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PATHOPHYSIOLOGY AND
PHYSIOLOGY OF
PRIMARY DYSMENORRHEA
DANETTE L. BILLINGS
NURS 530 APRN ADVANCED PHYSIOLOGYAND PATHOPHYSIOLOGY
WEST COAST UNIVERSITY
DR. GAYLA LOVE
JULY 30, 2017
DYSMENORRHEA • Just what is primary dysmenorrhea? McCance & Huether
(2014) define primary dysmenorrhea as painful menstruation
associated with the release of prostaglandins in ovulatory
cycles, but not with pelvic disease (in other words absent of
pelvic pathology).
• The American College of Obstetricians and Gynecologists
(ACOG) (2015) cited that “approximately 50% of all women
experience dysmenorrhea, 10% of whom are incapacitated for
1 to 3 days because of their pain severity”.
• “Primary dysmenorrhea usually begins with the onset of
ovulatory cycles, around age 15 or 16 years with prevalence
highest during adolescence. Often primary dysmenorrhea
starts shortly after a girl begins having menstrual periods”
(typically within 6 months) (McCance & Huether, 2014).
PATHOPHYSIOLOGY
“Primary dysmenorrhea is attributed to excessive endometrial
prostaglandin production. Prostaglandin is made within the
lining of the uterus or endometrium. Women with painful
periods produce 10 times as much prostaglandin F (pgf2α), a
potent myometrial stimulant and vasoconstrictor, as
asymptomatic women. Elevated levels of prostaglandins
(especially pgf2α and pge2α) cause uterine hypercontractility,
decreased blood flow to the uterus, and increased nerve
hypersensitivity, thus resulting in pain” (McCance &Huether,
2014). Pain usually occurs right before menstruation starts as
the level of prostaglandins increases in the lining of the uterus.
“The pain often radiates into the groin and may be
accompanied by backache, anorexia, vomiting, diarrhea,
syncope, and headache; these symptoms are caused by the
entrance of prostaglandins and prostaglandin metabolites into
the systemic circulation” (McCance & Huether, 2014).
PATHOPHYSIOLOGY CONT’D
On the first day of the menstrual period, the levels are very high. Calis (2016) states that “women
with dysmenorrhea may have up-regulated cyclo-oxygenase (COX) enzyme activity, which
contributes to increased synthesis of prostaglandins. Furthermore, leukotriene production is
elevated; contributing to increased and more intense levels of pain”. “Prostaglandins are primarily
released during the first 48 hours of menstruation, when symptoms are the most intense; but the
pain usually persists for the first 1 to 3 days of the menstrual flow” (McCance &Huether, 2014).
As menstruation continues and the lining of the uterus is shed, the levels decrease. Pain usually
decreases as the levels of prostaglandins decrease. “In many women with primary dysmenorrhea,
menstruation becomes less painful as they get older” (ACOG, 2015).
TREATMENT
• “Nonsteroidal anti-inflammatory
medication (NSAIDS, e.g., Ibuprofen) is
the treatment of choice as these reduce
COX enzyme activity, thus prostaglandin
production. NSAIDS work in the majority
of women with primary dysmenorrhea and
are most effective if started at the first sign
of bleeding or cramping” (ACOG,
2015)”. In women who desire
contraception, dysmenorrhea may be
relieved with hormonal contraceptives.
CONCLUSION
According to writings by McCance
&Huether (2014), hormonal contraception
stops ovulation and creates an atrophic
endometrium, thereby decreasing
prostaglandin synthesis and myometrial
contractility.
The state of an atrophic endometrium
simply put means a thinning of the
endometrium. This state is said to decrease
symptoms of primary dysmenorrhea
(ACOG, 2015) which makes it clear why
women commonly experience lessened
symptoms as they become older.
CONCLUSION CONT’D
“There are no tests specifically for the diagnosis of primary dysmenorrhea.
However a complete physical (including pelvic and rectal exams) should be
performed” (Calis, 2016). This is the most accurate method used to diagnose
primary dysmenorrhea. After diagnosis is confirmed the advanced practice nurse
(APN) must instruct the patient to proactively treat her symptoms, (by
implementing the interventions as the APN previously explained); thereby
creating the possibility for optimal patient outcome.
REFERENCES
American College of Obstetricians and Gynecologists, (2015) Dysmenorrhea: Painful
Periods-Frequently Asked Questions. Retrieved on July 26, 2017 from
https://www.Acog.Org/-/media/for-patients/faq046.Pdf
Calis, K.A. (2016) dysmenorrhea: practice essentials, background, pathophysiology.
