ANGGOTA:1.Yobi Syumarta2.Flora Oktavia3.Vella Paraditha4.Atika Sari Dewi5.Willy Valerian6.Amelia

1.DUB (Dysfunctional Uterine Bleeding) is abnormal bleeding from the vagina that is due to changes in hormone levels

2.PRC(Packed Red Cell) is also called "packed cells," are a preparation of red blood cell that are tranfused to correct low blood levels in anemic patients

3. Arcuate uterus is a form of a uterine anomaly or variation where the uterine fundus displays a concave contour towards the uterine cavity

4. USG Transrectal is A procedure in which a probe that sends out high-energy sound waves is inserted into the rectum. Transrectal ultrasound is used to look for abnormalities in the rectum and nearby structures, including the prostate

1. Why mrs.obesitaria menstruation prolonged for a month?

2. Interpretation of vital sign inpection, conjuntiva subanemis, TB 150 cm and weight 78 kg?

3. Predisposing factors of DUB? 4. What kind of anti-bleeding drug that may

be given?

5. Purpose of PRC transfution?6. Etiology of arcuate utery?7. What kind of supporting examinations to

establish diagnosis of DUB?

1. Because of the hormonal disorders, in which estrogen levels increase

2. Based on BMI calculation : BB/TB(m2) = 78/2,25m = 34,5 (obesitas) Because a lot of bleeding ,the patient was

pale, which is characterized by conjuntival subanemis

3. Cause of DUB are• Systemic disease, including

thrombocytopenia,hypothyroidism, hyperthyroidism, Cushing disease, liver disease, diabetes mellitus, and adrenal and other endocrine disorders, can present as abnormal uterine bleeding.

• Pregnancy and pregnancy-related conditions may be associated with vaginal bleeding.

• Trauma to the cervix, vulva, or vagina may cause abnormal bleeding.

Carcinomas of the vagina, cervix, uterus, and ovaries must always be considered in patients with the appropriate history and physical examination findings. Endometrial cancer is associated with obesity, diabetes mellitus, anovulatory cycles, nulliparity, and age older than 35 yers

• Other causes of abnormal uterine bleeding include structural disorders, such as functional ovarian cysts, cervicitis, endometritis, salpingitis, leiomyomas, and adenomyosis. Cervical dysplasia or other genital tract pathology may present as postcoital or irregular bleeding.

• Polycystic ovary disease results in excess estrogen production and commonly presents as abnormal uterine bleeding.

• Primary coagulation disorders, such as von Willebrand disease, myeloproliferative disorders, and immune thrombocytopenia, can present with menorrhagia.

• Excessive exercise, stress, and weight loss cause hypothalamic suppression leading to abnormal uterine bleeding due to disruption along the hypothalamus-pituitary-ovarian pathway.

• Bleeding disturbances are common with combination oral contraceptive pills as well as progestin-only methods of birth control. However, the incidence of bleeding decreases significantly with time.

• Contraceptive intrauterine devices (IUDs) can cause variable vaginal bleeding for the first few cycles after placement and intermittent spotting subsequently.

4. – first aid is blood transfusion to replace lost blood volume

- obat golongan estrogen: estradiol, etinil estradiol

- obat golongan progesteron: medroxi asetat, nortisteron, caprox hidroxi progesteron

5. packed red cells is widely used in the treatment of anemia, especially thalassemia, aplastic anemia, leukemia and anemia due to other malignancies. Giving transfusion aiming to improve tissue oxygenation and body tools. Usually achieved when Hb level was above 8 g%.

6. The uterus is formed during embryogenesis by the fusion of the two mullerian ducts.

During this fusion a resorption process eliminates the partition between the two ducts to create a single cavity. This process begins caudally and advances cranially, thus an arcuate uterus represents an in the final stage incomplete absorption process.

