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Reproductive System I > Menarche, Puberty, and Menstrual Disorders Lecture (Dr. Moulton) > Flashcards

Menarche, Puberty, and Menstrual Disorders Lecture (Dr. Moulton) Flashcards

1
Q

Menstrual Cycle

A
  • Menstrual Cycle occur with the MATURATION of the Hypothalamic- Pituitary- Ovarian Axis
  • Gonadotropin- Releasing Hormone (GnRH) from the Hypothalamus stimulate Follicle-Stimulating Hormones FSH and Luteinizing Hormone (LH) from the Anterior Pituitary, which stimulates ESTROGEN and PROGESTERONE from the Ovarian Follicle
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2
Q

Hypothalamic- Pituitary axis

A

PITUITARY GLAND
• Lies below the hypothalamus at the base of the brain within a bony cavity (SELLA TURCICA) & is separated from the cranial cavity by a condensation of dura matter covering the sella turcica (DIAPHRAGM SELLA)

• Is divided into 2 portions:
1.) ANTERIOR LOBE
• Can produce 6 hormones FSH,LH,TSH, Prolactin, Growth Hormone and Adrenocorticotropic Hormone (ACTH)
• FSH & LH are synthesized and stored in cells called Gonadotrophs

2.) POSTERIOR LOBE
• Vasopressin & Oxytocin

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3
Q

Hypothalamic-pituitary axis GONADOTROPIN SECTRETORY PATTERNS

A

• Normal ovulatory cycle can be divided into:
1) Follicular phase
• Begins with the onset of Menstruation and Culminates in the PREOVULATORY SURGE of LH

2) Luteal phase
• Begins with the onset of the Preovulatory LH surge and Ends with the first day of MENSES

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4
Q

Hypothalamic-pituitary axis GONADOTROPIN SECTRETORY PATTERNS Cont

A
  • Decreasing levels of Estradiol & Progesterone from the regressing CORPUS LUTEUM of the preceding cycle INITIATE an Increase in FSH by a Negative feed back mechanism, which stimulates Follicular Growth and Estradiol Secretion.
  • A Major Characteristic of Follicular Growth and Estradiol secretion is explained by the 2 Gonadotropin (LH & FSH), 2 cell (Theca cell and Granulosa cell) theory of Ovarian Follicular Development

Theory of Ovarian Follicular Development:
• Separate Ovarian functions in the Ovarian Follicle

  • LH stimulates the THECA Cells to produce ANDROGENS (Androstenedione & Testosterone)
  • FSH stimulates the GRANULOSA cells to convert these Androgens into ESTROGENS (E1 and E2)
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5
Q

Luteal Phase

A

• TheLH & FSH are significantly SUPPRESSED through the NEGATIVE FEEDBACK effect of the elevated circulating Estradiol and Progesterone

• If conception does NOT occur
Progesterone and Estradiol level DECLINE near the END of the Luteal Phase as a result of Corpus Luteal REGRESSION

• FSH will then RISE which Initiates new Follicular Growth for the next cycle

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6
Q

Hypothalamus

A

• 5 peptides or biogenic amines that affect the Reproductive Cycle have been Isolated from the hypothalamus:
1) Gonadotropin-Releasing Hormone (GnRH)

2) Thyrotropin-Releasing Hormone (TRH)
3) Somatotropin Release Inhibiting Factor (SRIF)or Somatostatin
4) Corticotropin-Releasing Factor(CRF)
5) Prolactin Release-Inhibiting Factor(PIF)

• All exert specific effects on the hormonal secretion of the Anterior Pituitary Gland.

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7
Q

Gonadotropin- Releasing Hormone (GnRH)

A
  • Decapeptide synthesized in the Arcuate Nucleus
  • Responsible for the Synthesis & Release of LH&FSH
  • Both LH & FSH are present in 2 different forms (releasable & storage) within the Pituitary Gonadotrophs
  • GnRH reaches the Anterior Pituitary & Stimulates the Synthesis & Release of FSH & LH into the circulation
  • ESTRADIOL appears to Enhance the Hypothalamic Release of GnRH and INDUCE the midcycle LH SURGE
  • Gonadotropins have an INHIBITORY effect on GnRH release
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8
Q

Ovarian Cycle Estrogens

A

A) ESTROGEN
• During early follicular development ESTRADIOL levels are LOW

• Approximately 1 week before ovulation, Estradiol levels begin to INCREASE

B) Estrogen levels generally reach a Maximum 1 day Before the Midcycle LH PEAK
• After the Peak and Before ovulation there is a marked & precipitous FALL.

