Menstrual disorders

Lentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.

Menstrual disorders


Menstrual disorders

• Abnormal uterine bleeding/ Heavy uterine bleeding

• Amenorrhea• Primary and Secondary

Dysmenorrhea, Premenstrual Syndrome (PMS), Premenstrual Dysphoric Disorder (PMDD)


ABNORMAL UTERINE BLEEDING


Abnormal Uterine Bleeding defined as changes in frequency of

menses, duration of flow or amount of blood loss


Definition of terms

Mean interval between menses is 28 days (±7 days)

Mean duration of menstrual flow is 4 days (>7 days is menorrhagia)

Mean amount of MBL in normal women is about 35 mL (>80 mL is menorrhagia)

DEFINITION OF MENSTRUAL CYCLE IRREGULARITIES: NO LONGER USED

IRREGULARITY DEFINITIONOLIGOMENORRHEA Infrequent IRREGULARLY timed episodes of

bleeding usually occurring at intervals of more than 35 days

POLYMENORRHEA Frequent but REGULARLY timed episodes of bleeding usually occuring at intervals of 21 days or less

MENORRHAGIA REGULARLY timed episodes of bleeding that are EXCESSIVE in amount (> 80 ml) and duration of flow (> 5 days)

METRORRHAGIA Irregularly timed bleeding or bleeding between periods

MENOMETRORRHAGIA

EXCESSIVE, PROLONGED bleeding that occurs at IRREGULARLY timed frequent intervals

HYPOMENORRHEA REGULARLY timed bleeding that is decreased in amount

INTERMENSTRUAL BLEEDING/SPOTTING

Bleeding usually not of an excessive amount that occurs between otherwise normal menstrual cycles


Etiology

Two major categoriesA. Organic

I. SystemicII. Reproductive Tract disease

B. DysfunctionalI. Anovulatory II. Ovulatory

A. Organic: Systemic Disease• Chronic systemic diseases e.g. hepatitis, renal

disease, cardiac disease, and coronary vascular disorders (usually from anovualtion due to hypothalamic cause or problem with estrogen metabolism)

• Disorders of blood coagulation e.g. von Willebrand's disease and prothrombin deficiency

• Disorders producing platelet deficiency e.g leukemia, severe sepsis, idiopathic thrombocytopenic purpura (ITP), and hypersplenism

• Drugs e.g.anticoagulants • Endocrine disorders e.g. hormonal disorders

involving thyroid, PRL, and cortisol Lentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.


A. Organic: Reproductive Tract Disease The most common cause: accidents of pregnancy Other causes: 1) Malignancy of the genital tract endometrial and cervical cancer – most common vaginal, vulvar, fallopian tube cancer – less common 2) Anatomic uterine abnormalities submucous myomas, endometrial polyps, adenomyosis (probably d/t abnormal vasculature and blood flow and increased inflammatory changes) 3) Cervical lesions erosions, polyps, cervicitis (postcoital bleeding)

ABNORMAL UTERINE BLEEDING: WORKUP

History– Timing of bleeding, quantity of bleeding, menstrual hx

including menarche and recent periods, associated sxs, family hx of bleeding disorders

Physical– Speculum exam to R/o vaginal or cervical source of bleeding– Bimanual exam may reveal bulky uterus/discrete fibroids– Assess for obesity, hirsutism, stigmata of thyroid disease

(hypothyroidism associated with anovulation), signs of hyperprolactinemia (visual field testing, galactorrhea)

– Pap smear– Endometrial biopsy, if appropriate

Pregnancy Test Imaging

– Pelvic ultrasound – Sonohystogram (SIS) or hysterosalpingogram (HSG)

Surgical– Endometrial biopsy (>35 y/o, long history of excessive

bleeding, EM >8mm)– Hysteroscopy– D & CLentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.

AUB: TREATMENT STRATEGIES Medical vs Surgical

– Depends on the ff. patient characteristic: age, desire to preserve fertility, coexisting medical conditions, and patient preference

Anovulatory DUB– For adolescents: Cyclic progestogen (MPA 10mg OD for10 days/month x 6 mos) – 1st line COCs – only 2nd line used if DUB persists beyond 6 mos. on cyclic progestogen, because it does not allow HPO to mature– For perimenopausal women: Low dose COCs (20ug EE) – 1st line Cyclic progestogen – only 2nd line, this will help the endometrium but not reliably control bleeding because of unpredictability of the hormonal situationLentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.

