinopathy.

88. Information that can be obtained by a limited ultrasound: -Determine fetalpresentation before or during labor

-Locate the placenta

-Confirm fetal heart rate activity

-Estimate amniotic fluid volume

-Diagnose multiple gestation

-Evaluate interval growth

-Evaluate the cervic

-Guide amniocentesis

89. Insulin and pregnancy: -first trimester: need decreased early

-during labor: need may increase due to increased energy needs and to balance IV glucose

-delivery of placenta: need decreases abruptly

90. Interpretation of NST: REACTIVE- Normal, there are 2 o r more fetal heart accwithin a 20 minute period. The FHR acceleration must be at least 15 beats per minutethe baseline and last 15 seconds from baseline to baseline.

NONREACTIVE- Abnormal, lacks sufficient FHR accelerations over a 40 minute pe

-Variable decelerations may be observed in up to 50% of NST's, if non repetitive and(less than 30 seconds) do not indicate fetal compromise nor the need for o bstetricintervention. However repetitive variable decelerations (at least 3 in 20 minutes) haveassociated with an increased risk of cesarean birth.

91. Intrapartal Management of DM: -Timing of birth: most go to term, but come copt to induce labor to avoid problems related to decreased profusion to the placenta. Csection may be indicated if evidence of nonreassuring fetal status exists. Induction mindicated when the mom has worsening hypertension, IUGR, or vascular changes.

- Lung maturity should be tested if there is evidence of macrosomia, fetal compromiselevated HbA1c. L/S ratio: 2-3.5

-Labor management: hourly glucose checks. druing active labor insulin may not be nLong-acting insulin should be reduced or stopped and regular insulin should be used meet most or all of moms needs. 2 IV lines: 5%dextrose and NaCl (if bolus is neededpiggyback insulin) IV insulin is d/c with the completion of the 3rd stage of labor.

92. INTRAPARTUM CLINICAL THERAPY-Eclampsia:• Hemodynamic monitoring- vascularly dry.. if oliguria, severe cardiac disease, severe renal disease, pulmonary edresulting in impaired maternal O2, refractory hypertension when given vasoactive dru

• Delivery when stable, BIRTH IS ONLY CURE!



93. INTRAPARTUM CLINICAL THERAPY-Preeclampsia:• Induction of labor w IV oxytocinwhen there is evidence of fetal maturity and cervical readiness. Woman may receive bothoxytocin and Mg SO. Epidural ONLY in absence of thrombocytopenia. Hyptotension majorconcern and can be avoided by careful technique and careful vol expansion. In total bodyfluid overload, the woman has depleted intravascular volume, making her prone tohypotension when vascular bed dilates from epidural.

• Cesarean delivery if severe

• Delivery in Sim's position, if lithotomy used wedge her w pillow, wedge w Csect as well

• O2 during labor

94. Iron Deficiency Anemia of Pregnancy: -Anemia is defined as hgb less than 11 g/dL in apregnant woman.

-Iron deficiency anemia is the most common medical complication of pregnancy, primarilyas a consequence of expansion of plasma volume without normal expansion of maternalhemoglobin mass.

95. Iron Deficiency Anemia of Pregnancy-Clinical therapy: pregnant women need to take atleast 27 mg supplement of iron daily. iron-rich diet, i f anemia is diagnosed dose shouldincrease to 60-120mg/day. with twins a larger dose is needed.

96. Iron Deficiency Anemia of P regnancy-Maternal Risks: may be asymptomatic, but moresusceptible to infection, may tire easily, has an increased chance of preeclampsia andpostpartal hemorhage, and tolerates poorly even minimal blood loss during birth. Healing of an episiotomy may be slowed. If hgb is less than 6, cardiac failure may happen.

97. Iron Deficiency Anemia of Pregnancy-Neonatal Risks: low birth weight, prematurity,stillbirth, and neonatal death in infants of women with severe iron deficiency anemia (6).infant is not iron defiecent at birth but is at an increased risk of developing iron deficiencyanemia during infancy.

98. Iron Deficiency Anemia of Pregnancy-Nursing considerations: teach womensupplements daily and with Vit C to increase absorption. GI upset if taken on an emptstomach. stool may turn black and formed. keep tabs out of reach of children as they fatal.

99.Methadone: -most commly used drug i n the treatment of women who are dependopioids

-benefits: blocks withdrawl symptoms and cravings

-crosses the placenta and fetal exposure in utero may result in neonatal abstinencesyndrome (NAS)

-GOAL: help mom recover from drug abuse, and optimize the long-term health of mobaby.

100. Mild Preeclampia Clincial Manifestations: • In normotensive mom BP of 14proteinuria = preeclampsia

• After 20wks a BP of 140/90 taken on 2 separate occasions 6 hrs apart in sitting posdiagnostic. they have 1 to 2+ protein on dipstick, 24 hr specimen then 300mg/dL to 1per liter of protein, more than 3 pound weight gain a month in 2nd tri, 1 pound a week3rd trimester

• Proteinuria- 300mg/L (1+ dipstick) and 1g/L (2+dipstick), in 24hr >300mg of proteabnormal

• she may be sent home on bed rest laying on left side so better perfusion on uterus aimproved CO, daily kick counts, low Na diet recommended , have to be able to self-mmust be able to determine signs of worsening condition and have a way to get to hospMag sulfate- to prevent seizure THAT IS THE ONLY REASON IT IS GIVEN, IT IS(blocks transmission of acetylcholine, relaxes uterus, relaxes arterioles- so a littleimprovement of BP), keep them on L side, can get up to bathroom and shower

101. NonStress Test: What is it, when is it done?: NST (3rd trimester)



-Noninvasive method of evaluating fetal status

-Involves using an external electronic fetal monitor to obtain a tracing of the feta heart rateand observation of acceleration of the FHR with fetal movement.

