Menstrual Abnormalities Flashcards

1
Q

PALM COEIN acronym for abnormal uterine bleeding

A
  • Polyps
  • Adenomyosis
  • Leiomyoma (fibroid)
  • Malignancy
  • Coagulopathy
  • Ovarian dysfunction
  • Endometrial process
  • Iatrogenic
  • Not yet classified
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2
Q

What is the most common cause of abnormal uterine bleeding in adolescent women

A

Ovulatory dysfunction

Specifically, anovulatory bleeding from immaturity of the HPO axis.

Regular periods are not usually established until 2-3 years post-menarche.

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3
Q

What is the most common cause of abnormal uterine bleeding in reproductive-age women?

A

Ovulatory dysfunction

Specifically PCOS in this population

However, you always need to remember to check a pregnancy test first!!!!!

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4
Q

Perimenopausal women have increased incidence of which causes of abnormal uterine bleeding?

A

The PALM group

Polyps, adenomyosis, leiomyoma (fibroid), and malignancy

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5
Q

Non-predictable or skipped periods suggests. . .

A

. . . ovulatory dysfunction

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6
Q

Bleeding in-between periods suggests. . .

A

. . . anatomic source (polyps, adenomyosis, leiomyoma, malignancy, or endometrial process)

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7
Q

In whom should you have a low threshold for endometrial biopsy?

A
  • Women over 40
  • Women w/ obesity
  • Women w/ diabetes
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8
Q

Therapies for abnormal uterine bleeding due to anovulation

A
  • Oral contraception
  • Cyclic progestin
  • Levonorgestrel IUD
  • Endometrial ablation (always need to perform endometrial biopsy first)
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9
Q

Primary dysmenorrhea

A

Not well understood

Tends to first occur around cycle 4-7 post menarche and then consistently. Incidence greatest in late teens/early twenties.

Thought to be due to excess production of prostaglandins (specifically F2a), leading to painful uterine muscle activity. This due to the surge in progesterone prior to menses, which in turn stimulates high levels of prostaglandins just prior to menses.

This is why ibuprofen works so well for menstrual cramping!

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10
Q

Secondary dysmenorrhea

A
  • Often caused by:
    • Endometriosis
    • Adenomyosis
    • Pelvic inflammatory disease
    • Leiomyoma(ta)
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11
Q

Prostaglandins vs progesterones in smooth muscle

A

Prostglandins result in smooth muscle contraction

Progesterones result in smooth muscle relaxation

However, progesterones also stimulate prostaglandin production in certain locations!

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12
Q

Secondary dysmenorrhea with a large and irregularly shaped uterus on exam suggests. . .

A

. . . uterine fibroids

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13
Q

Secondary dysmenorrhea with an regularly enlarged and boggy uterus suggests. . .

A

. . . adenomyosis

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14
Q

Secondary dysmenorrhea with painful uteroscral nodules and fixed uterus on exam suggests. . .

A

. . . endometriosis

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15
Q

Secondary dysmenorrhea with a history of high risk sexual behavior and vaginal discharge suggests. . .

A

. . . pelvic inflammatory disease

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16
Q

Therapy for secondary dysmenorrhea

A
  • Therapy should often be two-pronged: Symptomatic management and definitive
  • Symptom management / Conservative:
    • NSAIDs
    • Hot pads
    • Exercise
  • Definitive therapy:
    • OCP (suppress ovulation, stabilizes progesterone levels, less cramping)
    • Surgery (if there is a surgical indication)
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17
Q

Why do prostaglandins cause cramping pain?

A
  • Increased contraction of the myometrium
    • Resultant ischemia from vessel compression
  • Increased pain sensitivity via a direct effect on neuronal resting potential
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18
Q

Pattern of pain in primary vs secondary dysmenorrhea

A

Pain in primary dysmenorrhea usually occurs right before menses and decreases as menses progresses, since it is mediated by prostaglandins

Pain in secondary dysmenorrhea is less predictable, and often continues through menses and even after menses

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19
Q

Two “subtypes” of primary amenorrhea

A
  • Age 13, no adrenarche AND no menarche
  • Age 15, adrenarche BUT no menarche
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20
Q

