MENSTRUAL CYCLE PHASES
The menstrual cycle is a hormonally regulated process that prepares the uterus for potential
pregnancy. It is divided into four coordinated phases controlled by the
hypothalamic–pituitary–ovarian axis.
➢ Normal Cycle:25-35days Flow:4-5 Days Blood Loss:50-60ml
HORMONAL CONTROL
● GnRH (hypothalamus) → stimulates pituitary
● FSH & LH (pituitary) → stimulate ovaries
● Estrogen & Progesterone (ovaries) → act on endometrium and provide feedback
control
MENSTRUAL PHASE
Shedding of the endometrial lining due to withdrawal of estrogen and progesterone when
pregnancy does not occur.
Pathophysiology
● Corpus luteum regresses
● ↓ Estrogen and progesterone (fall rapidly)
● Endometrial blood vessels constrict → tissue breakdown and bleeding
Clinical Manifestations
● Vaginal bleeding
● Cramping (↑ prostaglandins)
● Fatigue, headache
PROLIFERATIVE PHASE
Phase in which estrogen stimulates regrowth and thickening of the endometrium.
Pathophysiology
● FSH stimulates ovarian follicle development
● Estrogen (steady increase) causes endometrial proliferation
○ Endometrium thickens and becomes more vascular
Key Event: Rising estrogen triggers LH surge → ovulation
, Secretory Phase
➢ Timing: Around Day 14
Release of a mature ovum from the ovary into the fallopian tube.
Pathophysiology
● LH low and Progesterone increasing
● Mature egg releases
● Ovum available for fertilization for ~24 hours
LUTEAL PHASE
Phase in which progesterone prepares the endometrium for implantation of a fertilized ovum.
Pathophysiology
● Corpus luteum forms and secretes progesterone
● Uterine lining thickens
● Endometrium becomes thick, vascular, and nutrient-rich
● If no pregnancy → corpus luteum degenerates → hormone levels fall → menstruation
begins
PERIMENOPAUSE & MENOPAUSE
Perimenopause is the transitional period leading up to menopause, characterized by fluctuating
and declining ovarian hormone production.
Menopause is defined as the permanent cessation of menstruation for 12 consecutive months
due to loss of ovarian follicular function.
Pathophysiology
● Progressive depletion of ovarian follicles
● Decreased estrogen and progesterone production
● Increased FSH and LH due to loss of negative feedback
Clinical Manifestations
● Vasomotor: hot flashes, night sweats
● Genitourinary: vaginal dryness, dyspareunia, urinary urgency, recurrent UTIs
● Neuropsychological: mood swings, anxiety, depression, sleep disturbances, memory
change
● Musculoskeletal: decreased bone density, joint pain
● Cardiovascular: increased risk of coronary artery disease
,Management
● Hormone therapy (estrogen ± progesterone if uterus present) for moderate to severe
symptoms
● Nonhormonal therapy: SSRIs, SNRIs, gabapentin, lifestyle modification
● Bone protection: calcium, vitamin D, weight-bearing exercise
● Cardiovascular risk reduction: smoking cessation, BP and lipid management
● Hot Flashes:vitamin b6, vitamin e, black cohash, ginseng, soy
Education
● Frequent sex maintins vaginal elasticity (use lube)
● Kegal daily
● Contraceptives for 1 year
● Drink6-8 glasses of water
● Report vaginal bleeding
ECTOPIC PREGNANCY
Implantation of a fertilized ovum outside the uterine cavity, usually in fallopian tube
Pathophysiology
● Delayed or impaired transport of the fertilized ovum through the fallopian tube
● Embryo implants in a narrow, highly vascular structure
● Progressive growth → tubal rupture → internal bleeding → shock
Risk Factors
● History of PID (chlamydia, gonorrhea)
● Prior ectopic pregnancy
● Tubal surgery or scarring
● Endometriosis
● Assisted reproductive technology
● Smoking
Clinical Manifestations
● Unilateral lower abdominal or pelvic pain
● Vaginal spotting or light bleeding
● Amenorrhea or missed period
● Shoulder pain (late sign)
● Dizziness or syncope
, ● Fallopien Tube: May rupture if not treated 4-6weeks
○ High risk of death
○ Horrible pain, dizzy, fatigue, N/V, faintness
○ Late Sign: hemorrahge, pain between shoulder blades & neck, dyspnea,
shock
Diagnostic/Assement
● Positive pregnancy test + NO intrauterine pregnancy on transvaginal ultrasound
● Serial β-hCG levels (rise abnormally slowly)
○ Should double every 3 days in early pregancy
● Vaginal assessment: often not abnormal but possible clotted blood collection behind
uterus
Medical Management
● Methotrexate (if stable and early, unruptured)
○ Will cause natural miscarriage (medical abortion)
● Surgical management: depending on location and size
○ Salpingotomy-Fallopian Tubes
○ Salpingo-oophorectomy-fallopian tubes and ovary
○ Complete hysterectomy
VULVITIS
➢ Inflammation of the vulva caused by infection, irritation, allergy, or trauma.
Pathophysiology
● Disruption of vulvar skin barrier leads to local inflammation and increased sensitivity
● May be infectious (yeast, bacteria, STIs) or noninfectious (chemical/physical irritants)
Common Causes / Risk Factors
● Poor hygiene or excessive washing
● Soaps, douches, scented products
● Tight or non-breathable clothing
● Yeast or bacterial infection
● STIs
● Diabetes mellitus
The menstrual cycle is a hormonally regulated process that prepares the uterus for potential
pregnancy. It is divided into four coordinated phases controlled by the
hypothalamic–pituitary–ovarian axis.