AUB: TREATMENT STRATEGIES Ovulatory DUB

Cyclic progestogen (MPA 10mg OD for 3 weeks/mo. ) – shorter duration do not workLocal progesterone exposure (LNG-IUS) – 80% MBL by 3 mos (lasts >5 yrs)NSAIDs – Mefenamic acid 500mg TID, Ibuprofen 400mg TID, Meclofenamate Na 100mg TID, Naproxen Na 550mg LD then 275mg q6Antifibrinolytic agents – 50% MBL EACA (ε-aminocaproic acid)18g/d x 3 days then 12g ,9g ,6g, 3g = total 48g AMCA (tranexamic acid) 6/d x 3 days then 4g, 3g, 2g, 1g,= total 22g PAMBA (para-amino methylbenzoic acid)COCs – 50% MBLAndrogenic steroids – Danazol 200-400mg/day x 12 weeks 60% MBL GnRH Agonists – given for 3 months, reserved for women with severe MBL with failed with other medicationLentz GM, Lobo RA, Gershenson DM, and Katz VL. Comprehensive Gynecology 2012. 6th Edition.

AUB: TREATMENT STRATEGIES Acute Bleeding Pharmacologic Agents vs. Surgical Therapy Dilatation and curettage – fastest way, best when EM is thick >10-12 mm and px is >35 y/o Estrogens – best when EM is thin <5mm Oral CEE 10mg/day in 4 divided doses

IV CEE 25mg q4-6 hrs. High dose OCPs(50ug EE) 4tabs OD, continued for 1week after bleeding stops Progestogens – no evidence in stopping acute bleeding, and can only be used after stabilization of the endometrium (after 2-3 days of estrogen) MPA 10mg/day x 10 days/month Norethindrone acetate 2.5-5mg/day in 4 divided dosesEndometrial ablation – used if medical therapy is not effective 22-55% amenorrhea success rate 86-99% satisfaction rate only 25% proceed to hysterectomy w/in 4 years

Hysterectomy – used to treat persistent ovulatory DUB when medical therapy has failed


The “MOST COMMON”• FOREIGN BODY IN

THE VAGINAMost common

cause of vaginal bleeding in CHILDHOOD

• ACCIDENTS OF PREGNANCY

Most common cause of vaginal

bleeding in REPRODUCTIVE

age women

• ATROPHIC ENDOMETRIUM

Most common cause of vaginal

bleeding in POSTMENOPAUSA

L women

Heavy Menstrual BleedingCharacteristics Descriptive

TermsNormal limits

Frequency of menses in days

Frequent Normal

Infrequent

<24 24-38 >38

Regularity of menses in days (cycle to cycle variation in a year)

Absent Regular Irregular

±2-20 >20

Duration of flow in days

Prolonged Normal

Shortened

>8 4.5-8 <4.5

Volume of monthly blood loss in mL

Heavy Normal Light

>80 5-80 <5

Fraser. International definitions of abnormal menstrual bleeding. Fertil Steril 2007 & Hum Reprod 2007

• Chronic AUB– bleeding from the uterine corpus that is

abnormal in volume, regularity, and/or timing that has been present for the majority of the last 6 months

• Acute AUB– episode of heavy bleeding that, in the opinion

of the clinician, is of sufficient severity to require immediate intervention to prevent further blood loss

Abnormal Uterine Bleeding

• Intermenstrual bleeding (IMB)• occurs between clearly defined cyclic and

predictable menses and includes both randomly occurring episodes as well as those that manifest predictably at the same time in each cycle

• Breakthrough bleeding (BTB)• unscheduled bleeding that occurs during

the use of exogenous gonadal steroid therapy

Abnormal Uterine Bleeding

PALM group– discrete structural abnormalities that can be

seen and measured by imaging techniques such as ultrasound or hysteroscopy

COEIN group– non-structural entities, not defined by

imaging or histopathology

Causes of Heavy Menstrual Bleeding

– Polyp– Adenomyosis– Leiomyoma– Malignancy/

Hyperplasia

Causes of Heavy Menstrual Bleeding

*FIGO classification system for causes of abnormal uterine bleeding in the reproductive years

