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Pathogenesis of Klinefelters

Seminiferous tubule destruction and hyalinization -> small, firm testes; Leydig cell damage


Klinefelters hormone levels

Serum inhibin low (S tubule dygenesis), low testosterone (Leydig dysfunction), high LH and FSH


Cryptorchidism hormone levels

Seminiferous tubules dmg'd but NOT leydig cells; Low inhibin levels and high FSH lvls; but LH and testosterone levels normal


Klinefelters clinical characteristics

Testicular atrophy, long extremities, gynecomastia, female hair distribution, presence of Barr bodies, mild ID


Cells of seminiferous tubules and functions

Spermatogonia (germ cells) - produce primary spermatocytes. Sertoli cells (non-germ) - secrete inhibin (-| FSH), androgen-binding protein (maintain local testosterone lvl), blood-testis barrier (via tight junctions), support spermatozoa, produce MIF. Leydig cells (endocrine) - secrete testosterone in presence of LH.


Temperature affects production of what in semineferous tubules?

Sertoli cells affected - decreased sperm production and decreased inhibin. Leydig cells NOT affected (testosterone levels okay)


Three main categories of drugs for BPH?

Alpha-adrenergic antagonists (terazosin, tamsulosin), 5-alpha-reductase inhibitors (finasteride, dutasteride), antimuscarinics (tolterodine)


Four possibilities when the urachus doesn't obliterate

Patent urachus (urine from umbilicus), vesicourachal diverticulum (out pouching of bladder), urachal sinus (adj to umbilicus), urachal cyst (often asymptomatic but can be infectious, adenoca)


Sertoli v. Leydig. What makes MIF?



Fetal anomalies associated with polyhydramnios?

Anencephaly, GI atresia


Turner's syndrome presentation

In neonate, lymphedema, cystic hygromas. Primary amenorrhea (streak ovaries), short statue, Coarctation of the aorta. Webbed neck, low hairline. Low estrogen, high LH and FSH.



Serous fluid in tunica vaginalis. See fluid in sac. Communicating if processus vaginalis (diverticulum from peritoneum) remains patent.


Complete mole vs. partial mole?

Complete - bleeding, enlarged uterus, PEC, Theca-lutein cysts, trophoblast only, no fetal tissue, 46 XX or XY (both paternal), with 15-20% risk of malignancy. Partial mole - bleeding, pain, fetus, cord, some enlarged villi, 69 XXX or XXY, with low risk malignancy.


Kallmann syndrome

Delayed pubery + anosmia. Etio - failure of GnRH-seceting neuron migration from olfactory placode to hypothalamus. Central hypogonadism and anosmia.


Male gonadotropin regulation

Hypothalamus secretes GnRH pulsatile which POS pituitary. Pituitary releases FSH and LH (ant. pituitary). LH stimulates release of testosterone from Leydig, which negatively feedbacks to LH.. FSH stimulates release of inhibin B from sertoli, which negatively feedback for FSH. Lute for Leydig for L'testosterone. FSH to Sertoli to inhibin B.


Metabolic effects of human placental lactogen?

Increases insulin resistance, stimulates proteolysis and lipolysis, inhibits gluconeogenesis.


What control breast development during pregnancy?

1st TM - corpus produces progesterone and estradiol. By 2nd TM, placenta produces progesterone and estradiol, while fetal adrenal helps w/ estradiol. Prolactin increases (ant. pituitary) but is prevented from lactogenesis b/c of high estrogen and progesterone levels. Once placenta separates, prolactin stimulates milk production.


Urge incontinence

Uninhibited bladder contractions (detrusor instability). M3 antagonists (e.g. oxybutynin) -> smooth muscle relaxation. (M3 is a Gq pathway, so drug dec. IP3 production).


Sheehan's syndrome

If significant hypotension occurs while pituitary is still enlarged (2/2 to high estrogen lvls, e.g. PPH) --> ischemic necrosis of pituitary --> panhypopituitarism -> prolactin deficiency for example


What day of separation leads to fetal membrane organization for monozygotic twins?

4,8,12. 4 Twins. FOUR is magic number. 0-4: di/di. 4-8:monochorionic/diamniotic; 8-12: mono/mono; >13: mono/mono conjoined


Histology changes in menstrual cycle

First half (proliferative phase). Estrogen stimulates proliferation of stratum FUNCTIONALE. Non-branching, non-budding EVENLY distributed. Tubular, narrow, pseudo stratified glands. Second half (secretory phase, begins with ovulation). Glands become LARGER and COILED w/ large vacuoles. Edematous stroma with SPIRAL arteries.


Deformation vs. malformation vs disruption?

Deformation occurs due to extrinsic mechanical forces (e.g. Potter sequence). Disruption refers to secondary breakdown of previously normal tissue (amniotic band syndrome). Malformation is primary defect of cells (intrinsic developmental abnormality) (e.g. holoprosencephaly).



Sign of infection with HPV. Immature squamous cell w/ dense, irregularly staining cytoplasm with PERINucLEAR clearing = halo. PYKNOTIC (apoptotic).


Parabasal cells

Round cells w/ HIGH N/C, basophilic cytoplasm. Dominate Pap smears of post-menopausal and postpartum women.


ABO disease

Must be IgG ab's (b/c only they cross placenta). Usually mothers make IgM uncless she is an O mom. Even so only 3% of O mom - X baby pregnancies have hemolytic disease of the newborn.



Constitutive activation (gain-of-function) of FGFR3. Sporadic mutation (adv. paternal age) in 85%, AD 15%. Homozygosity = death.


Urethral trauma

Posterior urethral injury is associated with pelvic trauma while anterior urethral injury is associated with straddle injuries. Inability to void w/ full bladder, high-riding boggy prostate, blood at urethral meatus. NO FOLEY.


What contains the ovarian nerves, arteries, veins, and lymphatics?

Suspensory ligament of the ovary


Treatment for hirsutism?

Spironolactone (blocks androgen receptors at hair follicles). Also flutamide (testosterone receptor antag) and finasteride (5-alpha-reductase inhibitor)


Vaginal adenosis?

Replacement of vaginal squamous epithelium with glandular columnar epithelium. Female children of women exposed to DES. Precursor to clear cell adenocarcinoma.