102. Normal glucose homeostasis: -insulin: enables glucose to move into muscles & liver--stored as glycogen

-blood glucose levels drop several hours after a meal

-pancrease releases glucagon

-glucagon stimulates conversion of glycogen to glucose--released into bloodstream

-glucagon stimulates sysnthesis of glucose from amino acids.

103. NST-Procedure: women are requested to be non-fasting and to have refrained fromrecent cigarette smoking because this can adversely affect test results. The NST is typicallyperformed with the women in the semi-Fowler's position with a small pillow or blanketunder the right hip to displace the uterus to the left. The FHR is monitored by the placementof an electronic fetal monitor.

-The FHR is usually monitored for 20 minutes, but monitoring may be extended to 40minutes if the fetus is in a sleep cycle.

104. NST: When do you use it?: -Can be used as an assessment tool in any pregnancy but isespecially useful in the presence of diabetes, preeclampsia, IUGR, SROM, multiple gestation,postdates, & other high risk pregnancy conditions. (most clinicians test twice weekly for highrisk patients and once a week for other conditions)

105. Nursing Care Management for CVS: nurse ascertains the woman's understanding of CVS, its uses, the procedure, and the possible results. The nurse supports the woman orcouple and encourages them to express any feeling and fears regarding the procedure andalso regarding the decision-making process if abortion is being considered.

106. Nursing Diagnoses for mom with DM: - Risk for imbalance nutrition: more trequirements r/t imbalance between intake and available insulin.

-risk for injury r/t possible complications secondary to hypoglycemia or hyperglycem

-Interrupted family process r/t the need for hospitalization secondary to GDM.

107. Nursing Diagnoses for Substance abusing moms: -Imbalance nutrition: lessrequirements r/t inadequate food intake secondary to substance abuse.

-risk for infection r/t use of i nadequately cleaned syringes and needles, secondary to use.

- ineffective health maintenence r/t lack of information about the impact of s ubstanceabuse on the fetus.

108. Patho of Preeclampsia/Eclampsia: • Vasospasm-(narrowing of vasculature) about Q organ sys, vasoconstriction of CNS/brain- headaches unrelieved by Tylenol,vasoconstriction of kidney, spots and stars, quick reflexes, vasoconstriction of gut, ofcontributes to IUGR

• PROSTAGLANDINS: Prostacyclin- vasodilator, prevents platelet aggregation Throvasoconstrictor, causes platelets to clump together imbalance

• Nitric oxide deficiency- it's a potent vasodilator and important regulator of materna

• Hyperhomocysteinemia- may play a role through oxidative stress and endothelialdysfunction

• Visual disturbances

109. Placenta Previa: - improper implantation of placenta



-unexplained bright red painless bleeding; exsanguination (after 7th month) - call for help.Fluid, type and cross, c-section, monitor fetus, US.

110. Placenta Previa- Nursing Management: bed rest w/ bathroom privileges only as long asthe woman is not bleeding, NO VAGINAL EXAMS, Monitoring blood loss, pain, uterinecontractility, evaluation of FHR with external monitor, monitoring

maternal vitals, complete lab evaluation: Hgb, Hct, Rh factor, urinalysis, IV fluids LR-monitor

drip rate, availability of 2 units of cross- matched blood for possible transfusion,administration of betamethasone to facilitate fetal lung maturity, Rh D immunoglobulin inRh D negative. Newborns hgb, cell volume, and erythrocyte count should be checkedimmediately after birth and then closely monitored, may require O2 and blood andadmission to the NICU

111. POSPARTAL CLINICAL THERAPY-Preeclampsia/Ecclamspia: o Magnesium sulfate- becautious on oral intake, will continue to receive for 24 hrs postpartum

o Antihypertensives

o Recurrence- some women develop late postpartum eclampsia (occurring more than 48hrsbut less than 4wks)- so important to educate. If BP, above 150/100 give antiHTN, shouldreturn to normal <12wks.

There is a genetic link to preeeclampsia, if the womans mother had preeclampsia, then sheis likely to develop preeclampsia as well.

MG SO NG CONSIDERATIONS

o It's a CNS depressant by dec acetylcholine, thereby blocking neuromuscular transmission.Relaxes smooth muscles so may dec BP, dec freq and intensity of uterine contractions, usedas tocolytic in preterm labor

o BP per protocol

o Serum MgSO4 levels- Q6- 8hrs, therapeutic range = 4-8 mg/dL, reflexes disapper b12, resp. depression at 14, cardiac arrest at 24-30

o Respiratory rate hourly <12= Mg toxicity developing

o Reflexes hourly- loss of reflexes= Mg toxicity

o Urinary output hourly - 30cc output or less= Mg toxicity

o MgSO4 antagonist= Ca gluconate 1gm IV over 3min

o Continue Mg SO for 24hrs after birth for prophylaxis

o Signs of toxicity= dec reflexes, oliguria, confusion, circulatory collapse, inc risk ofarrest, visual disturb, inc headache, epigastric pain, inc edema, dec urine o utput. Rapadministration of large doses= cardiac arrest.

o Newborn care- monitor Mg levels for 24-48hrs

o DIAGNOSTIC= Urinary output, DEC. reflexes, dec RR

o Generally given over 20min. VS Q5min, Check Levels if they have signs of mg tox

SO is nephrotoxic

112. Postpartum management of DM: -maternal insulin needs fall due to the decrleveld of gPL, progesterone, and estrogen.

-mom may not need insulin for 24 hrs or only 1/4 -1/2 her previous dose.