• During the Luteal Phase, Estradiol rises to a maximum 5 to 7 days after Ovulation & returns to baseline before Menstruation.

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9
Q

Ovarian Cycle Progestins

A
  • During follicular development the ovary secretes only a very small amount of Progesterone
  • The bulk of the Progesterone comes from the PERIPHERAL CONVERSION of the Adrenal Pregnenolone & Pregnenolone Sulfate.
  • Prior to Ovulation the Enraptured Luteinizing GRAAFIAN Follicle begins to produce INCREASING amounts of Progesterone.
  • Secretion of Progesterone by the Corpus Luteum reaches a maximum 5-7 days after Ovulation & returns to Baseline before Menstruation.
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10
Q

Ovarian Cycle Follicular Development

A
  • Primordial follicles undergo sequential Development, Differentiation, & Maturation until a Mature Graafian follicle is produced.
  • The follicle then rupture, releasing an Ovum
  • Subsequent Luteinization of the ruptured follicle produces the CORPUS LUTEUM.

• At about 8 to 10 weeks of fetal development, oocytes
become surrounded by precursor GRANULOSA Cells.

• This Oocyte-Granulosa cell complex is called a PRIMORDIAL FOLLICLE

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11
Q

Ovarian Cycle Follicular Development Cont

A
  • In the Adult Ovary, a Graafian follicle forms
  • The Innermost 3 to 4 layers of multiplying Granulosa cells become CUBOIDAL and Adherent to the Ovum this is known as the CUMULUS OOPHORUS!!!!!
  • A fluid filled ANTRUM forms among the Granulosa cells.
  • Antrum Enlarges & the Centrally located Primary Oocyte MIGRATES to the wall of the follicle.
  • The Innermost layer of the GRANULOSA Cells of the cumulus become Elongated and form the CORONA RADIATA.
  • The Corona Radiata is released with the Oocyte at Ovulation.
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12
Q

Ovarian Cycle Ovulation

A
  • Preovulatory LH SURGE initiates a sequence of biochemical and structural changes that result in OVULATION.
  • Cells on the follicular wall surface degenerate and a STIGMA forms, the Follicular Basement Membrane BULGES through the Stigma.
  • When this Ruptures the Oocyte is EXPELLED into the Peritoneal Cavity and OVULATION has occurred.
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13
Q

Ovarian cycle Lutenization & Corpus Luteum function

A
  • After ovulation the Granulosa Cells of the ruptured follicle undergo LUTEINIZATION.
  • The Lutenized Granulosa Cells, Theca cells, capillaries and connective tissue form the CORPUS LUTEUM.
  • Corpus Luteum produces copious amounts of PROGESTERONE & some Estradiol
  • Normal functional life span of Corpus Luteum is 9-10 days
  • If pregnancy does NOT occur, Menses ensues and the Corpus Luteum is gradually REPLACED by an avascular scar called CORPUS ALBICANS

*****During each cycle, many follicles develop but usually only 1 continues to Differentiation and Maturation and Ovulates

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14
Q

Full Cycle Summary

A

1) Corpus Luteum dies, Estrogen and Progesterone levels FALL
2) Pituitary responds to falling Estrogen and Progesterone by Increasing FSH Secretion
3) FASH recruits a Cohort of Large Antral Follicles to enter Rapid Growth Phase. Follicles SECRETE Low amounts of Estrogen and INHIBIT
4) Estrogen and Inhibit NEGATIVELY Feed Back on FSH
5) Declining FSH levels progressively cause Atresia of all but 1 Follicle - leading to Selection of Dominant Follicle, which produced HIGH levels of Estrogen
6) High Estrogen has a POSITIVE FEEDBACK on Gonadotropes - LH (and some FSH) SURGES!!!!
7) LH Surge induces MEIOTIC Maturation, Ovulation, and Luteinization. The Corpus Luteum produces HIGH P, along with E and INHIBIT
8) High P, E, and INHIBIT NEGATIVELY Feed Back on LH and FSH, returning them to BASAL LEVELS
9) The Corpus Luteum progressively becomes less Sensitive to Basal LH - DIES if levels of LH-like activity (Ex hCG) DO NOT Increase