7. PEMERIKSAAN GINEKOLOGI INSPEKSI Vulva : Tidak ada kelainan Ulkus -- darah  + PALPASINyeri tekan

Pemeriksaan Hematologi : ureun & kreatinin serum, Hb, trombosit, waktu pembekuan darah, dan faal hati

Ny.obesitaria

Haid tdk berhenti slm 1 bln,obesitas anemia, TD turun,pusing

Diagnosa : DUB USG : -Uterus arkuatus -Endometrium

tebal -Bentuk,ukuran

ovarium normalTransfusi PRC

1.Gangguan pembentukan dan perkembangan organ reproduksi wanita dan Penatalaksanaannya

2.Fisiologi siklus haid normal dan kelainan serta gangguan haid

3.Fisiologi endokrin yg berhubungan dengan reproduksi Penatalaksanaan

4. Kelainan endokrin yg berhubungan dengan reproduksi dan Penatalaksanaannya

5. Pemeriksaan penunjang pada gangguan reproduksi

1. Mengapa pasien didiagnosis menderita DUB,padahal dari pemeriksaan USG transrektal ditemukan adanya uterus arkuatus?

2. Perbedaan antara DUB dan PCOS?

1.Gangguan pembentukan dan perkembangan organ reproduksi wanita dan Penatalaksanaannya

2.Fisiologi siklus haid normal dan kelainan serta gangguan haid

3.Fisiologi endokrin yg berhubungan dengan reproduksi Penatalaksanaan

4. Kelainan endokrin yg berhubungan dengan reproduksi dan Penatalaksanaannya

5. Pemeriksaan penunjang pada gangguan reproduksi

1st LO

Based on its function (fisiobginya), female reproductive Afat has 3 functions, namely:1. Sexual Function2. Hormonal Function3. Reproductive Functions (continued descent.)

Sexual FunctionTool whose role is the vulva and vagina. Glands on the vulva that canremove fluid, is useful as a lubricant during intercourse. In addition, vulvar and vaginalalso serves as the birth canal.

Hormonal FunctionThat is called function is the role of the hormonal ovaries and uterus inmemperlahankan characteristics of femininity and menstruation settings. Changes in physical and psychic who happens throughout the life of a woman closely associated with ovarian function that produces the female hormones estrogen and progesterone.

Reproductive functionReproduction task performed by the ovaries, fallopian tubes and uterus. Eggs each month removed from the egg sac during the fertile period will be entered into the oviduct to then meet and blend with the spermatozoa to form a new organism.

Müllerian anomalyIn these circumstances, the vagina, cervix and uterus may not exist. Or in other circumstances, the uterus may exist but there is no cavity, or the presence of endometrial cavity but very little.

Ovarian DisordersOvarian abnormalities can cause primary or secondary amenorrhea. 30-40% of primary amenorrhea abnormal development of ovaries (gonadal dysgenesis). These patients may consist of patients with 45X karyotype (50%), mosaic (25%), 46XX (25%). Women with gonadal dysgenesis diseratai secondary amenorrhea associated with karyotype 46xx, mosaic, 47 xxx, and 45 × 9.

Turner SyndromeIn this syndrome occurs lose one X. X chromosome is active in oocytes to avoid accelerating the death of the follicle. Because in these patients there is a lack follicles, there is a lack gonadal sex hormones at puberty resulting in primary amenorrhea

2nd LO

What is the mean duration of the MC? Mean 28 days (only 15% of ♀) Range 21-35

What is the average duration of menses? 3-8 days

What is the normal estimated blood loss? Approximately 30 ml

When does ovulation occur? Usually day 14 36 hrs after the onset of mid-cycle LH surge

What regulate the phases of the MC & ovulation? Interaction between hypothalamus, pituitary &

ovaries

What is the mean age of menarche & menopause? Menarche 12.7 Menopause 51.4

Ovulation divides the MC into two phases:

1-FOLLICULAR PHASE -Begins with menses on day 1 of the

menstrual cycle & ends with ovulation

▲RECRUITMENT FSH maturation of a cohort of ovarian follicles “recruitment” only one reaches maturity

MATURATION OF THE FOLLICLE (FOLLICULOGENESIS)

♥ FSH primordial follicle (oocyte arrested in the diplotene stage of the 1st

meiotic division surrounded by a single layer of granulosa cells)

1ry follicle (oocyte surrounded by a single layer of granulosa

cells basement membrane & thica cells)