Retrieved on July 26, 2017 from
http://emedicine.Medscape.Com/article/253812-overview
McCance, K. L., Huether, S.E. (2014) pathophysiology: the biologic basis for disease in
Adults and children (7th ed.). St. Louis, MO: Elsevier -Mosby

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Pathophysiology of primary dysmenorrhea

  • 1. PATHOPHYSIOLOGY AND PHYSIOLOGY OF PRIMARY DYSMENORRHEA DANETTE L. BILLINGS NURS 530 APRN ADVANCED PHYSIOLOGYAND PATHOPHYSIOLOGY WEST COAST UNIVERSITY DR. GAYLA LOVE JULY 30, 2017
  • 2. DYSMENORRHEA • Just what is primary dysmenorrhea? McCance & Huether (2014) define primary dysmenorrhea as painful menstruation associated with the release of prostaglandins in ovulatory cycles, but not with pelvic disease (in other words absent of pelvic pathology). • The American College of Obstetricians and Gynecologists (ACOG) (2015) cited that “approximately 50% of all women experience dysmenorrhea, 10% of whom are incapacitated for 1 to 3 days because of their pain severity”. • “Primary dysmenorrhea usually begins with the onset of ovulatory cycles, around age 15 or 16 years with prevalence highest during adolescence. Often primary dysmenorrhea starts shortly after a girl begins having menstrual periods” (typically within 6 months) (McCance & Huether, 2014).
  • 3. PATHOPHYSIOLOGY “Primary dysmenorrhea is attributed to excessive endometrial prostaglandin production. Prostaglandin is made within the lining of the uterus or endometrium. Women with painful periods produce 10 times as much prostaglandin F (pgf2α), a potent myometrial stimulant and vasoconstrictor, as asymptomatic women. Elevated levels of prostaglandins (especially pgf2α and pge2α) cause uterine hypercontractility, decreased blood flow to the uterus, and increased nerve hypersensitivity, thus resulting in pain” (McCance &Huether, 2014). Pain usually occurs right before menstruation starts as the level of prostaglandins increases in the lining of the uterus. “The pain often radiates into the groin and may be accompanied by backache, anorexia, vomiting, diarrhea, syncope, and headache; these symptoms are caused by the entrance of prostaglandins and prostaglandin metabolites into the systemic circulation” (McCance & Huether, 2014).
  • 4. PATHOPHYSIOLOGY CONT’D On the first day of the menstrual period, the levels are very high. Calis (2016) states that “women with dysmenorrhea may have up-regulated cyclo-oxygenase (COX) enzyme activity, which contributes to increased synthesis of prostaglandins. Furthermore, leukotriene production is elevated; contributing to increased and more intense levels of pain”. “Prostaglandins are primarily released during the first 48 hours of menstruation, when symptoms are the most intense; but the pain usually persists for the first 1 to 3 days of the menstrual flow” (McCance &Huether, 2014). As menstruation continues and the lining of the uterus is shed, the levels decrease. Pain usually decreases as the levels of prostaglandins decrease. “In many women with primary dysmenorrhea, menstruation becomes less painful as they get older” (ACOG, 2015).
  • 5. TREATMENT • “Nonsteroidal anti-inflammatory medication (NSAIDS, e.g., Ibuprofen) is the treatment of choice as these reduce COX enzyme activity, thus prostaglandin production. NSAIDS work in the majority of women with primary dysmenorrhea and are most effective if started at the first sign of bleeding or cramping” (ACOG, 2015)”. In women who desire contraception, dysmenorrhea may be relieved with hormonal contraceptives.
  • 6. CONCLUSION According to writings by McCance &Huether (2014), hormonal contraception stops ovulation and creates an atrophic endometrium, thereby decreasing prostaglandin synthesis and myometrial contractility. The state of an atrophic endometrium simply put means a thinning of the endometrium. This state is said to decrease symptoms of primary dysmenorrhea (ACOG, 2015) which makes it clear why women commonly experience lessened symptoms as they become older.
  • 7. CONCLUSION CONT’D “There are no tests specifically for the diagnosis of primary dysmenorrhea. However a complete physical (including pelvic and rectal exams) should be performed” (Calis, 2016). This is the most accurate method used to diagnose primary dysmenorrhea. After diagnosis is confirmed the advanced practice nurse (APN) must instruct the patient to proactively treat her symptoms, (by implementing the interventions as the APN previously explained); thereby creating the possibility for optimal patient outcome.
  • 8. REFERENCES American College of Obstetricians and Gynecologists, (2015) Dysmenorrhea: Painful Periods-Frequently Asked Questions. Retrieved on July 26, 2017 from https://www.Acog.Org/-/media/for-patients/faq046.Pdf Calis, K.A. (2016) dysmenorrhea: practice essentials, background, pathophysiology. Retrieved on July 26, 2017 from http://emedicine.Medscape.Com/article/253812-overview McCance, K. L., Huether, S.E. (2014) pathophysiology: the biologic basis for disease in Adults and children (7th ed.). St. Louis, MO: Elsevier -Mosby