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15
Q

Histopathology of the Endometrium

A
  • Endometrium is responsive to circulating Progestins, Androgens, and Estrogens.
  • The Endometrium is divided into 2 zones:

1) Outer portion or FUNCTIONALIS:
a) This layer undergoes Cyclic Changes in Morphology during the Menstrual Cycle and is sloughed off at Menstruation.
b) Contains SPIRAL ARTERIS

2) Inner portion or BASALIS
a) This layer remains relatively unchanged during each cycle & after menstruation Provides Stem Cells for the renewal of the Functionalis
b) Contains Basal Arteries

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16
Q

Histophysiology of the endometrium

A

• The Cyclic Changes in histophysiology of the Endometrium can be divided into 3 stages:

1) Menstrual Phase
2) Proliferative or Estrogenic Phase
3) Secretory or Progestational Phase

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17
Q

Menstrual Phase

A
  • Is the only portion of the cycle that is visualized externally
  • The first day of menstruation is known as Cycle day 1

• During this Phase there is:
a) Disruption and disintegration of the Endometrial Glands & Stroma, Leukocyte Infiltration & Red Blood Cell Extravasation

b) Sloughing of the Functionalis Layer & Compression of the Basalis layer.

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18
Q

Proliferative phase

A
  • Characterized by Endometrial Growth secondary to Estrogenic Stimulation.
  • INCREASE in the Length of the Spiral Arteries & Numerous Mitoses can be seen in these tissues
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19
Q

Secretory Phase

A
  • Following Ovulation, Progesterone secretion by the Corpus Luteum stimulate the GLANDULAR CELLS to Secrete Mucus, Glycogen and other substances.
  • Glands become Tortuous & Lumens are Dilated and filled with these substances.
  • STROMA becomes Edematous
  • Mitosis are Rare
  • Spiral Arteries continue to extend into superficial layer of the endometrium and become CONVOLUTED
  • Endometrial lining reaches it’s maximal THICKNESS

• If conception does NOT occur by day 23:
a) The Corpus Luteum begins to REGRESS, secretion of Progesterone & Estradiol DECLINES, and the Endometrium undergoes ONVOLUTION.

• 1 day prior to the onset of Menstruation marked CONSTRICTION of the Spiral Arteries occurs resulting in ISCHEMIA of the Endometrium, leukocytes infiltration and RBC Extravasation.
a) The resulting NECROSIS causes sloughing of the Endometrium resulting in MENSTRUATION

• Thus the menstrual cycle is a TERMINAL Event of a Physiologic process that enables the uterus to be prepared to receive another Conceptus.

• Intact coagulation pathway is important in REGULATING Menstruation
A) Menstruation disrupts Blood Vessels, but with normal hemostasis, the injured vessels are rapidly Repaired
- Restoration of Blood Vessels require successful interaction of Platelets & Clotting Factors.
- Medications, such as Warfarin, Aspirin, Clopidogrel, can IMPAIR the Coagulation system & be associated with Heavy Bleeding.

20
Q

Initial reproductive health visit

A
  • Should occur between the ages of 13-15 years
  • Provides an opportunity to start Patient-Physician Relationship, build trust, & counsel pt’s and parents regarding healthy behavior.
  • Primary goal of this visit is to provide Preventative Health Care Services, including Educational information and guidance, rather then problem- focused care.
  • Age appropriate discussion regarding Reproductive Health-related topics

1) Pubertal development
2) Normal menses
3) Timing of Routine gynecology visits
4) Sexually transmitted infections (STI’s)
5) Pregnancy prevention
6) Sexual orientation & gender identity
7) Acquaintance rape prevention

• A general exam, Visual Breast Exam, & external pelvic exam may be Indicated.