2ry follicle or preantral follicle (oocyte surrounded by zona pellucida , several

layers of granulosa cells & thica cells)

tertiary or antral follicle 2ry follicle accumulate fluid in a cavity

“antrum” oocyte is in eccentric position surrounded by granulosa cells “cumulous

oophorus”

SELECTION ♥Selection of the dominant follicle occurs day

5-7 ♥It depends on - the intrinsic capacity of the follicle to synthesize estrogen -high est/and ratio in the follicular fluid ♥As the follicle mature estrogen FSH “-ve feed back on the pituitary” the follicle with the highest No. of FSH receptors will continue to thrive ♥ The other follicles “that were recruited” will become atretic

♥FSH ACTIONS -recruitement -mitogenic effect No. of granulosa cells FSH receptor -stimulates aromatase activity conversion

of androgens estrogens “estrone &

estradiol” - LH receptors ♥ ESTROGEN Acts synergistically with FSH to - induce LH receptors - induce FSH receptors in

granulosa & thica cells♥LH thica cells uptake of cholesterol & LDL androstenedione & testosterone

♥ NEGATIVE FEEDBACK ON THE PIUITARY - estradiol & inhibin -ve feed back on pituitary

FSH -This mechanism operating since childhood

♥ POSITIVE FEEDBACK ON THE PITUITARY estradiol (reaching a threshold concentration)

+ve feed back on the pituitary (facilitated by low

levels of progestrone) LH surge secretion of progestrone

Operates after puberty +ve feed back on pituitary FSH

LH SURGE Lasts for 48 hrs Ovulation occurs after 36 hrs Accompanied by rapid fall in estradiol level Triggers the resumption of meiosis Affects follicular wall follicular rupture Granulosa cells lutenization progestrone synthesis

The dominant follicle protrudes from the ovarian cortex

Gentle release of the oocyte surrounded by the cumulus

granulosa cells

Mechanism of follicular rupture 1- Follicular pressure Changes in composition of the antral fluid

colloid osmotic pressure2-Enzymatic rupture of the follicular wall LH & FSH granulosa cells production of

plasminogen activator plasmin fibrinolytic activity breake down of

F. wall LH prostglandin E plasminogen activator PG F2α lysosomes under follicular wall

LASTS 14 days

FORMATION OF THE CORPUS LUTEUM

After ovulation the point of rupture in the follicular wall seals

Vascular capillaries cross the basement

membrane & grow into the granulosa cells availability of LDL-cholestrole

LH LDL binding to receptors 3α OH steroid dehydrogenase activity progestrone

Marked in progestrone secretion Progestrone actions: -suppress follicular maturation on

the ipsilateral ovary -thermogenic activity basal body

temp -endometrial maturation Progestrone peak 8 days after ovulation (D22 MC) Corpus luteum is sustained by LH It looses its sensitivity to gonadotropins

luteolysis estrogen & progestrone level desquamation of

the endometrium “menses”

estrogen & progestrone FSH &LH The new cycle stars with the beginning of menses If prgnancy occurs hCG secreation maintain

the corpus luteum

1-Basal layer of the enometrium -Adjasent to the mometrium -Unresponsive to hormonal stimulation -Remains intact throughout the

menstrual cycle

2-Functional layer of the endometrium Composed of two layers: -zona compacta superficial

-Spongiosum layer

1-Follicular /proliferative phase Estrogen mitotic activity in the glands & stroma enometrial thickness from 2 to 8 mm (from basalis to opposed basalis layer)

2-Luteal /secretory phase Progestrone - Mitotic activity is severely restricted -Endometrial glands produce then

secrete glycogen rich vacules -Stromal edema -Stromal cells enlargement -Spiral arterioles develop, lengthen & coil

Periodic desquamation of the endometrium The external hallmark of the menstrual cycle Just before menses the endometrium is infiltrated

with leucocytes Prostaglandins are maximal in the endometrium

just before menses Prostaglandins constriction of the spiral

arterioles ischemia & desquamation Followed by arteriolar relaxation, bleeding &

tissue breakdown

The hypothalamus secretes GnRH in a pulsatile fashion

GnRH activity is first evident at puberty Follicular phase GnRH pulses occur hourly Luteal phase GnRH pulses occur every 90 minutes Loss of pulsatility down regulation of pituitary

receptors secretion of gonadotropins Release of GnRH is modulated by –ve feedback by: steroids gonadotropins Release of GnRH is modulated by external neural

signals

Menorrhagia Excessive (>80ml) uterine bleeding Prolonged (>7days) regular

DUB Abnormal Bleeding, no obvious organic cause usually anovulatory

Oligomenorrhea Uterine bleeding occurring at intervals between 35 days and 6 months

