GYN part 2 Flashcards
AMENORRHEA
Defined as pathological absence of menstruation.
Usu czed by an endocrine dysfxn resulting in anovulation
May also be caused by genital anatomic AbN (ovulatory amenorrhea)
Primary amenorrhea
lack of menarche at the age of 16, > 2yrs after the onset of puberty or if no signs of puberty by 14 yo
Most common cause of primary amenorrhea:
Physiologic/constitutional delay of puberty
Functional hypothalamic chronic anovulation (excessive exercise, eating d/os, stress)
Delayed growth may accompany these symptoms.
Chronic anovulation: complex causes in which diet, stresses, systemic disease, hypothalamic dysfxn, pituitary dysfxn, other endocrine dysfxn, exercise, environment, and body fat composition may play a part.
Secondary amenorrhea
menses cease > 3 - 6 months & the woman is not pregnant, lactating, or menopausal
Most common cause of secondary amenorrhea: pregnancy PCOS thyroid dysfunction ovarian insufficiency
etiology of amenorrhea
Typically divided into anovulatory & ovulatory
Anovulatory Amenorrhea
Both ovulation & menses are absent
Most common – results from functional causes
HP axis is intact, ovaries are functional, & gonadotropin secretion is ↓ → mild E deficiency.
Ovulatory Amenorrhea
Less common – results from anatomical genital AbN in women with normal hormonal function
Ovarian fxn is normal – external genitalia & secondary sex characteristics dev normally.
Causes of ovulatory amenorrhea
acquired - Asherman’s syndrome
congenital - Imperforate hymen
Cause of anovulatory amenorrhea
hypothalamic dysfunction - anorexia, excessive exercise, acute WT loss
pituitary dysfunction - galactorrhea
ovarian failure/dysfunction - AI, chemotherapy
endocrine disorders - hyperthyroidism, Cushing’s
Red flags for amenorrhea
Delayed puberty (R/O genetic disorder) Virilization (PCOS, Cushing’s syndrome, androgen secreting tumor) Visual field defects (prolactinoma)
DYSFUNCTIONAL UTERINE BLEEDING (DUB)
Definition - abnormal uterine bleeding in the absence of clinical or US evidence of structural AbN, inflammation, cancer, systemic d/o’s, pregnancy, complications of pregnancy, use of OC’s or certain drugs (dx of exclusion)
Most commonly occurs in women > 45 yo (> 50% of cases) & in puberty (20% of cases)
These are common periods in life when anovulation occurs.
PCOS is also a common cause of anovulation.
About 90% of cases are anovulatory and 10% are ovulatory
pathophysiology of DUB
Anovulatory – without progesterone secretion from the corpus luteum there is an excessive proliferation of the endometrium, eventually outgrowing its blood supply; it sloughs and bleeds incompletely, irregularly & sometimes profusely or for a long time. When this occurs repeatedly, the endometrium can become hyperplastic, sometimes with atypical or cancerous cells.
Ovulatory – progesterone secretion is prolonged; irregular shedding of endometrium results, most likely due to low estrogen levels – near threshold for bleeding like during menses. In obese women this can occur if estrogen levels are high, resulting in amenorrhea alternating with irregular or prolonged bleeding.
SSX of DUB
Polymenorrhea – menses < 21 days
Menorrhagia - > 7 days or > 80 ml
Metrorrhagia – occur frequently & irregularly between menses
Anovulatory DUB – tends to occur at unpredictable times & in unpredictable patterns & is not accompanied by cyclic changes in basal body temp.
Ovulatory DUB – tends to cause excessive bleeding during menstrual cycles – usually there are sxs of ovulation such as breast tenderness, midcycle cramping, change in basal body temp, & s/t dysmenorrhea.
History/PE/DX of DUB
Pregnancy test – even in young adolescent & perimenopause women CBC & ferritin – anemia Coagulation d/o’s should be R/O in adolescents who have DUB with anemia or require hospitalization for bleeding. Thyroid panel (FFT) & prolactin TVUS – R/O structural AbN Age ≥ 35 or if unopposed estrogen exposure in a younger woman Risk factors for endometrial cancer are present Bleeding continues despite use of empiric hormonal therapy.
DYSMENORRHEA
Definition: uterine pain associated with menses either primary or secondary
Etiology of dysmenorrhea
Primary (more common)
Secondary (due to pelvic abnormalities)
Primary Dysmenorrhea
Begins during adolescence, no underlying gynecological structural d/o.
Usually appears during adolescence and sometimes improves with age and pregnancy.
