WOMEN REPRODUCTIVE CYCLE

Hypothalamus-Pituitary-Ovary-uterus Interaction

Neural control Chemical control

Dopamine Norepinephrine Endorphines

(-) (+) (-)

Hypothalamus
Gn-RH
± Ant. pituitary ? –
FSH, LH
Estrogen Ovaries Progesterone

Uterus

2
Menses
 Physiology of Menstruation

• The first day of a typical menstrual cycle (day l) corresponds to the first day of menses.

• The menstrual phase usually lasts for 5 days and involves the disintegration and
sloughing of the functionalis layer of the endometrium.

• Involves the interplay of various prostaglandins in regulation of menstrual cycle.

• Prostaglandin F2-alpha causes myometrial contractions and vasoconstriction,

• Where as prostaglandin E2 causes vasodilatation and muscle relaxation.

• A typical menstrual cycle comprises of 28 days.

• The duration of bleeding is about 3–5 days.

• Estimated blood loss is between 50 and 200 mL (30-80).

• The regular cycle of 28 days is seen only in a small proportion of women.

• A deviation of 2 or 3 days from the 28-day rhythm is quite common.

• The menstrual rhythm depends on the H–P–O function,

• The amount of blood loss depends upon the uterine condition.

• Ovulation occurs in the middle of the menstrual cycle.

• The first 14 days of the cycle, before the menstruation occurs form the proliferative
phase, while the next 14 days of the cycle form the secretory phase.

• During the follicular phase of normal ovarian cycle (equivalent to the proliferative
phase of endometrial cycle), there is an increase in the blood levels of the hormone
estrogen.

• During this phase, the maturation of the dominant follicle takes place.
• At the midpoint of the cycle, ovulation occurs.
• Following the process of ovulation, the ruptured ovarian follicle
gets converted into corpus luteum (CL).
• During the luteal phase of the ovarian cycle (secretory phase of
endometrial cycle) as the CL matures, the main hormone produced
is progesterone.
• The endometrium during this phase gets transformed for
implantation of conceptus in anticipation of the pregnancy.
• If pregnancy occurs, the rising levels of human chorionic gonadotropin (hCG)
stimulates and rescues the endometrium.
• In case the pregnancy does not occur, the CL undergoes regression.

• The levels of estrogen and progesterone rapidly decline causing withdrawal of the
functional support of the endometrium.

• This results in menstrual bleeding, marking the end of one endometrial cycle and the
beginning of the other.
 The proliferative (follicular) phase

• The proliferative (follicular) phase extends from day 5 to day 14 of the

typical cycle.
• In this phase, the endometrial proliferation occurs under estrogen
stimulation.
• The estrogen is produced by the developing ovarian follicles under the
influence of follicle stimulating hormone (FSH).
• This causes marked cellular proliferation of the endometrium and an
increase in the length and tortuosity of the spiral arteries.
• Endometrial glands develop and contain some glycogen.
• This phase ends as ovulation occurs.
 Question???
• What changes exactly take place during proliferative phase of
menstrual cycle?.
 The secretory (luteal) phase

• This phase is marked by production of progesterone and less potent estrogens

by the corpus luteum.
• It extends from day 15 to day 28 of the typical cycle.
• The functionalis layer of the endometrium increases in thickness and the
stroma becomes edematous.
• The glands become tortuous with dilated lumens and stored glycogen.
• If pregnancy occurs, the placenta produces human chorionic gonadotropin
(hCG) to replace progesterone and the endometrium (and the accompanying
pregnancy) are maintained.
• If pregnancy does not occur, the estrogen and progesterone levels
cause negative feedback at the hypothalamus, resulting in the fall in
the levels of the hormones FSH and LH.
• The spiral arteries become coiled and have decreased blood flow.
• At the end of this period, they alternately contract and relax, causing
disintegration of the functionalis layer and eventually menses.
 AMENORRHEA

• Menses - is a physiologic uterine bleeding due to interplay of

hormones via hypothalmo-pituitary-ovarian axis.
• For menses to occur,
o Actively coordinated axis (H-P-O)

o Responsive endometrium

o Patent out-flow tract

 CNS-Hypothalamus-Pituitary
Ovary-uterus Interaction

Neural control Chemical control

Dopamine Norepinephrine Endorphines

(-) (+) (-)

Hypothalamus
Gn-RH
± Ant. pituitary ? –
FSH, LH
Estroge Ovaries Progesterone
n

Uterus

13
Menses
 AMENORRHEA
• Amenorrhea implies absence of menstrual periods.

• Amenorrhea can be of two types: Primary and secondary.

• Primary amenorrhea:- is absence of menstrual cycles in a woman who had never

experienced menstrual cycles before.

• Secondary amenorrhea:- is defined as the cessation of menstruation in a woman who had

been previously experiencing menstrual bleeding.

• This cessation must last for at least 6 months or for at least 3 of the previous 3-cycle
intervals.
• Secondary amenorrhea is more common than primary amenorrhea.
 Primary Amenorrhea

Primary amenorrhea can be defined as follows:

• Absence of menses by age of 13 or 14 years with the absence of growth or

development of secondary sexual characteristics.

• Or absence of menses by the age of 15 or 16 years with normal development

of secondary sexual characteristics.

• Seen in approximately 2.5% of the population.

 Pathophysiology of Menstrual Bleeding

• circulating estradiol levels in the body stimulates the growth of uterine endometrium.

• Progesterone, which is produced by the corpus luteum, is formed after ovulation.

• It transforms proliferating endometrium into a secretory one.

• If pregnancy does not occur, this secretory endometrium breaks down and sheds in the
form of menstrual bleeding.

• A complex interaction between the hypothalamic-pituitary-ovarian axis and the outflow

tract (uterus, cervix and vagina) is required for the normal menstrual bleeding to take place.
• For menstrual cycles to occur normally, there should be;
• An intact outflow tract: An intact outflow tract which connects the bleeding
occurring in the internal genitalia with the outside is essential for normal
menstrual flow.
• This requires a patent outflow tract and continuity in the vaginal orifice,
vaginal canal and endocervix with the uterine cavity.
• Normal endometrial development: Normal development of endometrial
lining which responds cyclically to stimulation by estrogen and
progesterone.
• Normal functioning ovaries: Proper functioning of the ovaries is required for
secretion and synthesis of estrogens and progesterone.
• The entire spectrum of follicle development, ovulation and formation of
corpus luteum occurs here.
• Normal functioning pituitary glands: The stimulus for the production of
ovarian hormones and ovarian follicles is provided by the hormones secreted
from anterior pituitary including hormones such as FSH and LH.
• Normal functioning hypothalamus: The secretion of these hormones is
dependent on secretion of GnRH by the hypothalamus.
• Any disruption of the interaction in above mentioned compartments can result
in amenorrhea.
 Causes of Primary Amenorrhea

• The causes of primary amenorrhea are related to defects in either of the four
compartments.