Amenorrhea No menses x at least 6 months

Metrorragia, Menometrorrhagia, Polymenorrhea

Anovulatory Oligo or Amenorrhea +/- Menorrhagia Ovulatory Regular menstrual cycles (plus premenstrual symptoms such

as dysmenorrhea and mastalgia

-Defn: Excessively heavy, prolonged or frequent bleeding of uterine origin that is not due to pregnancy, pelvic or systemic disease

-Diagnosis of exclusion- Anovulatory-Usually extremes of reproductive life and in

pts with PCOS

Disturbance in the HPO axis thus changes in length of menstrual cycle

No progesterone withdrawal from an estrogen-primed endometrium

Endometrium builds up with erratic bleeding as it breaks down.

5ft 7in, 105ibs, normal sec. sex xristics, pelvic normal

Menarche 14, 2 periods last year, heavy lasts 2 weeks, virginal.

I month hx of daily heavy vag bleeding with clots, 8 to 10 pads x day

No associated symptoms

Picture of teenager

HCG, CBC, TSH ? Coagulation workup Ensure pap smear UTD if appropriate >35 or Ca risk factors, tamoxifen use – sample endometrium

I/V or I/M conjugated estrogen therapy acute DUB--How ?!!!.

Usually followed by OCP or progestin Cyclic progestins for 10 to 12 days each

cycle, consider mirena IUD OCP D and C – old school, no longer

recommended.

-Heavy vaginal bleeding that is not DUB-Usually secondary to distortion of uterine

cavity- heavy with or without prolongation (anatomic).

Uterus unable to contract down on open venous sinuses in the zona basalis

-Other causes organic, endocrinologic, hemostatic and iatrogenic

-Usually ovulatory

5ft’5”, 155Ibs, husband ‘castrated’

Had normal 28 day cycles lasting 5 days

Last 1 year or so very heavy periods with clots and occ. ‘flooding’ in the first 3 days with need to use >8pads/day fully soaked, spots for up to 1 week after this.

Dysmenorrhea, severe, aching pain lower legs

Normal recent pap

Picture of middle aged woman

History Physical exam-anemia, obesity, androgen

excess e.g. hirsuitism, acne, ecchymosis/purpura, thyroid, galactorrhea, liver/spleen, Pelvic- Uterine, cervical and adnexal

HCG, CBC, TSH ? Coagulation workup Ensure pap smear UTD if appropriate >35 or Ca risk factors, tamoxifen use sample endometriumOther tests as INDICATED by HX and PE

Endometrial Endometrial BiopsyBiopsy

Sensitivity -91%Sensitivity -91%

False positive rate -False positive rate -2%2%

Office procedure, well tolerated, Office procedure, well tolerated, anesthesia and cervical dilation usually not anesthesia and cervical dilation usually not requiredrequired

Transvaginal Transvaginal Ultrasound Ultrasound (TVS)(TVS)

Sensitivity -88%Sensitivity -88% Good visualization of fibroids; may fail to Good visualization of fibroids; may fail to identify other intracavitary abnormalitiesidentify other intracavitary abnormalities

like polypslike polyps

Saline Infusion Saline Infusion Sonohysterosc-Sonohysterosc-

Opy (SIS)Opy (SIS)

Sensitvity -97%Sensitvity -97%

NPV -94%NPV -94%

Procedure of choice (detection and cost).Procedure of choice (detection and cost).

