Showing posts with label OB. Show all posts
Showing posts with label OB. Show all posts

Thursday, April 30, 2015

Innovation in Uganda

                                                         Healthcare In Africa? There's An App For That | TakePart World

Saturday, December 20, 2014

Overview of the Hormones of the Female Reproductive Cycle: E, PG, GnRH, FSH, LH

The human female reproductive system is guided by an incredible coordination of hormones. This is the first of a series of posts reviewing the hormones involved in the ovarian and uterine cycles.  It is important to realize 2 things: 1) that the ovarian and uterine cycles operate on the same hormone signals: estrogen, progesterone, GnRH, LH, FSH.  The production of these hormones are intertwined. 2) These hormones are free flowing in the blood, so, if there is an increase GnRH, there will be an increase in FSH and LH systemically, which means there will be an increase in estrogen and progesterone systemically, which means that both the ovaries and the uterus will be fluctuating/reacting at the same time.


http://ib.berkeley.edu/courses/ib140/ovarian%20cycle,%20uterine%20menstrual%20cycle,%20menstruation_files/image016.jpg


Gonad/o/tropin Releasing Hormone: GnRH is a hormone released by the hypothalamus, that stimulates the anterior pituitary to release LH and FSH, which are hormones that act upon the sex organs, also known as "gonads" (hence the name GONAD-o-TROPIN.)  In most cases, the presence of both estrogen and progesterone in the bloodstream at the same time will inhibit the hypothalamus from releasing GnRH.  This is a type of negative feedback.  (However, during a part of the uterine and ovarian cycle, estrogen actually becomes a positive feedback loop--no one really knows how this happens, but I will attempt to explain how to identify when this happens in a later post.)

Follicle Stimulating Hormone: As the name implies, this hormone stimulates the follicles.  Follicles are a generic term for any type of little sac, or cavity.  In the case of ovarian follicles, we're talking about the little sack that surrounds a single egg before it is released from the ovary into the fallopian tube.  All of a woman's oocyte first starts off as primordial follicles-- primary oocytes surrounded by a single layer of squamous granulosa cells.  FSH is the hormone that helps each primary oocyte begin developing into a mature follicle with a gigantic fluid filled antrum.  The antrum builds up so much pressure it explodes, jettisoning the oocyte out of the ovary during ovulation.
https://classconnection.s3.amazonaws.com/427/flashcards/1500427/jpg/picture21335761453346.jpg

Luteinizing Hormone: This hormone causes the follicles to complete maturation and undergo ovulation in the "LH surge."  Right as the oocyte has exploded out of the ovary and into the waiting arms of the fimbriae, LH causes the leftover follicle bits (mostly granulosa cells) to crumple up into the corpus luteum (the fact that luteinizing hormone has the same root word as corpus luteum, should not escape your notice).  These granulosa cells change into luteal cells, and supports the corpus luteum in its task to secrete large amounts of progesterone and some estrogen.

Estrogen: Estrogen is secreted by granulosa cells.  The primary reason for granulosa cells secrete estrogen is for a positive feedback loop with LH to induce a ovulation.  The secondary reason for estrogen secretion is to increase the number of progesterone receptors in the uterine lining.  This is necessary to increase progesterone sensitivity in the uterine lining so that the uterine lining can proliferate, becoming thicker with more blood vessels to create nice, nutrient rich lining for the potential embryo.

Progesterone: The pregnancy hormone.  Progesterone is secreted by the corpus luteum, and later by the chorionic villi, and then, when the placenta finally becomes functioning, it is secreted by the placenta.  In order for a pregnancy to remain viable, there has to be a consistent, elevated level of progesterone.  Progesterone does many things, which I will cover in a different post, but the most important one is, it relaxes the muscles of the body, causing a decrease chance of uterine contraction (which would lead to spontaneous abortion).


https://courses.stu.qmul.ac.uk/smd/kb/microanatomy/humandev/placenta/index.htm

Human chorionic gonadotropin:  The pregnancy test hormone.  Human chorionic gonadotropin is only released by the syncytiotrophoblast of the blastocyst (see the picture above).  More specifically it is secreted by the most superficial epithelial layer of the embryonic placental villi, so there has to be an embryo mature enough to be embedding into the uterus for this hormone to appear.   (You should remember that embedding of the embryo occurs about 8 days after fertilization, so hCG would appear around day 22 of a standard menstrual cycle).  HCG is like the little brother of luteinizing hormone.  You know how sometimes there are two siblings who play the same sport but the little one not only plays at the same level as the older, he also seems to be able to land all the tricks the older one can't?  If LH were the older brother, hCG would be the little brother who can do the same thing as LH, except better, because it is secreted even in the presence of elevated estrogen (remember elevated levels of estrogen causes a negative feedback repression of GnRH, which would cut off the supply of LH from the pituitary).  Sometimes LH is referred to as the pituitary analogue.  As the analogue, hCG continues to support the corpus luteum after LH has faded from the blood stream, ensuring that there is a steady release of progesterone and estrogen even after the high concentrations of progesterone and estrogen have caused the pituitary to stop releasing LH.  Additionally, FSH is also suppressed, which is good, because the woman's body doesn't need to be wasting energy maturing extra oocytes when there's already a pregnancy underway.