CoagulopathyOvulatory DisordersEndometrial

DisordersIatrogenic CausesNot Classified

PALM COEIN

P olypA denomyosisL eiomyomaM alignancy and

hyperplasia

PALMAUB-P

P olypA denomyosisL eiomyomaMalignancy and

hyperplasia

PALMAUB-A

P olyp

A denomyosis

L eiomyoma

M alignancy and hyperplasia

Submucousal

Other

PALM AUB-LSM

SM - Submucosal

0 Pedunculated intracavitary

(Wamsteker 1993) 1 <50% intramural

2 ≥50% intramuralO - Other Intramural,Subserous, Transmural

3 Contacts endometrium; 100% intramural

4 Intramural5 Subserosal; ≥50%

intramural6 Subserosal; <50%

intramural7 Subserosal

pedunculated8 Other (e.g. cervical,

parasitic)

Leiomyoma Subclassification System

P olypA denomyosisL eiomyomaM alignancy and

hyperplasia

PALM AUB-M

C oagulopathyO vulatory dysfunctionE ndometrialI atrogenicN ot yet classified

COEIN AUB-C

COEIN


Causes of Ovulatory Dysfunction

Luteal out of phase cyclesEndocrinopathies

PCOSHypothyroidismHyperprolactinemiaMental stress

ObesityAnorexiaWeight lossExtreme exercise

AUB-O

COEIN


Causes of Ovulatory Dysfunction

Systemic Pharmacotherapy Phenothiazines

Tricyclic antidepressants

AUB-O

COEIN


Primary disorder of local endometrial hemostasisEndometrial inflammation/infection

Abnormalities in the local inflammatory responseAberrations in endometrial vasculogenesis

AUB-E

COEIN


Gonadal Steroids

LNG-IUS

AUB-I


Arteriovenous malformationsMyometrial hypertrophyAssociations with some systemic diseasesOthers

COEIN AUB-N

How could this system be used?

– Polyp– Adenomyosis– Leiomyoma– Malignancy/

Hyperplasia

CoagulopathyOvulatory DisordersEndometrial

DisordersIatrogenic CausesNot Classified

PALM COEIN

Heavy menstrual bleeding (HMB) – volume of monthly blood loss of more

than 80 ml– management may be either medical or

surgical

Management of Heavy Menstrual Bleeding

MEDICAL MANAGEMENT SURGICAL MANAGEMENT

Acute HMB Chronic HMB

High dose Estrogen

LNG-IUS Dilatation and curettage

High dose COCs Antifibrinolytic agents

Endometrial ablation

Progestins NSAIDs HysterectomyTranexamic acid COCs

Cyclic progestogenDanazol

Management of Heavy Menstrual Bleeding


AMENORRHEA


Amenorrhea May be physiologic or pathologic which may include

primary and secondary causes Primary amenorrhea. No menses by age 14 in the absence of growth or

development of secondary sexual characteristics. Or No menses by age 16 with the appearance of

secondary sexual characteristics. Secondary amenorrhea.

In a menstruating women, the absence of menstruation for three previous cycle intervals or 6 months.

Evaluation of Amenorrhea

1. History2. Physical examination3. Diagnostics

Diagnostic Evaluation for Secondary Amenorrhea

Causes of Amenorrhea

1. Primary Amenorrhea2. Secondary Amenorrhea

Primary causes initially classified on whether absent uterus and/or breast development are also found


AmenorrheaPrimary causes initially classified on whether absent uterus and/or breast development are also found

BREASTS UTERUS CONDITION

ABSENT PRESENT With pituitary massesTURNER’S SYNDROME

PRESENT ABSENT TESTICULAR FEMINIZATION (XY) AND CONGENITAL ABSENCE OF THE UTERUS

ABSENT ABSENT MALE KARYOTYPE EITHER ENZYME DEFICIENCY OR AGONADISM

PRESENT PRESENT HYPOTHALAMIC CAUSES, PITUITARY, OVARIAN, UTERINE OR OUTFLOW TRACT PROBLEMS


Amenorrhea Secondary amenorrhea may be

physiologic or pathologic. Pathologic lesions include intra-uterine adhesions after curettage. Work up include: HYPOTHALAMIC CAUSES, PITUITARY, OVARIAN, UTERINE OR OUTFLOW TRACT PROBLEMS