21
Q

Initial visit

A

• Internal exam is not routinely performed unless indicated
- ACOG recommends first Pap test at the age of 21years!!!!!!!!!!!!

  • Review-Medical history, Family medical history, Immunizations (appropriate vaccinations should be provided)
  • Conversation regarding normal pubertal Development and Menstruation is VITAL!!!!!
  • It is important to Educate pt’s and parents regarding Expectations for normal menstrual variation.
22
Q

Menarche

A

• Median age of menarche is 12.43years

  • 10% of female menstruate at 11.11years
  • 90% are menstruating by 13.75 years

• Occurs within 2-3 years after THELARCHE (breast budding) at Tanner stage IV, RARE before Tanner stage III!!!!!!!!!

• By the age of 15 years old 98% of females will have had MENARCHE!!!!!!
- PRIMARY AMENORRHEA is defined as ABSENCE of menarche by age 13 years without Secondary Sexual Development OR by the age of 15 with Secondary Sexual Development!!!!!!!!!!!!!!!!!!!!!

23
Q

Cycle length & Ovulation

A
  • Menstrual cycles are often IRREGULAR throughout Adolescents, especially from first to the second cycle.
  • World Health Organization’s international & multicenter study of 3,703 girls
  • Median length of first cycle after Menarche was 34 days
  • Most females bled 2-7 days during FIRST Menstruation
  • Most normal cycles range from 21 to 45 days even in first Gynecologic year.
  • By the third year after Menarche approximately 80% of Menstrual Cycles are 21-35 days long, as is typical of adults.
24
Q

Prolonged Intervals between menstrual cycles

A

• SECONDARY AMENORRHEA is defined as the absence of Menstruation x 6 months

  • It is rare for girls & adolescents to remain Amenorrheic for more than 3 months!!!!!!!
    a) If > then 90 days further workup is indicated
    • Check urine or serum B-HCG to rule out Pregnancy!!!!!!!!

• IRREGULAR Cycles may be associated with many conditions

25
Q

Causes of Menstrual Irregulatiry

A

1) Pregnancy

2) Endocrine Causes:
- Poorly controlled Diabetes
- Mellitus Polycystic Ovary syndrome
- Cushing’s Disease
- Thyroid dysfunction
- Premature ovarian failure
- Late- onset Congenital Adrenal Hyperplasia

3) AQUIRED CONDITIONS:
- Stress-related hypothalamic dysfunction
- Medications
- Exercise- Induced Amenorrhea
- Eating Disorders (anorexia & bulimia)

4) TUMORS:
- Ovarian tumors
- Adrenal tumors
- Prolactinomas

26
Q

Excessive menstrual flow

A

• First Menses is usually reported as MEDIUM flow.

• Mean blood loss per menstrual period is 30cc!!!!!
- Most report changing a pad 3 to 6 times a day

• Greater then 80cc has been associated with ANEMIA
- Changing a pad q 1-2 hrs is considered EXCESSIVE especially if bleeding is lasting > 7 days.

27
Q

Primary Amenorrhea

A
  • No menstruation has occurred by the age of 13 WITHOUT Secondary Sexual development OR by the age of 15 WITH Secondary Sexual Development
28
Q

Secondary Amenorrhea

A
  • the Absence of Menses for 6months or more
29
Q

Polymenorrhea

A
  • Abnormally frequent Menses at intervals at
30
Q

Menorrhagia (hypermenorrhea)

A
  • Excessive and/or prolonged Menses (>80mL and > 7 days) occurring at Regular Intervals
31
Q

Metrorrhagia

A
  • Irregular episodes of Uterine Bleeding
32
Q

Menometrorrhagia

A
  • Heavy and Irregular uterine bleeding
33
Q

Intermenstrual bleeding

A
  • Scant bleeding at Ovulation for 1 or 2 days
34
Q

Oligomenorrhea

A
  • Menstrual Cycles at > 35 day cycles
35
Q

Dysfunctional Uterine Bleeding (DUB)