-when women is NOT br eastfeeding, oral antihyperglycemics may be used.

-follow up in 6wks, if her blood glucose levels are normal, then she should be reassesa minimum of 3 yr intervals.



-Breastfeeding is encouraged, as diabetes does not alter breast milk. blood glucose levelsmay be lowered because glucose is transferred from serum to breast to be converted toactose, and energy is expended in milk production.

113. Preeclampsia: 1ST trimester BP almost same, 2nd trimester BP drops, 3rd trimester BPgoes back up... Occurs after 20wks, 140/90, proteinuria. Only cure is the birth of fetus anddelivery of placenta!! Aspirin to prevent preeclampsia in "at-risk" women through low-dose(50-150mg daily) begun between 12-18wks gestation.

114. Premature Rupture of Membranes (PROM): -spontaneous ROM any time aftercompletion of 37 wks or before the onset of labor

-the earlier PROM; latent period is longer (the period of time between ROM and onset of labor)

-Causes: incompetent cervix, cervicitis, UTIs, asymptomatic bacteriuria, amniocentesis,placenta previa, abruption placentae, hydraminos, LEEP, multiple pregnancy, Genital tractanomalies.

115. Preterm Labor: -labor that occurs between 20 and 37 completed weeks of pregnancy

116. Preterm Labor-clinical therapy:: -identification and tx of infection.

-bedrest is ordered

-diagnosis: pt has 1 contraction in less than or equal to 10 min

-17P:given prophylactically but not once labor has started. IM beginning at 16 wks andcontinuing to 36 wks

-tocolysis : medicationally attempting to stop labor

-primary goal is to delay birth by 48 hrs so the maximum benefit of glucocorticoids can occurand decrease the incidence of RDS.

-beta adrenergic: can significantly affect maternal cardiovascular and metabolic physSerious effects: Hypotension, cardiac arrhythmia, tachycardia, palpitations, myocardiischemia, pulmonary edema, and maternal hyperglycemia.

-MgSO4: usually used in pt with preeclampsia. displaces intracellular calcium whichuterine contractions. monitor serum Mg level closely. Maternal Side effects: flushed, headache, nystagmus. Fetal S/E: hypotonia, lethargy, hypoglycemia, hypocalcemia. ndry mouth, and dizziness.

-Calcium channel blocker (Nifedipine) antagonize the action of calcium within themyometrial cells, which Reduces contractions. S/E are related to arterial vasodilationis, hypotension, tachycardia, facial flushing, and headache. Contraindicated: women wheart disease, cardiovascular compromise, intrauterine infection, multiple pregnancy,maternal hypotension.

-Prostaglanding synthetase inhibitors: inhibit contractions by interfering with PG synS/E: dyspepsia, n/v, depression, dizzy spells. Indomethacin not recommended after 34prevent premature PDA closure in the fetus.

-corticosteroids: bexamethasone for fetal lung maturation.

-monitor for s/s of PTL:abd pain, back pain, pelvic pain, menstrual like cramps, vaginbleeding (pinkish or mucus like), increased vaginal. Discharge, pelvic pressure, urinafrequency, diarrhea. Uterine contractions that occur q10min or less without pain, ROM

117. Preterm Labor-fetal risks: prematurity, mortality risk increased. maturationaldeficiencies (fat storage, heat regulation, immaturity of organ systems), immature lundevelopment.

118. Preterm Labor-maternal risks: (initial cause of PTL: antepartum hemorrhagematernal infection) multiple gestation, previous PTL with term birth. See Table 26-2 full list.

119. PROM Clinical Therapy: -diagnosis: complaints of watery vaginal discharge orgush of fluids ROM should be considered.



Ask about the time of initial fluid loss, if continuous leaking is occurring, any odor. Nitrazinetest should be tested on the leaking fluid blue=suggests ROM. Steril speculum exam, AVOIDdigital exam until PPROM is ruled out or plan had been determined. Ultrasound, GBS,gonorrhea, chlamidia test should be done at this time.

-amniocentesis

-bed rest with pelvic rest, bathroom privleges, fetal movement record, avoid intercourse,

douches, tampons.

-PT contacts Physician: has fever, uterine tenderness or contractions, increased leakage,decreased fetal

movement, or foul vaginal discharge.

-prophylactic abs: to any mom with unknown GBS status or history of + result.

-corticosteroids: bexamethasone; tocolytics within 24hrs to allow course of steroids to begiven.

120. PROM Fetal Assessment: q4hrs, fetal tachycardia suggests infection, fetal heart tracing,BPP (q24hrs), NST (qShift), fetal lung maturity test.

121. PROM Fetal/Neonatal Risks: mortality related to prematurity related to RDS,necrotizing enterocolitis, and intraventricular Hemorrhage, neonatal sepsis, fetal hypoxemia(cord prolapse or cord compression), oligohydraminos may result in fetal pulmonaryhypoplasia, facial anomalies, limb position defects, and fetal growth restriction.

122. PROM-maternal assessment: qShift , monitor temp. BP, HR (q4hrs), leaking?, CBC,urinalysis, position mom on her LEFT side for uteroplacental perfusion, hydrate if increasedtemp.

123. PROM-Maternal Risks: infection, chorioamnionitis, endometritis, abruption placentae,childbirth may be complicated by malpresentation and reduced amniotic fluid volume.

