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PHAR359 > Endometriosis > Flashcards

Endometriosis Flashcards

1
Q

What is endometriosis?

A

presence of endometrial tissue outside of the uterus
-can present anywhere, but is commonly limited to the pelvic area
-this can result in pain and/or infertility

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2
Q

When is the peak prevalence of endometriosis seen?

A

those 25-35 yo

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3
Q

What causes endometriosis?

A

exact cause remains unknown
-there are a few theories, however it is most likely multifactorial
theories:
-retrograde menstruation
-immunologic
-coelomic metaplasia (induction)
-vascular/lymphatic

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4
Q

Describe the 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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5
Q

Describe the immunologic theory.

A

an underlying, immunologic disorder is responsible
endometrial tissue is able to evade the immune system
this theory is supported by the presence of abnormal B & T cell function, and altered levels of cytokines & ILs in endometrial lesions
some of these changes may create an environment which is toxic to sperm

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6
Q

What is coelomic epithelium?

A

the coelomic epithelium is epithelial tissue that lines the surface of abdominal organs

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7
Q

Describe the coelomic metaplasia theory (induction theory).

A

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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8
Q

Describe the vascular/lymphatic theory.

A

endometrial cells are spread to distant locations via the lymphatic system or vascular pathway

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9
Q

What is going on in endometriosis?

A

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 increased E
decreased progesterone (P) receptors, hence P cant antagonize the effects of E (progesterone resistance)
overall, there is increased E stimulation of the endometriosis
stimulation by E can stimulate PGE2, COX-2 (pro-inflammatory)

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10
Q

How does estrogen fuel endometriosis pain?

A

proliferation of endometriotic lesions
inflammation

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11
Q

Describe the pain that might be seen in endometriosis.

A

inflammation:
-immune responses to the endometrial lesions may lead to increased levels of pro-inflammatory cytokines
neuropathic pain:
-endometrial lesions may compress nerve fibres or adjacent structures
central sensitization:
-persistent pain can alter response to stimuli, leading to central sensitization (increased pain perception)
bleeding from endometrial tissues

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12
Q

What are the hallmarks of the pathophysiology of endometriosis?

A

genetic predisposition
estrogen dependence
progesterone resistance
inflammation
may remain stable, regress, or progress

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13
Q

What are the risk factors for endometriosis?

A

European descent
1st degree maternal relative with endometriosis
not having children
early menarche (< 10 yo)
short monthly cycle (< 28 days)
heavy menses; > 5-6 days

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14
Q

What are the major symptoms of endometriosis?

A

pain
sub/infertility

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15
Q

What can be said about the variability of the symptoms of endometriosis?

A

symptoms vary from person to person, are unpredictable, and up to 1/3 may be asymptomatic
symptoms do not always correlate with extent of disease

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16
Q

Which symptoms contribute to the pain in endometriosis?

A

dysmenorrhea
chronic pelvic pain
-non-cyclical abdominal and pelvic pain > 6 months
dyspareunia
painful defecation/urination
lower back pain

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17
Q

Is the pain in endometriosis constant?

A

can be intermittent or constant; often occurs with menstrual cycle, but can occur anytime in cycle

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18
Q

What are some other signs and symptoms that might be seen in endometriosis?

A

symptoms:
-GI (urinary disturbances, constipation, bloating)
-premenstrual spotting, heavy/irregular bleed
-fatigue
signs:
-pelvic mass
-pelvic/adnexal tenderness
-subfertility

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19
Q

In which women should we suspect endometriosis?

A

women complaining of subfertility, dysmenorrhea, chronic pelvic pain, or dyspareunia

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20
Q

What are the impacts of endometriosis?

A

persistent pain - QoL
disrupt work/studies
physical/mental toll

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21
Q

How long is the average time between initial symptoms of endometriosis and the diagnosis?

A

average 6-12 years
-pain is shared with many diseases, leading to a delay

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22
Q

What is the gold standard for diagnosis of endometriosis?

A

laparoscopy and histological study
-can determine extent of disease, but is not required before treatment can be started

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23
Q

What is the cure for endometriosis?