References:

Perry, Shannon E., Marilyn J. Hockenberry, Deitra Leonard Lowdermilk, and David Wilson.  Maternal Child Nursing Care. St. Louis: Elsevier, 2014. 5th Ed.
Seeley, Rod, Cinnamon VanPutte, Jennifer Regan, Andrew Russo.  Seeley's Anatomy and Physiology. Boston: McGraw Hill, 2011. 9th Ed.
http://en.wikipedia.org/wiki/Syncytiotrophoblast


Wednesday, December 10, 2014

Magnesium sulfate and flushing

How I felt today:






Today was the OB ATI test.  70 questions in 70 minutes.  This was my question 68.  I was stumped, and tired, and frankly, by this point, didn't give two craps.  I just needed to get out of that room.  Now that I've finally got a few hours of sleep and had some time to think about it, I'm pretty sure I got it wrong, so I decided to do a post-mortem on it.

I'd like your input.

Here's the question:

A nurse is caring for a patient with preeclampsia with magnesium sulfate.  Which of these symptoms should you report to the provider?  Select all that apply.

a) Respiratory rate of 20 per minute
b) A urinary output of 400 mL/4hr
c) Epigastric pain
d) Facial flushing
e) Lack of deep tendon reflexes

I'm pretty confident I got this answer wrong, so what did you answer?  Why?  I'll give you a minute to think, and I'll explain my answer choices and reasonings below.

By the way, this is what a vial label for magnesium sulfate IM might look like:

http://dailymed.nlm.nih.gov/dailymed/image.cfm?id=59573&name=274e5d29-figure-02%2Ejpg

Ok, here's the question again:

A nurse is caring for a patient with preeclampsia with magnesium sulfate.  Which of these symptoms should you report to the provider?  Select all that apply.

a) Respiratory rate of 20 per minute
b) A urinary output of 400 mL/4hr
c) Epigastric pain
d) Facial flushing
e) Lack of deep tendon reflexes

I chose c) and e).  I think I should have chosen c), d), and e).

I had some confusion over this question for 2 reasons.  With the phrase "which of these symptoms" it was unclear to me whether the question was asking for the symptoms for preeclampsia progressing to eclampsia (essentially, the treatment was failing), or asking for the symptoms of magnesium sulfate overdose, or both.  In the moment my brain just thought: "Well, I'm going to report any potentially life threatening symptoms," because, you know, real life.  A good test taking tactic, if you don't know the answer to a question is to strike out the obviously WNL (within normal limits) answers.

a) Incorrect.  A respiratory rate of 20 breaths per minute is within normal range.
b) Incorrect.  An output of 30 mL/hour is "normal" on NCLEX questions.  30mL/hr x 4hrs = 120mL, so 400 mL/4hr is more than sufficient.
c) Epigastric pain.  Here's where it got a little confusing.  Was this question strictly about calling for signs of magnesium toxicity?  Or was it asking for what I should alert the doctor about in general?  Because epigastric pain, especially RUQ (right upper quadrant pain) is classic s/s of liver swelling, which happens with preeclampsia because the elevated blood pressure causes the blood to back up from the heart into the systemic circulation.  (The first organs to be affected by this systemic increase in blood pressure are your brain, heart, kidneys, and liver.)  This is why with preeclampsia and eclampsia, you'll see elevated liver enzymes.
d) Facial flushing.  I couldn't, for the life of me, remember with 100% certainty that facial flushing was a side effect of magnesium sulfate.  My gut said yes, but my brain was being a non-committing coward.  More on this later.
e) Magnesium sulfate classified as an anticonvulsant because it is a CNS depressant.  It blocks the transmission of Ach (acetylcholine), which decreases motor nerve impulse.  It would make sense, then, that if someone was given too much mag sulfate, that it would cause a cessation of motor nerve impulses, leading to a lack of deep tendon reflexes.  For a video explanation on how to perform deep tendon reflexes, click here.