Compartmental Systems Compartment I

– Disorders of the outflow tract Compartment II

– Disorders of the ovary Compartment III

– Disorders of the anterior pituitary Compartment IV

– Disorders of CNS (hypothalamic factors)

Compartment I: Disorders of the Outflow Tract or Uterus

Mullerian Anomalies– Imperforate hymen– Transverse vaginal septum

Mullerian agenesis (Mayer-Rokitansky-Kuster-Hauser syndrome)

Androgen insensitivity Ashermans syndrome

Imperforate Hymen•The hymen itself is formed from the proliferation of the sinovaginal bulbs, becoming perforate before or shortly after birth.

•Results when this sheet of tissue fails to completely canalize

•Translucent thin membrane just inferior to the urethral meatus that bulges with valsalva maneuver

Transverse vaginal septum•Horizontal wall of tissue that has formed during embryologic development and essentially creates a blockage in the vagina

• Occurs between the upper one-third and lower two-thirds of the vaginal canal.

•Resection of septum

Mayer-Rokitansky-Kuster-Hauser Syndrome (utero-vaginal agenesis)

15% of primary amenorrhea Normal secondary

development & external female genitalia

Normal female range testosterone level (20-80 ng/dl)

Absent uterus and upper vagina & normal ovaries

Karyotype 46XX 15-30% renal, skeletal and

middle ear anomalies• Treatment: Progressive

vaginal dilatation/vaginoplasty

Androgen Insensitivity Normal breasts but no

sexual hair Normal looking female

external genitalia Absent uterus and upper

vagina Karyotype 46, XY Testes present, male range

testosterone level (300 ng/dL to 800 ng/dL)

Treatment : gonadectomy after puberty + ERT

Androgen Insensitivity(Testicular feminization) 22% with Dysgerminoma or

Gonadoblastoma Gonadectomy once patient

undergoes spontaneous and complete natural breast development

Estrogen monotherapy to prevent osteoporosis and cardiovascular disease

Vaginal dilatation or create neovagina once sexually active

Differences between Mullerian agenesis and Androgen Insensitivity

Mullerian Agenesis Androgen Insensitivity

Karyotype 46, XX 46, XYHeredity Not known Maternal X-linked

recessive; 25% risk of affected child, 25% risk of carrier

Sexual hair Normal female Absent to sparseTestosterone level Normal female Normal to slightly

elevated maleOther anomalies Frequent RareGonadal neoplasia Normal incidence 5% incidence of

malignant tumors

Compartment II: Disorders of the Ovary

Gonadal Dysgenesis Chromosomally abnormal - Classic turner’s syndrome (45XO) - Turner variants (45XO/46XX),(46X-abnormal X) - Mixed gonadal dygenesis (45XO/46XY)

Chromosomally normal - 46XX (Perrault) - 46XY (Swyer’s syndrome)

Gonadal Dysgenesis Gonadal dysgenesis associated with a

normal karyotype is also linked to neurosensory deafness (Perrault syndrome)

Pure gonadal dysgenesis indicates the presence of bilateral streak gonads, regardless of karyotype.

Mixed gonadal dysgenesis indicates testicular tissue on one side and a streak gonad on the other.

Typical features of Turner Syndrome

XY Gonadal Dysgenesis Swyer’s syndrome

– Female patient with XY karyotype– Palpable mullerian system– Normal female testosterone level– Lack of sexual development

Mosaicism Multiple cell lines of varying sex

chromosome composition Appear normal, attaining normal

stature before premature menopause is experienced (accelerated atresia)

Patients are short

Gonadal Agenesis No complicated clinical problems

accompany the gonadal failure due to agenesis

Viral and metabolic influences in early gestation or undiscovered genetic mutations are suspected

Surgical removal of the gonadal streaks is necessary to avoid the possibility of neoplasia

Premature Ovarian Failure Early depletion of ovarian follicles

before the age of 40 Etiology : unknown but maybe due to

genetic disorder with an increased rate of follicle disappearance

Most common abnormalities: 45,X and 47, XXY followed by mosaicism

Hormonal therapy recommended

Radiation

Ovarian dose Sterilization effect

60 rads No effect150 rads Some risk over age 40

250-500 rads Ages 15-40: 60% sterilized

500-800 rads Ages 15-40: 60-70% sterilized

Over 800 rads 100% permanently sterilized

Chemotherapy Alkylating agents – very toxic to the

gonads

Inverse relationship between the dose required for ovarian failure and age at the start of therapy.

