exam 3 - dysmenorrhea and endometriosis Flashcards
(20 cards)
A 26 yo law student, G0 LMP 2 weeks ago c/o constant and severe dysmenorrhea beginning on the first day of menses x 2 years. She states the severity of the dysmenorrhea is worsening… She wonders if she should try birth control pills.
Your patient tries extended cycle oral contraceptives with minimal improvement of her dysmenorrhea. She undergoes laparoscopy with excision of all visible endometriosis, and then begins leuprolide thereafter. She notes significant improvement in her symptoms within 4-8 weeks after surgery.
primary dysmenorrhea
-80% of all patients at some point in reproductive life
-Caused by prostaglandin secretion
-No underlying pathology
-Is not disabling or incapacitating
-Clinical diagnosis based on history alone
-No findings on physical exam
-No need for imaging or other ancillary testing
-Treat with NSAID of choice
secondary dysmenorrhea
-caused by some type of underlying disorder
-common etiologies:
-Endometriosis
-Leiomyomata uteri
-Adhesions
-Adenomyosis
-Imperforate hymen
-Cervical stenosis
-other GI, GU, MSK, neuro processes
endometriosis definition and incidence
-Ectopic deposits of endometrial tissue
-Occurs in 10% of all patients AFAB
-Causes chronic pelvic pain and infertility
-MCC of chronic pelvic pain in reproductive-age women
-Inflammatory, estrogen-dependent process
-Estrogen receptor beta increases survival of lesions and inflammation
-Progesterone resistance due to reduced receptors in lesions
endometriosis risk factors
-Early menarche
-Short cycles (<27 days)
-Heavy menses
-1st degree relative with endometriosis (10x risk)
-Imperforate hymen
-Up to 30-40% of laparoscopy cases for pelvic pain/infertility show endometriosis
endometriosis pathophysiology
Theories:
- Sampson’s: Retrograde menstruation → peritoneal seeding
- Halban’s: Lymphatic/vascular dissemination → distant spread
- Meyer’s: Coelomic metaplasia → peritoneal cells transform
Genetic mutations
-Increased COX-2 → local overproduction of prostaglandins
-Increased aromatase → overproduction estrogen
-Progesterone resistance = increased estrogen effects
pain pathophysiology in endometriosis
-Chronic inflammation from lesions
-Proinflammatory cytokines (TNF-α, ILs)
-Increased prostaglandins
-Nerve growth and density increase
-Changes in uterine innervation
infertility association with endometriosis
-Cytokines may damage sperm DNA, oocyte cytoskeletons
-May cause tubal damage
symptoms: pain, GI, bladder, MSK
-Pain: dysmenorrhea, chronic pelvic pain, deep dyspareunia
-GI: perimenstrual tenesmus, dyschezia, hematochezia, diarrhea/constipation
-Bladder: perimenstrual dysuria
-MSK: back pain
-Other: syncope
physical exam findings
-Uterosacral nodularity on rectovaginal exam (classic, but often absent)
-Endometriomas may be present (adnexal mass or tenderness)
diagnosis of endometriosis
-Presumptive dx via hx, but confirmed via laparoscopy or biopsy
-Endometriotic implant may be visible in luteal phase
-US to rule out other causes and detect endometriomas
-Radio-tracer test fast-tracked by FDA for SPE
laparoscopy
-Minimally invasive abd surgery for dx or tx
-Carbon dioxide for pneumoperitoneum
-Less postop pain, faster recovery
-Higher risk: sepsis, atelectasis, pneumonia, DVT
surgical findings in endometriosis
-Dark red ‘powder burn’ or ‘mulberry’ lesions
-Endometriomas = ‘chocolate cysts’
-Most common sites: uterus surface, ovaries, tubes, pouch of Douglas, ligaments, rectovaginal septum
endometrioma
chocolate cyst
staging by ASRM
Stage I–IV (minimal to severe)
Based on:
- Lesion size/location
- Adhesions
- Ovarian involvement
initial medical management (pain + wants fertility)
-NSAIDs + oral contraceptives (especially extended cycle)
-Or medroxyprogesterone acetate (oral or depot)
-Progestins, GnRH agonists, androgens
medical management (pain + infertility)
-Surgery can improve fertility (excision of endometriomas)
-IVF is preferred treatment for infertility with endometriosis
when initial medical therapy fails
-GnRH antagonists up to 12 mo (Elagolix, Relugolix)
-Aromatase inhibitors + progestin or OCs
-SPRMs (mifepristone, asoprisnil, ulapristal)
-NSAIDs (celecoxib)
surgical management endometriosis
-Conservative: excision, ablation of visible ds
- adhesiolysis
-Presacral neurectomy for midline pain: can cause constipation and urinary dysfunction
Extirpative: total abdominal hysterectomy + bilateral salpingo-oophorectomy
- do salpingectomy when pt is having a hysterectomy
-Ovarian conservation → ↓ osteoporosis, ↑ recurrence
malignancy association
-Gene mutations (ARID1A, PIK3CA)
-Endometriomas → precursor to ovarian carcinoma
-↑ risk for endometrioid, clear cell carcinoma, ovarian cancer (1.46)
-No screening; best prevention = excision of all visible endometriotic implants
- Alternatively, hormonal therapy with oral contraceptives or other hormones may be used
-Salpingectomy ↓ ovarian cancer risk by 40%