Diagnostic criteria for secondary amenorrhea

A
  • Woman who was previously menstruating has not menstruated for 3-6 months or has missed 3 periods
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21
Q

Diagnostic criteria for oligomenorrhea

A
  • Woman who was a menstruation in cycles >40 days, but <6 months
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22
Q

1 cause of amenorrhea

A

Pregnancy

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23
Q

Most common pathological causes of amenorrhea

A
  1. Hypothalamic-pituitary axis dysfunction
  2. Ovarian dysfunction
  3. Anatomic abnormality
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24
Q

Functional causes of hypothalamic pituitary dysfunction that can cause amenorrhea

A
  1. Weight loss
  2. Excessive exercise
  3. Obesity
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25
Q

Ovarian failure and associated etiologies

A
  • Defined as resistance to LH/FSH or exhaustion of follicles
  • Causes:
    • Chromosomal abnormalities (Turner’s syndrome-associated ovarian dysgenesis)
    • Autoimmune ovarian failure
26
Q

Asherman’s syndrome

A
  • Most common cause of secondary amenorrhea
  • Obstruction of the outflow of the uterus due to formation of scar tissue or adhesions
  • May occur after:
    • Dilation and curretage
    • Infection
27
Q

Starting place for the workup of secondary amenorrhea

A

Progesterone withdrawal challenge

28
Q

Amenorrhea workup algorithm

A
29
Q

Hormonal contraception medications

A
30
Q

Non-hormonal contraception methods

A
31
Q

Lactational amenorrhea

A

Occurs when infant suckling interrupts GnRH secretion

32
Q

Active ingredient in spermicide

A
  • Either nonoxonyl-9 or octoxonyl-9
33
Q

Methodology of fertility awareness as a form of contraception

A

Relies heavily on a woman having regular cycles

Calculate cycle length and subtract 14 days to determine the time of ovulation.

The fertile period is 5 days prior to ovulation to 1 day after ovulation (the last 5 days of the follicular phase and the first day of the luteal phase).

34
Q

Emergency contraceptive pill

A
  • Ulipristol acetate or mifepristone
  • Selective progesterone receptor antagonists
    *
35
Q

Copper IUD as an emergency contraception method

A

Insertion of the copper IUD up to 5 days after unprotected sex can also work as a form of emergency contraception, and will continue to provide contraceptive benefits for up to 10 years.

It can easily be removed at any time to restore fertility.

36
Q

The multiple mechanisms of oral progestin as contraception (both OCP and alone)

A
  • Inhibits ovulation (95% of ovulations)
  • Thickens cervical mucous (prevents sperm from getting in)
  • Creates thin resting endometrium (hard for blastula to implant)
  • Interferes with fallopian tube peristalsis, hamper egg transport
37
Q

Major benefits of having estrogen in an OCP rather than progesterone alone

A
  • Potentiates the effects of progesterone
  • Further inhibits follicle recruitment
  • Allows for some endometrial thickening (this is really the key feature, as it prevents irregular bleeding from a thin atrophic endometrium as is sometimes seen in progesterone-only contraception)
38
Q

Meno-metrorrhagia

A

Frequent, heavy menstrual bleeding

39
Q

Dilation and curettage procedure

A

Basically the same as an endometrial biopsy

40
Q

“good” vs “bad” endometrial biopsy results

A

“Good”: Proliferative, atrophic, secretory

“Bad”: Hyperplasia, atypia, EIN, carcinoma

41
Q

Progestins in treatment of fibromas

A

Help with bleeding and pain due to their effects on the endometrium, but do nothing to reduce the size of the fibroids.

As such, bulk symptoms (urinary urgency, constipation) will not be affected, and it is not a definitive therapy.

42
Q

Deliveries after myomectomy for fibroids

A

Will likely need to be C sections from here on, as the uterus may rupture under the pressure of labor following uterine surgery.

43
Q

Definition of “chronic pelvic pain”

A

>6 months, non-cyclic

44
Q

Presence of dyspareunia suggests . . .

A

. . . secondary dysmenorrhea, as in endometriosis

45
Q

Age range for primary vs secondary dysmenorrhea

A

Primary: ~15-25

Secondary: 40+

46
Q

Dysmenorrhea with normal physical exam suggests. . .

