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PHAR 359 > Endometriosis > Flashcards

Endometriosis Flashcards

1
Q

What is endometriosis? Where can it present? What can it result in?

A

The presence of endometrial tissue outside of the uterus

It can present anywhere, but is commonly limited to the pelvic area

This can result in pain, and/or infertility (e.g. Endometrial tissue in fallopian tubes leading to blockage)

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2
Q

Describe the prevalence of endometriosis?

A

Affects ~10% of females of reproductive age

Affects up to 50% of women experiencing infertility

Affects ~70-80% of women experiencing chronic pelvic pain

Peak prevalence in those 25-35yo (Avg age at diagnosis is 27.9)

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3
Q

Describe the cause of endometriosis?

A

The exact cause remains unknown

There are a few theories, however it is most likely multi-factorial

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4
Q

Describe the theories for the cause of endometriosis

A
  1. Retrograde Menstruation Theory
  2. Immunologic Theory
  3. Coelomic Metaplasia Theory (Induction Theory)
  4. Vascular / Lymphatic Theory
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5
Q

Describe retrograde menstruation therapy

A

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

Rather than flowing out through the vagina

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6
Q

Describe the immunologic theory for endometriosis

A

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 (contributing to infertility)

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7
Q

Describe the coelomic metaplasia theory for endometriosis

A

Coelomic Metaplasia Theory (Induction Theory)

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

Metaplasia – Once cell type to another

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8
Q

Describe the vascular/lymphatic theory for endometriosis

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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9
Q

Describe the pathophysiology of 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 ↑ 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

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10
Q

Describe the relationship between estrogen and pain in endometriosis

A

Repetitive cycles of bleeding and inflammation may lead to adhesions and scarring on adjacent tissues

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11
Q

What are some of the reasons for pain in endometriosis?

A

Inflammation
Immune responses to the endometrial lesions may lead to ↑ levels of pro-inflammatory cytokines

Neuropathic Pain
Endometrial lesions may compress on nerve fibres or adjacent structures

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

Bleeding from endometrial tissues

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12
Q

Describe the relationship between pain and severity of endometriosis

A

Pain is not indicative of severity

e.g. a large amount of pain is not indicative of a severe pathology

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13
Q

Is endometriosis in regards to the experience of pain often diagnosed as endometriosis?

A

Endometriosis may not be discovered until one is investigated for infertiity

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14
Q

Describe the hallmarks of the pathophysiology of endometriosis? What is the course of endometriosis?

A

Genetic predisposition
Estrogen dependence
Progesterone resistance
Inflammation

Endometriosis may remain stable, regress, or progress (approximately 1/3 each)

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15
Q

What are some risk factors for endometriosis?

A
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16
Q

What are the major symptoms of endometriosis? Are the sx the same for everyone? Are sx indicative of the severity of the condition?

A

Pain

Sub/Infertility (reason why most seek MD)

Note: Sx’s vary from person to person, are unpredictable, and up to 1/3 may be asymptomatic

Sx’s also do not always correlate with extent of the disease

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17
Q

Describe the clinical presentation of endometriosis

A

Major symptom: pain
dysmenorrhea (80-90%)
chronic pelvic pain
–> Non-cyclical abdominal and pelvic pain ≥6 months
dyspareunia (30%)
painful defecation / urination
lower back pain

*** Can still worsen at times in the cycle – Can occur at any time in the cycle **

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18
Q

Describe the timeline of pain in endometriosis

A

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

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19
Q

What are some other signs and symptoms of endometriosis that an individual may experience?

A
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20
Q

In what other conditions should endometriosis be suspected?

