CC: 18yo, no menses, small uterus, no gonads palpable, webbed neck, low hairline, shield chest, wide nipple. T1 breast T2 hair. She's sort
- High gonadotropins (FSH and LH)
(but 10% of having eggs if young)
- Low estrogen
IMAGING: Can't see gonads. Uterus looks small.
GENETIC: Often abnormal karyotype (eg: 45,X)
- often the case when high gonadotropins.
- only one X chromosome. Turner's.
ALSO CALLED: Ovarian failure (secondary or primary)
--- No more eggs
--- No hormone production
(Non-Turner CAUSE: idiopathic, cancer, mumps, anything. more likely genetic. )
SYMPTOMS: cardiac, thyroid issues, berry aneurisms.
TX: E/P Treatment (breasts, bone, uterus, periods)
Fertility: Egg donation (maybe not for Turners b/c may have anuerism).
CC: Secondary AM. Mom hirstuism, father has diabetes. She's obese.
LABS: LH higher than FSH, Low Progesterone (no ovulation), increased androgens.
- more symptoms the higher your androgen level.
- virillism worst
ULTRASOUND: string of pearls of cysts- they are actually cysts. Tend to be a large ovary. Black = sign of anovulation.
ANDROGENS IN WOMEN:
50% of T/androstenedione from ovary, rest from adrenal.
DHEA - 90% from adrenal, rest from ovar.
. Androgens converted to estrogens in fat (by aromatase)
. More fat, more conversion
. Estrogens ~↑ LH . LH ↑ ovarian androgens
. Estrogens (low levels) ↓FSH
COMPLICATIONS: They are already overweight.
PCOS have an innate insulin resistance. More insulin to try to overcome - IGF1 - goes to ovary and leads to higher androgen levels (and that feeds back to more IGF-1)
- Insulin also leads to less SHBG (free androgen sucked up) - therefore tons of free androgen/testosterone.
- Insulin also drives LH up
- Note: metformin actually lowers androgen levels.
RISKS: -Risk obesity, hypertension, diabetes, endometrial
SYMPTOMS: Acanthosis nigricans- dirty neck.
Provide Estrogen / Progestin treatment
(eg: oral contraceptive pills)
-Cycles endometrium, prevents hyperplasia
-Lowers LH (from PG) and FSH
-Prevents ovarian cysts
-Increases SHBG (via estrogen)
¨Decreases free androgens
-Ovulation induction, Clomiphene citrate (tricks brian to think no E- induces more FSH) , Gonadotropins (FSH)
* Note: there are some higher brain centers than just the hypothalamus.
* Hypothalamus- the pulse generator/big boss/president
- GnRH: released in pulses from GnRH neurons to portal system...turns on FSH (egg food- causes follicles/cysts to grows)- makes the ovar make estrogen
-- E feeds back so we don't have a litter.
-- at some point, so high, causes a release/maturation of egg. leftover are lutenized. If yellow= making steroid.
-- now favors progesterone secretion
--- this goes to help out the uterine lining, stabilizing, prevents it from overgrowing, and makes it receptive for an embroy. Causes a secretory chanbe to the endometrium. If pregant, the placenta ends up takine this over. If not pregrant, without LH, will die after a few weeks. E and LH fell, and uterine lining shed.s As long as you have an open cervix, vagina, hymen, blood will come out.
FSH also induces production of inhibin. What's so wonderful about this is that it inhibits FSH. It's another mechanism to ensure that we are only one-egg ovulating species.
LH also leads to male hormones.