So I got home and researched magnesium sulfate, and this is why I think I should have picked d):
http://www.healthline.com/health/pregnancy/preterm-labor-magnesium-sulfate#Overview1
Basically, it would have similar results to a calcium channel blocker.  It does not have the same mechanism of action, but if you think about it, calcium channel blockers block the calcium channels in smooth vascular muscles, prevent an influx of calcium, which causes vasodilation (hence, why a side effect of nifedipine is orthostatic hypotension).  Similarly, if you decrease the calcium blood levels by administering magnesium sulfate, there won't be an influx of calcium through channels on the smooth vascular muscles, so your body will be unable to vasoconstrict.  The vessels will remain vasodilated.  What else happens with vasodilation?  Flushing!  You get red.  When it's hot outside, or when you work out, or when you are embarrassed, your blood vessels dilate, causing flushing.

I'm not 100% sure, but it makes sense, right?  And, in the words of Ms. Soberano, "If you can defend your reasoning, then it's a good answer."

Now, if I could figure out why we use calcium gluconate as the antidote...

References:
http://www.drugs.com/sfx/magnesium-sulfate-side-effects.html
http://www.rxlist.com/magnesium-sulfate-side-effects-drug-center.htm
http://www.surgeryencyclopedia.com/La-Pa/Laxatives.html
http://en.wikipedia.org/wiki/Magnesium_sulfate
http://www.healthline.com/health/pregnancy/preterm-labor-magnesium-sulfate#Overview1
http://www.ncbi.nlm.nih.gov/pubmed/1331782
Mosby's 2013 Nursing Drug Reference
https://www.youtube.com/watch?v=0sqCIzuotWo
http://en.wikipedia.org/wiki/Calcium_channel_blocker
http://www.drugs.com/nifedipine.html

Cramming for exams: Prioritizing at its finest

Quick.  You have, for whatever reason, not kept up with the reading for a class.  Tomorrow is the final, and you don't know what you're doing.

(Bear with me.  I pulled an involuntary all-nighter--my brain just would not stop racing.  Granted, that's not all that uncommon while in school, still, I am not sure I'll write what I mean to write, so, if something sounds nonsensical, it probably is.  Hopefully that'll add to the post since I'm assuming you're reading this post because you're cramming, probably with an all-nighter.)

I've been reading my Asinine Testing Insanity book for this OB test tomorrow, trying to cram the whole thing into one night of reading, which, I'll admit, isn't the best plan I've had this year, but, we do what we gotta do.  (I mean, they did say it doesn't count, right?)  By now, you've taken at minimum, one test, usually more like 4, and you know where your weak spots are.   For example, I know that the question about normal neonate head circumference always gets me (it is, by the way, 32-36.8 cm or 12.6-14.5 in, which sound like numbers people made up just to make me mad, but they aren't), and I always forget what "telangiectatic nevi" is (stork bites, or flat red marks that blanch, found around the infant's face, that are benign and fade by second year).

Lab values are maddening, but one of the best things to capitalize on.  They change from source to source.  My tip?  Memorize the ATI values (vs the professor's values) because these questions will only pop up once or twice on a 50 question exam from your professor, and you can afford to miss 2 points on a unit exam, but you don't want to mess up on the ATI and have to repeat the course--and standardized tests love to screw you on lab values.

Data you just need to know cold.  There's no way around it.  Some data you're just going to have to route memorize.  For me it was just repeating it, writing it, posting it next to light switches and on bathroom mirrors over and over and over, one fact per day, like memorizing a series of phone numbers (remember back in the day when people actually had to remember phone numbers?  I can still recite my childhood home number from over 20 years ago: 312-985-4715).  And sure, I forget it, but if I glance at them before an exam I can still recall them.

And that's not to say I've got everything memorized.  Like today, I've only got 20% of neonatal data memorized.  But you know what?  Honestly, there are general things you should know, like VS, and the rest will come on a printout when you're at work, so don't sweat it.

Speaking to my classmates, I don't have these memorized, and I'm betting not many of you have these memorized either, so here's the ATI version:

For term babies
Expected VS:
BP: 60-80/40-50mmHg** NOTE: this is different than our professor's ranges of 60-80/45-55mmHg
HR: 100-160/min ** NOTE: this is different than our professor's range of 110-160bpm
Resp: 30-60 c up to 15 seconds of apnea
Temp: 36.5-37.2C or 97.7-98.9F axillary

Expected reference ranges of physical measurements:
Weight: 2,500-4,000 g
Length: 45-55cm
Head circumference: 32-36.8cm (or about 2-3 cm larger than chest circumference due to cephalocaudal development)
Chest circumference: 30-33cm

Expected lab values: 
Hgb: 14-24 g/dL
Hct: 44-64%
RBC: 4,800-7,100,000/mm3
Leukocyte: 9,000-30,000mm3
Platelets: 150,000-300,000/mm3
Glucose: 40-60
Bilirubin: 0-6 mg/dL on day 1; 8mg/dL or less on day 2; 12 mg/dL or less on day 3

Good luck today!