Sterile isotonic fluid is instilled into the Sterile isotonic fluid is instilled into the uterus under continuous visualization of uterus under continuous visualization of

endometrium with TVSendometrium with TVS

HysteroscopyHysteroscopy Sensitivity -100%Sensitivity -100% Highest cost. Better in pre-menopausal Highest cost. Better in pre-menopausal women. Does not reduce hysterectomy women. Does not reduce hysterectomy rate even without intracavitary path. Used rate even without intracavitary path. Used as gold standard for other proceduresas gold standard for other procedures

NSAID’s, 1st line, 5 days, decrease prostaglandins Danazol, Androgen and prog. competitor , amenorrhea in 4-6

weeks, androgenic side effects OCP’s, esp. if contraception desired, up to 60% dec. supp. HP

axis Continous OCP’s Oral continous progestins (day 5 to 26),

most prescribed, antiestrogen, downregulates endormetrium Levonorgestrel IUD (Mirena), High satisfaction

rate that approaches surgical techniques GnRH agonists, Inhibit FSH and LH release–

hypogonadism, bone Conjugated estrogens for acute bleeding Other treatments as indicated e.g. DDAVP for coagulation

defects

Tailor treatment to individual patient. Consider patients age, coexisting medical

diseases, FH, desire for fertility, cost of rx and adverse effects

Surgical management reserved for organic causes (e.g fibroids) or when medical management fails to alleviate symptoms

Male gender Prepubertal female Pregnant female Postmenopausal female

Absence of menses by age 14 with absence of SSC (e.g. breast development) or absence by age 16 with normal SSC

Only 3 conditions unique to primary, other causes of amenorrhea can cause either

-Vaginal agenesis-Androgen insensitivity syndrome-Turners syndrome (45, X0)

Generalized pubertal delay e.g. Turner syndrome

Normal puberty e.g. PCOS Abnormalities of the genital tract e.g.

Ashermans syndrome

Hx. PE- These are probably the most important

aspects in diagnosis Remember to always rule out pregnancy H & P suggests- Ovarian-axis problem- TSH, prolactin, FSH,

LH- Hirsuitism-Testosterone, DHEAS,

androstenedione and 17-OH progesterone- Chronic ds.- ESR, LFT’s, BUN, cr and UA- CNS- MRI

If H and P gives no clues to diagnosis-exciting

Use step wise approach to diagnosis

Evaluation of Secondary Amenorrhea

TABLE 4Causes of Amenorrhea

Hyperprolactinemia Prolactin ≤ 100 ng per mL (100 mcg per L) Altered metabolism

Liver failure Renal failure

Ectopic production Bronchogenic (e.g., carcinoma) Gonadoblastoma Hypopharynx Ovarian dermoid cyst Renal cell carcinoma Teratoma

Breastfeeding Breast stimulation Hypothyroidism Medications

Oral contraceptive pills Antipsychotics Antidepressants Antihypertensives

Histamine H2

receptor blockers Opiates, cocaine

Prolactin > 100 ng per mL Empty sella syndrome Pituitary adenoma

Hypergonadotropic hypogonadism Gonadal dysgenesis

Turner's syndrome* Other*

Postmenopausal ovarian failure Premature ovarian failure

Autoimmune Chemotherapy Galactosemia Genetic 17-hydroxylase deficiency syndrome Idiopathic Mumps Pelvic radiation

Hypogonadotropic hypogonadism Anorexia or bulimia nervosa Central nervous system tumor Constitutional delay of growth and puberty* Chronic illness

Chronic liver disease Chronic renal insufficiency Diabetes Immunodeficiency Inflammatory bowel disease Thyroid disease Severe depression or psychosocial stressors

Cranial radiation

Hypogonadotropic hypogonadism (continued) Excessive exercise Excessive weight loss or malnutrition Hypothalamic or pituitary destruction Kallmann syndrome* Sheehan's syndrome Normogonadotropic Congenital

Androgen insensitivity syndrome* Müllerian agenesis*

Hyperandrogenic anovulation Acromegaly Androgen-secreting tumor (ovarian or adrenal) Cushing's disease Exogenous androgens Nonclassic congenital adrenal hyperplasia Polycystic ovary syndrome Thyroid disease

Outflow tract obstruction Asherman's syndrome Cervical stenosis Imperforate hymen* Transverse vaginal septum*

Other Pregnancy Thyroid disease

*-Causes of primary amenorrhea only.Information from references 3, 6, and 15.