124. PTL-Nursing: monitor FHR, vitals, bed rest, I&Os, UCs, place mom on her LEFmaternal fetal circulation,

vaginal exams at a minimum, watch for adverse effects if tocolytics are used. Decreamoms axiety , use

empathetic communication, help with coping mechanisms, prepare parents for birth iimminent.

-provide psychological support: arrange consult for neonatologist, social worker, or hchaplin if requested.

-NO attempt is made to stop labor if: Fetal demise, lethal fetal anomaly, severepreeclampsia/eclampsia,

hemorrhage/abruption placentae, chorioamnionitis, severe fatal growth restriction, fetmaturity, acute reassuring fetal status.

125. Rh Sensitation: o An antigen-antibody reaction

• Rh (-) mother with Rh (+) fetus

• Exposure can occur in termination by miscarriage or induced abortion, blood transfexperiences an Rh positive tubal pregnancy, amniocentesis, or experiences any traumevent. Or during birth

• Maternal IgG anti-D antibodies produced= MOM HAS BEEN SENSITIZED, alsoalloimmunization and isoimmunization

• Second exposure to Rh (+) RBC's leads to hemolysis

126. Rh Sensitation-Fetal Risks: • Erythroblastosis fetalis- severe hemolytic diseashemolysis caused by the maternal IgG antibodies in the fetus creates fetal anemia, fetresponds by increasing RBC production



• Hydrops fetalis- fetal edema, congestive heart failure may result

• Icterus gravis- hyperbilirubinemia and jaundice because of RBC destruction, which canlead to

127. RhoGam: Rho gam given during invasive procedures or if woman has bleeding. Or at28wks preg, if she has another procedure, and after pregnancy.

MANAGEMENTo An FYI: the goal of medical management is the birth of a mature fetus who has notdeveloped severe hemolysis in utero. This requires early identification and tx of maternalconditions that predispose the infant to hemolytic disease, coordinated obstetric pediatrictx for the seriously affected newborn, and prevention of Rh sensitization if none present.

o Antepartum

• Rh immune globulin given prophylactically at 28wks. And for any time a blood transfusionoccurs.

• 2 interventions to aid fetus whose blood cells are being destroyed by maternal antibodies:

Ø Early delivery

Ø Intrauterine transfusion- done to correct the anemia produced by the RBC hemolysis andthereby improve fetal oxygenation. Done IV through PUBS or intraperitoneally as early as18wks.

o Postpartum

• Prevent sensitization

Ø RhoGAM

Ø If you don't know if mom is sensitized, give anyway, it will cause no harm.

• Treat isommune hemolytic disease in newborn

128. Rubella: o Teratogenic during 1st trimester, defects rare after 20wks gestation.

o Fetal/neonatal risks- if newborn twin has congenital rubella they need to be isolatedshed virus for 12mon.

o Diagnosis- presence of congenital cataracts sensorineural deafness and congenital h

defects (PDA). Mental retardation, cerebral palsy may become evident in i nfancy. Diamade in presence of the conditions and an presence of of IgM antirubella antibody tit

o Treatment-prevention!! by live attenuated vaccine. mom immunized after delivery. preg. woman becomes infected in 1st tri. therapeutic abortion may be alternative L

o Asymptomatic or signs of mild infection, macupapular rash, lymphadenopathy, muachiness, and joint pain.

129. SCREENING FOR Rh INCOMPATIBILITY & SENTIZATION-Fetal assessmentpercutaneous umbilical cord blood sampling requires highly skilled physician, directof assessing Rh status of fetus.

• Amniocentesis- less risk than PUBS

• Ultrasound- to follow fetal progress. Presence of ascites and subcutaneous edema asigns of severe fetal involvement (fetal hydrops). Other indicators: inc. in fetal heart shydramnios and placental thickness and texture.

130. SCREENING FOR Rh INCOMPATIBILITY & SENTIZATION-Maternal assessmIndirect Coomb's- an antibody screen, it measures the number of Rh- positive antibodthe maternal blood

• Direct Coomb's - done on the infant's blood to detect antibody coated Rh-positive R

• If sensitized:



Ø Anti-D antibody titer Q2-4wks beginning at 16 to 18wks, biweekly during 3rd trimester,and the week before the due date. If test shows 1:16 or less late in pregnancy, birth at 38wks or spontaneous labor at term can be anticipated. Negative antibody titers canconsistently identify the fetus not at risk.

Ø Delta optical density . If Anti-D antibody titer test shows titer of 1:16 or greater, the deltaoptical density analysis of amniotic fluid is performed. Determines amount of bilirubinpigment found in the amniotic fluid, it Serves as an indirect predictor of the severity of fetal

anemia.

131. Self-care measures to prevent PTL:: rest 2-3x , laying on your side, increase fluids, avoidcaffeine, empty bladder q2hrs while awake, avoid lifting heavy objects, pace yourself toavoid overexertion, stop sexual activity.

132. Severe Preeclampsia- Clinical M anifestations: 160/110 on 2 occasions, taken 6hrs apartwhile on bed rest (cannot get up to bathroom or shower), 5 or more grams per liter of protein in 24 hr specimen or 3+ dipstick, ol iguria= urinary output <equal to 500mL in 24 hr,pulmonary edema , vasoconstriction of liver- epigastric pain upper R quad pain, blurry/spotsvision, thrombocytopenia <100,000, usually hospitalized, daily weights, sometimeselectrolytes, cerebral or visual disturbances, cyanosis, impaired liver function (inc AST/ALT),thrombocytopenia, fetal growth restriction, pitting edema of low extremities while on bedrest, irritability, and emotional tension.

133. Sickle Cell Anemia: -recessive autosomal disorder

-hgb A is abnormally formed.