• Compartment I: Outflow tract and the uterus.

• Compartment II: Defect in ovulation.

• Compartment III: Defect at the level of pituitary gland.

• Compartment IV: Defect at the level of hypothalamus and central nervous

system.
 I. Outflow obstruction

Acquired causes
Congenital causes
Müllerian anomalies Asherman's syndrome
Secondary to prior surgeries
Transverse vaginal septum Cesarean section
Mayer– Rokitansky –Küster–Hauser Myomectomy
syndrome Currettage, especially postpartum
Absent endometrium Secondary to infections
Pelvic inflammatory disease
Cervical agenesis IUD–related
Imperforate hymen Tuberculosis
Schistosomiasis
Androgen insensitivity Cervical stenosis
True hermaphrodites Cone biopsy
Loop electro excision procedure
20
 Out flow contd.

Imperforate hymen
• Is one of the most common obstructive lesions of the female genital tract
• At birth, infants may have a bulging introitus due to mucocolpos from vaginal secretions
stimulated by maternal estradiol.
• If the diagnosis is not made in the newborn period and the hymen remains imperforate, the
mucus will be reabsorbed and the child usually remains asymptomatic until menarche.
• Adolescent girls present with cyclic abdominal or pelvic pain & hematocolpos, which
gives the hymenal membrane a bluish discoloration.
• Marked distension of the vagina may also result in back pain, pain with defection, or
difficulties with urination.
• Retrograde menstruation may lead to development of endometriosis. 21
 Treatment
• Hymenectomy or Cruciate incision

• Repair of the hymen can be performed at any age; however, the repair is
facilitated if the tissues have undergone estrogen stimulation.

• Therefore, surgery is ideal in the newborn, post pubertal, or premenarchal

periods.

• Give certificate to the child.

24
 Out flow contd.
Transverse vaginal septum
• Results when there is failure of fusion and/or canalization of the urogenital sinus
and müllerian ducts.
• Occurs in approximately 1 in 30,000 to 1 in 80,000 women.
• These septa may be located at various levels in the vagina;
• Approximately 46 % are found in the upper vagina, 35 to 40 % in the middle
portion, and 15 to 20 % in the lower vagina.
• The septa are generally less than 1 centimeter in thickness and may have a small
central or eccentric perforation.
• The external genitalia appear normal, but internally the vagina is shortened (a blind
pouch). 25
Treatment — Excision and complete removal of the septum.

26
 Mayer – Rokitansky-Küster-Hauser syndrome (Utero-vaginal – Agenesis)

• 15% of 1ry amenorrhea

• Normal breasts and Sexual Hair development & Normal

looking external female genitalia

• Normal female range testosterone level

• Absent uterus and upper vagina & Normal ovaries

• Karyotype 46-XX

• 15-30% renal, skeletal and middle ear anomalies

• Treatment : STERILE Vaginal creation ( Dilatation VS

Vaginoplasty.
27
 Androgen insensitivity Syndrome
(Testicular feminization syndrome)
• X-linked trait
• Absent cytosol receptors
• Normal breasts but no sexual hair
• Normal looking female external genitalia
• Absent uterus and upper vagina
• Karyotype 46, XY
• Male range testosterone level
• Treatment : Gonadectomy after puberty + HRT
• Vaginal creation (dilatation VS Vaginoplasty )

28
 Absent endometrium

• This abnormality is rare

• Physical findings are normal.

• Absence of the endometrium is suspected in patients With:

1. Primary amenorrhea and

2. Normal secondary sexual characteristics

3. Hormone levels are normal and

4. No withdrawal bleeding after combined estrogen & progesterone replacement .

29
 True Hermaphroditism

• A true hermaphrodite has both ovarian and testicular gonadal tissue.

• The most common karyotype associated with true hermaphroditism is 46,XX, followed by
46,XX/46,XY.
• The phenotype of a 46,XX true hermaphrodite includes a unilateral ovotestis with a
contralateral ovary or testis, or bilateral ovotestes.
• The gonadal location varies from abdominal ,inguinal to scrotal.
• External genitalia are usually ambiguous and usually are under masculinized due to an
inadequate amount of testosterone.
• These individuals are not usually diagnosed until puberty or during an evaluation for infertility.
• The testes are usually small and may be cryptorchid.
• Semen analysis reveals azoospermia due to absent spermatogenesis. 30
 Asherman's syndrome
• It is diagnosed by performing hysterosalpingography, saline infusion ultrasonography, or hysteroscopy.
• There is complete obliteration or multiple filling defects caused by synechiae.
• If tuberculosis or schistosomiasis is suspected, do endometrial cultures.

Treatment
• Adhesions released using hysteroscopic resection with scissors or electrocautery.
• A pediatric Foley catheter is placed in the uterine cavity for 7 to 10 days postoperatively.
• Systemic administration of broad–spectrum antibiotic therapy
• 2–month course of high– dose estrogen therapy with monthly progesterone withdrawal is used to prevent
reformation of adhesions.
• 80% of patients treated achieve pregnancy , Complications including miscarriage, preterm labor, placenta
previa, & placenta accreta occur.
• Cervical stenosis can be treated by cervical dilation. 31
 Ovarian Failure
• Primary dysfunction at the level of the ovary.
• Termed premature menopause or premature ovarian failure (POF).
• POF is preferable, as it better describes the pathophysiology of this condition.
• Due to lack of negative feedback, the gonadotropins, LH and FSH, have increased levels
(hypergonadotropic).
• Premature ovarian failure is defined as loss of oocytes and the surrounding support cells
prior to age 40 years.
• The diagnosis is determined by two serum FSH levels greater than 40 Miu /mL that are
obtained at least 1 month apart.
• Incidence 1 in 1,000 women less than 30 years, and 1 in 100 women less than 40 years.
• In most cases, the etiology of POF is not determined. 32
 Ovarian Failure contd.
3. Acquired Abnormalities
1. Chromosomal Disorders
• Iatrogenic causes
e.g. Turner Syndrome
e.g. Radiation
2. Specific Genetic Defects • Infections(mumps oophoritis)
e.g. Mutations in the LH & FSH • Autoimmune disorders
receptors
• Cigarette smoking
(impair follicular health)
• Polycystic ovarian syndrome
• Feminizing tumor of the ovary
• Masculinizing tumor of the ovary
• Idiopathic
33
Polycystic ovarian syndrome

34
 Characteristic Findings in Women with Turner Syndrome

Height 142–147 cm Lack of breast development

Micrognathia Areola widely spaced
Epicanthal folds Coarctation of the aorta
Low-set ears Short fourth metacarpal
Sensorineural hearing loss Cubitus valgus
Otitis media  conductive loss Renal abnormalities
High-arched palate Autoimmune disorders
Webbing of the neck Autoimmune thyroiditis
Chest square and shield-like Diabetes mellitus
Edema

35
 Turner’s syndrome

(Classic 45-XO) Mosaic (46-XX / 45-XO)

36
Ovarian dysgenesis

37
Ovarian Failure contd.

Mutations in the LH and FSH receptors:

These mutations prevent normal response of ovaries to circulating
gonadotropins, a condition termed resistant ovary syndrome
(Savage's syndrome).