Always R/O pregnancy, check pap Try to differentiate anovulatory from ovulatory

bleeding Good history and physical is key( this applies to

amenorrhea as well) Do a focused work up based on your H & P rather

than a random set of studies In amenorrhea, where no indication of cause

based on H & P, follow the stepwise algorithm for

diagnosis Know the INDICATIONS for endometrial sampling

3rd LO

◦ Infertility 75%◦ Hyperandrogenism 70%◦ Amenorrhea 50%◦ Obesity 60-80%◦ Abnormal uterine bleeding 30%◦ Normal menstruation 20% 

Exact etiology of PCOS is still unknown ◦ likely due to a steady state of high estrogen,

androgens, luteinizing hormone (LH) and insulin levels.

High estrogen levels can cause suppression of pituitary FSH and relative increase in LH.

Increased LH stimulates the ovary, which results in anovulation, multiple cysts and theca cell hyperplasia with excess androgen output.

High insulin levels may also increase the production of testosterone by the ovaries.

No single confirmatory test for PCOS. It is a clinical diagnosis. Ovarian cysts are not required for

diagnosis. Cysts are present on ultrasound in more

than 90% of women with PCOS but also present in up to 25% of normal women.

◦Hyperandrogenism Elevated serum androgen levels or Biological expression of hyperandrogenism (acne or hirsutism)

◦Ovarian Dysfunction Anovulation or oligo-ovulation or Polycystic ovaries

◦Absence of other causes of anovulation Thyroid disorders Hyperprolactinemia Cushing’s syndrome Late onset congenital adrenal hyperplasia (CAH) Ovarian and adrenal tumors

◦ Elevated androgen (i.e. testosterone > 60 or free testosterone >0.75) levels

◦ Elevated LH:FSH ratio > 2:1◦ Insulin resistance with hyperinsulinemia

Prolactin level Testosterone level LH and FSH TSH Fasting glucose level or 2 hr OGTT Lipid profile, including total, LDL,HDL 17-hydroxyprogesterone level*

*--Fasting level to r/o CAH

Hirsuitism, Acne

Women who desire contraception

Combination OCPs

Treatment

Lifestyle modification

Depilatory/electrolysis/laser GlucophageEflornithine HCl creamSpironolactoneFlutamideFinasteride

Glucophage,TZDsInsulin Resistance,Oligomenorrhea

Obesity

Hirsuitism, Acne

Women who desire pregnancy/ovulation induction

Glucophage Clomiphene citrate Gonadotropins Ovarian drilling

Treatment

Lifestyle modification

Depilatory/electrolysis/laser Glucophage

GlucophageInsulin Resistance,Oligomenorrhea

Obesity

◦ Infertility 75%◦ Hyperandrogenism 70%◦ Amenorrhea 50%◦ Obesity 60-80%◦ Abnormal uterine bleeding 30%◦ Normal menstruation 20% 

Exact etiology of PCOS is still unknown ◦ likely due to a steady state of high estrogen,

androgens, luteinizing hormone (LH) and insulin levels.

High estrogen levels can cause suppression of pituitary FSH and relative increase in LH.

Increased LH stimulates the ovary, which results in anovulation, multiple cysts and theca cell hyperplasia with excess androgen output.

High insulin levels may also increase the production of testosterone by the ovaries.

No single confirmatory test for PCOS. It is a clinical diagnosis. Ovarian cysts are not required for

diagnosis. Cysts are present on ultrasound in more

than 90% of women with PCOS but also present in up to 25% of normal women.

◦Hyperandrogenism Elevated serum androgen levels or Biological expression of hyperandrogenism (acne or hirsutism)

◦Ovarian Dysfunction Anovulation or oligo-ovulation or Polycystic ovaries

◦Absence of other causes of anovulation Thyroid disorders Hyperprolactinemia Cushing’s syndrome Late onset congenital adrenal hyperplasia (CAH) Ovarian and adrenal tumors

◦ Elevated androgen (i.e. testosterone > 60 or free testosterone >0.75) levels

◦ Elevated LH:FSH ratio > 2:1◦ Insulin resistance with hyperinsulinemia

Prolactin level Testosterone level LH and FSH TSH Fasting glucose level or 2 hr OGTT Lipid profile, including total, LDL,HDL 17-hydroxyprogesterone level*

