The ATI will be on Tues Locke 313 at 1100. The N8 Final will follow. Then the theory and clinical evaluations are to be turned in.
The ATI results are usually back within 24 hours up to 2 days max. We have to score at least a 40th percentile in the program or retake the home version and score at least an 85% before our pinning and before we can get a grade. Recommends taking the ATI and then going home and taking the unsecured version just in case. Cannot be taken ahead because it is timed.
The Final will worth 50 points.
Test only covers complications covered in the last 2 lectures.
It will contain multiple multiples and not a lot of writing. It is one of the shorter tests and is usually finished in an hour or less.
Here is the final review typed from a recording. It is not necessarily in the order given but is grouped by subject. I will post the answers with the page numbers in the comments soon. Please contribute your findings and thoughts
NST testing. (4 points)
How many beats should it go up to be considered reactive?
How long do they last?
How many times in how many minutes?
Need to tell if it is reactive or non reactive.
What does a positive contraction stress test mean?
You are not going to have a strip but you need to know it means if it is positive or negative.
What causes GDM?
What are the 2 things that the placenta produces that can predispose a woman to GDM?
Which one is a hormone and which is an enzyme?
How is GDM diagnosed?
What test is done to diagnose it?
How do you manage GDMs?
How often do you need to do ultrasounds?
How often would you do a FSBS?
What kind of diet?
What is a GDM mom at risk for?
Will more or less insulin be needed if insulin dependent as the pregnancy progresses?
Why does a baby for a GDM mom develop hypoglycemia?
How will you handle this baby?
Why do DM babies have RDS?
Know the warning signs of PIH.
Know if it is getting worse.
Know what normal edema is and what is not.
What are the vision symptoms?
How do you know if the pt has a clear understanding? Will have to pick out the true and false statements
PIH treatment at home
What is the rationale for increasing your dietary protein?
What happens in PIH that you would have to do that?
Is increasing the intake of water good or bad?
Treatment of MgSO4
How do you know that it is doing the job?
What is its primary focus, why is it given?
It does have other side effects that help, but what is the primary reason that MgSo4 is given in the hospital setting?
Review assessments and interventions.
How often do you do reflex checks?
How often do you do urine checks and what should the urine be?
How often would you check MgSo4 levels?
What drug do you give if there is MgSO4 toxicity?
If a PIH mom has a seizure and there is ROM and meconium, know why this happened.
What do you do with a woman in labor, which the fetal baseline goes down and you have persistent late decelerations?
What are all of things that you do like turn them on their side; give them O2, bolus and all that stuff.
If this happens with a woman who has PIH, would these same things done?
Do you turn her on her side; give O2 and a fluid bolus?
Is there anything different in the way that you treat her?
What is the cause of PIH?
Does it usually reoccur?
What are the complications that a baby would have if they were IUGR (a small baby)?
What kind of problems would they have?
What do you have to do before increasing the dose of pitocin for a woman who is being induced for labor?
Does pitocin need to be run through a pump or can it be free flowing?
When should you discontinue pitocin?
Under what criteria?
What might be going on with the mom that you would stop it?
How do you diagnose if somebody is really in preterm labor?
How do you know, what is happening with her that makes you think that she really is in labor that early?
How do you take care of a pt on terbutaline, which is a tocolytic?
What side effects does the medication have?
How high do you let certain levels go, like HR?
Does terbutaline affect any other lab values?
Why do you give preterm labor moms betamethasone?
If a woman is in preterm labor, what test might they do to see if the baby has mature enough lungs?
What problem do preemies have with the RDS?
What happens initially?
What happens later?
What is the pathophysiology of RDS?
What are some side effects of giving too much O2 to babies?
How do monitor that?
What can you do to prevent some of those problems related to giving O2 to babies?
Know about Rh negative moms and Rh positive babies.
When is jaundice normal?
When would it be abnormal?
What kind of tests might you run on a baby that is jaundiced?
What is the difference between placenta previa and abruptio placenta?
What is the procedure called when you have an incompetent cervix and they fix you so that the baby doesn’t fall out?
3 comments:
What is the purpose of a NST?
To evaluate the FHR in response to fetal movements (pg 105 and 105a in Study Guide and Pg 231 in Text)
(Kick counts) Should have at least 2 fetal movements within 20 minutes that cause an acceleration of the FHR of at least 15 beats above baseline and which last for at least 15 seconds. If these criteria are met the test is considered reactive.