38
 Pituitary Failure

Acquired Abnormalities Inherited Abnormalities

Pitutary adenomas
Septoptic dysplasia
Sheehan syndrome
Mutations in GnRH receptor
Inflammation
Mutations in LH /FSH subunits
Infiltrative disease

Metastatic lesions

surgical removal or

Radiation treatment of pituitary adenomas.

39
 Pituitary contd.

Acquired Pituitary Dysfunction

• Most pituitary dysfunction is acquired after menarche, and therefore, women
present with normal pubertal development followed by secondary amenorrhea.

• Nevertheless, in rare cases, these disorders may develop prior to puberty,

resulting in delayed pubertal development and primary amenorrhea

• Pituitary adenomas are the most common cause of acquired pituitary

dysfunction.
40
 Pituitary contd.

Pitutary adenomas
• Cause amenorrhea in two ways
1. Prolactin secretion
• Elevated prolactin levels are associated with a reflex increase in central
dopamine production, which alters GnRH neuronal function.
2. Mass effect
• This mass may compress neighboring gonadotropes or may damage the
pituitary stalk, disrupting dopamine inhibition of prolactin secretion.
• As many as one tenth of amenorrheic women have increased levels of serum
prolactin (the "galactorrhea-amenorrhea syndrome").
41
 Pituitary cont …

• Sheehan syndrome refers to panhypopituitarism that develops after massive

postpartum hemorrhage complicated by hypotension.
• Loss of gonadotrope activity results in anovulation and subsequent
amenorrhea.
• Damage to the other pituitary cell types may present as failure to lactate, loss of
sexual and axillary hair, hypothyroidism, and adrenal insufficiency.
• The pituitary cell types are differentially sensitive to damage.
• Prolactin secretion deficiency is the most common, followed by loss of
gonadotropin and growth hormone release, loss of ACTH, and least commonly,
by decreases in thyroid-stimulating hormone (TSH) secretion
42
 Hypothalamic failure
Acquired abnormalities
Inherited Abnormalities Eating disorders
Extreme exercise
Idiopathic hypogonadotropic
Stress
hypogonadism Chronic disease
Kallmann syndrome Anatomic Destruction
Radiation

43
 Hypothalamic failure contd.

Inherited Abnormalities
• Inherited hypothalamic abnormalities primarily consist of those patients with
idiopathic hypogonadotropic hypogonadism (IHH).

• Of these patients, a subset has associated defects in the ability to smell

(hyposmia or anosmia) and are said to have Kallmann syndrome.

44
 Hypothalamic failure contd.

Acquired Hypothalamic Dysfunction

• Functional Disorders or Hypothalamic Amenorrhea
• Most frequently, gonadotropin deficiency leading to chronic anovulation is believed to
arise from functional disorders of the hypothalamus or higher brain centers.
• Also called hypothalamic amenorrhea, this diagnosis encompasses three main
categories: eating disorders, extreme exercise, chronic disease and stress.
• Each woman appears to have her own hypothalamic "set-point" or sensitivity to
environmental factors.
• For example, individual women can tolerate significantly different amounts of stress
without developing amenorrhea. 45
 Hypothalamic failure contd.

Eating Disorders
• Anorexia nervosa and bulimia, result in amenorrhea.

• Anorexia nervosa patient have abnormal body image, intense fear

of weight gain, often engaged in compulsive exercise, mean age
onset 13-14 yrs (range 10-21 yrs)

• Low estradiol  risk of osteoporosis

46
 Hypothalamic failure contd.

Exercise-Induced Amenorrhea
• Seen in women whose exercise
regimen is associated with significant
loss of fat, such as ballet, gymnastics,
and long-distance running.

47
 Hypothalamic failure contd.

Stress-Induced Amenorrhea
• This may be associated with leaving for college, taking examinations,
wedding planning, or traumatic life events, such as death of a family
member or divorce.

• Eating disorders, exercise, and stress may alter menstrual function through
overlapping mechanisms.
48
 Hypothalamic failure contd.

Pathophysiology of Functional Hypothalamic Amenorrhea

• Exercise increases levels of endogenous opioids endorphins, producing the so-
called "runner's high".
• Opioids alter GnRH pulsatility as demonstrated by treatment of humans and
animal models with anti-opiates, such as naloxone.
• As part of the stress response, each of these conditions may lead to an increase
in corticotropin-releasing hormone (CRH) release by the hypothalamus, which
in turn results in cortisol secretion by the adrenal gland.
• Corticotropin-releasing hormone alters the pattern of pulsatile GnRH
secretion, whereas cortisol may act directly or indirectly to disrupt GnRH
neuronal function.
49
 Hypothalamic failure contd.

• Eating disorders are thought to disrupt

ovulatory function through a number of
hormonal factors including insulin,
glucagon, and leptin.
• Patients with anorexia nervosa have
been found to have low circulating
leptin levels.
• Decrease in leptin secondarily stimulate
neuropeptide Y, which is known to
stimulate hunger and alter GnRH
pulsatility.
Anorexia nervosa
50
 Hypothalamic failure contd.

Pseudocysesis
• Pseuodocyesis exemplifies the ability of the mind to control physiologic processes.
• Approximately 550 cases have been reported in the medical literature in women ranging
from 6 to 79 years.
• These patients fervently believe that they are pregnant and subsequently demonstrate a
number of the signs and symptoms of pregnancy.
• Endocrine evaluation shows inconsistent pattern of hormonal derangements.
• A common link in these patients is a history of severe grief, such as recent miscarriage or
infant death.
• Psychiatric treatment to treat the associated depression, which is often exacerbated when the
patient is informed that she is not pregnant 51
 Patient Approach

• History
• Age, parity
• Previous menstrual history
• Mode of onset-Sudden, Gradual
• Family history
• Past medical history or recent illnesses
• Weight fluctuation
• History of any stressful events
• History of drug intake
• Radiation exposure
• History of uterine curettage or uterine surgeries
• History of PPH or shock or infection
• Acne, hirsute
• Inappropriate galactorrhea
• Headache or visual disturbances
• Symptoms of estrogen deficiency 52
 Approach Contd.