MOA: ↓ progesterone → lysosome breakdown → enzymes → ↑ prostaglandins in the uterus (endometrium/menstrual fluid) → ↑ uterine contractions & ischemia.
Secondary Dysmenorrhea
Usually beginning in adulthood Due to an underlying pelvic AbN causing pain with menstruation commonly: Most common causes: Endometriosis – most common Adenomyosis Fibroids
Red Flags for dysmenorrhe
New or sudden-onset pain
Unremitting pain
Fever
Vaginal d/c
PMS (PREMENSTRUAL SYNDROME)
Definition: symptoms that occur during the second half of the cycle (luteal phase 7-10 days before menses) and are relieved with the onset of the flow
Some common symptoms and signs of PMS
weight gain bloating breast swelling and pain
headache fatigue lethargy anxiety anger
irritability depression insomnia salt/sugar cravings
emotional lability pelvic heaviness/pressure backache
Etiology of PMS
Related to AbN responses to fluctuations of E and P
Fluid retaining effects of E, P, aldosterone and ADH
There are definite changes in CHO metabolism in the luteal phase, and in
adrenal production of corticosteroids
Possible hypoglycemia, and hyperprolactinemia
Possible serotonin connection
PMDD (PREMENSTRUAL DYSPHORIC DISORDER)
Definition/Presentation:
Severe PMS sxs occurring only during the 2nd half of the menstrual cycle ending with onset of menses or shortly thereafter
Mood is markedly depressed and anxiety, irritability, and emotional liability are pronounced
Suicidal thoughts may be present
Interest in daily activities is greatly decreased
Sxs are severe enough to interfere with routine daily activities or overall fxn
Diagnosis is clinical for Premenstrual Dysphoric Disorder (PMDD)
PMS - have her fill out PMS diary for 2-3 months
PMDD – a diary for 2 or more cycles to determine whether sever sxs occur regularly.
Must have ≥5 of the following sxs for most of the week before menses and at least 1 sx must be from the first 4 on the list:
Feelings of sadness, hopelessness, or self-depreciation
A tense (on edge) feeling or anxiety
Emotional liability with frequent tearfulness
Irritability or anger that persists leading to ↑ interpersonal conflicts
Loss of interest in daily activities, possibly causing withdrawal
↓ concentration
Fatigue, lethargy, or lack of energy
Changes in eating habits, including binging
Insomnia or hypersomnia
Feelings of being overwhelmed or out of control
Physical sxs associated with PMS
Also, the sx pattern must have occurred for most of the previous 12 months and sxs must be severe enough to interfere with daily activities and fxn
N LABS INDICATED
POLYCYSTIC OVARY SYNDROME (PCOS)
Overview:
Common female endocrinopathy – occurring 5%-10% of women
It is usually defined as a clinical syndrome
There may or may not be ovarian pathology – the ovaries may be enlarged and contain many 2-9mm follicular cysts containing atretic cells
Presents with anovulation & androgen excess causes - multiple metabolic AbN (hyperinsulinemia/glucose issues, lipid AbN, obesity, metabolic syndrome, ↑ E & T, ↓ P, AbN FSH:LH ratio [1:3 instead of normal 3:1])
The pivotal underlying issue is the woman’s inability to process insulin in the liver and muscles due to a probable genetic susceptibility that causes hyperinsulinemia, all other factors are considered to be downstream*
SSX of PCOS
Sxs usually start with menarche & worsen with time
Irregular menses – oligomenorrhea, polymenorrhea, amenorrhea
Hirsutism, acne, temporal balding
Acanthosis nigricans
Mild to severe obesity
May have enlarged ovaries/cystic ovaries
Diagnosis can be made clinically if signs of anovulation & hyperandrogenism are present
Serious sequelae will occur if not dx & treated – CVD, DM II, metabolic syndrome, endometrial carcinoma, possibly breast cancer (due to ↑ E and T, hyperinsulinemia and ↓ P)
Labs/Imaging/Dx for PCOS
Clinical criteria
Pregnancy test
Salivary or serum E, P, T, DHEA, cortisol
Serum FSH/LH
Thyroid studies (FFT) and Abs
Prolactin
Fasting glucose/insulin or (GITT) & lipids
TVUS – may show multiple follicles 2-9mm on the periphery of ovary (string of pearls) – is not diagnostic without anovulation being present.
