menstrual disorders

1. ETIOLOGY,
DIAGNOSIS AND
MANAGEMENT OF
MENSTRUAL
DISODERS
DR. FATMA MRISHO

2. Outline
Introduction
Physiology of the menstrual cycle
Dysmenorrhea
Premenstrual syndrome
Amenorrhea
Abnormal uterine bleeding
References

3. MENSTRUATION
 Refers to visible manifestation of cyclic physiologic uterine
bleeding due to shedding of the endometrium following
invisible interplay of hormones mainly through hypothalamo-
pituitary ovarian axis.
 For the menstruation to occur, the axis must be actively
coordinated, endometrium must be responsive to the ovarian
hormones (estrogen and progesterone) and the outflow tract
must be patent.

4. Hypothalamus-pituitary–Ovaryax

5. Under the influence of the Hypothalamus which produces
gonadotrophin-releasing hormone,
The anterior pituitary gland secretes 2 gonadotrophins, FSH
and LH.
GnRH is released in a series of pulses about an hour apart
and the gonadotrophins like wise are secreted in a pulsatile
manner.
This is crucial to the normal pattern of the menstrual cycle.

6. FSH
Causes several graafian follicles to develop and enlarge,
one enlarges more than others.
FSH stimulates the granulosa cells and theca to secrete
estrogen.
The level of estrogen rises in the first half of the cycle and
when it reaches a certain point its production is stopped.

7. Luteinizing hormone (LH)
Receptors exist primarily on the theca cells at all stages of
the cycle and on granulosa cells after the follicle matures
under the influence of FSH and estradiol.
Stimulates androgen synthesis by the theca cells.
theca tissue produces androgens that are converted through
FSH induced aromatization to estrogen in the granulosa cells.
With enough LH receptors on granulosa cells , LH act directly
on the granulosa cells to cause lutenization and production
of progesterone.

8. Ovarian hormones:
Estrogen:
Sec sex characteristics--- female shape, breast
development and hair distribution.
Cervical mucus production,vaginal epithelium that
encourages growth of lactobacilli and promote vaginal
acidity.
Estrogen causes proliferation of uterine endometrium
and encourages fluid retention.
It inhibits FSH.

9. Progesterone
Only acts on tissues previously affected by estrogen.
Responsible for secretory changes in the
endometrial lining, Increasing tortuousity of glands
and enriching blood supply in readiness for possible
arrival of fertilised ovum.
Causes temperature rise by 0.5 degrees centigrade.
Tingling and fullness of breasts prior to menses due
to Progesterone effect.

10. DEFINITION OF NORMAL
UTERINE BLEEDING
The four parameters used to define normal
uterine bleeding are frequency, regularity, duration,
and volume.
Assessment is generally based on the patient's
bleeding pattern during the previous six months
and applies to patients who are not taking local or
systemic medications (eg, progestin-based
contraceptives with or without estrogen,
gonadotropin-releasing hormone agonists or
antagonists,etc

12. MENSTRUAL CYCLE
The normal menstrual cycle is a tightly coordinated cycle of
stimulatory and inhibitory effects that results in the release of
a single mature oocyte from a pool of hundreds of thousands
of primordial oocytes.
A variety of factors contribute to the regulation of this
process, including hormones and paracrine and autocrine
factors

13. NORMAL MENSTRUAL CYCLE

The period extending from the beginning of a menstruation
to the beginning of the next.
The first menstruation (menarche)

Once the menstruation starts, it continues cyclically at
intervals of 24–38 days.
It ceases between the age 45–55 years when menopause
sets in.

The duration of menstruation is about 3- 7 days
The amount of blood loss is estimated to be 20 to 80 mL
per cycle.

14. ……
It is divided into:
1.Ovarian cycle
-Follicular phase
-Luteal phase
2.Uterine cycle
-Proliferative phase
-Secretory phase

16. Phases of the Ovarian cycle
 The ovarian cycle is divided into two phases: follicular and
luteal.
The follicular phase begins with the onset of menses and
ends on the day before the luteinizing hormone (LH) surge.
The luteal phase begins on the day of the LH surge and ends
at the onset of the next menses.

