Contraception Myths

Some highlights from my contraception mythbusting crusade.  If only I could get to the Supreme Court…

“The good thing about science is that it’s true whether or not you believe in it.” Neil deGrasse Tyson

For combined Estrogen and Progesterone contraceptives: These prevent ovulation, primarily with the progesterone.  The normal menstrual cycle is below, the cyclic fall and rise of progesterone triggers the LH surge. By keeping this high, negative feedback to the hypothalamus is washed out. No LH surge, no ovulation.  The estrogen is there to recruit more progesterone receptors (so less progesterone is needed), and stabilize the endometrium (less breakthrough bleeding).

menstrual cycle

Ovulation happens at the LH surge. LH is surging because progesterone is low.

Large doses of progesterone only contraceptives (DepoProvera, the MiniPill, and Implants) is enough progesterone to prevent ovulation.  The lower dose progesterone only contraceptives (Mirena/Skyla IUDs, the MiniPill) work by thickening cervical mucus, reduce fallopian tube motility, and thinning the endometrium.

IUDs are not abortifacients.  They actually prevent conception from ever happening: the IUD creates a sterile inflammatory response that is toxic to sperm and ova.  This has been shown in vivo with tubal flushing studies.  Women who are not on contraception can be found to have sperm, non fertilized eggs, and even fertilized, but nonviable eggs in the tubes.  Women with IUDs have fewer of all three: the sperm never get there and fertilization doesn’t happen.

IUDs do not increase the risk of STIs or PID.  There is a slightly higher risk of infection in the first 20 days after insertion. This is either from incompletely sterile technique or if the woman is already infected when the IUD is placed. So make sure your patient is free from cervicitis before inserting an IUD. After that, the risk is no different.  This myth comes from an old IUD, the Dalkon Shield (that parasite-looking thing in the picture below), which DID increase the risk of PID, because it had a multifilament string that acted as a bacterial superhighway.   IUDs

Emergency Contraception is not an abortifacient either.  The EC pills are mostly large doses of progesterone- which works to prevent ovulation, thicken cervical mucus, and impair motility in the fallopian tubes.  Women do not get pregnant if they have had intercourse after ovulation. Sperm lives in the female reproductive tract for up to 6 days after intercourse, and all that time it is making its way up to the fallopian tubes, where fertilization happens.  EC pills prevent ovulation, and are more effective the sooner after unprotected intercourse they are taken (this is why it is helpful for a woman to have it at home before something goes wrong).  If a woman does get pregnant despite taking EC, the pills will not harm the pregnancy.  

Here’s a great table to use when talking about contraception with your patients. Aim to pick a method from the top row: these are the most effective with typical use (because they don’t require the woman to think about anything once in place).  As you move down the rows, preventing pregnancy gets closer and closer to just luck.  And we can do better than that!

contraception effectiveness

Advertisements

Life is Pain, Highness

Noon conference this week was about safe opiate prescribing. I hope that some of you were there and enjoyed it.  As I was making the talk, I felt that I also wanted to learn/teach more about chronic pain and how to treat it.

Most of this information comes from a great TMS (no really) course on Complex Chronic Pain.  If you are interested in the topic, I recommend the course. TMS is here, and you can find the course by searching for V07 Complex Chronic Pain Course. Of course you have to be a VA employee to access TMS.

Do you have patients in your clinic that carry a diagnosis of “Chronic Pain.” Not chronic back pain, or osteoarthritis, or fibromyalgia, but just “chronic pain.” It has been a pet peeve of mine, to label the pain but not the etiology, but turns out that it is a real thing, and our traditional biomedical model just doesn’t do a great job at addressing the issue. We start out with the right things: history and physical, careful testing, conservative treatment. When that doesn’t work, we might refer to a specialist, or PT, or send the patient for injections. Slowly we tread into unproven, non-evidence based therapies, which often don’t work either. Or, the patient feels a little better; often because they felt that they were heard and they believe in the treatment plan, not because the therapy worked.  We keep doing the same things and expecting a different result. the patient feels that their life is on hold while their doctor gets their pain under control. Eventually, the patient gets frustrated with us, we get frustrated with the patient, and the relationship becomes strained.  Often, the patient finds a new doctor and the cycle starts over again.  We are all frustrated and unsatisfied, and we resolve not to do that again.  But we do, because the tools we have are insufficient for the problem

.Components of Chronic Pain

A new way to think about this is from a biopsychosocial model. The root cause of the pain is as much psychosocial and emotional as it is biological, and emotional and social stressors make it worse, just as lifting a refrigerator would. In this model, the doctor has to give up some control, it is really up to the patient to get better. We become the coach, the therapist, rather than the omniscient expert with the prescription pad.  The goal shifts from relieving pain to restoring function and improving health.  Patients move away from a focus on ending pain and minimizing symptoms to “expecting pain” and living their life in spite of that.  The office visit is less about pain control and more about setting and achieving functional goals.  Your job is to teach patients that you hear their frustration and believe that they have pain, but there isn’t a medical solution to this problem, and the two of you are going to work together to help them move on with their life.

there are no magic pills

Chronic pain is aggravated by a variety of things. If you can identify these in your patient, you may be able to help them move forward in recovery. The first is deconditioning: think like an athlete in spring training, they don’t expect to come in at mid-season form. Second is poor coping skills and ineffective stress managment techniques. We should teach that pain is not necessarily leading to more damage, but represents a bump in the road that they will move past.  Pain is inevitable, but misery is optional. Finally, outright mood disorders can aggravate pain. It is reasonable to aggresively seek out and treat these, but in such a way so that the patient doesn’t come away feeling that you don’t believe their pain.