Dx is suspected if women have at least 2 typical symptoms
Dx requires at least 2 of the 3 following criteria:
Ovulatory dysfunction causing menstrual irregularity
Clinical or biochemical evidence of hyperandrogenism
More than 10 follicles per ovary on TVUS, usually occurring in the periphery, resembling a string of pearls
Women meeting the criteria need serum cortisol to exclude Cushing’s syndrome
To exclude adrenal virilism, run a fasting serum 17-hydroxyprogesterone
PREMATURE OVARIAN FAILURE/INSUFFICIENCY (POF/POI)
Definition – ovaries do not produce enough estrogen despite high levels of gonadotropin hormones (esp. FSH) in women < 40 yo
Etiology for Premature Ovarian Failure/Insufficiency
Autoimmune d/o’s Congenital thymic aplasia Galactosemia Gonadal dysgenesis – d/o’s that confer a Y Physical and environmental factors: Chemotherapy & pelvic irradiation Cigarette smoking Viral infxns (mumps)
SSX for POF/POI
Amenorrhea or irregular blding
Sxs of E deficiency – osteoporosis (fractures), atrophic vaginitis, ↓ libido
Dx is suspected in women < 40 yo with the above sxs
Labs for POF/POI
Pregnancy test
Serum FSH, estradiol – if FSH is > 20 IU/mL (but usually >30mIU/mL) & E < 20 pg/mL repeat in 1 mos if findings are the same ovarian failure is confirmed
MENOPAUSE
Definition - physiological or iatrogenic cessation of menses due to ↓ ovarian function
Physiologic menopause occurs when menses is absent for 1 yr.
Average age for cessation of menses in the US is 51, with the normal
range from 45-55.
PERIMENOPAUSE
refers to the yrs before & 1 yr after LMP
Initially ↑ frequency of menses followed by ↓ freq (oligomenorrhea) – hallmark of this aspect of the transition.
Conception is still possible at this time
Pathophysiology of menopause
Ovaries – follicles ↓ in # & in ability to respond to FSH & LH → initially causing a shorter follicular phase, fewer ovulations, and ↓ P production, then follicles do not respond → ↓ estradiol (E2) & inhibin, but estrone (E1) is produced by peripheral conversion from androgens.
Testosterone – continues to be produced by stroma of ovary and adrenal gland
With the continued decreased levels of inhibin and E → ↑ LH & FSH
S/SX for perimenopause/menopause
Changes in bleeding patterns with menses (hallmark of perimenopause) becoming closer together, then further apart and eventually stopping – usu begin in 40’s
Estrogen – daily fluctuations occur ≈ 1 yr before menopause & cause sxs
Sxs – can last 6 mos – 10 yrs & range from none – severe.
Hot flashes & sweating
Common & due to vasomotor instability – affect 75%-85% of women
Last > 1 yr in most women & > 5 yrs in 50%
Low estrogen & high gonadotropins (FSH/LH) cause these.
Vaginal dryness, atrophy (atrophic vaginitis), dyspareunia, dysuria
Neuropsychiatric changes - nervousness, irritability, depression, anxiety, poor conc, memory loss (generally depression & anxiety occur in women with a history of this in their lifetime)
Recurrent night sweats - fatigue, insomnia, irritability & poor conc
Light-headedness, palpitations, numbness and tingling
Atrophic changes - urinary frequency, incontinence
GI disturbances - nausea, constipation, diarrhea
Musculoskeletal changes - back pain, arthralgias, myalgias & cold hands & feet
Lack of libido
Health problems accelerated by menopause
Osteoporosis
Dt ↓ E → ↑ bone resorption by osteoclasts
Most rapid loss occurs in 1st 2 yrs after E begins to ↓
Cardiovascular Dz
↑ chol, LDL, Tg’s, ↓ HDL, HTN, ↑ fasting blood glucose
Breast Cancer – with each decade of life there is ↑ risk of breast cancer
Management/Dx for menopause
Dx is clinical – with cessation of menses in women > 50 with a hx of irregular menses & no other AbN findings – no dx testing is necessary
FSH - consistently ↑ levels predict menopause
Post menopausal women with risk factors for osteoporosis & all women > 65 should be screened for bone loss – DEXA (dual x-ray absorptiometry) – measured at hip & lumbar vertebrae.
BMD – measured in T-scores (refers to the number of standard deviations from the young adult mean BMD)
Normal = T score above –1
Osteopenia = T-score bt –1 & -2.5
Osteoporosis = T-score at or below –2.5
Risk factors for osteoporosis
cigarette smoking
sedentary lifestyle
weight less than 127 lbs or BMI <21
VAGINITIS
Definition: Infectious or non-infectious inflammation of the vaginal mucosa and sometimes the vulva
- Many causes: most are infectious or due to normal flora imbalances
Normally (in women of reproductive age), Lactobacillus sp is the predominant constituent of normal vaginal flora. Colonization maintains the vaginal pH at 3.5-4.5, thereby preventing overgrowth of pathogenic bacteria.
