Sept17 A3-Gynecological-Chronic-Pain Flashcards
most common cause of chronic pelvic pain (CPP)
endometriosis
problem in chronic pain
- nociceptive signals form peripheral nerves to CNS
- signals are interpreted by the brain as danger
- BUT pain is not accurate indication of the danger
factors that can modify pain experience
- mood, stress
- environment
- past experiences
- meaning of pain
- spine and brain have mechanisms to amplify or diminish pain*
sensitization def
PNS and CNS are overxited and get huge amount of synapses firing in resp to one stimulation
- peripheral sensitization OR
- central sensitization
crpss-sensitization def
somato-visceral or viscero-visceral convergence
why some people remain functional with endometriosis and some don’t
in certain people, the brain can adapt to a certain level but in others, there is sensitization
most common sx of endometriosis (BUT NOT CPP)
dysmenorrhea
(IMP) 2most imp components of central sensitization
- hyperlagesia (uncomfortable stimulus becomes painful)
- allodynia (not uncomfortable stimulus becomes painful)
how central sensitization occurs
normal descending inhibitory pathwys are gone
pain is not a good indicator of:
- the problem
- where the problem is (bc of cross sensitization)
- how dangerous the problem is (degree of tissue damage)
positive thing with chronic pain
neuroplasticity
- possibility to retrain brain to desensitize
- pain does not necessarily mean danger
- empower the patient
CPP def
at least 3-6 months
- episodic or constant
- no cyclical pain like dysmenorrhea
- in anatomic pelvis (between umbilicus and inguinal lig)
- can cause functional disability
- unrelated to pregnancy
- requires tx
common causes of CPP (that also often coexist)
- gyn (ENDOMETRIOSIS, adenomyosis, chronic pelvic infections, fibroids)
- urologic (interstitial cystitis or painful bladder syndrome)
- GI (IBS = irritable bowel syndrome)
endometriosis def
presence of endo glands and stroma outside of normal location
endometriosis most common location
on pelvic peritoneum
pathophgy of endometriosis
- retrograde menstruation (most accepted theory) = endometrial cells pass through fallopian tubes and within peritoneal cavity
- coelomic metaplasia (PMD (Muellerian duct)) from highly pluripotential coelomic epith formed endometrium in ectopic places
- lymphatic or vascular spread
why endometriosis happens to some women and not to others (nbr of women with retrograde menstruation >nbr with endometriosis)
- immune system dysfunction contributes to genesis of endometriosis
- NK cells, macrophages and lymphocytes usually get rid of endometrial tissue*
hormone role in endometriosis
estrogen
-ectopic tissue is deficient in enzymes inactivating estrogens (progesterone responsive enzymes in normal endo)
-it expresses aromatase to make estrogen (normal endo doesn’t)
END RESULT: estrogen makes the endometriosis grow. (E = fertilizer. P = lawn mower)
classic sx of endometriosis
- severe dysmenorrhea
- severe dyspareunia
- chronic pelvic pain
- dysuria
- dyschezia (painful bowel mvmts)
endometriosis possible PE findings
- non mobile tender uterus
- adnexal mass (endometrioma)
- tender nodules in posterior cul de sac (Douglas)
- can be normal PE with no pain (good inhibition in brain). but still some infertility
how imaging helps for endometriosis
can only detected ADVANCED stage endometriosis or LARGE nodules using
- pelvic US
- MRI
gold std (best sensitivity) to dx endometriosis
laparoscopy and pathologic confirmation
why does endometriosis cause CPP
mostly bc of inflammation (for ex bc of pressure caused by a nodule)
medical endometriosis tx
- pain control with NSAID or tylenol)
- OCPs (stops from ovulating so no more E produced + OCP contains P), progestins, GnRH agonists