PRIMARY AND SECONDARY DYSMENORRHEA,
PREMENSTRUAL SYNDROME, PREMENSTRUAL DYSPHORIC DISORDER
Dr. Vallega | March 22, 2022
OUTLINE
I. Dysmenorrhea
II. Primary Dysmenorrhea
III. Secondary Dysmenorrhea
IV. Premenstrual Syndrome vs Premenstrual Dysphoric
Disorder
Words in gray were transcribed from the audio within the
powerpoint of the lecturer
 It starts with an immature follicle and then it matures until
eventually ovulation occurs and what is left of the follicle
becomes the corpus luteum.
 There is also a correlation between the body temperature and
what happens during the menstrual cycle. At about the time of
ovulation, there is a spike or rise in body temperature.
 The hormonal levels - before ovulation, there is a peak of
estradiol and luteinzing hormone. In the follicular phase, there
is a gradually increasing level of estradiol followed by some
degree of decrease while the progesterone (black line) is
relatively low during the follicular phase but becomes more
predominant during the luteal phase
 At the start of the menses, the endometrium will start to
rapidly thin out followed by a gradual growth again but 14
days after ovulation if there’s no fertilization that occurs in the
egg cell then there will be menstruation.
DYSMENORRHEA
 Cyclic, painful cramping sensation in the lower abdomen
 Often accompanied by other biologic symptoms including
sweating, tachycardia, headaches, nausea, vomiting, diarrhea,
tremulousness
 Usually occurs just before or during menses
PRIMARY DYSMENORRHEA
 The menstrual cramps that happen usually at the age of 20.
 There is no specific or known cause for the dysmenorrhea.
There’s no structural cause for it.
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Incidence and Epidemiology
 16-90% incidence
 Swedish study:
○ 72.4% suffered from dysmenorrhea
○ 34.3% mild
○ 22.7% moderate requiring analgesia
○ 15.4% severe dysmenorrhea that inhibited working
ability
 Canada study:
○ 60% had primary dysmenorrhea
○ 60% reported pain as moderate or severe
 Risk of developing dysmenorrhea is reduced with:
○ Younger age at first childbirth
○ Higher parity
○ Physical exercise
 Risk of developing dysmenorrhea is increased with:
○ Age less than 30; BMI less than 20
○ PMS
○ PID
○ Sterilization - ex. Tubal ligation
○ History of sexual assault
 Other factors:
○ Positive correlation between the severity of
dysmenorrhea and duration of menstrual flow,
amount of menstrual flow and early menarche
○ 38.3% reported dysmenorrhea for the first time
within the first year of menarche
○ Family history - mother and sisters
Pathogenesis
 Close association between elevated prostaglandin F2a levels in
the secretory endometrium and the secretory endometrium
and the symptoms of dysmenorrhea
 Arachidonic acid is converted PGF2a, PGE2 and leukotrienes
involved in increasing myometrial contractions
○ Because there’s an increase of these substances in
the body during menstruation, there is sort of
hypercontractility. The smooth muscles of the
uterus contract causing cramps and pain.
Diagnosis
 Diagnosis is made largely by history and PE
 Midline, crampy, lower abdominal pain usually at the start of
menstruation
○ Sometimes even a few days before the start of the
menstrual flow there could already be some
discomfort in the lower abdomen and sometimes
even at the lower back
 Pain can be severe and can also involve the low back and
thighs
 Pain does not occur at times other than menses and only
occurs in ovulatory cycles
 Normal pelvic exam
 No labs of imaging modalities
 If you have regular ovulatory cycles then that means you have
the normal fluctuations of the reproductive hormones then
usually you would experience dysmenorrhea. If you have very
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 irregular menstruation especially if you have anovulatory
cycles or not ovulating, commonly you would not experience
dysmenorrhea.
Treatment
 Provide patient education and reassurance
 Individualized, supportive therapy
 Exercise
 Heat therapy - lower abdomen or lower back can help alleviate
the symptoms
 Behavioral interventions: biofeedback, Lamaze, hypnotherapy,
imagery, coping strategies, desensitization procedures
 Vitamins and diet: Vit E, Vit B, fish oil supplements
 NSAIDs
○ First line
○ Prostagandin synthesis inhibitors that have been
demonstrated to alleviate symptoms
○ 2 types:
 Arylcarboxylic acids (aspirin, mefenamic acid)
 Arylalkanoic acids (iburprofen, naproxen)
 COX 2 inhibitors
○ Decreased expression of COX2 with continuous
OCP use - reduction of uterine muscular
contractility
 Cochrane review - NSAIDs were substantially more effective
than placebo in pain reduction
 Progesterone
○ DMPA (Depot Medroxyprogesterone acetate)
 Most common and cheapest
 A type of contraception that is an injection, a
depot preparation of Medroxyprogesterone
acetate
 There is a tablet preparation but what is used for
long term treatment or for contraception is
the depot which is an IM injection
 Some would discourage the use of DMPA