17. Events during the menstrual cycle
Early follicular phase —is the time when the ovary is the
least hormonally active, resulting in low serum estradiol and
progesterone concentrations .
A results in a late luteal/early follicular phase increase in
gonadotropin-releasing hormone (GnRH) pulse frequency and
a subsequent increase in serum follicle-stimulating hormone
(FSH) concentrations.
 This small increase in FSH secretion appears to be required
for the recruitment of the next cohort of developing follicles.

18. ……
 Ovaries and endometrium — the ovary is quiescent in the
early follicular phase, except for the occasionally visible
resolving corpus luteum from the previous cycle.
The endometrium is relatively indistinct during menses and
then becomes a thin line once menses is complete.
Mid-follicular phase — The modest increase in follicle-
stimulating hormone (FSH) secretion in the early follicular
phase gradually stimulates folliculogenesis and estradiol
production, leading to progressive growth of the cohort of
follicles selected that cycle

19. ……
The increase in estradiol production feeds back negatively on
the hypothalamus and pituitary, resulting in suppression of
mean serum FSH and luteinizing hormone (LH) concentrations.
Ovarian and endometrial changes — Within approximately
seven days from the onset of menses, several 9 to 10 mm
antral follicles are visible on ovarian ultrasonography.
The rising serum estradiol concentrations result in
proliferation of the uterine endometrium, which becomes
thicker, with an increase in the number of glands

20. ……...
Late follicular phase — The serum concentrations of
estradiol and inhibin A increase daily during the week before
ovulation due to release from the growing follicle. Serum
follicle-stimulating hormone (FSH) and luteinizing hormone
(LH) concentrations are falling at this time due to negative
feedback effects of estradiol and perhaps other hormones
released from the ovary
Ovarian, endometrial, and cervical mucus changes — By
the late follicular phase, a single dominant follicle has been
selected, while the rest of the growing cohort of follicles
gradually stop developing and undergo atresia.

21. ……
Rising serum estradiol concentrations result in gradual
thickening of the uterine endometrium and an increase in the
amount of the cervical mucus.
Midcycle surge and ovulation — Serum estradiol
concentrations continue to rise until they reach a peak
approximately one day before ovulation. Then, a unique
neuroendocrine phenomenon occurs: the midcycle surge.
The surge represents a switch from negative feedback control
of LH secretion by ovarian hormones to a sudden positive
feedback effect, resulting in a 10-fold increase in serum LH
concentrations and a smaller rise in serum FSH.

22.  Ovarian changes — The LH surge initiates substantial
changes in the ovary. The oocyte in the dominant follicle
completes its first meiotic division.
 The oocyte is released from the follicle at the surface of the
ovary approximately 36 hours after the LH surge.
There is a close relation of follicular rupture and oocyte
release to the LH surge; as a result, measurements of serum or
urine LH can be used to estimate the time of ovulation.
Luteal phase — Progesterone secretion from the corpus
luteum results in gradually rising progesterone concentrations
in the middle to late luteal phase. This leads to progressive
slowing of LH .

23. …….
In the late luteal phase, a decrease in LH secretion results in a gradual
fall in progesterone and estradiol production by the corpus luteum in
the absence of a fertilized oocyte.
If, however, the oocyte becomes fertilized, it implants in the
endometrium several days after ovulation.
The early embryo begins to make chorionic gonadotropin, which
maintains the corpus luteum and progesterone production.
Endometrial changes — The decline in estradiol and progesterone
release from the resolving corpus luteum results sequentially in the
loss of endometrial blood supply, endometrial sloughing, and the onset
of menses approximately 14 days after the LH surge.
Menses is a relatively imprecise marker of hormonal events in the
menstrual cycle

25. DYSMENORRHEA
Defined as painful menstruation of sufficient magnitude that interferes
with day to day activities.
Dysmenorrhea can be primary or secondary.
Primary or idiopathic dysmenorrhea is menstrual pain without
identifiable pelvic pathology.
Secondary dysmenorrhea is painful menstruation in the presence of
pelvic pathology.