Compartment III: Disorders of the Anterior Pituitary

Hypogonadism and delayed puberty warrant brain evaluation by MRI

Nonfunctioning adenoma: microadenoma Pituitary prolactin secreting adenomas Sheehan’s syndrome

– Acute infarction and necrosis of the pituitary gland due to post partum hemorrhage and shock

– Failure of lactation and loss of pubic and axillary hair

Constitutional Delayed Puberty

10-30% of cases with delayed puberty

Physiologic variant in development

Short stature, appropriate bone maturation delay

Delayed secondary sexual characteristics

Familial pattern

Late but otherwise normal growth pattern and adult reproductive function

Compartment IV: Central Nervous System Disorders

Hypothalamic amenorrhea (hypogonadotropic hypogonadism)– Deficiency in GnRH pulsatile secretion– Frequently associated with stress– Higher proportion of underweight

women and previous menstrual irregularity

– Displays the endocrine, metabolic, and psychological characteristics suggesting the presence of a subclinical eating disorder

Compartment IV: Central Nervous System Disorders

– Chronic hypothalamic anovulation Stress Increased exercise levels Anorexia nervosa

– Head trauma– Space-occupying lesions

Exercise and Female Athlete Triad

Disordered eating, amenorrhea, and osteoporosis

↑ endogenous opioids, ACTH, prolactin, adrenal androgens, cortisol, and melatonin

Minimum of 17% body fat required for the initiation of menses and 22% body fat for the maintenance of menses (Frisch. Science 1974)

Exercise and Female Athlete Triad

Low caloric intake during strenuous exercise more important than body fat (Laughlin. J. Clin Endocrinol Metab 1997)

Suboptimal amount of body fat→ estrogens to inactivate catecholestrogens

Stress-induced Hypothalamic Amenorrhea

Potential mediators:– Opioid (β-endorphins)– Dopaminergic (Prolactin)

Activation of H-P-A axis and the stress inhibition of the H-P-G axis

↑ CRF→ ↑ ACTH → ↓ GnRH-LH secretion → ↓steroid biosynthesis

Space-Occupying Lesions Craniopharyngiomas, gliomas,

dermoid cysts Peak incidence: ages 6 and 14 Disruption of tonic inhibition of

dopamine on PRL release Neurological symptoms (headache,

visual field defects) Cranial imaging: Abnormal sella and

calcifications

Kallman’s Syndrome Rare (1:50,000) Autosomal dominant or x-linked

recessive Congenital absence of GnRH

neurons, partial or complete agenesis of olfactory bulb

Sexual infantilism, primary amenorrhea, anosmia

Normal height for their age

Anorexia Nervosa Affects 1-3% of adolescents and young

adults

Diagnostic criteria:– Refusal to maintain body weight at or above

normal weight for height and age– Intense fear of gaining weight or being fat, even

though underweight– Denial of seriousness of current low body weight– Amenorrhea

Anorexia Nervosa Restrictive Type

– W eight is mainly controlled by restricting oral intake

B inge-eating/Purging subtype– Self-induced vomiting– Misuse of laxative

Anorexia Nervosa (Physical examination)

B radycardia, hypothermia, abnormal response to heat and cold

Dry skin, yellow skin (hypercarotenemia) Scaphoid abdomen, loss of subcutaneous

fat Submandibular adenopathy or parotid

gland enlargement Cardiac murmur Prepubertal appearing vaginal mucosa

(hypoestrogenemia)

Anorexia Nervosa (Laboratory Findings)

Low Normal HighFSH TSH Serum total

cortisol

LH Prolactin Serum free cortisol

Estradiol ACTH 24 hour urinary free cortisol

Leptin

IGF-I

DHEAS

Anorexia Nervosa and Leptin Ideal sensor of energy deficiency Concentration increases with obesity

and decreases rapidly during fasting Regulates the synthesis and

secretion of GnRH, gonadotropins, and sex steroids

Low leptin levels in anorexia nervosa significantly correlated with low IGF-I levels