Physical examination
• V/S
• Weight, Height , BMI
• Assess thyroid gland, breast
• Signs of acromegaly
• Signs of Cushing’s disease
• Presence of normal reproductive tract
• Presence of secondary sexual characteristics
• Axillary and pubic hair growth
• Neurological examinations and determination of visual field

53
 Amenorrhea
Pelvic
Absent uterus Sexual hair
examination
Normal
Yes No
Negative HCG +Ve
Müllerian Agenesis AIS
ANC

Prolactin TSH FSH

Increased Increased See next slide

Dopamine Vs
Thyroid
surgery
replacement

54
 FSH

Decreased Increased Normal

Stress, exercise & Gonadal failure

eating disorders Testosterone DHEAS 17-OH-
P
Karyotype
Increased Increased
Yes Increased
No
MRI Adrenal CA
POF Vs Gonadal Ultrasound
treat tumors H
MRI dysgenesis for ovarian
tumor
Abnormal
Normal

Tumor IHH,
Kallman 55
 Approach Contd.

Step 1
• Patient with amenorrhea & pelvic examination normal ,then
• Do urine HCG, if positive to ANC, if negative , then
• Determine serum TSH, FSH and Prolactin level , If normal, do progestational challenge test
• Progesterone challenge (withdrawal) test give medroxyprogesterone acetate, 10 mg, po, daily for
5 days
• Purpose: To assess level of endogenous estrogens and patency of of the out flow tract.
• Within 2-7 days after the completion of the medication the patient will either have withdrawal
bleeding or not.
• Withdrawal bleeding indicates - Functional out flow tract & estrogen primed endometrium is
confirmed.
• No withdrawal bleeding, either the target organ outflow tract is inoperative or preliminary
estrogen proliferation of the endometrium has not occurred.
• No withdrawal bleeding go to Step 2. 56
 Approach Contd.

Step 2
Estrogen-Progesterone Challenge Test
Give 1.25 mg conjugated estrogens or 2 mg estradiol daily for 21 days, then
medroxyprogesterone acetate 10 mg daily for the last 5 days is necessary to achieve
withdrawal bleeding.
The patient with amenorrhea will either bleed or not bleed.
If there is no withdrawal flow, the diagnosis of a defect in the Compartment I systems
(endometrium, outflow tract) can be made.
If withdrawal bleeding does occur, one can assume that Compartment I systems have
normal functional abilities if properly stimulated by estrogen.

57
 Approach Contd.

Step 3
Step 3 is designed to determine whether the lack of estrogen is due to a fault in the follicle
(Compartment II) or in the CNS-pituitary axis (Compartments III and IV).
In order to produce estrogen, ovaries containing a normal follicular apparatus and sufficient
pituitary gonadotropins to stimulate that apparatus are required.
This step involves an assay of the level of gonadotropins in the patient.
Because Step 2 involved administration of exogenous estrogen, endogenous gonadotropin levels
may be artificially and temporarily altered from their true baseline concentrations.
Hence, a delay of 2 weeks following Step 2 must ensue before doing Step 3, the gonadotropin assay.
The gonadotropin assay will be abnormally high( ovarian failure) or abnormally low (pituitary or
hypothalamic failure), or in the normal range(absent endometrium).
58
Approach Contd.

Clinical state Serum FSH Serum LH

Normal 5-20 IU/L 5-20 IU/L

Hypogonadotropic <5 <5

Hypergonadotrophic >20 >40

59
 Approach Contd.

Step 4
• To differentiate whether the cause of hypogonadotropic is pituitary or hypothalamic
failure.

• With GnRH administration:

• Pituitary gonadotropin
• Increased: Hypothalamic failure

• Not increased: Pituitary failure 60

 Summary of
AN APPROACH FOR DIAGNOSIS
of AMENORRHOEA
• HISTORY
• PHYSICAL EXAMINATION
• ULTRASOUND EXAMINATION

Exclude Pregnancy
Exclude Cryptomenorrhea

61
Summary of General Principles
of management of Amenorrhea
. Attempts to restore ovulatory function
. If this is not possible HRT (oestrogen and progesterone) is
given to hypo-estrogenic amenorrheic women (to prevent
osteoporosis; atherogenesis)
. Periodic progestogen should be taken by euestrogenic
amenorrheic women (to avoid endometrial cancer)
. If Y chromosome is present gonadectomy is indicated
. Many cases require frequent re-evaluation

62
 Hormonal treatment
Primary Amenorrhea with absent secondary sexual characteristics

To achieve pubertal development

Premarin 5mg D1-D25 + provera 10mg D15-D25 X 3 months;  2.5mg

Premarin X 3 months and  1.25mg Premarin X 3 months

Maintenance therapy

0.625mg Premarin + provera OR ready HRT preparation OR 30µg oral

contraceptive pill
63
 Final message
• Although the work-up of amenorrhea may seem to be complex, a carefully
conducted physical examination with the history, and Looking to the patient as a
bioassay for endocrine abnormalities, should permit the clinician to narrow the
diagnostic possibilities and an accurate diagnosis can be obtained quickly.

• Management aims at restoring ovulatory cycles if possible, replacing estrogen

when deficient and Progestrone to protect endometrium from unopposed estrogen.

• Frequent re-evaluation and reassurance of the patient.

64
MENOPAUSE
 MENOPAUSE
• Definition: permanent cessation of menstruation at the end of reproductive life due to loss of
ovarian follicular activity.
• It is the point of time when last and final menstruation occurs.
• It takes 12 months of amenorrhoea to confirm that menopause has set in, and therefore it is a
retrospective diagnosis.
• Premenopause: Refers to the period prior to menopause.
• Climacteric is the period of time during which a woman passes from the reproductive to the
non reproductive stage.
• May begin 2–3 years before menopause and continue for 2–5 years after it.
• This phase covers 5–10 years on either side of menopause.
 Menopause…

• Perimenopause is the part of the climacteric when the menstrual cycle is likely to be
irregular.
• Postmenopause is the phase of life that comes after the menopause.
• Premature ovarian failure: Menopause occurring prior to age 40 years
• Late menopause: If menopause occurs after age 55 years.
• Age at which menopause occurs is genetically predetermined.
• The age of menopause is not related to age of menarche or last pregnancy, number of
pregnancy, lactation, use of oral pill, socioeconomic condition, race, height or weight.
• Thinner women may have early menopause.
• However, cigarette smoking and severe malnutrition may cause early menopause.
• The age of menopause ranges between 45–55 years, average being 50 years.
 Pathophysiology of menopause

• Initially, ovulation fails, no corpus luteum forms and no progesterone is secreted

by the ovary.
• Therefore, the premenopausal menstrual cycles are often anovulatory and
irregular.
• Later, Graafian follicles also fail to develop, oestrogenic activity is reduced and
endometrial atrophy leads to amenorrhoea.
• Cessation of ovarian activity and a fall in the oestrogen and inhibin levels cause a
rebound increase in the secretion of FSH and LH by the anterior pituitary gland.
• The FSH level may rise as much as 50-fold and LH 3–4 fold.
• With further advancing years, gonadotropin activity of the pituitary gland also
ceases, and a fall in FSH level eventually occurs.
 Changes during Menopause

• Ovaries shrink in size, become wrinkled and white.