26. Primary Dysmenorrhea
No obvious organic cause, but it may be explained by the following;

27. Primary Dysmenorrhea
Role of prostaglandin
Uterine myometrial hyperactivity and
dysperistalsis
Imbalance in the autonomic nervous
control of uterine muscle
Psychosomatic factors such as stress,
tension

28. Diagnosis
Thorough history taking;
 Menstrual hx
 CFs; timing of pain, Associated symptoms (N&V, fatigue, diarrhea,
headache, tachycardia)
 Sexual hx
On physical examination and pelvic examination there are no obvious
abnormalities
 Laboratory testing
 imaging i.e. pelvic USS
Laparoscopy

29. Treatment
Non-Pharmacological
Psychotherapy (Explanation and assurance)
Heat pack and exercise
Pharmacological
NSAIDs such as ibuprofen
Prostaglandin synthetase inhibitors such as
indomethacin
Oral contraceptives (combined estrogen and
progesterone).

30. Secondary Dysmenorrhea
Causes
 endometriosis
 adenomyosis
cervical stenosis
pelvic adhesions
PID
uterine fibroids
 uterine polyps

31. Diagnosis
 Hx of pain (the pain is dull, situated in the back and front,
non radiating)
 It usually appears 3–5 days prior to the period, relieves
with the start of bleeding, response to NSAIDS?
No systemic discomfort however there are symptoms of
associated pelvic pathology.
Menstrual hx, Impact of dysmenorrhea on daily
activities,

32. Dx cont.
On pelvic examination
External genitalia; rashes, swelling, discharge
cervix; for mass and signs of infection
Bimanual examination; for cervical tenderness, uterine or
adnexa tenderness or masses.
Laboratory Testing
 FBP
 Gonococcal and chlamydial cultures
 HCG to exclude ectopic pregnancy
 Urinalysis to exclude UTI
Imaging
 Abdominal or Trans vaginal US - detecting adnexal masses

33. Management
Treat the underlying organic cause
Preventive measures(Life style modification) - physical
exercise, cessation of smoking.

34. PREMENSTRUAL SYNDROME(PMS)
PMS- presence of both physical and behavioral symptoms
that occur repetitively in the second half of the menstrual cycle
and interfere with some aspects of the woman’s life.
resolve after menstruation ceases.
It occurs in almost all women of reproductive age.
 The symptoms appears during the last 7–10 days of the
menstrual cycle

35. Etiology
The cause is unknown to explain all symptomatology.
Changes in levels of estrogen and progesterone.
Neuroendocrine factors including serotonin and
endorphins and GABA
Psychosocial and psychological factors
Others including TRH, prolactin, renin, aldosterone,
prostaglandin.

36. Symptoms

37. Diagnosis
Based on symptom chart to be filled by the patient so as to
determine exact point at which symptoms arise and when they
resolve.
Not related to any organic lesion
Occurring regularly at luteal phase of menstruation
Interferes with normal life style
There should be symptoms free period

38. Management
Non pharmacological management
 Life modification- Stress reduction, alcohol& caffeine
reduction, avoidance of salty diet, exercise
Psychotherapy by reassurance and cognitive behavioral therapy.
pharmacological management
Anxiolytic agents i.e. Alprazolam 0.25 mg, bid
Selective Serotonin Reuptake Inhibitors (SSRI) and
Noradrenaline Reuptake Inhibitors (SNRI).
Oral contraceptives
Bromocriptine
spironolactone

39. AMENORRHEA
Transient, intermittent or permanent absence of menses
resulting from dysfunction of the hypothalamus, pituitary, ovaries,
uterus or vagina
Its classified as primary amenorrhea and secondary amenorrhea.
Primary amenorrhea, Absence of menstruation by the age of
14years in the absence of secondary sexual characteristics or by
the age of 16years if they are present.
Secondary amenorrhea, cessation of menstruation for more than
3 cycle intervals or six months in women who were previously
menstruating.