A

• DUB is DEFINED as abnormal Uterine bleeding that CANNOT be attributed to:
1) MEDICATIONS: Exogenous Estrogen, ASA, Heparin, Tamoxifen, IUD

2) BLOOD DYSCARASIAS: Thrombocytopenia, Leukemia, Autoimmune Disease,
Von Willebrand’s

3) SYSTEMIC DISEASE: Thyroid Disease, Hepatic Disease (impaired metabolism of estrogen), Renal Disease (hyperprolactinemia)
4) TRAUMA: Lacerations, Abrasions, Foreign body
5) ORGANIC CONDITIONS: Pregnancy, Fibroids, Polyps, Adenomyosis, Cervical or Uterine Cancer

  • Usually caused by ABERRATIONS in the H-P-O axis resulting in ANOVULATION!!!!!!
  • Most DUB occurs around the years of Menarche (11 to 14 years) or Perimenopause (45 to 50 years old)
36
Q

PALM- Co Classification System for Abnormal Bleeding in Reproductive-Aged Woman

A

PALM: STRUCTURAL CAUSES
1) Poly (AUB-P)

2) Adenomyosis (AUB-A)

3) Leiomyoma (AUB-L)
- Submucosal Myoma (AUB-L sm) or Other Myoma (AUB-L o)

4) Malignancy and Hyperplasia (AUB-M)

COEIN: NONSTRUCTURAL CAUSES
1) Coagulalopathy (AUB-C)

2) Ovulatory Dysfunction (AUB-O)
3) Endometrial (AUB-E)
4) Iatrogenic (AUB-I)
5) Not yet classified (AUB -N)

37
Q

Adenomyosis (AUB-A)

A
  • Histologic illustration of Adenomyosis causing the ENLARGEMENT of the Uterus
  • A HYPERPLASTIC Nodule of Myometrium is seen. Note the Endometrial Glands and STROMA
38
Q

COEIN- Nonstructural Causes

A

1) Coagulopathies (AUB-C)
• Associated with heavy flow
- i.e. Von Willebrand disease

2) Ovulatory Dysfunction(AUB-O)
• Associated with unpredictable menses with variable flow.
- i.e. polycystic ovarian syndrome

3) Endometrial Causes (AUB-E)
- i.e. infection

4) Iatrogenic (AUB-I)
- IUD, IUS, exogenous hormones

5) NotYetClassified(AUB-N)
• Reserved for entities that are poorly defined &/or not well examined
- i.e. Arteriovenous Malformation

39
Q

Diagnostic evaluation of Abnormal uterine bleeding

A 
1) MEDICAL HISTORY:
• Age of Menarche & Menopause
• Menstrual bleeding patterns
• Severity of bleeding (clots or flooding)
• Pain (severity & treatment)
• Medical conditions
• Surgical history
• Use of medications
• Symptoms & Signs of possible hemostatic disorders
2) PHYSICAL EXAM:
• General exam
• Pelvic exam
• External
• Speculum with Pap if needed 
• Bimanual
3) LABORATORY TESTS
• Pregnancy test (blood or Urine)
• CBC
• Targeted screening for bleeding disorders
- Von Willebrands profile
- PT and PTT
• TSH
• Chlamydia trachoma's
4) AVAILABLE DIAGNOSTIC OR IMAGING TESTS (When Indicated)
• Transvaginal Ultrasonography
• Saline Infusion Sonohysterography
• Magnetic Resonance Imaging
• Hysteroscopy

5) AVAILABLE TISSUE SAMPLING METHODS (When Indicated)
• Office Endometrial Biopsy
• Hysteroscopy directed endometrial sampling

40
Q

Puberty

A

1) Encompasses the development of secondary sexual characteristics & the acquisition of reproductive capability.