• Fallopian tubes show feature of atrophy and the muscle coat becomes thinner, the cilia
disappear.
• The uterus becomes smaller and the ratio between the body and the cervix reverts to the 1:1
ratio.
• The endometrium becomes thin and atrophic and cervical secretion becomes scanty.
• The vagina becomes narrower due to gradual loss of elasticity and vaginal pH becomes
alkaline.
• The vulva shows features of atrophy.
• The labia becomes flattened and the pubic hair becomes scantier.
• The end result is a narrow introitus.
 Changes..

• Breast fat is reabsorbed and the glands atrophy.

• The nipples decrease in size. Ultimately, the breasts become flat and pendulous.
• Bladder and urethra undergo similar changes to those of the vagina.
• The epithelium becomes thin and is more prone to damage and infection.
• There may be dysuria, frequency, urge or even stress incontinence.
• Loss of muscle tone leads to pelvic relaxation, uterine descent and anatomic
changes in the urethra and neck of the bladder.
• The pelvic cellular tissues become scanty and the ligaments supporting the
uterus and vagina lose their tone.
 Cont.…

• Following menopause, there is loss of bone mass by about 3–5% per year.
This is due to deficiency of estrogen.

• Risk of cardiovascular disease is high in postmenopausal women due to

deficiency of estrogen.
 Patterns of Menstruation prior to Menopause

• Abrupt cessation of menstruation (rare).

• Gradual decrease in both amount and duration.

• It may be spotting or delayed and ultimately lead to cessation.

• Irregular with or without excessive bleeding.

• One should exclude genital malignancy prior to declare it as the usual

premenopausal pattern.
 Common symptom in menopause
• Cessation of menstruation are the most common and evident. Some of the symptom that
appear in some women are:
• Vasomotor symptoms
• Urogenital atrophy
• Osteoporosis and fracture
• CVS disease
• Cerebrovascular disease
• Psychological Changes
• Skin and Hair
• Sexual Dysfunction
• Dementia and cognitive decline
 Diagnosis
• Women over age 45 years
• Change in intermenstrual interval with or without menopausal symptoms.
• 12 months of amenorrhea in the absence of other biological or physiological causes.
• Women between the ages of 40 and 45 years
• The dx is the same as >45 years but menstrual cycle dysfunction must first be ruled
out (hCG, TSH)
• Women <40 years
• Should no be diagnosed as MT/menopause
• Primary ovarian insufficiency (premature ovarian failure)
 Stages of Reproductive Aging workshop (STRAW)

• These staging criteria are guides rather than strictly applied diagnoses.

• Every stage may not manifest in all women

• The anchor stage is the FMP

• Five stages precede and two stages follow the FMP.

 STRAW..
• Stage -5:early reproductive period

• Stage -4:reproductive peak

• Stage -3:late reproductive period

• Stage -2is the early MT , and

• Stage -1is the late MT.

• Stage +1a: the first year after FMP

• Stage +1b: 2 to 5 years Postmenopause, and

• Stage +2:later postmenopausal years.

 Management

Prevention
• Spontaneous menopause is unavoidable.
• However, artificial menopause induced by surgery (bilateral oophorectomy) or
by radiation (gonadal) during reproductive period can to some extent be
preventable or delayed.
• Counseling: Every woman with postmenopausal symptoms should be
adequately explained about the physiologic events.
• This will remove her fears, and minimize or dispel the symptoms of anxiety,
depression and insomnia. Reassurance is essential.
 TREATMENT
Non-hormonal Treatment
• Lifestyle modification includes: Physical activity (weight bearing), reducing high coffee
intake, smoking and excessive alcohol.
• There should be adequate calcium intake (300 mL of milk), reducing medications that causes
bone loss (corticosteroids).
• Nutritious diet-balanced with calcium and protein is helpful.
• Supplementary calcium-daily intake of 1–1.5 g can reduce osteoporosis and fracture
• Exercise-weight bearing exercises, walking, jogging
• Vitamin D-supplementation of vitamin D3 (1500–2000 IU/day) along with calcium can reduce
osteoporosis and fractures.
 Hormone replacement
therapy (HRT)
• The HRT is indicated in menopausal women to overcome the short-term and
long-term consequences of estrogen deficiency.

Indication of Hormone Replacement Therapy

• Relief of menopausal symptoms.

• Prevention of osteoporosis.

• To maintain the quality of life in menopausal years.

 HRT….

Special group of women to whom HRT should be prescribed:

• Premature ovarian failure

• Gonadal dysgenesis

• Surgical or radiation menopause

 Benefits of hormone replacement therapy (HRT)

• Improvement of vasomotor symptoms (70–80%)

• Improvement urogenital atrophy

• Increase in bone mineral density (2–5%)

• Decreased risk in vertebral and hip fractures (25–50%)

• Reduction in colorectal cancer (20%)

• possibly cardioprotection.
 Risks of Hormone Replacement Therapy
• Endometrial cancer: When estrogen is given alone to a woman with intact
uterus, it causes endometrial proliferation, hyperplasia and carcinoma.
• It is therefore advised that a progesterone should be added to ERT to counter
balance such risks.
• Breast cancer: Combined estrogen and progestin replacement therapy, increases
the risk of breast cancer slightly.
• Adverse effects of hormone therapy are related to the dose and duration of
therapy.
• Venous thromboembolic (VTE) disease has been found to be increased with the
use of combined oral estrogen and progestin.
• Transdermal estrogen use does not have the same risk compared to oral estrogen
 HRT….

• Coronary heart disease (CHD): Combined HRT therapy shows a relative

hazard of CHD.

• Hypertension has not been observed to be a risk of HRT.

• Lipid metabolism: An increased incidence of gallbladder disease has been

observed following ERT due to rise in cholesterol (in bile).

• Dementia, Alzheimer disease are increased.