-primarily in African Americans

134. Sickle Cell Anemia-Clinical Therapy: additional folic acid supplement (4mg/day).Maternal infection should be treated immediately. Rehydration with IV fluids, administer o2,antibiotics, and analgesics. Fetal heart monitoring, antiembolism hose in postpartum. if

vasooclusive crisis occurs during labor keep woman in a LEFT LATERAL position, may be used, as well as episiotomy and forceps to shorten delivery time.

135. Sickle Cell Anemia-Fetal/neonatal risks: -Fetal/neonatal risks prematurity anfetal death due to sickling in placenta.

136. Sickle Cell Anemia-Maternal Risks: increased risk for nephritis, bacteriuria, ahematuria, anemia. low o2 pressure- caused by high temps, dehydration, infection, or

acidosis may precipitate a vaso-occlusive crisis (occur more often in second half of pregnancy). may require blood transfusion, c-section, develop acute chest syndrome, or acute renal failure.

137. Signs & Symptoms of PTL: abd pain, back pain, pelvic pain, menstrual like cravaginal bleeding (pinkish or mucus like), increased vaginal. Discharge, pelvic pressuurinary frequency, diarrhea. Uterine contractions that occur q10min or less without pROM.

138. Signs of Substance abuse: Behavioral signs: -memory lapses, mood swings,hallucinations

-pattern of frequently missed appointments.

-frequent accidents, falls

-signs of depression, agitation, euphoria

-suicidal gestures

139. Signs of Substance abuse: History: -vague or unusual medical complaints

-family hx of alcoholism/addiction

-hx of childhood physical, sexual, emotional abuse.

-hx of cirrhosis, pancreatitis, hepatitis, gastritis, STI's, or unusual infections such as cor endocarditis



140. Signs of Substance abuse: Physical signs: -dilated or constricted pupils

-inflamed nasal mucosa

-evidence of needle "track marks" or absecesses

-poor nutritional status

-slurred speech or staggereing gait

-odor of alcohol on breath

141. Sono/US are Used to assess: gestational sac, the presence or absence of a yolk sac orembryo, the crown rump length to most accurately determine gestational age, the presenceof cardiac motion, and fetal number. It also can most accurately identify shortened cervicallength and cervical funneling (indicating cervical incompetence or risk of preterm labor)

-The FDA states that obstetric sonograms fall within an acceptable level of safey becausethey use low-intensity ultrasound, however they do not approve of nonmedical uses such asvideos and pictures for "keepsakes."

142. Sonogram/Ultrasound: -All 3 Trimesters

-Ultrasound is a diagnostic procedure that used high- frequency sound waves exceeding20,000 cycles per second, to produce and image that varies based on the density of thestructure under the transducer.

-Ultrasound can be used to produce images called SONOGRAMS in several different ways.(Motion mode, brightness modulation, & 3 dimensional)

-Limited ultrasound may be used to address a specific question, or determine specificinformation. (this should not take the place of a standard ultrasound evaluation)

143. Spontaeous Abortion- Nursing: amount and appearance of vag bleeding, VS, and pain,moms bld type and antibody status. If pregnancy is 10-12wks or more FHR should bedetermined w Doppler. Provide emotional support.

144. Spontaneous Abortion: oPregnancy termination before 20 weeks

oReliable indicators= pelvic cramping and backache

145. Spontaneous Abortion- Classifications: • Threatened- unexplained bleeding,or backache. Cervix is closed. Followed by partial or complete expulsion or it may rew/out threatening fetus.

• Imminent- inc bleed and cramp. Internal cervical os dilates. ROM. The term inevitaabortion applies.

• Incomplete- part of the placenta are r etained, internal cervical os dilated.

• Complete- all products of conception expelled. Uterus is contracted and cervical osclosed.

• Missed- fetus dies in utero but not expelled. DIC may develop if fetus retained beyowks

• Recurrent pregnancy loss- abortion occurs consecutively in 3 or more pregnancies.

• Septic- presence of infection

146. Spontaneous Abortion-Causes: -over half in 1st trimester r/t chromosomalabnormalities, teratogenic drugs, faulty implantation due to abnormalities of the femareproductive tract, weakend cervix, placental abnormalities, chronic maternal diseaseendocrine imbalances, and maternal infections. Jaczzi users 2x's more likely.

-Advanced maternal age is the most significant risk factor

147. Spontaneous Abotion- Causes for early/late: o Early- chromosomal defectsweeks 4 - 8 , insufficient or excessive hormonal levels will result in loss by 10 wks, iand environmental factors



o Late- cervical insufficiency or maternal disease

148. Standard ultrasound: examination is performed during the 2nd or 3rd trimester. Itincludes the evaluation of fetal presentation, fetal number, amniotic fluid volume, placentalposition, cardiac activity, fetal biometry, & anatomic survey.

149. Substance abuse: Indiscriminate use of drugs during the pregnancy, particularly the firsttrimester, may adversly affect the health of the woman and the growth of the fetus.

(cocaine/ alcohol, methadone) 150. SURGERY DURING PREGNANCY:o Risk of spontaneous AB & PTL

o In 1st tri= inc. risk of SA, best time is in 2nd tri. or postpartum, in 3 rd its difficult becauseof enlarging uterus and inc risk of preterm labor.

o Recommended procedures- appendicitis, cholecystitis, bowel obstruction, melanoma,ovarian disorders, breast or cervical disease or trauma.

o Essential to avoid

• maternal hypoxia, pneumonia, thrombophlebitis

For woman who receiving surgery we need to consider HTN, wedge pt on table, you needSCD, need to consider that gastric content may be elevated because of uterus- so they willlikely have an NG tube, foley. Fetal heart tones monitored before during and after.