High E levels maintain vaginal wall thickness, bolstering local defenses.
Predisposing factors to vaginal bacterial pathogens:
Use of antibiotics (→ ↓ lactobacilli)
Alkaline vaginal pH due to menstrual blood, semen, or ↓ in lactobacilli
Poor hygiene
Frequent douching
Pregnancy
DM
HIV
S/SX of vaginitis
presents with an abnormal vaginal discharge (most common complaint with or without vulvar irritation)
irritation
pruritis
erythema
Vaginitis is one of the most common gynecological disorders. Called vulvitis when affects the vulva alone. If it affects the vulva and vagina it is called vulvovaginitis
Vaginal discharge is abnormal when:
odor is offensive
when pruritis or irritation occurs
burning, pain, blood in discharge
when the amount of discharge is distressing to the woman
needs to be distinguished from normal discharge
Normal discharge
Common when estrogen levels are high
First two weeks of life, first few months before menarche
Milky white/mucoid, odorless, non-irritating
Dysuria or dyspareunia may occur with vaginitis
Vulvitis: can cause erythema, pruritis, tenderness and discharge from the vulva
Discharge that is watery, bloody or both may result from uterine, ovarian, vulvar or vaginal cancers, DES related tumors
Etiology of vaginitis in Children:
Infection usually involves GI tract flora
Girls age 2-6: common contributing factors are poor perineal hygiene (wiping back to front), not wiping hands after BM, fingering the area in response to pruritis
Chemicals in bubble baths and soaps can cause inflammation
Foreign bodies: may cause non-specific vaginitis with bloody discharge
Sexual abuse: Trichomonas
S/t specific pathogens: strep, staph, candida, occ’l. pinworms and E.Coli
Etiology of vaginitis in Reproductive age women:
Usually is infectious
Most common types are trichomonas vaginitis (STI), Bacterial Vaginosis (BV), also Candida,
Factors that dispose to overgrowth of bacteria and fungus Things that ↑ pH such as: menstrual blood, semen, tight non-porous underclothing, poor hygiene, frequent douching and diaphragm/spermicide use Foreign bodies (forgotten tampons)
Etiology of vaginitis in menopausal women:
Usually atrophic or inflammatory vaginitis, can have an overlapping BV or candida
Decrease in estrogen causes vaginal thinning → ↓ lactobacillus → ↑ vaginal pH increasing vulnerability to infection and inflammation
Poor hygiene (patients who are incontinent or bed-ridden)
PE for vaginitis
Palpate inguinal lymph nodes
Examine external genitalia, vaginal mucosa, glands and urethra, cervix for erythema, edema, excoriation & lesions, amount of d/c, color & odor, speculum exam
Bimanual – assess for CMT, adnexal or uterine tenderness
Assess vaginal pH
Lab for vaginitis
Wet prep, culture and vaginal pH
Consider DNA culture for BV, Candida, Trichomonas in chronic conditions
Red flags for vaginitis
Trichomonal vaginitis in children (suggesting sexual abuse) Fecal discharge (suggesting a fistula, even if not seen)
DDX for vaginitis
lichen sclerosus, lichen simplex chronicus
paget’s disease
Bacterial vaginosis or BV
Definition & Etiology
Most common infectious vaginitis
Due to alteration of vaginal flora ↓ lactobacillus → ↑ anaerobic bacteria
Increase in concentration 10-100 fold and decrease normal protective lactobacillus (its all about the ecosystem!)