 Contraindications to HRT

• Undiagnosed genital tract bleeding

• Estrogen dependent neoplasm in the body

• History of venous thromboembolism

• Active liver disease

• Gallbladder disease
 Available preparations for HRT

• The principal hormone used in HRT is estrogen.

• Ideal for a woman who had her uterus removed (hysterectomy) already.
• But in a woman with an intact uterus, only estrogen therapy leads to endometrial
hyperplasia and even endometrial carcinoma.
• Addition of progestins for last 12–14 days each month can prevent this problem.
• Commonly used estrogens are conjugated estrogen (0.625–1.25 mg/day) or
micronized estradiol (1–2 mg/day).
• Progestins used are medroxyprogesterone acetate (2.5–5 mg/ day), micronized
progesterone (100–300 mg/day) or dydrogesterone (5–10 mg/day).
 HRT…
• Considering the risks, hormone therapy should be used with the lowest effective dose
and for a short period of time.

• Low dose oral conjugated estrogen 0.3 mg daily is effective and has got minimal side
effects.

• Dose interval may be modified as daily for initial 2–3 months then it may be changed to
every other day for another 2–3 months and then every third day for the next 2–3 months.

• It may be stopped there after if symptoms are controlled.

 HRT…

• Oral estrogen regime: Estrogen - conjugated equine estrogen 0.3 mg or

0.625 mg is given daily for woman who had hysterectomy.

• Estrogen and cyclic progestin: For a woman with intact uterus estrogen is
given continuously for 25 days and progestin is added for last 12–14 days.

• Continuous estrogen and progestin therapy Continued combined therapy

can prevent endometrial hyperplasia.

• There may be irregular bleeding with this regimen.

THANK YOU!!!
ABNORMAL UTERINE BLEEDING
 Abnormal Uterine Bleeding (AUB)
• Definition:- Is defined as bleeding from the genital tract that is out of the normal menstrual cycle in terms of

o Duration of stay
o Frequency
o Amount
o Quality
• Normal menstrual cycle
 Comes every 21-35days
 Stays for 3-7days
 Amount is 20-80ml
 It doesn’t clot.
 Parameters for normal and abnormal menstrual
blood loss
Normal Abnormal
Duration 4-6 days Less than 2 or more than 7 days.

Volume 30 ml Less than 30 ml or >80 ml.

Interval 21-35 days Less than 21 days or more than 35 days

 Incidence

• 10 -30% in reproductive aged women

• 50% of perimenopausal women

 Types of abnormal uterine bleeding
• Menorrhagia:- Excessive and prolonged bleeding

• Metrorrhagia :- Irregular or intermenstural bleeding

• Menometrorrhagia :- Menorrhagia+ Metrorrhagia

• Polymenorrhea:- When menstruation comes in less than 21days

• Oligomenorrhea:- When menstruation comes in greater than 35 days

• Hypomenorrhea (Cryptomenorrhea) :- Small bleeding

• Contact bleeding:- Bleeding following sexual intercourse or after examination

Terms Definition

Menorrhagia Prolonged or excessive menstrual blood loss (>80 ml) at

regular intervals.

Polymenorrhea Regular bleeding at intervals of less than 21 days

Oligomenorrhea Infrequent menstruation at intervals greater than every

35 days

Amenorrhea No uterine bleeding for at least 6 months

Intermenstrual bleeding (spotting) Episodes of uterine bleeding of varying amounts

occurring between the regular menstrual periods

Menometrorrhagia Combination of both menorrhagia and Metrorrhagia,

associated with prolonged or excessive bleeding (> 80
ml) at irregular intervals.

Metrorrhagia Irregular, frequent uterine bleeding of varying amounts,

but not excessive, at irregular intervals.

Hypomenorrhea Scanty menstruation

 Causes of AUB

• The causes of abnormal uterine bleeding can be divided into

• Structural causes -Ovulatory

• Level of sex hormones and gonadotropins are normal

• Mensus is cyclic.
 Cont.…
• Hormonal causes -Anovulatory

• Sex steroids are produced, but not cyclically so bleeding is irregular.

• Chronic estrogen production unopposed by adequate progesterone

production allows continued proliferation of the endometrium which leads to
breakthrough bleeding
 Causes of anovulatory bleeding
• Hypothyroidism

• Hyperprolactinemia

• Hormone producing ovarian tumors

• Polycystic ovarian syndrome

• Chronic liver or renal disease

• Congenital adrenal hyperplasia

• Side effect of contraception

 Causes of ovulatory bleeding
A. Pregnancy associated complications

B. Anatomic uterine lesions

• Neoplasm -Leiomyoma, polyp, endometrial hyperplasia, cancer, cervical cancer

• Atrophic endometrium

• Infection -sexually transmitted disease, tuberculosis

• Mechanical causes -intrauterine device, perforation

• Partial outflow obstruction -congenital müllerian defect, Asherman syndrome

 Dysfunctional uterine bleeding (DUB)
• It is abnormal uterine bleeding with out any structural abnormality in the genital
tract

• So the cause is said to be hormonal abnormality

• Reflects a disturbance in normal ovulatory function

• It is a manifestation of abnormal hormonal stimulation of the endometrial lining of

the uterus.

• 50% of AUB

• 80-90% is due to dysfunction of the H-P-O axis

 Pathophysiology
no ovulation
↓
no corpus luteum
↓
no progesterone secretion
↓
unopposed estrogen stimulation of endometrium
↓
endometrium become out of phase and start to shade
 Evaluation and Diagnosis of Abnormal Uterine
Bleeding

• History

• Physical examination

• Laboratory studies

• Pregnancy test

• Complete blood count

• Thyroid-stimulating hormone (TSH) and prolactin.

• Coagulation profile
 Cont.…
• P/E focus on
• V/s
• HEENT( anemia)
• Abdomen
• Mass and enlarged irregular uterus suggests myoma
• Symmetrically enlarged ux is more typical of Adenomyosis or endometrial CA
• GUS
• Consistency and surface of CX
• Any mass on the CX or VX
• Adnexal mass
 Diagnostic procedures

o Ultrasonography

o Endometrial biopsy

o Hysteroscopy
 Cytologic Examination

• Cervical and endometrial cancers can cause AUB

• Pap smear

• Depending on the cytological results, colposcopy or endometrial biopsy or

both may be indicated
 Endometrial Biopsy

• AUB in a woman above 35 years

• AUB not responding to conservative measures

 ULTRASONOGRAPHY
• In post menopausal mothers endometrial thickness <4mm excludes
endometrial Ca in 95-97%.

• Endometrial thicknesses >5 mm warrant additional evaluation with

hysteroscopy, or endometrial biopsy.