Anorexia Nervosa and Skeletal System

Decreased bone formation and increased resorption → increased rates of osteopenia and osteoporosis

44-92% patients with osteopenia with amenorrhea of < 24 months

Normalization of B MD with weight recovery noted in some cross-sectional studies

Anorexia Nervosa and Skeletal System

Osteopenia improves but does not resolve with weight gain in recent prospective studies

OC and recombinant human IGF-I with significant positive effect on B MD

Hypothalamic Amenorrhea (Hypothalamic hypogonadism)

Most common cause of primary and secondary amenorrhea

Abnormalities of GnRH secretion and disruption of H-P-O axis

Low levels of FSH, LH, estrogen

Diagnosis by exclusion of pituitary lesions

Hypothalamic Amenorrhea (Hypogonadotropic hypogonadism)

Mild suppression: marginal effect on reproduction, inadequate luteal phase

Moderate suppression: anovulation with menstrual irregularity

Profound suppression: Hypothalamic amenorrhea– W eight loss, exercise, stress

Hypothalamic Amenorrhea (Hypogonadotropic hypogonadism)

83% resumed menses once precipitating cause of amenorrhea is reversed(Perkins et al. Hum Reprod 16: 2198, 2001)


The “MOST COMMON”• ANOREXIA NERVOSA

Most common cause of

amenorrhea in adolescents

• GONADAL FAILUREMost common

cause of PRIMARY

amenorrhe

• SERUM FSHTest to confirm gonadal failure


DYSMENORRHEA

Dysmenorrhea Primary Dysmenorrhea – pain with no obvious pathologic

disease (usually <20 y.o) Secondary Dysmenorrhea – associated with pelvic

conditions or pathology causing pelvic pain in conjunction with menses (most often >20 y/o)


CAUSES OF SECONDARY DYSMENORRHEAGynecologic Pathology Non-gynecologic

Disorders Causing Pelvic Pain

Cervical stenosis Endometriosis and adenomyosis Pelvic infection and adhesions Uterine polyps or fibroids Ovarian cyst or mass Pelvic congestion Congenital obstructed mullerian malformations

Conditioned behavior Bowel disease Irritable bowel syndrome Inflammatory bowel disease Celiac sprue (?) Lactose intolerance (?)Urinary tract disease Ureteral obstruction Interstitial cystitis Nephrolithiasis

Differences between Primary and Secondary DysmenorrheaPrimary Dysmenorrhea Secondary

DysmenorrheaCause Effects of endogenous prostaglandin Secondary to pelvic pathology

Hx Midline crampy lower abdominal pain w/c gradually resolves over 12-72 hrs and does not occur at times other than menses

Pain not responding to NSAIDs and OCsOccur after many years of painless menses

Associated symptom

DiarrheaHeadacheFatigue or Malaise

+/- Urinary and Bowel symptoms

PE Normal pelvic examAdolescents with dysmenorrhea in first 6 months of menarche – consider obstructive genital tract malformation

(+) physical finding associated with: cervical stenosis, endometriosis, adenomyosis, fibroids, ovarian cyst, nongynecologic disorders (bowel disease or urinary tract disease)

Treatment

NSAIDs (Fenamates>ibuprofen, naproxen, indomethacin)COX-2 inhibitorsOCs, LNG-IUS, TENS, Nifedipine, Narcotic analgesic - last resort

Treat underlying disease



Primary Dysmenorrhea: Pathogenesis

Arachidonic acid PGF2α uterine hypercontractility uterine blood flow Ischemia Sensitization of pain fibers

Endometrial PGF2α and PGE2 correlates with severity of dysmenorrhea and may affect other organs (bowel causing N/V and diarrhea)


PREMENSTRUAL DISORDERS:

Premenstrual Syndrome (PMS) Premenstrual Dysphoric Disorder (PMDD)


Premenstrual Disorders: PMS and PMDD

Premenstrual Syndrome (PMS)

Premenstrual Disphoric Disorder (PMDD)

Definition is defined as a group of mild to moderate symptoms, physical and behavioral, that occur in the 2nd half of the menstrual cycle and that may interfere with work and personal relationships, followed by an entirely symptom-free period.

represents a more severe disease, with marked behavioral and emotional symptoms.