A

Endometriosis should be suspected in women complaining of subfertilty, dysmenorrhea, dyspareunia, or chronic pelvic pain

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21
Q

Describe the impact of endometriosis

A

Functional impairments across domains: Psychological, Social, Occupational, and Academic

Persistent pain and decreased QOL

Disruption in work and studies

Physical and mental toll

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22
Q

Describe the diagnosis of endometriosis

A

Average 6-12yrs between initial sx’s and diagnosis
–> Pain is shared with many diseases, leading to a delay

The diagnosis is based on a thorough history, physical exam, and imaging assessments

The gold standard is visualization at laparoscopy and histological study**
–> Can determine extent of dx, but is not required before treatment can be started

** Histological examination of endometrial lesions**

23
Q

Describe the staging of endometriosis. Issue with staging?

A

Limited clinical usefulness - Does not correlate with sx severity

24
Q

Is there a cure for endometriosis?

A

There is no cure, so treatment is aimed at management

25
Q

Describe the goals of therapy for endometriosis

A

The goals of treatment will vary depending on the person’s desired outcomes:

Relieve symptoms
Improve fertility

26
Q

What are the tx options for endometriosis? What is treatment based on?

A

Tx options: surgery, pharmacotherapy, or both

Treat based on symptoms, preference, and priorities

27
Q

Describe the management of sx associated with suspected or confirmed endometriosis?

A

Diagnosis made and then patient decides if sx control or fertility

28
Q

Describe the first line pharamcotherapy options for endometriosis. Benefit?

A

1st line:
Hormonal therapies
Combined hormonal contraceptives (CHC)
Progestins
Oral, IM, SC implants, IUD

Similarly effective to later treatment options but with fewer AEs and less $

NSAIDs: can help for dysmenorrhea

29
Q

Describe the goals of hormonal therapy

A

1) Supress the menstrual cycle
2) Create amenorhhea
3) Stop ovulation if that process is painful

30
Q

Describe the role of combined hormonal contraceptives?

A

Suppress ovulation and the growth of implants

They decrease hormone levels, & they keep the menstrual cycle regular, shorter, and lighter

31
Q

With oral combined hormonal contraceptives, does the estrogen component stimulate endometrial tissue growth?

A

The estrogen used (ethinyl estradiol) has less estrogenic activity than endogenous estradiol, and the progestin helps prevent a rise in estradiol

Does not cause endometrial lesions to grow

32
Q

Describe who oral combined hormonal contraceptive is useful for

A

Ideal for people with no current desire to get pregnant

33
Q

Describe the dosing of CHC’s in endometriosis

A

They can be used cyclically or continuously

Some evidence favours continuous use

34
Q

Describe the evidence for the use of CHC’s in endometriosis? Safety?

A

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

35
Q

What are some of the side effects of CHC?

A

SE’s (i.e. breast tenderness, h/a, nausea, weight gain, mood changes), precautions (i.e DVT risk), and contraindications

36
Q

Describe the tolerability of CHC compared to other hormonal therapies in endometriosis

A

CHCs are considerably better tolerated than alternative hormonal options (and less $)

37
Q

What are some of the initial potential adverse effects of COC? Management of the side effects?

A

Common in first 3 months of starting pill:

Breakthrough bleeding (BTB) (Spotting – Not a full on period)
–> Check adherence
–> If lasts >6 months look for other causes (STIs) – check at how they are taking the pill, if forgetting, different times
–> Change to pill with ↑ estrogen/progestin (depending when BTB occurs in cycle)

Breast tenderness
–> If lasts longer than first 3 months, look for other causes
Change to pill with ↓ estrogen

Nausea
Take at HS or with food
Change to pill with ↓ estrogen

Weight gain (controversial)
Some notice ↑ appetite in first month, but overall little or minimal weight gain
Remember weight fluctuates with age and water retention

Headache or migraine
Can be hormone-related
Can either ↓ or ↑ with use

Mood changes – Depression
–> Observational study
Acne
Can worsen initially…but…
Usually improves with long-term use

Several OC have official indications for acne…but all combined OC can be beneficial
–> Lowers amount of endogenous androgens produced or (bio)available (androgens stimulate sebum production → acne)
If a continued problem, change to pill with ↓ androgenic activity
Or use topical therapy

38
Q

What are some of the potential risks of COC?