•Definition: inflammation of vulvar and vaginal tissues
-MOST common prepubertal GYN complaint
-Anatomic: no pubic hair, no labial fat pads, close to rectum
-Poor hygiene: wipe front to back, diapers
-Hormonal: thin atropic vagina pH more basic than adults
-Others: obesity, diabetes, other vulvar skin issues, immune status
•Differentiate from normal
- make sure not Leukorrhea of newborn (desquamation of vaginal and cervical epithelium
(Gone by 7 - 10 days)
-Premenarchal after thelarche
-Discharge (50%), dysuria, pruritis, pain, genital irritation, erythema, excoriation
- Ask: Duration, color, wiping (demonstrate), bedwetting, bubble baths, soaps, medications, ?sexual abuse
- 70% premenarchal vulvovaginitis
- Secondary to urinary/fecal hygiene
- Mixed bacterial (ecoli)
- Enteric: Shigella
- Respiratory: Haemophilus influenzae
- Skin: staph, strep
- STD: SEXUAL ABUSE, Neisseria gonorrhoeae, Chlamydia trachomatis
- Candida: RARE vaginitis, newborns or diapers, diabetics, prolonged antibiotics, immunocompromised
- Pinworm = Enterobius vermicularis:
scotch tape test
• Poorly understood
• Involving multiple chromosomes and genes:
- Ch. Loses: 8p, 10q, 13q, 16q
- Ch. Gains: 7p, 7q, 8q, Xq
- Germline mutations: RANSEL, MSR1
- Somatic alterations: GSTP1, NKX3.1, PTEN,
CDKN1B (p27), AR
= • Androgen receptor amplification in 1/3 of the hormonerefractory
• Recurrent fusion of TMPRSS2 to ERG or
1) Well circumscribed,compact glands
2) Less circumscribed, Loosely packed
3) Infiltrating, discrete glands, variable in size, well formed lumen
4) Infiltrating, fused glands, No lumen, cords
5) Infiltrating, diffuse sheets, individual tumor cells
Primordial germ cells (46,2N) arrive in testes at week 4 of embryonic development and remain dormant until puberty
Occurs in the seminiferous tubules
Type A Spermatogonia
At puberty, primordial germ cells differentiate into type A spermatogonia (46,2N)
Type A Spermatogonia undergo mitosis to provide a continuous supply of stem cells through the reproductive life of the male
Some type A spermatogonia differentiate into type B spermatogonia (46,2N)
Type B spermatogonia enter interphase and undergo DNA replication, and then enter mitosis to form primary spermatocytes (46,4N)
Primary spermatocytes complete meiosis I to form two secondary spermatocytes (23,2N)
Secondary spermatocytes complete meiosis II to form four spermatids (23,1N)
Spermatids undergo spermiogenesis which includes formation of acrosome, condensation of nucleus, and formation of the head, neck and tail (sperm 23,1N)
The total time for sperm formation is approximately 64 days
Prolactin is produced by the maternal adenohypophysis, fetal adenohypophysis, and decidual tissue of the uterus.
3 major actions of prolactin:
1) ↑ proliferation of mammary ducts at puberty and during pregnancy (with help of estrogen and progesterone)
2) ↑ milk production and secretion in breast in response to suckling by inducing synthesis of milk components: lactose, casein (the protein of milk), and lipids
3) ↓ synthesis and release of GnRH
During pregnancy, levels of prolactin, estrogen and progesterone increase. But estrogen and progesterone down-regulate prolactin receptors, preventing lactation from occurring during pregnancy
At parturition, there is a precipitous drop in estrogen and progesterone → prolactin receptors are no longer down-regulated, allowing the high levels of prolactin seen during pregnancy to take action → lactation can occur
Suckling is required to maintain milk production as increased nerve stimulation increases oxytocin and prolactin levels 
↓ Synthesis and release of GnRH → ↓ FSH and LH ∴ no LH surge ∴ inhibits ovulation → ↓ fertility while breast-feeding [Breastfeeding only provides 6 weeks of birth control protection] 
The ↓ fertility following parturition is only temporary. In lactating women, ovulation may return within 10 weeks postpartum, and the birth control protection afforded by lactation is ensured for only 6 weeks 
Males with high prolactin (e.g. prolactinoma) → ↓ GnRH → ↓ FSH and ↓ LH. Decreased FSH compromises spermatogenesis by Sertoli cells → infertility. Decreased LH → ↓ testosterone production by Leydig cells → ↓ energy, ↓ libido, impotence
Menopause is the cessation of estrogen production with age-linked decline in number of ovarian follicles
The average age of menopause in the western world is 51 years old (earlier in smokers). Typical range is 45-55 years old
Hormonal changes include: very high follicle stimulating hormone, elevated luteinizing hormone, elevated gonadotropin hormone, and decreased estrogen
Symptoms of menopause include: hot flashes, atrophy of the vagina, osteoporosis, coronary artery disease, decreased libido, and insomnia
Premature Ovarian Failure: loss of function of the ovaries before age 40. A commonly cited triad for the diagnosis is amenorrhea, hypergonadotropinism (high levels of follicle stimulating hormone), and hypoestrogenism
especially assoc. w/ HPV 16, 18, 31, 33
Risk factors: early sexual intercourse, multiple partners, smoking, birth control pills, immunodeficiency
HPV infects immature basal cells of squamous epithelium and immature metaplastic squamous cells at the squamocolumnar junction.