Reactive is the desired outcome to continue an at risk pregnancies If not reactive further evaluation is needed..
Remember to state whether reactive or non reactive
Reactive NST – 4 pts for 4 things
1. How many beats FHR(above baseline)
2. How long did they last
3. How many times in how many minutes
4. Was it reactive or non reactive
Basically looking to see if the baby’s HR goes up when it moves.
What does a positive contraction stress test mean? (pg 106 in SG and 231 in T)
A positive contraction stress test is a warning sign of fetal compromise and has fewer false-positives than a NST.
Contractions will produce late decelerations in the FHR if there is uteroplacental insufficiency.
We are not going to have a strip but will need to know what it means if it is positive or negative.
Contractions are caused by stimulation of the breast nipples or with pitocin.
Positive – Persistent and consistent late decels with more than half of the uterine contractions.
Negative – No decels within a minimum of 3 contractions X 40-60 seconds in 10 minutes.
What causes GDM? (pg 109, 114 SG, 330-333 T)
GDM is caused by a borderline functioning pancreas’ inability to compensate with increased insulin production in response to the placentas production of HPL and insulinase which reduces the mother’s ability to transport glucose into her cells.
What are the 2 things that the placenta produces that can predispose a woman to GDM? (pg 109 SG, 198 T)
The placenta secretes a hormone called hPL (human placental lactogen) also called hCS (human chorionic somatomammotropin) which interferes with the ability of insulin to transport glucose into muscle and adipose tissue cells.
The placenta also secretes an enzyme called insulinase which accelerates the breakdown of insulin which decreases its effectiveness.
Which one is a hormone and which is an enzyme? (pg 109 SG)
hPL(aka hCS) is a hormone and insulinase is an enzyme
How is GDM diagnosed? (330 T)
GDM is any degree of glucose intolerance with its onset or first recognition during pregnancy and is diagnosed through signs and symptoms which lead the health care provider to order a glucose tolerance test.
What test is done to diagnose it? (pg 330 T, Tabors GDM, 114 SG)
GDM is diagnosed through a fasting glucose tolerance test.
How do you manage GDMs? (pg 110-114 SG, 330, 333-338 T)
Assessments
- Hx of family DM, obstetrical, personal health
- Physical assessments same as pregestational
- Age of onset
- Type of control
- Cardiovascular (atherosclerosis, BP)
- Eyes (retinopathy)
- Kidneys (nephropathy)
- Nerves (neuropathy)
- Infections (UTI, monilial vaginitis)
- All other routine prenatal assessments
Fetal surveillance of GDM (SG 111)
- Ultrasound
- AFP 17-20 weeks for increased chance of neural tube defects
- Urine and serum estriole levels
- Weekly NST from 34 weeks: CST if NST abnormal
- Biophysical profile( NST, AFI (amniotic fluid index), fetal tone, fetal breathing movements
- Amniocentesis at 12-16 weeks for genetic analysis and 3rd trimester for PG level and L/S ratios
Labs
- 24 hour urine collection
- urinalysis for , UTI, ketones
- Thyroid function
- Accuchecks QID
- HgbA1C (3 month glucose measurement)
How often do you need to do ultrasounds? (T 338, SG 111)
During 1st trimester to determine EDB and throughout the pregnancy as often as every 4-6 weeks, but at least 2 times.
How often would you do a FSBS? (T 337, SG 112)
BS levels should be checked as ordered by healthcare provider which could be fasting and after meals.