Epidural/Spinal anesthesia preferred because local anesthetics are not associated w birthdefects. But may cause hypotension, can be prevented w 900 to 1000 mL infusion beforeprocedure.

Fluid replacement from bld loss is done w electrolyte solution and/or whole blood.

151. Thalassemia During Pregnancy: -group of autosomal recessive disor ders characterizedby a defect in the sys=nthesis of alpha or beta chains in hgb. beta-thalassemia is mostcommon in US.

152. Thalassemia During Pregnancy-Clinical Therapy & Nursing: - folic acid supmay need transfusion or chelation therapy. Care is similar to sickle cell anemia.

-genetic counseling

153. Thalassemia During Pregnancy-Maternal/fetal/neonatal risks: -Maternal/fetal/neonatal risks:pregnancy is rare in women with b -thal. major. in womeb-thal. minor has mild anemia with microcytic red cells. she should not recieve iron i

not iron deficient. she has normal serum ferritin levels. newborns may not have sympfor months, once infants start to produce adult type hemoglobin (HbA) they develop anemia and are dependent on transufions, iron chelation therapy may be needed.

154. The MODIFIED Biophysical Profile: (more cost & labor efficient) test consistsand a measurement of the AFI, both of which reflect long term uteroplacental functiomodified BPP is considered NORMAL if the amniotic fluid volume is greater than 5 the NST is reactive. The test is ABNORMAL if either the NST is nonreactive or the Aor less.

155. TORCH: TAXOPLASMOSIS:o Protozoan Toxoplasma gondii

o Contracted through eating raw meat, unpasturized goat's milk, contact with feces ofinfected cats

o Fetal risks- if in 1st tri often ends in SA, Mainly contracted in last month of preg, aninfants born w/out clinical signs of infection. In mild cases infant will have retinocho(inflame. Of the retina and choroid layer of the eye). Severe neonatal - convulsions, cmicrocephaly and hydrocephalus. Infant w severe infection may die soon after birth.Survivors are often blind, deaf, and severly retarted.

o Diagnosis-serologic testing IgM and IgG florescent antibody cream. PCR for T.gonamniotic fluid is the best way to diagnose fetal infection.

o Treatment spiramycin to decrease the frequency of fetal transmission, in 1st tri. doetreat an established infection. If infection is suspected, pyrimethamin/sulfadiazine/folacid after 18th wk pregnancy.



o Moms who aquire this are asympotomatic, myalgia, malaise, splenomegaly, might have alittle rash a little fever, headache, and enlarged posterior cervical lymph nodes.

156. Trauma During Surgery: o Greater volume of blood loss before signs of shock

• Preg woman w large amount of blood loss is able to maintain hemodynamic stabilitytemporarily by dec uteroplacental perfusion, thereby compromising fetal status

o Normal physiologic changes of pregnancy place woman at greater risk of hypoxia,thrombosis, DIC, abruption, ROM

o Nursing considerations

• Maintenance of cardiorespiratory functioning

• Stabilize injury

• Avoid development of supine hypotension

• Evaluate for placental abruption

Partner violence or car wreak... Oh I'll give my life for my baby- you treat mom first... Payattention of uterine tone... Get mom under control then you worry about baby

157. Two most common methods of ultrasound scanning are transabdominal &transvaginal.: -Transabdominal: transducer is moved across the abdomen. The woman isusually scanned with a full bladder, except when ultrasound is used to localize the plcaentabefore amniocentesis. The woman may feel discomfort from pressure applied over a fullbladder.

-Transvaginal: uses a probe inserted into the vagina. Once inserted, the transvaginal probe isclose to the structures being imaged and so produces a better, clearer image.

158. What can CVS detect?: fetal karyotype, hemoglobinopathies, phenylketonuria,antitrypsin deficiency, down syndrome, duchenne muscular dystrophy, and factor IXdeficiency.

159. When can an Amniocentesis be performed and what can it detect?: Amnperformed between 15 & 20 weeks gestation. Amniocentesis can make chromosomalbiochemical determinations (enzyme analysis, AFP measurement for neural tube defeblood typing, or cytogenetic, metabolic, or other DNA testing) and can validate

abnormalities detected by ultrasound. Later in pregnancy, from about 30 to 39 weeksgestation, amniocentesis may be done for lung maturity studies, such as LS ratio.

160. When is CVS performed?: performed between 10 and 12 weeks. The CVS resuobtained in 24 hours if the direct pr eparation method is used and in 7 to 10 days whentissue culture is used.

161. When is insulin therapy indicated?: when dietary management fails to meet apostprandial level less than 120 or fasting glucose less than 95.

OB - Blueprints OBGYN Part 1

1.At what beta-hCG level should an IUP be seen?: between 1,500 and 2,000.

2.At what gestational age does the closure of the neural tube happen?

- what are the most common NTD?

- #1 risk factor for NTD?: week 6 according to LMP

- spina bifida (posterior NT) and anencephaly (anterior NT)

- #1 risk factor: low levels of maternal folate

3.Besides symptomatically, how can ROM be diagnosed?: - NITRAZINE PAPEblue (basic) if amniotic fluid is present, normal vaginal secretion is acidic (red)



- FERNING under the microscope due to crystalization of the amniotic fluid from theestrogen that is present in it.

