Repro Flashcards
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?
Sertoli
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.
Hydrocele
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).
Koilocyte
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.
Achondroplasia
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.
Ambiguous external genitalia in female infant and maternal virilization?
Aromatase deficiency. AR. High androgen and low estrogen. Aromatase converts Androstenedione to estrone and testosterone to estradiol.
Tamoxifen
SERM that used for tx of osteoporosis and breast cancer. But associated with increased incidence of endometrial cancer and thromboembolic disease
Raloxifene
Also a SERM. Agonist on bone, CV, and blood lipoproteins. Antagonist to BREAST and UTERUS. Decreases incidence of breast cancer and osteoporosis
Complete androgen insensitivity
Lack of androgen receptors in the body. 46,XY. Testosterone -> estradiol -> external female genitalia. Blind pouch vagina. Testes in the abdomen. Serum testosterone high, LH high, FSH normal.
Role of androgen binding protein (ABP)?
To ensure high lvls of testosterone in the seminiferous tubules to allow spermatogenesis to occur.
PCOS hormones
LH thought to be high. Causing theca-cells to make lots of androgens and estrogens, suppressing FSH.
Absolute contraindications to OCPs?
Prior hx of DVT/PE. Hx of estrogen-dependent rumor. Women > 35 who smoke heavily. HyperTG. Decompensated or active lier disease. Pregnancy.
Appendages in wrong locations?
Homeobox gnes
Gene involved in limb lengthening?
FGF gene. Produced at apical ectodermal ridge -> mitosis of underlying mesoderm
Gene mutation that can cause holoprosencephaly?
Sonic hedgehog gene
Dorsal-ventral axis vs. anterior-posterior axis organization genes?
Shh (BASE) for ant-post. Wnt-6 (apical ectodermal ridge) for dorsal-ventral.
Bilaminar vs. trilaminar timeline?
2 weeks vs. 3 weeks
Morula timeline?
Day 3
Implantation occurs when?
About 1 week after fertilization
When do the genitalia differentiate?
Week 10
When is fetal cardiac activity seen on US?
Week 6 (heart actually begins to beat at wk 4)
When do the limb buds form?
Week 4
Mesodermal defect acronym?
VACTERL - Vertebral defects, anal atresia, cardiac defects, tracheo-esophageal fistula, renal defects, limb defects (bone and muscle)
Thyroid embryo derivative?
Endoderm (follicular) and neural crest (parafollicular C cells)
Craniopharyngioma
Benign Rathke pouch (surface ectoderm) tumor with cholesterol crystals and calcifications
Deformation vs. malformation?
Deformation is extrinsic occurring after “embryonic period,” whereas malformation is intrinsic (w 3-8)
Alkylating agent teratogenicity
Absence of digits, multiple anomalies
ACEi teratogenicity
Renal damage
Aminoglycosides teratogenicity
CN VIII tox
Carbamazepine teratogenicity
Neural tube, craniofacial, fingernail hypoplasia, dvpt delay, IUGR
DES teratogenicity
Vaginal clear cell adnocarcinoma, congenital Mulerian
Folate antagonists teratogenicity
Neural tube
Lithium teratogenicity
Ebstein anomaly (atrialized RV)
Methimazole teratogenicity
Aplasia cutis congenita (congenital absence of skin)
Phenytoin teratogenicity
Fetal hydantoin syndrome = microcephaly, dysmorphic craniofacial, hypoplastic neails, cardiac, IUGR, intellectual
Thalidomide teratogenicity
Limb defects - phocomelia
Valproate teratogenicity
Neural tube defects
Warfarin teratogenicity
Bone deformities, fetal emorrhage, abortion, optho
Cocaine teratogenicity
Abnormal fetal growth, fetal addiction, placental abruption
Smoking teratogenicity
LOW birth rate. Preterm labor. Placental problems.