• Endometrial thickness of >12mm independent of cycle in premenopausal

mother endometrial Ca should be ruled out by endometrial biopsy.
 Treatment of Abnormal Uterine Bleeding

• The cause of the abnormal bleeding should determine the treatment options
available to the patient.

• Hormonal or medical conditions causing the bleeding should be addressed

• Structural causes are often addressed surgically.

Management of AUB due to organic lesion
• Depends on the type of lesion
 Management of DUB
• The management of DUB has several goals

1.Maintenance of hemodynamic stability

2.Correction of acute or chronic anemia
3.Return to a pattern of normal menstrual cycles
4.Prevention of recurrence
5.Prevention of long-term consequences of anovulation
 Cont.…
• How hormone therapy stops bleeding in DUB

• Estrogen-proliferation at site of the bleeding

• Progesterone-stabilize & promote expulsion

• More than 90% of adolescent respond to this RX.

 Management for mild DUB

• Management of mild DUB consists of observation and reassurance.

• They should follow-up in three to six months

• Although hemoglobin concentration is usually normal (>12 mg/dL) in mild

DUB iron should be given
 Mx of moderate DUB
1) Not in Active bleeding

• Managed in the outpatient setting

• Combined OCP

• Progesterone only pills

• Medroxyprogesterone 10 mg po/d from in the last 10days of the cycle

2) Currently bleeding -a combination of estrogen and progestin rather than to

progestin-only preparations, as estrogen provides hemostasis
 Cont.…

• Different recommendation

• 1tab TID until the bleeding stops

• 1tab BID for 5 days

• 1tab daily to complete 21 days course

• If the bleeding persist despite 3month hormonal RX other causes should be

ruled out
 MX of sever DUB

• Hospitalization

• Stabilization

• Hematological tests before transfusion (PT ,PTT)

• Hormone RX
 Cont.…
• Combined OCP with high dose estrogen (50mcg estradiol /0.5 mg norgestrel.

• 1tab qid for 4 day

• 1tab tid for 3 day

• 1tab bid for 21 day

 Hemostatic therapy
• Patients with DUB have high concentration of fibrinolytic activity in the
endometrial vessels this drug block the lysine binding site of plasminogen

• Anti fibrinolytic drugs

aminocaproic acid

desmopresin
 Surgical methods

• Are last options in a lady who doesn’t respond to hormonal therapy

• D&C

• Endometrial destructive procedures

• Hysterectomy
THANK YOU!
INFERTILITY
 Definition and Epidemiology

• Infertility is defined as a failure to conceive within one or more years of regular

unprotected coitus.

• Primary infertility denotes those patients who have never conceived.

• Secondary infertility indicates previous pregnancy but failure to conceive

subsequently.

• Fecundability is defined as the probability of achieving a pregnancy within one

menstrual cycle.

• Fecundity is the probability of achieving a live birth within a single cycle.

 INCIDENCE

• 80 % of the couples achieve conception if they so desire, within one year of having regular
intercourse with adequate frequency.

• 10 % will achieve the objective by the end of second year.

• 10 % percent remain infertile by the end of second year.

• Infertility is common and affects 10 to 15 percent of reproductive aged couples.

• Even without treatment, approximately half of women will conceive in the second year of
attempting.
 Factors Essential for Conception.
• Healthy spermatozoa should be deposited high in the vagina at or near the cervix (male factor).
• The spermatozoa should undergo changes (capacitation, acrosome reaction) and acquire motility (cervical
factor).
• The motile spermatozoa should ascend through the cervix into the uterine cavity and the fallopian tubes.
• There should be ovulation (ovarian factor).
• The fallopian tubes should be patent and the oocyte should be picked up by the fimbriated end of the tube (tubal
factor).
• The spermatozoa should fertilize the oocyte at the ampulla of the tube.
• The embryo should reach the uterine cavity after 3–4 days of fertilization.
• The endometrium should be receptive (by estrogen, progesterone) for implantation, and the corpus luteum
should function adequately.
 Causes of Fertility
• The male is directly responsible in about 30–40 percent.

• The female in about 40–55 percent

• Both are responsible in about 10 percent cases.

• The remaining 10 percent, is unexplained.

• 4 out of 10 patients of unexplained category become pregnant within 3 years without having any
specific treatment.

• NB: The basic investigations that should be performed before starting any infertility treatment are
semen analysis, confirmation of ovulation, and the documentation of tubal patency.
 Investigation

 Seminal analysis

o most important male fertility evaluation

o normal result exclude male factor
 Prerequisites for sperm analysis

• Test should be done after 3-7 days abstinence

• It should be examined within 1 hr. of collection

 Normal parameters of sperm analysis

• Volume 2-5 ml

• Total sperm count – >20 million/ml

• Sperm motility of > 50-60%

• Morphology > 50% normal

• PH 7.2 -7.8

• Of which sperm count & motility are the most important factor
 Male factor

• Absence of spermatozoa in the seminal fluid

 Testicular Azoospermia- abnormality may be in the tests,

hypothalamus or pituitary.
 Obstruction of vas deference
o Post testicular Azoospermia-H-P-Tests is normal
 Cont.…
• Testicular Azoospermia
• Gonadal failure is the hallmark of testicular Azoospermia.
• Causes of this condition
congenital or genetic (e.g., Klinefelter syndrome, micro deletion of Y
chromosome)
acquired(e.g., radiation therapy, chemotherapy, testicular torsion, or mumps
orchitis, undescended tests)
 Treatment of male infertility

• For hypothalmo pituitary dysfunction (hypogonadotropic hypogonadism)

 Hormonal treatment is effective

o pulsatile gonadotropin–releasing hormone (GnRH) therapy is effective

• For post testicular Azoospermia

 Micro surgery to correct the obstruction

 Surgical Sperm Recovery for Intracytoplasmic Sperm Injection

• For gonadal failure

 Donor Insemination may be used

 Female infertility

 Common causes

o An ovulation

o Tubal obstruction

o Uterine & cervical factors

 Investigation of female infertility
• Documentation of ovulation
• By Luteinizing Hormone Monitoring using serum or urine kit
• By following pattern of basal Body Temperature
• Following the cervical mucus pattern
• Following the size of the dominant follicle by ultrasound

• Documentation of tubal patency

• by hysteronsalphingeogram.
 Ovulatory factor
• Is due to anovulation
• Cause Could be
– Hypothalamus
– Pituitary
– Ovary
• Gonadal dysgenesis
• Premature ovarian failure
• Ovarian failure due to chemotherapy, radiotherapy, infections
• polycystic ovarian syndrome
 Cont.…

• Treatment depends on the specific cause

o Transient abnormalities which affect the axis should be corrected

o Stress

o Very strong exercise

o Malnutrition

o Disease like hypothyroidism& Hyperprolactinemia should be treated accordingly

o Abnormality in hypothalamus & pituitary

o pulsatile gonadotropin–releasing hormone (GnRH) therapy

 Cont.…

• Ovulation induction

 By chlomepine Citrate- A functional hypothalamic–pituitary–ovarian

axis is required

• For ovarian failure

 Use of donor oocyte

 Tubal factor
• Obstruction of the fallopian tubes

 PID is the commonest one

• 12% of women will be infertile after a single episode of PID

 Congenital

• Diagnosis will be confirmed by hysterosalphingogram.