40. CAUSES OF PRIMARYAMENORRHEA
Obstructed outflow tract; imperforate hymen, transverse
vaginal septum, absence uterus and asherman’s syndrome,
mayer-rokitansky-kuster-hauser syndrome.
Ovarian dysfunction; anovulation, turners syndrome and
menopause.
Adrenal dysfunction; congenital adrenal hyperplasia,
Cushing disease
Thyroid dysfunction; hyperthyroidism
Hypothalamus-Pituitary dysfunction: hyperprolactinemia,
contraceptive agents, psychotropic drugs, Sheehan’s
syndrome, Cushing’s, anorexia nervosa, athletes, severe
stress, Kallman’s syndrome, injury, prior infection

41. DIAGNOSIS
Inquire about the duration of amenorrhea, pattern before
secondary amenorrhea, contraceptive use and sexual activity
Headache, visual disturbance and galactorrhea.
Development of secondary sexual characteristics like breast
enlargement and hair distribution
Stigmata of chromosomal anomalies
Life style; exercise, diet, stress
Past medical history
Vaginal examination

42. Investigation
Urinary pregnancy test
Progesterone challenge test; give medroxyprogesterone
10mg twice daily for 10 days.
Serum HCG, FSH, TSH, PRL, estrogen, T4 and LH
Karyotype
Reproductive hormone profile; SHBG, testosterone,
DHEAS, hydroxyprogesterone.
Pelvic USS and/or MRI

43. TREATMENT
Treatment depends on the cause
Psychological counselling
Consult the expert on sub specialization
Hormonal replacement therapy
Surgical reconstruction

44. ABNORMAL UTERINE BLEEDING (AUB)
AUB is a term that describes any symptomatic variation from
normal menstruation, it includes intermenstrual bleeding,
prolonged bleeding and extremely heavy bleeding.
It is characterized by variations from normal frequency,
regularity, duration and volume of menses.

45. AUB Classification
Etiological classification PALM COEIN based on
Structural (PALM) and Non-Structural(COEIN) related
etiologies of abnormal uterine bleeding was introduced
by FIGO in 2011.
This is specific for abnormal uterine bleeding in
nonpregnant reproductive age women

46. PALM- COEIN

47. AUB-P, Polyps
Are overgrowths of endometrial glands that typically protrude
unto the uterine cavity.

Sometimes can be long enough to protrude through cervix.
Symptoms
Abnormal uterine bleeding
Post menopausal bleeding
Risk factors
Tamoxifen therapy
Obesity
Hypertension, Diabetes
Increased patient age
Hormone replacement therapy

48. Polyps cont.
Diagnosis
 Transvaginal ultrasound
 Hysteroscopy
Treatment
Watchful waiting; Asymptomatic small polyps may regress
spontaneously.
Symptomatic polyps must be removed
Progesterone hormonal therapy
Polypectomy

49. AUB-A, Adenomyosis
Endometrial glands and stroma invade the
myometrium.
30-40years
Symptoms
• Heavy prolonged menstrual bleeding
• Dysmenorrhea
• Chronic pelvic pain
Risk factors:
Previous c/s, D&C multiparity, estrogen effects

50. Diagnosis
Bimanual examination may reveal a large boggy uterus
Ix: Transvaginal Ultrasound
Treatment
Medical; NSAIDS, hormonal medication
(Levonorgestrel releasing IUD)
Surgical; Uterine artery embolization, hysterectomy

51. AUB-L, Leiomyoma
Most common benign pelvic tumors arising from the
smooth muscle cells of the uterus.
Can be submucosal, intramural or sub serosal
Symptoms
• Abnormal uterine bleeding
• Pelvic pressure and/or heaviness
• Urinary frequency
• Dysmenorrhea
Abdominal enlargement
•Pregnancy loss

52. Risk factors
Nulliparity
 Obesity
 Family history
 Hypertension
African-American
Diet (red meats)

53. Diagnosis

Bimanual examination may reveal large fibroid.