Iodine teratogenicity
Congenital goiter or hypothyroidism
Maternal diabetes teratogenicity
Caudal regression syndrome: anal atresia to sirenomelia; congenital heart, neural tube
Vitamin A excess teratogenicity
Spontaneous abortions and birth defects (cleft palate, cardiac)
X-ray teratogenicity
Microcephaly, ID
Fetal alcohol syndrome
ID, developmental retardation, microcephaly, holoprosencephaly, facial abnormalities (smooth philtrum, thin upper lib, small palpebral fissures, hyper telorism), limb dislocation, heart defects
Cleavage at 0-4 days of monozygotic cell leads to
Fused OR separate placenta. But dichorionic diamniotic
Cleavage at 4-8 days of monozygotic cell
Monochorionic, diamniotic (most common)
Cleavage at 8-12 days of monozygotic cell
Monochorionic, monoamniotic
Cleavage >13 days of monozygotic cel
Likely mono-mono but CONJOINED twins
Cytotrophobloast vs. Syncytiotrophobloast
cyto = inner layer of chorionic villi. Syncytio = outer layer that secretes hCG
When does the vitelline duct obliterate?
Week 7
Aortic arch 1
Part of maxillary artery
Aortic arch 2
Stapedial artery
Aortic arch 3
Common carotid arteries and beginning of internal carotics
Aortic arch 4
Part of AA, part of right subclavian artery
Aortic arch 6
Proximal part of pulmonary arteries and the ductus arterosus
What do the branchial clefts do?
Branchial cleft 1 becomes external auditory meatus. Rest involute via temporary cervical sinus. If persist- > cyst in lateral neck
Branchial arch 1 nerve and abnormality
Nerve is V3. Treacher Collins syndrome -> mandibular hypoplasia and facial abnormalities
Branchial arch 2 nerve and abnormality
Nerve is VII. Abnormality is congenital pharyngocutaneous fistula = fistula between tonsillar area and lateral neck
Branchial arch 3 nerve
Nerve is IX.
Branchial arch 4-6 nerve
Nerve is X + recurrent X
Muscles of branchial arch 1
Muscles of mastication (temporalis, masseter, lateral and medial pterygoid, mylohyoid), ant. belly of digastric, tensor tympani, tensor veli palatini
Muscles of branchial arch 2
Facial expression, Stapedius, Stylohyoid, platysma, and post. belly of digastric
Muscles of branchial arch 3
Stylopharyngeus
Muscles of branchial arches 4,6
Pharyngeal, laryngeal
Cartilages of branchial arch 1
Meckel cartilage: Mandible, Malleus, incus, spheno-mandibular ligament
Cartilages of branchial arch 2
Stapes, sytloid process, lesser horn of hyoid, stylohyoid
Cartilage of branchial arch 3
Greater horn of the hyoid
Cartilages of 4,6th branchial arch
Thyroid, cricoid, arytenoids, croniculate, cuneiform
Branchial pouch 1
Middle ear, eustachian tube, mastoid air cells. ENDODERM
Branchial pouch 2
Epithelial lining of palatine tonsil
Branchial pouch 3
Dorsal - inferior parathyroid. Ventral - thymus.
Branchial pouch 4
Dorsal - superior parathyroids. Ventral - C-cells of thyroid gland.
Two mechanisms for cleft palate
Failure to fuse 2 lateral palatine processes. Fusion of one or more lateral palatine processes with the nasal septum and/or median palatine process
Cleft lip mech
Failure of fusion of maxillary and medial NASAL processes
Other names of Mullerian and Wolffian ducts?
Mullerian = parameonephric. Wolffian = mesonephric (renal)
Components of the Wolffian duct
SEED (Seminal vesicles, epididymis, ejaculatory duct, ductus deferens). NOT prostate.
What internal and external genitalia result in a XY has no MIF working?
Both male AND female internal genitalia. But male external genitalia (DHT going strong)
What internal and external genitalia results in a XY with 5alpha reductase deficiency?
Male internal genitalia but ambiguous external genitalia until puberty
Homolog of scrotum?
Labia majora
Homolog of Prostate gland?
Urethral and paraurethral glands of Skene
Homolog of Bartholin gland?
Bublourethral glands of Cowper
Homolog of Corpus cavernous and spongiosum?
Vestibular bulbs
Homolog of the labia minor?
Ventral shaft of penis
Hypospadia vs. epispadia
Ventral vs. dorsal. Failure to close fold vs. faulty positioning of genital tubercle.