4.Classic caharacteristics of Edward Syndrome: Trisomy 18

- clenched fists

- overlapping digits

- rocker bottom feet

- omphalocele

- tetralogy of fallot

5.Classic characteristics of Patau Syndrome: Trisomy 13

- holoprosencephaly

- cleft lip/palate

- overlapping fingers, polydactaly

- clubfoot

6.Dates of 1st, 2nd and 3rd t rimester: 1st: 0 - 14 weeks

2nd: 15 - 28 weeks

3rd: 29 - delivery

7.Define and describe Nagele's rule: Used to estimate date of delivery:

- subtract 3 months from LMP and add 7 days.

8.Define episiotomy: incision in the perineum to facilitate delivery.

9.Define labor: Labor: regular contractions that cause cervical change in dilation oreffacement.

10.Define PROM (premature rupture of membranes).

- define prolonged PROM.

- define PPROM (preterm premature rupture of membranes): - PROM: rupturmembranes at least 1 hour prior to the onset of labor.

- Pronlonged PROM: when PROM occurs more than 18 hours before labor.

- PPROM: when PROM occurs before 37 weeks gestation.

11. Define Recurrent Abortions.

- most common cause?: Def: 3 or more consecutives SABs.

- #1 cause if antiphospholipid antibody syndrome

- #2 cause is luteal phase defect and lack of adequate progesterone to carry the pregna

12.Define Spontaneous Abortion: pregnancy that ends before 20 weeks gestation

13.Define Stage 1 of labor.

- what are the phases of the first stage of labor?: DEF: onset of labor to compleof the cervix.

- latent phase: labor onset - 4 cm di lation

- active phase: 5 cm - 9 cm

14.Define Stage 2 of labor: DEF: complete dilation of cervix/10 cm to delivery of b

15.Define Stage 3 of labor: Starts after delivery of the baby, until delivery of the pl



16.Define:

- placenta accreta

- placenta increta

- placenta percreta: ACCRETA: invasion of the placenta superficially i nto the myometrium

INCRETA: invasion of the placenta well deep into the myometrium

PERCRETA: invasion of the placenta through the myometrium and into the serosa

17.Defininiton preterm birth: prior to 38 weeks.

18.Describe the 4 degrees of perineal lacerations after a delivery:: - 1st: skin only

- 2nd: extends into the PERINEAL BODY but does not involve the anal sphincter

- 3rd: extends into and through the ANAL SPHINCTER

- 4th: ANAL MUCOSA itself is entered.

19.Describe the following types of spontaneous abortions according to CERVIX, BLEEDING,products of conceptions POC:

- threatened

- inevitable

- incomplete

- complete

- missed: THREATENED: closed os, painless bleeding, poc in uterus with normal heart tones

INEVITABLE: open os, painful bleeding, poc in uterus

INCOMPLETE: open os, painful bleeding, partial poc in uterus and in vagina/cervix

COMPLETE: closed os, +/- bleeding, no poc in uterus

MISSED: closed os, +/- bleeding, poc in uterus without heart tones

20.Describe the m anagement of recurrent spontaneous abortions: 1. karyotyparents

2. hysterosalpingogram for maternal anatomy

3. screening tests for THYROID, APA syndrome, SLE, HYPERCOAGULABE STATleiden, protein S/C deficiency)

4. progresterone levels

21.Describe the NST.

- describe the normal/reactive results.

- how should an obgyn proceed if NST is non-reactive?: NST is a test for fetal h

- Reactive: two accelerations of fetal heart rate in 20 minutes that are at least 15 beatsabove the baseline heart rate for at least 15 seconds each.

- Nonreactive: proceed with ultrasound

22.How are NTDs screened for?: Quad screen:

- MSAFP levels will be high

- hCG levels will be low

23.How can labor be mechanically and chemically induced?: MECHANICALLamniotomy, by using a hook to puncture the amniotic sac



CHEMICALLY: with Pitocin

24.How is Down Syndrome screened for in utero with labs and us?

- what are the results associated with Down Syndrome?: LABS:

- Quad Screen: maternal-serum AFP (low), hCG (high), estriol (low), inhibin A

- plasma protein A

US: nuchal translucency

- @ 15 - 20 weeks

25.How is fetal lung maturity assessed?: Via the lecithin/sphingomyelin ratio (L/S ratio).

- normal ratio is > 2 and indicates low risk of respiratory distress syndrome (RDS).

26.How is placenta previa diagnosed?

- how is placenta previa managed?: Via abdominal US.

MANAGEMENT:

- abdominal US should be repeated in the third trimester to see if placenta has moved andplacenta previa has resolved.

- strict pelvic rest

27.How should beta-hCG levels behave with a normal pregnancy?: they should doubleevery 48 hours

28.MEDICAL therapy for an ectopic pregnancy: methotrexate

29.Most common cause of 1st trimester abortions.

- 2nd trimester abortions: 1st: chromosomal abnormalities

2nd: anatomical abnormalities (uterus or cervix/incopetent cervix)

30.Most common location of ectopic pregnancy.

- what are some ectopic pregnancy risk factors?: fallopian tube

- risk factors:

1. scarring of the tube due to STIs, PIDs, endometriosis

2. use of IUD

3. hx of prior ectopic pregnancies

31.Normal fetal HR: 110 - 160

32.Placenta Previa

- define

- #1 risk factor for it

- classical clinical sx: DEF: abnormal implantation of the placenta over the internal o

- may be complete, partial or marginal.

RISK FACTOR: hx of prior uterine surgeries

SX: painless vaginal bleeding after 28 weeks gestation ("sentinel bleed")

33.Plancetal Abruption

- def



- risk factors

- clinical presentation/sx: DEF: premature separation of the placenta from the uterus

RISK FACTORS: htn (#1), cocaine use, trauma, prior hx of abruption

SX: 3rd trimester severely painful bleeding

34.sx:How is placenta abruption diagnosed?: mostly clinically

35.Treatment for incompetent cervix: betamethasone, strict bed rest and cervical cerclageat 12-14 weeks until 36 - 38 weeks.