A

Contraceptive failure
Especially if missed pills with <20mcg estrogen (less s/e; however, need good adherence)

Venous thromboembolism (VTE)
Risk is 2-3x higher than in non-users
Risk ↑ with age, smoking, ↑ estrogen dose
Controversy whether drospirenone increases risk

MI and stroke (arterial thrombosis)
↑ risk associated with estrogen >50mcg day, age >35 years, smoking, HTN and other CVD risks

39
Q

What are some of the early signs of the risks associated with COC?

A

A – Abdominal pain (severe)
Gallbladder, pancreatitis, thrombosis
C – Chest pain (severe) or shortness of breath
Pulmonary embolus or myocardial infarction
H – Headaches (severe)
Stroke, hypertension, migraine
E – Eye problems (blurring, flashing, vision loss)
Stroke, hypertension, vascular insufficiency
S – Severe leg pain (calf or thigh)
DVT

40
Q

What are some drug interactions that alter the levels of COC? How can they be managed?

A

CPY450 3A4 inducers
Anticonvulsants (carbamezapine, phenytoin)
Anti-infectives (rifampin)
Herbals (St John’s wort)

Management:
Use product with higher estrogen levels (>30ug EE)
Use extended dosing (skip HFIs)
Use alternative to interacting drug or other method of birth control

41
Q

What drugs metabolism is altered by combined OC? Management?

A

Metabolism altered by oral contraceptives

Lamotrigine (significantly ↓ levels – induction of lamotrigine glucuronidation)

Management

Use alternative to interacting drug or other method of birth control

42
Q

What are some of the contraindications of COC?

A

Thromboembolic disease
Current or past VTE
Hypertension (>160/100mmHg)
Ischemic heart disease / Stroke
Known or suspected breast cancer
Migraine with aura
Severe / active liver disease
Post-partum
–> Wait least 3-6 weeks post-partum b/c increased risk of VTE
Smokers (>15 cigs/day)
Over 35 years old

43
Q

What are the two types of the progestin-only pills?

A

Norethindrone 35mcg daily (no HFI)

Drospirenone 4mg OD x 24 days then 4 placebo pills

44
Q

Describe the MOA of norethindrine?

A

Alters cervical mucus and endometrium (main moa)

45
Q

Describe the MOA of drosperinone?

A

Primarily suppresses ovulation

46
Q

Describe the indication of progestin-only contraceptives?

A

Estrogen contraindicated
History/risk of blood clots (VTE)
Smoker >35 years old
Obese
Migraine
Breastfeeding – won’t decrease milk supply

47
Q

What are the adverse effects of progestin only pills?

A

Irregular bleeding (more so in first months)
Headache
Bloating, wgt gain (water)
Acne
Breast tenderness
Potential to ↑ K+ (monitor if risk for hyperkalemia) –> Drosperinone, monitor it

48
Q

What are some contraindications of the progestin only pills?

A

Liver disease
Breast cancer
Drug interactions similar to combined OC

49
Q

What are some of the progestins hormonal therapy? How do they work?

A

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

Can help with dysmenorrhea symptoms

50
Q

Describe the efficacy of progestins compared to other contraceptives in endometriosis?

A

Similar efficacy to other hormonal therapies

51
Q

What are some adverse effects of progestin contraceptives in endometriosis?

A

AE’s - breakthrough bleeding, weight gain/fluid retention, mood changes, h/a

Depot: may delay the return in ovulation, and decraesed BMD with prolonged use

Dienogest: may be detrimental to BMD (especially adolescants, adults can be reversed), associated with less anti-androgenic effects, requires non-hormonal contraception

IUS: risk of expulsion; long-term effect on BMD unknown

52
Q

Counselling point regarding contraception in endometriosis

A

A minimum of a 3 month trial should be tried prior to moving on to subsequent treatment options for pain control

53
Q

Describe the MOA of NSAID’s in endometriosis

A

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

PHAR 359 (3 decks)

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