Processus vaginalis
It is an evagination of the peritoneum that forms the tunica vaginalis in men and obliterates in women.
Gubernaculum?
The anchor that brings down the testes during its descent OR what becomes the ovarian ligament and round ligament of the uterus
What’s weird about the venous drainage of the gonads?
The left side always goes from L gonadal vein into the L renal vein to IVC, whereas the R gonadal vein goes directly into the IVC.
Where are the uterine vessels located?
In the cardinal ligament. (Cervix to side wall of pelvis). Be careful of the ureters
Where are the ovarian vessels located?
Suspensory ligament of the ovaries. Be careful of the ureters.
Broad ligament contains what?
Ovaries, fallopian tubes, round ligament of the uterus
Round ligament connects what?
Uterine fundus to the labia major. (Round ligament pain)
Ovarian ligament connects what?
Medial pole of the ovary to the lateral uterus. Not in the broad ligament.
Histology of the female reproductive tract.
Stratified epithelium from vagina to transformation jone. Now simple columnar epithelium up into fallopian tubes. Ovaries have simple cuboidal epithelium on the outer surface.
Pathway of sperm?
Seminiferous tubules, Epididymis, Vas deferens, Ejaculatory ducts, (Nothing), Urethra, Penis. SEVEN UP.
Physiology of erection
PNS (pelvic). NO leads to increased cGMP -> SMC RELAX = blood filling. With sympathetic tone, NE -> increased Ca2+ which leads to SMC contraction and vasoconstriction = flaccid.
What nerves responsible for “shoot?”
SNS’ hypogastric n. for emission. Pudendal nerve for ejaculation.
Theca cell role?
Desmolase converts cholesterol into androstenedione.
Granulosa cell role
Aromatase converts androstendeione from theca cells into estrogen.
Potency of estrogen-family hormones?
Estradiol (ovary) > estrone (peripheral) > estriol (placenta), which btw, is an indicator for fetal well being
What makes progesterone?
Corpus luteum, placenta, adrenal gland, testes
Function of progesterone
Endometrial glandular secretion, spinal artery development, maintain pregnancy, dec. myometrial excitability, thick cervical mucus to inhibit sperm entry, inhibits LH, FSH, uterine smooth muscle relaxation, dec. estrogen receptor expressivity, prevents endometrial hyperplasia
Tanner II vs. III vs IV
II is pubarche and telarche. III is darkening, curling, enlargement. But IV has darker scrotal skin, development of the glans, and raised areolae
Arrested development of oocytes where?
Meiosis is begun in fetal life but stops at Prophase 1 until selected for ovulation. As primary oocyte, finishes meiosis I and becomes secondary oocyte. It is arrested in METAphase II until fertilization. Must fertilize within ONE day.
Mittelschmerz
Transient mid-cycle ovulatory pain classicularlly associated with peritoneal irritation.
Exclusively breast fed infants require what vitamin supplementation?
Vitamin D
hCG role
Made by syncytiotrophoblast and acts like LH in 1st TM, which is required for the luteal cell to continue making progesterone (maintaining the pregnancy). In 2nd-3rd TM, corpus luteum degenerates.
hCG subunit for pregnancy test?
Beta subunit b/c alpha subunit is identical to LH, FSH, and TSH.
How to diagnosis menopause?
FSH increased (very specific)
Symptoms of menopause?
HAVOCS - Hot flashes, atrophy of the vagina, osteoporosis, coronary artery disease, sleep disturbances
How long does spermatogenesis take?
2 months
Spermatogonia vs. spertazooa?
Going to tbe a pserm. Zooa have acrosomal cap and loss of cytoplasm = zooming.
Potency of androgens?
DHT > tesosterone > androstenedione
Where do androgens get converted into estrogens in men?
Adipose and testis (Cytochrome P-450 aromatase)
Function of DHT?
Early on, in differentiation of male external genitalia plus prostate. Late - involved in prostate growth, balding, sebaceous gland activity
Function of testosterone
Differentiation of epididymis, vas, seminal vesicles. Growth spurt. Voice deepening. Closure of epiphyseal plates. Libido.