Similarity Manifest in the LUTEAL PHASE of menstrual cycle Resolve during menses

Differences

Severity of symptomMust have one severe affective symptom which occur regularly during the last week of the luteal phase:Markedly depressed mood or hopelessnessAnxiety or tensionAffective labilityPersistent anger5 of 11 symptom in the DSM-IV criteria


Key symptoms of PMS AND PMDD

Somatic symptoms Affective symptoms

Abdominal bloating, swelling, weight gain Aches Increased appetite, food cravings Breast pain or tendernessHeadache Dizziness, poor coordination, clumsiness Cramps, change in bowel habits Fatigue

Depressed mood+ Irritability, persistent anger+

Mood lability, crying, social withdrawal+ Anxiety, tension+ Feeling hopeless or guilty Poor impulse control or feeling out of control Decreased interest, change in libido Insomnia Loss of concentration, confusion+ being severe before menstruation starts and mild or absent after menstruation

Severe PMS or PMDD is based on at least five symptoms, including one of four core psychological symptoms

Modified from the American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th ed, text revision (DSM-IV-TR). Washington, DC, 2000, American Psychiatric

Association, pp. 771-774.




PROPOSED CAUSES OF PMS AND PMDD

In summary, the cause of PMS and PMDD is associated with ovarian steroids and ovulation, which seems to produce alterations in neurohormones and neurotransmitters that lead to a reduction of serotonergic function during the luteal phase. Beta-endorphin, GABA, the autonomic nervous system, and social expectations may also play a role in these complex disorders.

Premenstrual Disorders: PMS and PMDDPremenstrual Syndrome

(PMS)Premenstrual Disphoric Disorder

(PMDD)Diagnosis Made by history of 2 consecutive menstrual cycles demonstrating luteal phase symptoms

Medical problems influencing symptomatology must be ruled out (by history and PE)

Differential Diagnosis

Endometriosis Dysmenorrhea Physical disorders with premenstrual exacerbations Autoimmune disordersDiabetes mellitus Anemia

Hypothyroidism Psychiatric disorders with luteal phase exacerbation DepressionAnxiety Dysthymic disorder Bipolar disorder

Treatment

1. Diet, Exercise, and Lifestyle Changes - complex CHO diet (tryptophan as source of serotonin), low fat vegetable diet (SHBG to decrease active estrogen), high-intensity aerobic exercise, Calcium (1200mg/day x 3 months), Vit B6 (50mg/d), Mg (200-400mg/d)

2. Cognitive Behavioral Therapy – less effective as primary therapy, usually as supportive adjunct to managing symptoms of PMS through group psychoeducation and relaxation therapy

3. Pharmacologic agents Diuretics – for bloating, fluid retention and perceived change in body habitus; use K-sparing diuretic (Spirinolactone 100mg/d) Psychoactive drugs – SSRIs are extremely effective (luteal phase or continuous) – caution if px has anxiety symptoms (FDA approved for PMDD: Fluoxetine HCl/Sarafem 20mg/d, Sertraline HCl/Zoloft 50mg/d, Paroxetine HCl/ Paxil CR 12.5mg/d); Alprazolam 025mg TID Day 20-28/cycle; Buspirinone less addictive potential vs Alprazolam Oral Contraceptives – mainly for physical symptoms: breast pain, bloating, acne, and appetite. (Monophasic OCs with shortened hormone-free interval (3-4 days) – better; FDA approved for PMDD: Ethinyl estradiol 20 ug, drosperinone 3mg/ YAZ NSAIDs – for cramping and other systemic symptoms (i.e. aches, diarrhea, or heat intolerance) Danazol – for premenstrual mastalgia 200mg/day Day 20-28/cycle Bromocriptine – for cyclic mastalgia at 2.5-5 mg/day during the luteal phase GnRH agonists – ovulation suppression, treatment of PMS and physical symptoms of PMDD4. Surgical Treatment: Total Hysterectomy and Bilateral oophorectomy – if all other

treatment regimens have failed.

Thank you !

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