Viral proteins E6, E7 inactivate cell cycle regulation at p53 (E6) and Rb (E7).
CIN (cervical intraepithelial neoplasia) → subtype CIN 1, CIN 2, or CIN 3. Parallel classification includes low- or high-grade squamous epithelial lesions (LSIL or HSIL).
CIN 1/LSIL: dysplasia involving lower 1/3 of the epithelium.
CIN 2/HSIL: dysplasia involving lower 2/3 of the epithelium.
CIN 3: defined as carcinoma in situ (CIS).
Histopathology: Cervical dysplasia is characterized by disordered epithelial growth → loss of polarity. Koilocytes are seen → (clear halo surrounding hyperchromatic, atypical nuclei) beginning at the basal layer and extending outward
Carcinoma in situ is characterized by atypical changes extending through the entire thickness of the epithelium
Vaccine: Gardasil (tetravalent) is now FDA approved for both males and females
Preeclampsia: defined clinically as hypertension and proteinuria with or without edema which develop during the third trimester
Definitive treatment for preeclampsia or eclampsia is delivery of the baby
In less severe illness, symptomatic treatments include bed rest, salt restriction, and monitoring and treatment of hypertension
Eclampsia: add grand mal seizures to the preeclampsia triad
Affects 7% of pregnant women from 20 weeks gestation to 6 weeks postpartum (before 20 weeks suggests molar pregnancy-hydatidiform mole)
There is an increased incidence in patients with preexisting diabetes mellitus, hypertension, chronic renal disease, and autoimmune disorders
Etiology involves placental ischemia secondary to lack of trophoblastic invasion of the spiral arteries in the myometrium
Clinical symptoms include blurred vision, abdominal pain, edema of the face and extremities, altered mentation, and hyperreflexia. The presence of seizures makes the diagnosis eclampsia.
Laboratory findings include thrombocytopenia and hyperuricemia
Can be associated with HELLP syndrome (Hemolysis, Elevated Liver function tests, Low Platelets)
Eclampsia is a medical emergency requiring intravenous magnesium sulfate and diazepam
Enlargement of the male breast, usually in response to relative hyperestrinism
Commonly seen in patients with cirrhosis. Can also occur with certain types of testicular tumor (especially Leydig cell), as well as with puberty, old age, and Klinefelter's syndrome.
The gynecomastia in cirrhosis is due to decreased breakdown of estrogen secondary to decreased metabolic capacity of the fibrotic liver.
Drugs causing gynecomastia: estrogen, marijuana, heroin, psychoactive drugs, spironolactone, digitalis, cimetidine, alcohol, and ketoconazole
Agonist at androgen receptors
Clinically it is used for treating hypogonadism by promoting secondary sexual characteristics, stimulates anabolism to promote recovery after severe burns or from chronic debilitating diseases, promote skeletal growth in prepubertal boys with pituitary dwarfism, and treat endometriosis
Adverse effects in males (excess androgens) include priapism, impotence, decreased spermatogenesis, gynecomastia, reduces intratesticular testosterone by inhibiting Leydig cells leading to gonadal atrophy, hepatic abnormalities, and increased aggression/psychotic episodes
Adverse effects in females (excess androgens) include masculinization with acne, growth of facial hair, deepening of the voice, male pattern baldness, excessive muscle development, and menstrual irregularities
Adverse effects in children include growth disturbances from premature closure of the epiphyseal plates and abnormal sexual maturation
Excess androgens increases serum LDL and lowers serum HDL, thereby increasing LDL/HDL ratio leading to increased risk for premature coronary heart disease