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Endometriosis Flashcards

1
Q

What is endometriosis?

A

The presence of endometrial tissue outside of the uterus
- This can result in pain, and/or infertility

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2
Q

What are 4 theories as to the causes of endometriosis?

A
  1. Retrograde Menstruation Theory
  2. Immunologic Theory
  3. Coelomic Metaplasia Theory (Induction Theory)
  4. Vascular/Lymphatic Theory
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3
Q

What is retrograde menstruation theory?

A

Endometrium shed during menstruation flows back through the fallopian tubes and becomes implanted on organs/tissues in the pelvic area

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4
Q

What is immunulogic theory? (4)

A
  1. An underlying, immunologic disorder is responsible
  2. Endometrial tissue is able to evade the immune system (deficient cell-mediated immunity)
  3. This theory is supported by the presence of abnormal B & T cell function, and altered levels of cytokines & IL’s in endometrial lesions
  4. Some of these changes may create an environment which is toxic to sperm
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5
Q

What is coelomic metaplasia theory? (2)

A
  1. The coelomic epithelium is epithelial tissue that lines the surface of the abdominal organs
  2. Lesions develop when cells covering the peritoneum undergo metaplasia (i.e., normal peritoneal tissue transforms via metaplastic transition to ectopic endometrial-like tissue)
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6
Q

What is vascular/lymphatic theory?

A

Endometrial cells are spread to distant locations via the lymphatic system or vascular pathways (i.e., to the lung, brain, eyes)

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7
Q

What is the pathophysiology of endometriosis? (6)

A
  1. Endometrial tissue deposits outside the uterus (likely via retrograde menstruation)
  2. These implants are dependent on estrogen (E) - they can grow & bleed similar to the uterine lining during a menstruation cycle
  3. Aromatase is present in lesions, leading to ↑ E
  4. Decreased progesterone (P) receptors, hence P can’t antagonize the effects of E: “progesterone-resistance”
  5. Overall, there is ↑ E stimulation of the endometriosis
  6. Stimulation by E can stimulate PGE2, COX2 – i.e. can have pro-inflammatory effects
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8
Q

Go through the estrogen/pain cycle of endometriosis?

A

Estrogen fuels endometriosis pain by promoting:
- Proliferation of endometriotic lesions
- Inflammation

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9
Q

Describe inflammation pain in endometriosis

A

Immune response to the endometrial lesions may lead to increased levels of pro-inflammatory cytokines

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10
Q

Describe neuropathic pain in endometriosis

A

Endometrial lesions may compress on nerve fibres or adjacent structures

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11
Q

Describe central sensitization in endometriosis

A

Persistent pain can alter response to stimuli, leading to central sensitization (i.e., increased pain perception)

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12
Q

What are the 4 hallmarks of endometriosis pathophysiology?

A
  1. Genetic predisposition
  2. Estrogen dependence
  3. Progesterone resistance
  4. Inflammation
    (Endometriosis may remain stable, regress, or progress (approximately 1/3 each))
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13
Q

What are some risk factors for endometriosis? (6)

A
  1. European descent
  2. 1st degree maternal relative with endometriosis (7-10x)
  3. Not having children
  4. Early menarche
  5. Short monthly cycle (<28 days)
  6. Heavy menses; >=5-6 days
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14
Q

What are the 2 major symptoms of endometriosis?

A
  1. Pain
  2. 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)
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15
Q

What is the clinical presentation of pain in endometriosis? (5)

A
  1. Dysmenorrhea
  2. Chronic pelvic pain
    - Non-cyclical abdominal and pelvic pain 6+ months
  3. Dyspareunia
  4. Painful defecation/urination
  5. Lower back pain
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16
Q

What are the “other” signs and symptoms of endometriosis? (6)

A
  1. GI (urinary disturbances, constipation), abdominal bloating
  2. Premenstrual spotting, heavy, irregular bleed
  3. Fatigue
  4. Pelvic mass
  5. Pelvic/adnexal tenderness
  6. Subfertility
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17
Q

What is the impact of endometriosis on someone’s life? (3)

A
  1. Persistent pain - QOL
  2. Disrupt work/studies
  3. Physical/mental toll
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18
Q

What is the gold standard of endometriosis diagnosis?