Ix:
Transvaginal ultrasound
Transvaginal sonohysterography
MRI
Treatment

Medical: gonadotrophin releasing hormone analogue for
3months eg

Followed by combined therapy (estrogen and progestin)

Hysteroscopic myomectomy, uterine artery embolization,
hysterectomy

54. AUB-M, Malignancy/Hyperplasia
RFs
Obesity
Prolonged anovulation
Unopposed estrogen
 Tamoxifen
Family history
 Hypertension
Diabetes.
Lynch syndrome
Cause- Endometrial Ca/hyperplasia or Uterine sarcoma

55. Diagnosis
Consider endometrial hyperplasia in any
women >45yrs or <45yrs with a Hx of obesity,
PCOS or unopposed estrogen
All women with post menopausal bleeding need
a referral for uss and biopsy
Endometrial biopsy has high overall accuracy in
diagnosing endometrial cancer when an adequate
specimen is obtained.

56. Investigations;
Endometrial biopsy
Treatment options include:
 Hysterectomy
Radiotherapy
Combined therapy

57. AUB-C, Coagulopathy
Spectrum of systemic disorders of hemostasis 20% of
AUB in adolescent.
Examples
 Von Willebrand disease (13%)
Idiopathic thrombocytopenia purpura
 Platelet dysfunctions
Leukemia
 Liver dysfunction

58. Diagnosis
Hx
P/E
Investigation
FBP (platelets, Hb)
Bleeding indices; prothrombin time, and partial
thromboplastin time.
Depending on the results of the initial tests,
specific tests for von Willebrand disease or other
coagulopathies may be indicated.

59. Treatment options
Antifibrinolytic agent (e.g. Tranexamic acid)
Endometrial ablation

60. AUB-O, Ovulatory Disorders
When a woman is not ovulating or has infrequent ovulation. Most
often seen in adolescent and perimenopausal women.
This causes luteal-out of phase events (LOOP) i.e. Low luteal
phase progesterone and high estradiol, disruption in ovulation.
Symptoms
Irregular and heavy bleeding patterns
Amenorrhea
Possible causes
 Hypo/hyperthyroidism & hyperprolactinemia
 Polycystic ovary syndrome (PCOS)
 Hypothalamic dysfunction( Stress, exercise & Weight loss)

61. Diagnostic approach
 UPT, FBP
Endocrine tests i.e. Thyroid function test,
Prolactin level, Androgens level, FSH, LH etc.
Treatment options include:
 Oral Progestin therapy or LNG IUD
Surgery- Endometrial ablation

62. AUB-E, Endometrial Disorders
Patient have normal ovulatory cycles and structurally normal
uterine cavity may have associated breast tenderness, abdominal
bloating and pelvic pain.
Diagnosis is made in patient with heavy menstrual bleeding and
no other identified abnormalities. (Diagnosis of exclusion)
Treatment options include:
Medical therapy; gonadal steroids,
surgical therapy; endometrial ablation, hysterectomy

63. AUB-I, Iatrogenic
Examples
Anticoagulants
IUDs
Breakthrough bleeding due to use of COC, erratic use of pills
or contraceptive steroids.
Drugs causing hyperprolactinemia. e.g. haloperidol,
Fluphenazine..
Diagnosis
proper history taking
Treatment
Treat the underlying cause

64. AUB-N ,Not otherwise Classified
The causes are either poorly defined , inadequately
examined or are extremely rare.
Not yet classified

65. References
1. Text book of gynecology by D.C Dutta’s
2. Obstetric and gynecological disorders MNH guideline
3. Up-to-date
4. Medscape

66. THANK YOU