Endometriosis Flashcards
(50 cards)
What is endometriosis?
The presence of endometrial tissue outside of the uterus
- This can result in pain, and/or infertility
What are 4 theories as to the causes of endometriosis?
- Retrograde Menstruation Theory
- Immunologic Theory
- Coelomic Metaplasia Theory (Induction Theory)
- Vascular/Lymphatic Theory
What is retrograde menstruation theory?
Endometrium shed during menstruation flows back through the fallopian tubes and becomes implanted on organs/tissues in the pelvic area
What is immunulogic theory? (4)
- An underlying, immunologic disorder is responsible
- Endometrial tissue is able to evade the immune system (deficient cell-mediated immunity)
- This theory is supported by the presence of abnormal B & T cell function, and altered levels of cytokines & IL’s in endometrial lesions
- Some of these changes may create an environment which is toxic to sperm
What is coelomic metaplasia theory? (2)
- The coelomic epithelium is epithelial tissue that lines the surface of the abdominal organs
- Lesions develop when cells covering the peritoneum undergo metaplasia (i.e., normal peritoneal tissue transforms via metaplastic transition to ectopic endometrial-like tissue)
What is vascular/lymphatic theory?
Endometrial cells are spread to distant locations via the lymphatic system or vascular pathways (i.e., to the lung, brain, eyes)
What is the pathophysiology of endometriosis? (6)
- Endometrial tissue deposits outside the uterus (likely via retrograde menstruation)
- These implants are dependent on estrogen (E) - they can grow & bleed similar to the uterine lining during a menstruation cycle
- Aromatase is present in lesions, leading to ↑ E
- Decreased progesterone (P) receptors, hence P can’t antagonize the effects of E: “progesterone-resistance”
- Overall, there is ↑ E stimulation of the endometriosis
- Stimulation by E can stimulate PGE2, COX2 – i.e. can have pro-inflammatory effects
Go through the estrogen/pain cycle of endometriosis?
Estrogen fuels endometriosis pain by promoting:
- Proliferation of endometriotic lesions
- Inflammation
Describe inflammation pain in endometriosis
Immune response to the endometrial lesions may lead to increased levels of pro-inflammatory cytokines
Describe neuropathic pain in endometriosis
Endometrial lesions may compress on nerve fibres or adjacent structures
Describe central sensitization in endometriosis
Persistent pain can alter response to stimuli, leading to central sensitization (i.e., increased pain perception)
What are the 4 hallmarks of endometriosis pathophysiology?
- Genetic predisposition
- Estrogen dependence
- Progesterone resistance
- Inflammation
(Endometriosis may remain stable, regress, or progress (approximately 1/3 each))
What are some risk factors for endometriosis? (6)
- European descent
- 1st degree maternal relative with endometriosis (7-10x)
- Not having children
- Early menarche
- Short monthly cycle (<28 days)
- Heavy menses; >=5-6 days
What are the 2 major symptoms of endometriosis?
- Pain
- Sub/Infertility
(Symptoms vary from person to person, are unpredictable, and up to 1/3 may be asymptomatic)
(Symptoms also do not always correlate with extent of the disease)
What is the clinical presentation of pain in endometriosis? (5)
- Dysmenorrhea
- Chronic pelvic pain
- Non-cyclical abdominal and pelvic pain 6+ months - Dyspareunia
- Painful defecation/urination
- Lower back pain
What are the “other” signs and symptoms of endometriosis? (6)
- GI (urinary disturbances, constipation), abdominal bloating
- Premenstrual spotting, heavy, irregular bleed
- Fatigue
- Pelvic mass
- Pelvic/adnexal tenderness
- Subfertility
What is the impact of endometriosis on someone’s life? (3)
- Persistent pain - QOL
- Disrupt work/studies
- Physical/mental toll
What is the gold standard of endometriosis diagnosis?
Visualization at laparoscopy and histological study
- Can determine extent of diagnosis, but is not required before treatment can be started
There is no cure to endometriosis, so what are the goals of treatment? (2)
- Relieve symptoms
- Improve fertility
What is 1st line pharmacotherapy for endometriosis? (3)
Hormonal therapies
1. Combined hormonal contraceptives
2. Progestins
- Oral, IM, SC, implants, IUD
NSAIDs: can help for dysmenorrhea
What are the goals of hormonal therapy for endometriosis? (3)
- Suppress the menstrual cycle
- Create amenorrhea
- Stop ovulation if that process is painful
What is the MOA of hormonal therapy (CHCs) for endometriosis? (4)
- Suppress ovulation and the growth of implants
- They decrease hormone levels, & they keep the menstrual cycle regular, shorter, and lighter
- ”But doesn’t estrogen stimulate growths?”
- The estrogen used (ethinyl estradiol) has less estrogenic activity than endogenous estradiol, and the progestin helps prevent a rise in estradiol - Ideal for people with no current desire to get pregnant
What are some useful tips to know about CHC use in endometriosis? (5)
(Use, efficacy, safety, SEs, tolerability)
- They can be used cyclically or continuously
- Trials show clinically significant ↓ in endo-related pain
- Evidence primarily with OCPs (but patch or vaginal ring are options as well) - They are safe and can be used long-term
- SE’s (i.e. breast tenderness, h/a, nausea, weight gain, mood changes), precautions (i.e DVT risk), and contraindications
- CHCs are considerably better tolerated than alternative hormonal options (and less $)
What is the MOA of progestins for endometriosis?
They help prevent the rise in estradiol, without estrogen related stimulation of endometriotic growth, and induce a hypoestrogenic environment