because of adverse effects
○ LNG-IUS (Mirena, Levonorgestrel releasing
intrauterine system)
○ Single rod etonorgestrel-releasing contraceptive
(Implanon)
 Usually inserted in the inner upper arm and it is
made of thin rod which contains progestogen
within it
 These are slow releasing, hormone containing
devices that are applied for sustain release
 If we give continuous progesterone, these
progestogenic agents will inhibit ovulation. If
you don’t ovulate and menstruate, it will not
allow withdrawal bleeding or monthly
bleeding. If you do not menstruate, you will
not experience dysmenorrhea.
 Other treatments
○ Transcutaneous electrical nerve stimulation
○ Acupuncture, acupressure
○ LUNA - Laparoscopic Uterine Nerve Ablation
○ LPSN - Laparoscopy Presacral Neurectomy
○ Nifedipine
 In obstetrics, it is used as a tocolytic because it
has been demonstrated to decrease or
prevent uterine contractions
 A high dose is needed up to 40mg to prevent
dysmenorrhea and this can result to adverse
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reactions like flushing/redness of the face,
tachycardia and headache
SECONDARY DYSMENORRHEA
 Should be considered in patients with dysmenorrhea that does
not respond to NSAID
 Due to pelvic pathology and may occur at any age and may
include cervical stenosis, endometriosis, adenomyosis, pelvic
inflammation, pelvic congestion syndrome, mental health
condition, functional bowel disease
Cervical Stenosis
 Severe narrowing of cervical canal at the level of the internal
os; impedes menstrual flow and causing increased intrauterine
pressure at the time of menses
○ The walls of the uterus stretches during the time of
menses causing pain
 May also cause retrograde menstrual flow; and is associated
with endometriosis
 Treated by dilating the cervix or removing the obstruction
(polyp, mass, myoma)
Endometriosis
 The presence of endometrial glands and stroma outside of the
endometrial cavity
 Affects 6-10% of women; cause of 70-80% of chronic pelvic
pain
 History: pain becoming more severe during menses
 PE: uterosacral ligament nodules, lateral displacement of the
cervix as a result of adhesions caused by the repeated trauma
to the peritoneum to the pelvis
Adenomyosis
 The presence of endometrial glands and stroma in the
myometrium
○ When adenomyosis is present, there’s a high
chance the patient also has endometriosis
 Heavy, painful menses
 Significantly higher levels of prostaglandin found
Pelvic Inflammation
 Infection caused by chlamydia, gonorrhea and other pelvic
infections can cause pelvic adhesions and tubal damage
(because of abscess formation) and pain is aggravated during
menses
Pelvic Congestion Syndrome
 Engorgement of pelvic vasculature, vasocongestion
 Global tenderness of cervix, uterus and adnexal - nonspecific
 Diagnosed history and imaging
PREMENSTRUAL SYNDROME vs
PREMENSTRUAL DYSPHORIC DISORDER
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 PMS  For adenomyosis especially those with abnormal
○ More common and milder uterine bleeding, the first line of treatment is
○ A group of mild to moderate symptoms (physical levnorgestrel releasing intrauterine system or
and behavioral) that occur in the second half of the the mirena
menstrual cycle or the luteal phase and that may ○ NSAIDs for pain
interfere with work and personal relationships ○ Diuretics for bloatedness
○ They can have breast tenderness, bloatedness, ○ Bromocriptine for mastalgia
water retention, headache, irritability, anxiety, and  If all else fails, you can offer surgery only for those who are in
depression the perimenopause who still have severe symptoms of PMDD
○ Usually after menses, there is a symptom free  Alternative therapies:
period then 2-3 weeks after you’ll start to have ○ Yoga
symptoms again ○ Acupuncture
○ More easily controlled and managed compared to ○ Massage
PMDD ○ Biofeedback
 PMDD
○ Less prevalent END OF TRANSCRIPTION
○ More severe sort of PMS
○ With marked behavioral and emotional symptoms -
depressed mood, feeling of hopelessness, more
anxious, there’s tension and labile affect,
sometimes even feeling of anger

Causes
 Was initially attributed to estrogen excess, or an imbalance of
estrogen and progesterone, however studies have not been
able to show a definite or consistent correlation
 Multifactorial psychoendocrine disorder - as evidenced by
successful clinical trials using SSRIs

Treatment
 Diet, supplement and exercise
○ Reduction or elimination of sugar, alcohol, caffeine,
salty food and red meat during this period
○ Vitamin B6 supplementation may also help
 Cognitive Behavioral Therapy - may be added
 Pharmacologic agents:
○ Psychoactive drugs - SSRIs, alprazolam
 Help improve the dysphoric or depressive
symptoms
 Sometimes given cyclically - if patient has regular
menses, start at day 14 of the cycle up to the
time the patient menstruates (give SSRIs)
○ Progesterone, OCPs
 Depot, IUD, or subdermal implant
 Induce pseudo-pregnancy state ‘

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