A

Visualization at laparoscopy and histological study
- Can determine extent of diagnosis, but is not required before treatment can be started

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19
Q

There is no cure to endometriosis, so what are the goals of treatment? (2)

A
  1. Relieve symptoms
  2. Improve fertility
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20
Q

What is 1st line pharmacotherapy for endometriosis? (3)

A

Hormonal therapies
1. Combined hormonal contraceptives
2. Progestins
- Oral, IM, SC, implants, IUD
NSAIDs: can help for dysmenorrhea

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21
Q

What are the goals of hormonal therapy for endometriosis? (3)

A
  1. Suppress the menstrual cycle
  2. Create amenorrhea
  3. Stop ovulation if that process is painful
22
Q

What is the MOA of hormonal therapy (CHCs) for endometriosis? (4)

A
  1. Suppress ovulation and the growth of implants
  2. They decrease hormone levels, & they keep the menstrual cycle regular, shorter, and lighter
  3. ”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
  4. Ideal for people with no current desire to get pregnant
23
Q

What are some useful tips to know about CHC use in endometriosis? (5)
(Use, efficacy, safety, SEs, tolerability)

A
  1. They can be used cyclically or continuously
  2. Trials show clinically significant ↓ in endo-related pain
    - Evidence primarily with OCPs (but patch or vaginal ring are options as well)
  3. They are safe and can be used long-term
  4. SE’s (i.e. breast tenderness, h/a, nausea, weight gain, mood changes), precautions (i.e DVT risk), and contraindications
  5. CHCs are considerably better tolerated than alternative hormonal options (and less $)
24
Q

What is the MOA of progestins for endometriosis?

A

They help prevent the rise in estradiol, without estrogen related stimulation of endometriotic growth, and induce a hypoestrogenic environment

25
Q

True or False? Progestins have similar efficacy to other hormonal therapies for endometriosis

A

t

26
Q

What are the adverse effects of progestins?
(Depot, Dienogest, IUS) (4)

A
  1. Breakthrough bleeding, weight gain/fluid retention, mood
    changes, headache
  2. Depot: may delay the return in ovulation, and decreased BMD with prolonged use
  3. Dienogest: may be detrimental to BMD, associated with less anti-androgenic effects, requires non-hormonal contraception
  4. IUS: risk of expulsion; long-term effect on BMD unknown
27
Q

A minimum of a _ _____ trial should be tried prior to moving on to subsequent treatment options for pain control

A

3 month

28
Q

What is the MOA of NSAIDs in endometriosis?

A

Interfere with PG synthesis (which is overexpressed in endometrial lesions)

29
Q

When are NSAIDs most appropriate in endometriosis? (2)

A
  1. Appropriate 1st choice if sx’s are mild & women do not want to take a hormonal treatment option
  2. Appropriate to use in conjunction with hormonal tx options
30
Q

What is the MOA of Gonadotropin-Releasing Hormone (GnRH) Agonists? (3)

A
  1. Bind to GnRH receptors in the pituitary, and initially cause an increased release of LH/FSH
  2. Due to their long t½ , down-regulation of the hypothalamic-pituitary-ovarian axis occurs
  3. This prevents the release of endogenous GnRH from the hypothalamus, blocking the release of FSH/LH, and results in a hypoestrogenic state, endometrial atrophy, and amenorrhea
31
Q

True or False? When doing progestin therapy for endometriosis, symptoms may temporarily worsen after the first dose

A

True - should decrease within the first month

32
Q

What are the side effects of GnRH agonists? (4)

A
  1. Bone loss
  2. Vasomotor symptoms –> hot flashes, night sweats, vaginal dryness, insomnia, decreased libido
  3. Headache/migraine
  4. Mood swings
33
Q

What is add-back treatment?