A

there is no cure, so treatment is aimed at management

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24
Q

What are the goals of therapy for endometriosis?

A

the goals of treatment will vary depending on the persons desired outcomes
-relieve symptoms
-improve fertility

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25
Q

What are the treatment options for endometriosis?

A

surgery
pharmacotherapy
or both

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26
Q

What are the goals of therapy for pain-associated endometriosis?

A

suppress the menstrual cycle
create amenorrhea
stop ovulation if that process is painful

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27
Q

What are the 1st line pharmacotherapy options for pain-associated endometriosis?

A

hormonal therapies
-combined hormonal contraceptives
-progestins

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28
Q

Which symptoms of endometriosis can NSAIDs help with?

A

dysmenorrhea

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29
Q

How does the efficacy of hormonal therapies compare to newer therapies for pain-associated endometriosis?

A

similarly effective
-fewer AEs and less $$

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30
Q

What is the MOA of CHC in endometriosis?

A

suppress ovulation and the growth of implants
-they decrease hormone levels & keep the menstrual cycle regular, shorter, and lighter
they help prevent the rise in estradiol, without estrogen related stimulation of endometriotic growth, & induce a hypoestrogenic environment

31
Q

How come ethinyl estradiol in CHC doesnt stimulate growth of implants?

A

EE has less estrogenic activity than endogenous estradiol and the progestin helps prevent a rise in estradiol

32
Q

For which endometriosis patients is CHC an ideal option?

A

no current desire to get pregnant

33
Q

How should CHCs be used in endometriosis?

A

cyclically or continuously
-some evidence favours continuous use

34
Q

What is the evidence for CHCs in endometriosis?

A

trials show clinically significant decrease in endo-related pain
-evidence primarily with OCPs (but patch or ring are options)

35
Q

What are some common adverse effects of CHCs?

A

breast tenderness
headache
nausea
weight gain
mood changes
safe and can be used long-term
considerably better tolerated than alt hormonal options and less $$

36
Q

What is the efficacy of progestins in endometriosis-associated pain?

A

similar efficacy to other hormonal options

37
Q

What are some common adverse effects of progestins?

A

breakthrough bleeding
weight gain/fluid retention
mood changes
headache
Depot: delay return in ovulation, decreased BMD (long use)
dienogest: may be detrimental to BMD, associated with less anti-androgenic effects, require non-hormonal contraception
IUS: risk of expulsion, long-term effect on BMD unknown

38
Q

How long should CHC/progestins be trialed before moving onto another option for pain control in endometriosis?

A

a minimum of a 3 month trial

39
Q

What is the MOA of NSAIDs in endometriosis?

A

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

40
Q

What is the evidence for NSAIDs in endometriosis?

A

lack of high-quality evidence assessing their efficacy
no evidence favouring one over another

41
Q

When are NSAIDs an appropriate choice in endometriosis?

A

symptoms are mild & women do not want to take a hormonal treatment option
in conjunction with hormonal treatment options

42
Q

How are NSAIDs dosed in endometriosis?

A

on a scheduled basis
-can administer intermittently or continuously

43
Q

What is the MOA of GnRH agonists?

A

bind to GnRH receptors in the pituitary, and initially cause an increased release of LH and FSH
due to their long t1/2, down-regulation of the HPO axis occurs
-this prevents the release of endogenous GnRH from the hypothalamus, blocking the release of LH/FSH, and results in a hypoestrogenic state, endometrial atrophy, and amenorrhea

44
Q

What is seen with the first injection of a GnRH agonist depot?

A

temporary increase in estrogen levels
-temporary worsening of symptoms for ~ 1 month

45
Q

What are examples of GnRH agonists?

A

buserelin
goserelin
leuprolide
nafarelin
triptorelin

46
Q

What are side effects of GnRH agonists?

A

hypoestrogenic AEs
-bone loss (reversible on d/c)
-vasomotor symptoms
-headache/migraine
-mood swings
the AEs are analogous to menopause due to E depletion

47
Q

What can be used to combat the adverse effects of GnRH agonists?

A

add back therapy

48
Q

What should be ruled out before starting a GnRH agonist?

A

pregnancy

49
Q

What kind of birth control should be used while on a GnRH agonist?