- Before breakfast, lunch and dinner
- 2 hours after meals
- At bedtime
- In the middle of the night
What kind of diet? (SG 112, 334 T)
- ADA diet
- 2000-2200 calories daily
- Based on blood sugar levels
- 3 meals and 3 snacks (1 substantial bedtime snack)
- 50% CHO, 30% fats and 20% proteins
- Prescribed prenatal vitamins and iron
- High fiber
- Reduce amounts of refined sugar, saturated fats, cholesterol,
- Avoid alcohol, caffeine,
What is a GDM mom at risk for? (T 332, SG 110)
- HTN
- PIH
- Abruptio placenta from PIH
- Increased prenatal visits
- Monilial vaginitis
- UTI
- Infections
- Dystocia (difficult labor)
- C Section delivery (T 338 – 45%)
- Polydramnios
- Emotional stressors
- Increased testing
- Hospitalization during pregnancy
- Loss of fetus (stillbirth and congenital anomalies)
- Fetal abnormalities (congenital) especially cardiac and neuro
- Fetal need for NICU
- Fetal RDS
- Fetal macrosomia or IUGR
- Neonatal hypoglycemia, polycythemia and hyperbilirubinemia
Will more or less insulin be needed if insulin dependent as the pregnancy progresses? (113a SG)
Most GDMs do not require insulin, but if insulin dependant will require…
- 1st trimester a decrease in need for insulin R/T increase in insulin production by the pancreas and increased peripheral sensitivity to insulin, nausea, vomiting and decreased food intake (T 331)
- 2nd and 3rd trimester insulin need increases (double to triple) R/T increasing levels of hPL(aka hCS), estrogen, progesterone, prolactin, cortisol, and insulinase. (T 331)
Why does a baby for a GDM mom develop hypoglycemia?
The fetus of a DM mom compensates for the increased glucose levels from mom by increasing its own insulin production. When mom’s glucose supply is cut off with the clamping of the cord, the still elevated insulin levels of the baby move the remaining glucose into the cells which cause hypoglycemia until the baby’s insulin production can adjust to the decreased glucose levels.
How will you handle this baby? (SG 116, 132, T 821 )
Assess IDM babies for…
- Hyperinsulinemia - watch for hypoglycemia within 1-3 hours
- Hypoglycemia - accucheck protocol< feed
- Congenital anomalies – report abnormal physical and/or reflex activity
- Macrosomia
- Birth trauma
- Perinatal asphyxia
- RDS – nasal flaring, expiratory grunting, chest retractions
- Hypocalcemia – suspect if jittery and accucheck nomal and neg drug screen, apnea, tetany; replace Calcium via formula or IV fluids
- Hypomagnesemia
- Cardiomyopathy
- Hyperbilirubinemia -
- Polycythemia – hct > 65%, risk for jaundice
Why do DM babies have RDS? (T 200, 814, SG 116)
The increased insulin levels in the fetus required to handle to increased glucose levels from mom directly inhibits the production of lecithin an alveolar surfactant which is needed to keep the lungs inflated and predisposes the neonate to progressive atelectasis which is known
PIH
What is the cause? (SG 118, T 371- )
Unknown cause
How does it progress? (SG 117a)
Vascular sensitivity – HTN – Renal Ischemia – Proteinuria – Intravascular to Interstitial shift – Edema – Hemoconcentration
Progression can then lead to severe preeclampsia, HELLP syndrome or eclampsia
Does it recur?
Yes, higher incidence if have had previously
Warning signs of PIH (SG 118)
- HTN
- Proteinuria
- Edema (upper body, face, hands) Normal edema is in the legs and ankles.
- Increase of 30mmHg systolic or 15mmHg diastolic over baseline X 2 assessment within a 6 hour time frame
Signs of getting worse
- HA (especially after reading)
- BP continues to rise
- Epigastric pain (from a hypoxic liver which can lead to HELLP syndrome)
- Hyperreflexia
- Blurred vision
- Scomata (blind spots)
- Increase in proteinuria
PIH Tx at home (T 379,)
- Bed rest or move to couch with BR privileges
- Gentle exercises
- Increase fluids to at least glasses a day
- Encourage family participation in care
- Use relaxation to cope with stress
- (Education BIG regarding preeclampsia for motivation to follow plan) Make sure mom understands what is going on, why, what to do and what subjective and objective sign to report to healthcare provider
- Rest on L lateral side
- Home health visit 2 or 3x a week
- Self assessments of urine dipstick for protein, weight, BP, baby’s activity daily
- Keep at antenatal visits 2x a week.
- Ultrasound q 3 weeks and amniocentesis to check lung maturity in 3rd trimester.
- NST once or twice a week as needed
Why increase dietary protein?
To replace albumin that was lost in the urine and tissues which results in hypovolemia
Is it good or bad to increase your water intake?
Good since there could be a vascular hypovolemia R/T fluids moving into tissues
Diet (T 381)
- Regular diet to start
- Increased protein to replace albumin lost which will increase oncotic pull in the vasculature to pull the fluid back in from edematous tissues
- Increased fluids (restricted with severe eclampsia R/T severe vasoconstriction)
- Moderate salt
- No Diuretics (Even with edema can still be hypovolemic)
Rest on L lateral recumbent
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