A

To counter bone loss and vasomotor symptoms from GnRH agonist, a low dose estrogen and/or progestin should be added
E.g. Estrace 1mg + MPA 2.5mg od
E.g. CES 0.625mg + norethindrone acetate 5mg od
E.g. Norethindrone acetate 5mg od
(Note: not combined oral contraceptives)

34
Q

True or False? Add-back treatment increases efficacy of GnRH agonists

A

False - maintains efficacy but decreases the AE’s

35
Q

What class is Elagolix?

A

GnRH receptor ANTAGONIST

36
Q

What is the MOA of elagolix?

A

Oral GnRH receptor antagonist –> competitively binds to GnRH in the pituitary and suppresses gonadotropins and causes rapid, reversible, dose-dependent hypoestrogenic state

37
Q

How should elagolix be administered?

A

Can be taken with or without food. Begin at time of menstruation; patients should use an effective method of contraception not containing estrogen

38
Q

What are the ADEs of elagolix? (7)

A
  1. Hot flashes
  2. Headache
  3. Insomnia
  4. Nausea
  5. Amenorrhea
  6. Mood swings
  7. Night sweats
39
Q

Why do we prefer to use lower doses of elagolix unless necessary?

A

Dose-dependent increases in TC, LDL, TG, and decrease in BMD

40
Q

What are some considerations/counseling tips for elagolix? (4)

A
  1. Rule out pregnancy before beginning
    - Use a non-estrogen contraceptive
  2. 200mg BID x 6mos is max use due to BMD concerns / not studied beyond 1 year
    - Ensure adequate calcium and Vitamin D intake
  3. Can cause alterations in bleeding patterns
  4. Common side effects – hot flashes, headache, nausea, insomnia, mood changes
41
Q

What endometriosis pharmacotherapy is no longer routinely recommended anymore?

A

Aromatase inhibitors
(anastrozole, letrozole, exemestane)

42
Q

What was the previous drug of choice for endometriosis? Why not anymore?

A

Danazol
Not well tolerated (but was very good at controlling symptoms)

43
Q

Surgical management of endometriosis is for those: (2)

A
  1. Who are infertile and desire pregnancy
  2. Not responding to pharmacologic therapies
44
Q

What effect does laparoscopy have on fertility? (2)

A
  1. Can help improve fertility in women with minimal/mild endometriosis
  2. Effect on deeply infiltrating endometriosis is unclear
45
Q

What effect does laparoscopy have on pain? (3)

A
  1. Recurrence of pain in up to 50% of patients 5 years post-surgery
  2. Some will require repeat surgery
  3. Consider long-term post-op hormonal suppression to decrease risk of recurrent pain
46
Q

Aside from laparoscopy, what are the other surgical managements for endometriosis? (2)

A
  1. Hysterectomy with or without oophorectomy
  2. TAH-BSO (total abdominal hysterectomy - bilateral salpingo-oophorectomy) + removal of all visible endometriosis
47
Q

What to know about pregnancy/fertility in endometriosis? (2)

A
  1. Generally recommended waiting 1 month after d/c medical therapy before trying to conceive
  2. If pregnancy occurs, endometriosis generally enters remission with pregnancy
48
Q

What are some of the proposed explanations for infertility-associated endometriosis? (6)

A
  1. Changes in characteristics of peritoneal fluid
  2. Extensive scarring from endometrial lesions distorts pelvic anatomy causing mechanical obstruction
  3. Autoimmune mechanisms
  4. Increased concentrations of inflammatory cells; hostile environment to sperm/embryo
  5. Increased uterine peristaltic activity, which may prevent embryo implantation
  6. Irregularities in menstrual cycle
49
Q

What are the 4 management options for infertility-associated endometriosis?

A
  1. Watchful waiting
  2. NSAIDs for pain relief
  3. Conservational surgery (minimal endometriosis)
  4. Ovarian stimulation or In Vitro fertilization
50
Q

What are the GnRH agonists available in Canada? (5)

A
  1. Buserelin acetate nasal solution
  2. Goserelin acetate (SC)
  3. Leuprolide acetate (IM)
  4. Nafarelin acetate nasal solution
  5. Triptorelin pamoate (IM)

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