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PHARMACOTHERAPY PRINCIPLES AND PRACTICE CARE PLANS & CASES

LEARNING OBJECTIVES

LEARNING OBJECTIVES

Upon completion of the chapter, the reader will be able to:

  1. Describe the underlying etiology and pathophysiology of dysmenorrhea, amenorrhea, anovulatory bleeding, and menorrhagia and how they relate to selecting effective treatment modalities.

  2. Describe the clinical presentation of dysmenorrhea, amenorrhea, anovulatory bleeding, and menorrhagia.

  3. Recommend appropriate nonpharmacologic and pharmacologic interventions for patients with dysmenorrhea, amenorrhea, anovulatory bleeding, and menorrhagia.

  4. Identify the desired therapeutic outcomes for patients with dysmenorrhea, amenorrhea, anovulatory bleeding, and menorrhagia.

  5. Design a monitoring plan to assess the effectiveness and adverse effects of pharmacotherapy for dysmenorrhea, amenorrhea, anovulatory bleeding, and menorrhagia.

INTRODUCTION

The most common menstruation-related disorders include dysmenorrhea, amenorrhea, anovulatory bleeding, and menorrhagia. These disorders negatively affect quality of life, reproductive health, work productivity, and may lead to adverse long-term health consequences, such as osteoporosis or polycystic ovarian syndrome.

DYSMENORRHEA

Dysmenorrhea is pelvic pain, generally described as cramping, that occurs during or just prior to menstruation. Primary dysmenorrhea is pain in the setting of normal pelvic anatomy and physiology, whereas secondary dysmenorrhea is associated with underlying pelvic pathology.1

Epidemiology and Etiology

Rates of dysmenorrhea range from 16% to 90%.2 Around 8% to 15% percent of women with dysmenorrhea report limited daily activities or missed days in work or school.1,3 Risk factors for dysmenorrhea include irregular or heavy menses, age less than 30, menarche prior to age 12, body mass index (BMI) less than 20 kg/m2, history of sterilization or sexual abuse, and smoking.1,2 Causes of secondary dysmenorrhea may include endometriosis, pelvic inflammatory disease, uterine or cervical polyps, and uterine fibroids.1,4,5

Pathophysiology

KEY CONCEPT In primary dysmenorrhea, elevated arachidonic acid levels in the menstrual fluid lead to increased concentrations of prostaglandins and leukotrienes in the uterus. This induces uterine contractions, stimulating pain fibers, reducing uterine blood flow, and causing uterine hypoxia.1,3,4

Treatment

Desired Outcomes

Desired treatment outcomes (Figure 49–1) are relief of pelvic pain, improved quality of life, and fewer lost days at school and work.

FIGURE 49–1.

Treatment algorithm for dysmenorrhea. (CHC, combination hormonal contraceptive; IUD, intrauterine device; MPA, medroxyprogesterone acetate; NSAID, nonsteroidal anti-inflammatory drug.)

Nonpharmacologic Therapy

Nonpharmacologic interventions which diminish dysmenorrhea symptoms include topical heat therapy, regular exercise, transcutaneous electric nerve stimulation (TENS), and acupuncture.1,3,5 In addition, a low-fat vegetarian diet has been shown to lessen the intensity and duration of dysmenorrhea.5

Pharmacologic Therapy

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