• Treatment

 Tuboplasty –surgical technique used to correct tubal patency

 If the surgery fails artificial reproductive technique is recommended

 Cont.…
• Treatment of Unexplained Infertility
• Clomiphene Citrate for ovulation induction followed by Intrauterine
Insemination
PELVIC ORGAN PROLAPSE
 Pelvic Organ Prolapse
• Pelvic organ prolapse (POP), is the herniation of the pelvic organs to or beyond the
vaginal walls, is a common condition.

• Descent of pelvic organs from their normal place due to weakness in their supporting
structures.

• Supporting structures of pelvic organs

• Bony pelvis

• Perineal muscles( levator ani muscles)

• Endopelvic facia & its condensations

• Ligaments (e.g. Uterosacral and cardinal ligament)

 Risk factors for pelvic organ prolapse

• Vaginal childbirth

• Risk increases with number of deliveries & if the labor and delivery was
difficult

• Obesity, chronic cough, and chronic constipation may cause increased intra-
abdominal pressures which will increase the risk of pelvic organ prolapse

• A genetic predisposition for pelvic organ prolapse may exist in some women
 Terminologies used in POP
• Cystocele is protrusion of the bladder with the anterior vaginal wall to wards the vaginal
canal

• Rectocele is protrusion of the rectum with the posterior vaginal wall towards the vaginal
canal

• Uterine prolapse is descent of the uterus into the lower part of the vagina or through
the vaginal opening

• Vaginal vault prolapse is descent of the vaginal apex after hysterectomy.

• Enterocele is protrusion of small bowel behind the upper vaginal wall into the vaginal
canal
 Symptoms

• Bulge of tissue protruding through the vaginal opening

• Pelvic or vaginal pressure, especially after prolonged standing

• Urinary incontinence or urine retention

Cont. ..
 Pelvic organ prolapse staging

• Different ways of staging

• Traditional method of staging
 First degree-Most distal portion of the prolapse is bellow the ischial spines (for
uterus).
 Second degree Most distal portion of the prolapse is at the level of the hymeneal ring

 Third degree-when the uterus is totally out of the vaginal canal

 Treatment of pelvic organ prolapse
• Depends on
o The degree of prolapse

o Age of the patient and medical condition of the patient

o Type of prolapse
• For mild to moderate degree of prolapse
 Pelvic floor muscle (Kegel) exercises may improve symptoms

 Pessaries are devices placed in the vagina that support prolapse can be used
 Gelhorn pessaries

The short stem Gelhorn pessaries can be useful for women with
a short vagina
 Cont.….

• Surgery
• Reconstructive

• Obliterative –in very old woman sexually in active

• The surgical procedure and approach can be

• Abdominal

• Vaginal
 Cont.…
• For uterine prolapse
 Conservative procedures- Uterosacral ligament suspension or sacrospinous ligament suspension

 Vaginal Hysterectomy

• For cystocele
 anterior corporrhapy-repairing the defect in the anterior vaginal wall

• For rectocele
 posterior corporrhapy-repairing the defect in the posterior vaginal wall

• For enterocele-a true hernia

 Excision of the sac, returning the content of the sac back, closing the defect
Urinary Incontinence
 Types

• Stress urinary incontinence

• Urge incontinence

• Mixed incontinence

• Overflow incontinence

• Extra urethral sources of urine including genitourinary fistulas

 Stress urinary incontinence (SUI)

• Is involuntary loss of urine that occurs with increased abdominal pressure, such
as coughing or straining

• SUI is the result of loss of anatomic support of the urethra.

• It most commonly occurs following pelvic floor muscle and nerve damage that
resulted from childbearing

• Urethral hyper mobility.

 Urge incontinence

• Is defined by involuntary loss of urine following strong need or urgency to void

• It is a common cause of incontinence in elderly women.

• Urge incontinence includes the following subtypes:

– Detrusor over activity (DO), is caused by involuntary detrusor contractions. Its cause is usually

unknown.

– Neurogenic DO is involuntary detrusor contractions associated with a neurologic disorder (e.g.,

stroke, spinal cord injury, )

– In younger women may be due to interstitial cystitis

 Mixed incontinence

• Is the combination of urge and stress incontinence

• Represent the overlap of two mechanisms, detrusor over activity and impaired
urethral sphincter function

• Is the complaint of involuntary leakage associated with urgency and also with
exertion

• Patients vary in the predominance, severity, and/or bother of urge versus stress
leakage
 Overflow incontinence

• Dribbling and/or continuous leakage associated with incomplete bladder

emptying, due to impaired detrusor contractility and/or bladder outlet
obstruction

• This form of incontinence is associated with retention of urine

 Cont. …

• Etiologies of detrusor underactivity include smooth muscle damage, fibrosis,

low estrogen, aging, peripheral neuropathy

• Obstruction in women may be caused by scarring from prior anti-incontinence

surgery or significant pelvic organ prolapse, when the prolapsed uterus kinks the
urethra.
 Evaluation

• A detailed history is essential and should include:

– Urinary symptoms, including the presence of voiding frequency, nocturia,

urgency, precipitating events, and frequency of loss.

– Obstetric history, including parity, birth weights, and mode of delivery

– CNS or spinal cord disorders

 Cont.…

• Physical examination may detect:

– Exacerbating conditions, such as chronic obstructive pulmonary disease,

obesity, or intra-abdominal mass

– Hypermobility of the urethra

– Pelvic organ prolapse

– Neurologic disorders
 Diagnostic tests

• urinalysis or culture

• stress test

• Post void residual urine volume should be measured (by ultrasound or catheterization)
after the patient has voided.

• post void residual urine volume is less than 50

• The Q-tip test is an indirect measure of the urethra

• Urodynamic testing-not routinely recommended

 Treatment
• Treatment of exacerbating factors such as excess weight, chronic cough, or
constipation may improve SUI
• Pelvic muscle rehabilitation may be helpful for SUI
– Kegel exercises
–Pessaries
• Drug therapy is the mainstay of treatment for urge incontinence but is of
limited value in treating SUI.
–Antispasmodic agents
• Surgery-mainly for stress incontinence
• Procedures to support the urethra