➢ Normal Cycle:25-35days Flow:4-5 Days Blood Loss:50-60ml
HORMONAL CONTROL
● GnRH (hypothalamus) → stimulates pituitary
● FSH & LH (pituitary) → stimulate ovaries
● Estrogen & Progesterone (ovaries) → act on endometrium and provide feedback
control
MENSTRUAL PHASE
Shedding of the endometrial lining due to withdrawal of estrogen and progesterone when
pregnancy does not occur.
Pathophysiology
● Corpus luteum regresses
● ↓ Estrogen and progesterone (fall rapidly)
● Endometrial blood vessels constrict → tissue breakdown and bleeding
Clinical Manifestations
● Vaginal bleeding
● Cramping (↑ prostaglandins)
● Fatigue, headache
PROLIFERATIVE PHASE
Phase in which estrogen stimulates regrowth and thickening of the endometrium.
Pathophysiology
● FSH stimulates ovarian follicle development
● Estrogen (steady increase) causes endometrial proliferation
○ Endometrium thickens and becomes more vascular
Key Event: Rising estrogen triggers LH surge → ovulation
, Secretory Phase
➢ Timing: Around Day 14
Release of a mature ovum from the ovary into the fallopian tube.
Pathophysiology
● LH low and Progesterone increasing
● Mature egg releases
● Ovum available for fertilization for ~24 hours
LUTEAL PHASE
Phase in which progesterone prepares the endometrium for implantation of a fertilized ovum.
Pathophysiology
● Corpus luteum forms and secretes progesterone
● Uterine lining thickens
● Endometrium becomes thick, vascular, and nutrient-rich
● If no pregnancy → corpus luteum degenerates → hormone levels fall → menstruation
begins
PERIMENOPAUSE & MENOPAUSE
Perimenopause is the transitional period leading up to menopause, characterized by fluctuating
and declining ovarian hormone production.
Menopause is defined as the permanent cessation of menstruation for 12 consecutive months
due to loss of ovarian follicular function.
Pathophysiology
● Progressive depletion of ovarian follicles
● Decreased estrogen and progesterone production
● Increased FSH and LH due to loss of negative feedback
Clinical Manifestations
● Vasomotor: hot flashes, night sweats
● Genitourinary: vaginal dryness, dyspareunia, urinary urgency, recurrent UTIs
● Neuropsychological: mood swings, anxiety, depression, sleep disturbances, memory
change
● Musculoskeletal: decreased bone density, joint pain
● Cardiovascular: increased risk of coronary artery disease
,Management
● Hormone therapy (estrogen ± progesterone if uterus present) for moderate to severe
symptoms
● Nonhormonal therapy: SSRIs, SNRIs, gabapentin, lifestyle modification
● Bone protection: calcium, vitamin D, weight-bearing exercise
● Cardiovascular risk reduction: smoking cessation, BP and lipid management
● Hot Flashes:vitamin b6, vitamin e, black cohash, ginseng, soy
Education
● Frequent sex maintins vaginal elasticity (use lube)
● Kegal daily
● Contraceptives for 1 year
● Drink6-8 glasses of water
● Report vaginal bleeding
ECTOPIC PREGNANCY
Implantation of a fertilized ovum outside the uterine cavity, usually in fallopian tube
Pathophysiology
● Delayed or impaired transport of the fertilized ovum through the fallopian tube
● Embryo implants in a narrow, highly vascular structure
● Progressive growth → tubal rupture → internal bleeding → shock
Risk Factors
● History of PID (chlamydia, gonorrhea)
● Prior ectopic pregnancy
● Tubal surgery or scarring
● Endometriosis
● Assisted reproductive technology
● Smoking
Clinical Manifestations
● Unilateral lower abdominal or pelvic pain
● Vaginal spotting or light bleeding
● Amenorrhea or missed period
● Shoulder pain (late sign)
● Dizziness or syncope
, ● Fallopien Tube: May rupture if not treated 4-6weeks
○ High risk of death
○ Horrible pain, dizzy, fatigue, N/V, faintness
○ Late Sign: hemorrahge, pain between shoulder blades & neck, dyspnea,
shock
Diagnostic/Assement
● Positive pregnancy test + NO intrauterine pregnancy on transvaginal ultrasound
● Serial β-hCG levels (rise abnormally slowly)
○ Should double every 3 days in early pregancy
● Vaginal assessment: often not abnormal but possible clotted blood collection behind
uterus
Medical Management
● Methotrexate (if stable and early, unruptured)
○ Will cause natural miscarriage (medical abortion)
● Surgical management: depending on location and size
○ Salpingotomy-Fallopian Tubes
○ Salpingo-oophorectomy-fallopian tubes and ovary
○ Complete hysterectomy
VULVITIS
➢ Inflammation of the vulva caused by infection, irritation, allergy, or trauma.
Pathophysiology
● Disruption of vulvar skin barrier leads to local inflammation and increased sensitivity
● May be infectious (yeast, bacteria, STIs) or noninfectious (chemical/physical irritants)
Common Causes / Risk Factors
● Poor hygiene or excessive washing
● Soaps, douches, scented products
● Tight or non-breathable clothing
● Yeast or bacterial infection
● STIs
● Diabetes mellitus