How to help the patient set goals. These need to come from the patient, not you.  Ask about what they want to do, but can’t now.  Listen carefully and pick up on anything that the patient identifies, then try and troubleshoot the barriers.  If they want to exercise, but always have increasing pain, then try and reduce the intensity back to a level that they can acheive. Set goals that seem too easy, too simple, so that you can build on successes- first you have to have successes.  If the patient is not even getting dressed every day, make that a first step. Later they can work toward the gym membership, but if you try and do it all at once, they will end up hurting and less likely to try again.

Goals need to be acheivable, almost easy for the patient. Then build on success.

If you have access, pain psychology or mental health providers can help with cognitive behavioral therapy around coping mechanisms, goal setting, and stress managment techniques.  You can also teach your patient some simple stress managment. Deep breathing and meditation is a simple concept to understand and provides a coping strategy for the patient to deal with pain.  There is an app “Breathe 2 Relax” that teaches deep breathing and website calm.com that does guided imagery relaxation.

6b71f548f5feffd1eff285ddb315e09b

The trick for all of this is getting patients to buy in. They are doing all of the work and the motivation has to come from within. So long as you really listen to their pain story, and have done an adequate evaluation, you don’t necessarily change the treatment plan because of resistance. However, don’t become confrontational, don’t fight.  Pushing hard for patient self managment strategies will often backfire.  Use your best Motivational Interviewing jujitsu to roll with resistance and put the onus to change back onthe patient. They can certainly stay the same, but you might point out that isn’t getting them anywhere.

Chronic Kidney Disease for the Generalist

 

Protect those nephrons!  From AMR this week, a handy primer on CKD for your continuity clinic.  

When do your patients have CKD? Decline in GFR for >3 months PLUS Evidence of Kidney Disease (evidenced by one of the following)

  • ›Albuminuria
  • ›Urine sediment abnormalities
  • ›Electrolyte and other abnormalities due to tubular disorders
  • ›Abnormalities detected by histology
  • ›Structural abnormalities detected by imaging
  • ›History of kidney transplantation

Figure out what caused it: 75% are HTN and/or Diabetes

  • Glomerular disease
  • Obstructive uropathy
  • Vascular diseases
  • Hepatorenal/cardiorenal syndromes
  • Congenital disease: PKD

Do the workup:

  • GET THE UA  Active sediment/proteinuria vs a bland UA will be a major branch point in your evaluation, so you have to get a UA.  Spot urine protein and creatinine are also useful.
  • US Looking for cystic kidneys, hydronephrosis, asymmetry, or even symmetric evidence of “medical renal disease” is useful.
  • Based on historical clues, you can also check: HIV, hepatitis serologies, SPEP/UPEP, ANA, ANCAs

Stage it: based on GFR. VGFR- MDRD and CKD-EPI are most commonly used formulas. Here’s a handy calculator that gives you both, plus the stage.

Stage Description GFR
1 Kidney damage with nl GFR >90
2 Kidney damage with increased GFR 89-60
3a Moderately decreased GFR 59-45
3b 44-30
4 Severely decreased GFR 29-15
5 Kidney failure <14 or on dialysis

 

Call for Backup: Nephrology Referral

  • You don’t know why the patient has kidney disease
  • It is progressing quickly (loss of 50% of their GFR within one year)
  • Nephrosis: Lots of proteinuria (>3g/day)
  • Nephritis: active urine sediment with blood, protein, casts
  • Dialysis planning: sometime during stage3b is probably ideal, certainly by the time patient has GFR <30
    • Mortality benefit for patients that see nephrology earlier.

OK, now what?  Manage it:

  • Fix reversible causes: remove nephrotoxins, relieve obstruction, treat CHF/Cirrhosis/HIV/Hepatitis
  • Slow progression
    • HTN: JNC8 guidelines recommend goal 140/90
    • DM: ACCORD trial showed benefit with treatment to HbA1c <7.5
    • Add an ACE-inhibitor or ARB if there is proteinuria
  • Aggressive cardiovascular risk reduction (Cardiovascular disease is going to kill these patients before the renal disease does- see graph below)
  • Deal with the complications

CV mortality in CKD

Sarnak M J et al. Circulation. 2003;108:2154-2169

What Complications?

  • Hyperkalemia: Lasix helps
  • Anemia: Replace Iron, consider EPO if Hgb <10
  • Acidosis: consider when serum bicarb <22
  • Volume Overload: Lasix helps
  • Mineral Bone Disease: replace Vitamin D, bind PO4

Great posts by our own Dr.Centor on CKD here (don’t miss the comments) and here.

2012 KDIGO Guidelines for the evaluation and management of CKD.