A

non-hormonal

50
Q

What is add-back treatment?

A

low dose estrogen +/or progestin to counter bone loss and vasomotor symptoms
-not CHC

51
Q

What is the benefit of add-back treatment in endometriosis?

A

decrease AE of GnRH agonists yet maintain efficacy
-how? theory: there is an estrogen threshold effect

52
Q

What is the MOA of elagolix?

A

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

53
Q

How is elagolix dosed?

A

start at lower doses as there is dose-dependent decrease in BMD; adjust based on symptoms
-partial estradiol suppression: 150 mg daily
-nearly full estradiol suppression: 200 mg BID

54
Q

How should elagolix be administered?

A

can be taken with or without food
begin at time of menstruation
use effective method of contraception not containing estrogen

55
Q

What are the adverse effects of elagolix?

A

hot flashes
headache
insomnia
nausea
amenorrhea
mood swings
night sweats
dose-dependent increases in TC, LDL, TG, and decrease in BMD

56
Q

What are drug interactions of elagolix?

A

CYP
-CYP inducer
-3A4 substrate

57
Q

What needs to be ruled out before starting elagolix?

A

pregnancy

58
Q

What is the max dose and duration of use for elagolix?

A

200 mg BID x 6 months
-due to BMD concerns/not studied beyond 1 year

59
Q

What are examples of aromatase inhibitors?

A

anastrozole
letrozole
exemestane

60
Q

What is the MOA of aromatase inhibitors?

A

inhibiting aromatase, lowering overall estrogen
-aromatase is a key enzyme in the conversion of adrenal androgens to estrogens

61
Q

What is the efficacy evidence for aromatase inhibitors?

A

not a lot of evidence available
-some signals they decrease pain alone or in combo with CHCs, progestins, and GnRH agonists

62
Q

What are the adverse effects of aromatase inhibitors?

A

headache
nausea
diarrhea
hot flash
vaginal dryness
long-term may impact BMD
less than GnRH agonists

63
Q

What can be considered to combat adverse effects of aromatase inhibitors?

A

add-back therapy

64
Q

What is the MOA of danazol?

A

induces a pseudomenopausal state by increasing androgen levels & decreasing estrogen levels (it suppresses the production of LH & FSH)
-estradiol suppression will cause anovulation, amenorrhea, and atrophy of the endometrial tissue
-a synthetic androgen derived from 17-ethinyl testosterone

65
Q

Describe the efficacy of danazol.

A

80-90% achieve symptomatic improvement
-however, use is no longer supported due to androgenic AE

66
Q

When is surgical management considered for endometriosis?

A

infertile and desire pregnancy
not responding to pharmacologic therapies

67
Q

What is the typical surgical option for endometriosis?

A

laparoscopy

68
Q

What are the benefits of laparoscopy?

A

fertility:
-can help improve fertility in women with minimal/mild endometriosis
-effect on deeply infiltrating endometriosis is unclear
pain:
-recurrence of pain in up to 50% 5yrs post-surgery
-some will require repeat surgery

69
Q

What should be considered post-op for endometriosis?

A

long-term hormonal suppression to reduce risk of recurrent pain

70
Q

What is the most definitive surgical option for endometriosis?

A

hysterectomy

71
Q

Upon discontinuing medical therapy, how long should a women wait to conceive?

A

1 month after d/c medical therapy

72
Q

What generally occurs to endometriosis with pregnancy?

A

endometriosis generally enters remission
-can recur after birth

73
Q

What are the multiple proposed explanations for why endometriosis causes infertility?

A

changes in characteristics of peritoneal fluid
extensive scarring from endometrial lesions distorts pelvic anatomy causing mechanical obstruction
autoimmune mechanisms
increased concentrations of inflammatory cells; hostile environment to sperm//embryo
increased uterine peristaltic activity, which may prevent embryo implantation
irregularities in menstrual cycle

74
Q

What are the management options for infertility-associated endometriosis?

A

watchful waiting
NSAIDs for pain relief
conservational surgery (minimal endometriosis)
ovarian stimulation or in vitro fertilization

PHAR359 (3 decks)

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