A

. . . primary dysmenorrhea

47
Q

Therapy for primary dysmenorrhea

A
  • Conservative:
    • Heat pads
    • Exercise
    • NSAIDs
    • Oral contraceptive (to induce anovulation)
  • Surgical:
    • Presacral neurectomy (disruption of superior hypogastric plexus, only for refractory cases)
48
Q

Carnett Sign

A

Tensing of abdominal wall with raise of legs or chin in supine position

Indicates myofascial pelvic pain

49
Q

Most common chronic pelvic pain etiologies

A
  • IBS
  • Interstitial cystitis
  • Endometriosis
  • Adhesions
  • PID
  • STIs
50
Q

Interstitial cystitis

A
  • Chronic inflammation of the bladder
  • Pelvic pain, urinary urgency and frequency, dyspareunia.
  • Possibly due to disruption of glycosaminoglycan layer protecting bladder epithelium
  • Diagnosis:
    • Exclusion of other diagnoses
    • Cystoscopy w/ biopsy showing gross puncta of blood on the bladder wall, Hunner’s ulcers, lymphocytic infiltrate on histology.
51
Q

Initial management for new diagnosis of chronic pelvic pain

A

First addressed with a therapeutic challenge for most likely etiology.

Otherwise, GnRH agonist trial can rule out ovarian/menstrual process. If IBS symptoms predominate, referral to GI.

52
Q

If no identifiable source is found for chronic pelvic pain, __ often provides relief.

A

If no identifiable source is found for chronic pelvic pain, hysterectomy often provides relief.

53
Q

Diagnosis of PMS

A
  • Reporting of one or more of the following symptoms 5 days before menses of 3 cycles:
    • Depression
    • Angry outbursts
    • Irritability
    • Anxiety/confusion/social withdrawal
    • Breast tenderness
    • Headache
    • Abdominal bloating
    • Swelling of extremities
54
Q

Pre-menstrual dysmorphic disorder diagnosis (per DSM IV)

A
  • Presence of 5/11 symptoms with at least one core symptom, along with functional impairment and/or morbidity
  • Cycles with luteal phase, but symptom free follicular phase
  • Core symptoms:
    • Depressed mood
    • Anxiety or tension
    • Irritability
    • Anhedonia
  • Additional symptoms:
    • Difficulty concentrating
    • Lack of energy
    • Marked change in appetite
    • Sleep changes
    • Feeling overwhelmed/out of control
    • Somatic symptoms
55
Q

Two mechanisms of progestin (in progestin only or OCP therapy) that prevent dysmenorrhea

A
  1. Inhibition of ovulation
  2. Induction of atrophy in the endometrium (even when estrogen is present)
    • Remember that prostaglandins are produced in the endometrium, so inducing endometrial differentiation and atrophy prevents prostaglandin production
56
Q

Syndrome of an endometrial polyp

A
  • Often occur in women ages 40-50, pre-menopausally
  • Symptoms: Menorrhagia, cramping, spotting
  • Significantly more common than endometriosis
57
Q

Tranexamic acid

A
  • Inhibitor of plasminogen and thereby fibrinogenolysis
  • Second-line therapy for menorrhagia (irrespective of etiology)
  • Useful for cases where hormonal medications are contraindicated (patient wants to become pregnant, high risk of VTE, etc)
  • Useful for women who wish to become pregnant soon
  • Acts within 2–3 hours of administration and should not be used in women at a high risk of thrombosis.
58
Q

Signs of anorexia nervosa

A
  • Enlargement of salivary glands (parotids, submandibulars)
  • Presence of lanugo body hair
59
Q

Mittelschmerz

A
  • A common, benign phenomenon in women of reproductive age that is caused by follicular enlargement or rupture of the follicular cyst during ovulation, which leads to the release of small amounts of intraperitoneal fluid and subsequent peritoneal irritation. The pain is self-limited and usually subsides within hours to two days.
  • Patients should be reassured and receive symptomatic treatment with NSAIDs as needed.
  • Especially common during adolescence
60
Q

___ has been shown to improve psychological and emotional symptoms in PMS when used as sole therapy or as adjunctive therapy to standard treatments

A

Supplementation with 1200 mg calcium daily has been shown to improve psychological and emotional symptoms in PMS when used as sole therapy or as adjunctive therapy to standard treatments