36.Uterine Rupture

- at what setting do m ost of them occur?

- #1 risk factor?

- sx: Setting: most will occur during labor

Risk factor: uterine scar from hx of uterine surgery

Sx: intense abdominal pain, vaginal bleeding -> hypotension if severe, cessation of uterinecontractions

37.What are the 3 signs of soon-to-be placental delivery?

- how long does the placenta have to be delivered before a patient is diagnosed with aretained placenta?: 1. cord lengthening.

2. gush of blood

3. uterus will contract and become firm

- must be delivered in 30 minutes.

** do not attempt to deliver the placenta untill all 3 signs are present

38.What are the 5 components of cervical examination for labor?

- describe each one.: - dilation

- effacement (how thin the cervix is as it is compressed by baby's head)

- fetal station (relation of baby's head to mom's ischial spine; negative when above, pwhen below)

- cervical position

- consistency of the cervix (firm, soft)

39.What are the cardinal movements of labor, in order?: - ENGAGEMENT

- FLEXION

- DESCENT of the head into the pelvis

- INTERNAL ROTATION so that the sagital suture is parallel to the anteroposterior dof the pelvis

- EXTENSION and EXTERNAL ROTATION

40.what are the components of a BPP?

- what is a normal score?: 1. amniotic fluid levels

2. fetal tone



3. fetal activity

4. fetal breathing movements

5. nonstress test (NST)/fetal heart rate

Normal score in between 8-10

41.What are the genetic diseases where every baby is screened for?: - CF

- sickle cell

- Tay Sachs

- thalassemias

42.What are the most common sex chromosomal abnormalities?: - Turner (45 XO)

- Kleinfelter (47, XXY)

43.What are the most common tocolytics?

- what are they used for?: TERBUTALINE and MG SULFATE

- used as labor supressants; will inhibit uterine contractions

44.What are the types of decel?

- for each type, describe what it LOOKS LIKE IN FETAL TRACING MONITOR and CAUSES OFIT.:EARLY: head compression.

- mirror image with mother's contraction

VARIABLE: cord compression

- no relation to mom's contraction but will look li ke "w" or "jagged carrot".

LATE: hypoxia due to placental insufficiency.

- may or may not be associated with loss of variability.

- will occur after mom's contraction

45.What is IMP to KIM about the physical exam in a patient with placenta previa?:digital exam should be performed!!!

46.What is the Bishop score?

- describe.: For each component of the cervical examniation during labor, there is a 2 points for a grand total of 10 points.

- a Bishop score is the summation of all points.

- a score > 8 indicates favorable conditions for spontaneous labor.

47.What is the maximum number of days by which EDD can differe between LMP andUS?: 7 days.

- When the difference is more than 7 days, the US predominates.

48.What is the uterine fundal height when the fundus of the uterus reaches the level of the umbilicus?: 20 cm

- at 15 cm it will be halfway between pubic symphysis and umbilicus

49.What type of decels are commonly seen in the second stage of labor?: Eacompression) and Variable (cord compression).



50.When during the process of labor is an epidural administered?: during the active phaseof the first stage of labor.

51.When in the pregnancy can fetal heart tones be heard?: 10 - 14 weeks

52.When is amniocentesis performed?

- when is chorionic villus sampling performed?: Amnio: 15 weeks

CVS: 9 - 12 weeks

53.when is GBS screened for?

- tx if positve.: between 35 and 37 weeks, cerca 36 weeks.

- penicilin is drug of choice.

- if mom is allergic, second choice is cefazolin.

- if cefazolin r esistant, attempt clindamycin

54.When looking at a fetal heart tracing monitor (such as NST), what must be present fordiagnoses of a reassurant (but not necessarily reactive) tracing?: VARIABILITY and HR withinnormal limits.

- presence of variability is the jaggedness of the line.

55.Which shoulder is delivered first?: anterior first by pushing baby down.

- posterior second by bringing baby up after anterior shoulder has been delivered

Obstetrics: Teratogens + Defects

1.ACEIs:Oligohydramnios, fetal renal damage

2.Aminoglycosides (gentomycin, neomycin, streptomycin): Deafness

3.Carbamazepine: Fingernail hypoplasia, craniofacial defects

4.Cocaine: Cerebral infarcts, mental retardation, bowel atresias

5.DES:Clear cell vaginal cancer, adenosis, cervical incompetence

6.Diazepam: Cleft lip and/or palate

7.Iodine: Goiter, mental retardation

8.Isotretinoin: Ear, CNS, craniofacial, and CV defects

9.Lithium: Cardiac (Ebstein's) anomalies

10.Maternal diabetes: macro or microsomia and ___: CV malformations, cleft lip and/or palate, caregression (lower half of body incompletely formed), neural tube defects, left colon hypoplasia

11. OCPs: VACTERL syndrome

12.Phenytoin: Craniofacial, limb, and cerebrovascular defects, mental retardation

13.Progesterone: masculinization of female fetus

14.Quinolones: cartilage damage

15.Sulfonamides (thiazides, TMP-SMX): kernicterus

16.Tetracyclines (doxycycline): Yellow or brown teeth

17.Thalidomide: Phocomelia (absence of long bones and flipper-like hands)

18.Valproate: Spina bifida, hypospadias

19.Warfarin: Craniofacial, CNS malformation, IUGR, stillbirth

Documents

Abnormal OB