Risk Factors for BV
IUD’s Low vitamin D Poor nutritional status Douching No condom use Anal sex before vaginal intercourse/sex/penetration Sex with uncircumcised male partners Spermicides New male partner Increased number of sexual partners Smoking Non-white ethnicity BV increases the risk for the following conditions PID, HPV Post-abortion and post-partum endometritis Post-hysterectomy vaginal cuff infections Chorioamnionitis Pre-mature rupture of membranes (PROM) Pre-term labor & pre-term birth
SSX of BV
Mild and often asymptomatic
Vaginal discharge is usually malodorous (fishy odor), white/gray, thin and profuse
Odor becomes stronger after menses and intercourse (pH more alkaline)
Pruritus and irritation are common
Erythema and edema are uncommon
Candida
Definition:
most fungal vaginitis is caused by Candida species, usually albicans
Risk factors for Candida
use of antibiotics or corticosteroids pregnancy constrictive undergarments immunocompromised use of IUD OC’s or vaginal ring Diabetes, HIV
SSX for Candida
Thick white cottage cheese like vaginal discharge that adheres to vaginal wall
Vaginal or vulvar pruritus, burning or irritation - mb worse from vaginal penetration
Dyspareunia is common
Sx. Increase the week before menses
Erythema, edema and excoriation are common, s/t fissures at introitus
DX for Candida
Wet prep
pH will be normal < 4.5
DDX for Candida
Contact irritation
Paget’s
Cytolytic disease
Atrophic/Inflammatory Vaginitis
Definition
vaginal inflammation with the absence of usual causes of infectious vaginitis
Risk factors for Atrophic/Inflammatory Vaginitis
Estrogen loss d/t menopause or premature ovarian failure or insufficiency
Genital atrophy predisposes to inflammatory vaginitis and increases risk of recurrence
Signs/Sxs for Atrophic/Inflammatory Vaginitis
Vaginal pruritus, erythema, burning, pain or minor bleeding
Thin and dry vaginal mucosa
DX for Atrophic/Inflammatory Vaginitis
pH >6
wet prep: Increased WBC’s, decreased lactobacillus, parabasal cells
–> ruling out infectious cause
DDX for Atrophic/Inflammatory Vaginitis
erosive lichen planus (intense erosion of tissue)
Trichomonas
Definition & Etiology
caused by trichomod protozoa
is a STI (requires the you report it and treat partner)
Signs/Sxs of Trichomonas
copious yellow/green frothy discharge soreness of vulva and perineum dyspareunia, dysuria edema of the labia may be present vaginal walls and surface of the cervix may have punctate red (strawberry) spots
DX for Trichomonas
Wet Prep: Elevated WBC’s, flagellated trichomod
Cytolytic Vaginosis
Definition:
- Overgrowth of lactobacillus strain (lyses if becomes overgrown)
DX for Cytolytic Vaginosis
wet prep: small amount WBC’s, increased rods, false/atypical clue cells (look like clue cells of BV except the rods are long not short)
Pelvic Inflammatory Disease (PID)
Definition:
infection of the upper female genital tract-the cervix, uterus, fallopian tubes, and ovaries
Etiology of PID
microorganisms ascending from the vagina/cervix into endometrium, fallopian tubes commonly If severe, infection can spread to the ovaries and then to the peritoneum Is a polymicroorganism etiology Neisseria Gonorrhea (GC) and Chlamydia trachomatis (CT) are common causes and STI’s
Risk factors for PID
Hx of STI’s
Hx of PID
IUD in women >35
Signs and sxs for PID
Lower abdominal pain: radiation to the back/sacrum
Cervical discharge
Dysuria
Nausea/ vomiting are common
PE for PID
Cervical motion tenderness (CMT)
Uterine and adnexal (unilateral or bilateral) tenderness
can pretty much DX based on SSX
DX for PID
High index of suspicion (CMT or fundal tenderness or adnexal tenderness on exam)
Wet prep: > 10 WBC’s/hpf
CBC: WBC count elevated
ESR increased >15 mm/hr
If all of the above are negative it probably excludes endometritis/PID
Complications of PID
Adhesions & tubal scarring
Infertility
Treatment of PID
MUST be treated with 2 or 3 antibiotics depending on history (SAVE THE TUBES!!!)
Endometriosis
Definition – noncancerous d/o where endometrial tissue are found outside the uterine cavity.
Most commonly found on peritoneal & serosal surfaces – broad ligaments, posterior cul-de-sac, uterosacral ligaments, and ovaries.
Less commonly found on surfaces of small & lg intestines, ureters, bladder, vagina, cx, surgical scars, pleura, & pericardium.
SSX of endometriosis
Generally pain & infertility are the most common sxs seen
Pelvic pain – dysmenorrhea (esp after several yrs of pain free menses), deep dyspareunia
Pelvic mass – endometriomas
Dyschezia – pain during BM’s, esp. during menses
Dysuria, suprapubic pain
Infertility-About 25-50% of infertile women have endometriosis
Stages of Endometriosis
Stage I – Minimal – A few superficial implants
Stage II – Mild–More, slightly deeper implants
Stage III – Moderate–Many deep implants, small endometriomas on ≥ ovaries, & some filmy adhesions
Stage IV – Severe–Many deep implants, large endometriomas ≥ ovary, & many dense adhesions, s/t with the rectum adhering to the uterus
Pathogenesis of Endometriosis
*Bleeding from implants initiates inflammation → fibrin deposition → adhesion formation → scarring which distorts peritoneal surfaces of organs and pelvic anatomy