*--Fasting level to r/o CAH

Hirsuitism, Acne

Women who desire contraception

Combination OCPs

Treatment

Lifestyle modification

Depilatory/electrolysis/laser GlucophageEflornithine HCl creamSpironolactoneFlutamideFinasteride

Glucophage,TZDsInsulin Resistance,Oligomenorrhea

Obesity

Hirsuitism, Acne

Women who desire pregnancy/ovulation induction

Glucophage Clomiphene citrate Gonadotropins Ovarian drilling

Treatment

Lifestyle modification

Depilatory/electrolysis/laser Glucophage

GlucophageInsulin Resistance,Oligomenorrhea

Obesity

Endometriosis is a condition in which the tissue that behaves like the cells lining the uterus (endometrium) grows in other areas of the body, causing pain, irregular bleeding, and possible infertility

The tissue growth (implant) typically occurs in the pelvic area, outside of the uterus, on the ovaries, bowel, rectum, bladder, and the delicate lining of the pelvis. However, the implants can occur in other areas of the body, too.

Each month a woman's ovaries produce hormones that stimulate the cells of the uterine lining (endometrium) to multiply and prepare for a fertilized egg. The lining swells and gets thicker.

If these cells (called endometrial cells) grow outside the uterus, endometriosis results. Unlike cells normally found in the uterus that are shed during menstruation, the ones outside the uterus stay in place. They sometimes bleed a little bit, but they heal and are stimulated again during the next cycle

This ongoing process leads to symptoms of endometriosis (pain) and can cause scars (adhesions) on the tubes, ovaries, and surrounding structures in the pelvis.

The cause of endometriosis is unknown, but there are a number of theories. One theory is that the endometrial cells loosened during menstruation may "back up" through the fallopian tubes into the pelvis. Once there, they implant and grow in the pelvic or abdominal cavities.

This happens in many women, but there may be something different about the immune system in women who develop endometriosis compared to those who do not get the condition.

Endometriosis is a common problem. Sometimes, it may run in the family. Although endometriosis is typically diagnosed between ages 25 - 35, the condition probably begins about the time that regular menstruation begins.

A woman who has a mother or sister with endometriosis is six times more likely to develop endometriosis than women in the general population.

Other possible risk factors include: Starting menstruation at an early age Never having had children Frequent menstrual cycles Periods that last 7 or more days Problems such as a closed hyman, which block the

flow of menstrual blood during the period

Pain is the main symptom for women with endometriosis.

This can include: Painful periods Pain in the lower abdomen or pelvic cramps

that can be felt for a week or two before menstruation

Pain in the lower abdomen felt during menstruation (the pain and cramps may be steady and dull or severe)

Pain with bowel movements Pelvic or low back pain that may occur at

any time during the menstrual cycle Pain during or following sexual intercourse

Test that are done to diagnose endometrosis include:

Pelvic exam Transvaginal ultrasound Pelvic laparoscopy

Treatment options include: Medications to control pain Medications to stop the endometriosis from

getting worse Surgery to remove the areas of

endometriosis Hysterectomy with removal of both ovaries

definition: Relates to abnormal bleeding as a result of hormonal

changes directly affecting the menstrual cycle in the absence of any identified organic, systemic, or structural disease

Anovulatory (90% of cases) Common in women at beginning/end of reproductive life

Estrogen secreted, but ovum doesn’t ripen

Progesterone not produced to counteract uterine lining proliferation

Ovulatory More likely to occur during peak reproductive years

Associated with prolonged progesterone secretion or prostaglandin release

Leads to heavy but predictable bleeding

Age under 20 or over 40

Overweight/extreme weight loss or gain

Excessive exercise

High stress levels

Polycystic ovarian syndrome

Obtain detailed gynecologic/obstetric history

Medication history

Physical assessment to include vital signs, height and weight, thyroid gland

Past medical history

Mainstay for DUB is combination oral contraceptive therapy containing estrogen and progesterone or cyclical progesterone

Generally prescribed for at least 3 months before other options are considered

Teach patient to take drug 1 to 2 days before she expects her period

Continue taking it throughout her menses as prescribed