2) Usually occurs between 10-16 y/o ( mean is 12.4 )
• Onset of puberty is determined primarily by:
A) Genetic factors including race
- African American and Hispanic girls usually begin puberty EARLIER

B) Geographic location
- Girls that live in Metropolitan areas, at Altitudes NEAR SEA level begin puberty EALIER

C) Nutritional status

  • Obese children have EARLIER onset of Puberty
  • Malnourished, chronically ill w/ weight loss will have a LATER onset of menses
  • Invariant mean weight of 48kg (106lbs) is Essential to START MENARCHE
41
Q

Fetal/ Newborn and Childhood Period

A
  • Female infant acquires the lifetime peak number of oocytes of 6-7 million by Mid-Gestation (16-20 weeks)
  • Hypothalamic-Pituitary-Ovarian (H-P-O) axis is SUPPRESSED between the ages of 4-10 years old
  • The Hypothalamic–Pituitary System regulating gonadotropin release is termed the GONADOSTAT.

• LOW levels of Gonadotropins & Sex steroids during this Prepubertal period are a function of 2 mechanisms:
1) Gonadostat sensitivity to the NEGATIVE FEEDBACK of low circulating Estradiol

2) Intrinsic Central Nervous System INHIBITION of the Hypothalamic Gonadotropin-Releasing Hormone (GnRH) Secretion

42
Q

Late childhood

A
  • Between the ages of 8-11, there is an INCREASE serum concentrations of Dehydroepiandrosterone (DHEA), a Dehydroepiandrosterone Sulfate (DHEA-S), & Androstenedione
  • In general, Adrenal Androgen production and differentiation by the ZONA RETICULARIS of the Adrenal Cortex are the INITIAL Endocrine CHANGES associated w/ Puberty.
  • Rise in Adrenal Androgens causes GROWTH of Axillary and Pubic Hair (adrenarche or pubarche)
43
Q

Onset of Puberty

A

• Around 11 years of age
- There is a Gradual LOSS of sensitivity by the Gonadostat to the NEGATIVE FEEDBACK of Sex Steroids. In combination w/ the INTRINSIC LOSS of Central Nervous system INHIBITION of Hypothalamic GnRH release

  • Sleep-associated INCREASES in GnRH secretion Occur and gradually shift into adult type secretory patterns.
  • Increase in GnRH promotes Ovarian Follicular Maturation and sex steroid Production, which leads to the Development of SECONDARY Sexual Characteristics.
  • By mid to late Puberty, the POSITIVE-FEEDBACK Mechanism of Estradiol on LH release from the Anterior Pituitary gland is COMPLETE and Ovulatory Cycles are ESTABLISHED.
44
Q

Stages of Normal Pubertal Development

A

A) THELARCHE (breast development)
• First Physical Sign of Puberty
• Unilateral Development & slight tenderness in first 6months is not Uncommon
• Requires ESTROGEN

B) PUBARCHE/ ADRENARCHE (Pubic Hair/Axillary Hair Development)
• Requires ANDROGENS

C) MAXIMAL GROWTH OR PEAK HEIGH VELOCITY
• Occurs 2 years EARLIER in Girls
• Occurs about 1 year before onset of Menses

D) MENARCHE (onset of menses)
• Requires Pulsatile GnRH from the Hypothalamus, FSH and LH from the Pituitary, Estrogen and Progesterone from the Ovaries, normal outflow tract

45
Q

Tanner Staging

Breast Development

A
  • Stages of breast development as defined by Marshall and Tanner.

STAGE 1: Preadolescent; elevation of papilla only.

STAGE 2: Breast BUD stage; Elevation of Breast and Papilla as a small mound with enlargement of the Areolar region.

STAGE 3: Further Enlargement of Breast and Areola WITHOUT separation of their contours.

STAGE 4: PROJECTION of Areola and Papilla to form a SECONDARY MOUND above the level of the breast.

STAGE 5: MATURE STAGE; Projection of papilla only, resulting from recession of the areola to the general contour of the breast.

46
Q

Tanner Staging

Pubic Hair

A

STAGE 1: Preadolescent; ABSENCE of Pubic Hair.

STAGE 2: SPARSE Hair along the Labia; hair downy with slight pigment.

STAGE 3: Hair SPREADS SPARSELY over the junction of the pubes; hair is darker and coarser.

STAGE 4: ADULT-type HAIR; there is NO spread to the medial surface of the thighs.

STAGE 5: ADULT-type HAIR with SPREAD to the Medial Thighs assuming an INVERTED Triangle pattern.

Reproductive System I (18 decks)

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