XYY Presentation
Pheno normal. Tall, acne, antisocial in 1-2%. Normal fertility.
Men: Testosterone down, LH down?
Hypogonadotropic hypogonadism
Men: Testosterone down, LH up?
Primary hypogonadism
Men: Testosterone up, LH down?
Exogenous testosterone (tumor, drugs)
Men: Testosterone up, LH up?
Androgen receptor defect
Most common etiology of a male pseudohermaphrodite?
Androgen insensitivity syndrome. Testes present but external genitalia are female/ambiguous.
Most common etiology of a female pseudohermaphrodite?
Congenital adrenal hyperpasia or exogenous androgens during pregnancy. Ovaries present but virilized/ambiguous external genitalia.
Aromatase deficiency
Can’t make estrogens from androgens -> masculization of females (ambiguous genitalia) +/- maternal virilization during pregnancy because fetal androgens cross the placenta. Increased serum testosterone and androstenedione.
Androgen insensitivity syndrome
46 XY that is a normal appearing female with female external genitalia with rudimentary vagina. NO uterus or fallopian tubes. Testes (often found in labia majora). Increased testosterone, estrogen, and LH.
5alpha-reductase deficiency
AR and only limited in phenotype to males. Inability to convert testosterone -> DHT means ambiguous genitalia until puberty when increased testosterone -> masculinization and growth of external genitalia. NORMAL testosterone/estrogen. LH normal or increased. Internal genitalia are normal.
Kallmann syndrome
Hypogonadtropic hypogonadism 2/2 defect of GnRH migration. Decreased GnRH, decreased FSH, LH, testosterone, infertility. Anosmia.
Etiology of complete vs. partial mole?
Complete mole is completely paternal (which duplicates its genome) + enucleated egg. Partial mole = 2 sperm + egg.
Week cut-off for diagnosing gestational HTN?
Wk 20. HTN before week 20 suggests a molar pregnancy.
Treatment for gestational HTN?
alpha-methyldopa, labetalol, hydralazine, nefidipine; delivery at 39 weeks
Preeclampsia?
HTN > 20th week + proteinuria (>300 mg/24h). Severe features are Bp > 160/110, end-rgan damage. Caused by ABNL Spiral Arteries -> maternal endothelial dysf(x), vasoconstriction, and hyperreflexia
HELLP syndrome?
Hemolysis, elevated liver (enzymes), Low platelet count. Tx = immediate delivery
Tx differences between pre-eclampsia and eclampsia?
Both give antihypertensives, IV MgSO4. But immediately deliver in ecclampsia b/c of risk of maternal death 2/2 stroke w/ intracranial hemorrhage or ARDS
Increased incidence of PEC found with what conditions?
Pre-exisitng HTN, DM, chronic renal disease, or autoimmune disorders
Abnormal placental detachment types?
Placenta accreta attaches to myometrium w/o penetrating. Placenta increta penetrates into myometrium. Placenta percreta penetrates into uterine seroa —> rectal or bladder attachment.
Presentation of placental abruption?
Abrupt, painful bleeding (concealed or apparent) in 3rd TM. Maternal DIC, shock, fetal distress.
Placenta previa
Attachment of placenta near the cervical os -> inc. risk of bleeding. RF’s = multiparty, prior C-section
Presentation of ectopic pregnancy?
Sudden lower abdominal pain w/ or w/o vaginal bleeding. Amenorrhea. Lower-than-expected bCG rise. r/o appi. US diagnosis.
Pathophysiology of HPV virus -> cervical carcinoma?
HPV 16 and 18 produce two proteins: E6 and E7. E6 inhibits p53 while E7 inhibits RB. The virus, therefore, inhibits tumor suppressor genes
Endometritis inflammatory picture? What cells?
Plasma cells and lymphocytes.
Treatment of endometriosis?
NSAIDs, OCPs, progestins, GnRH agonists, surgery.
Adenomyosis
Extension of endometrial tissue into the myometrium. Presents with dysmenorrhea, menorrhagia. ENLARGED, soft uterus. Tx = hysterectomy.
RF’s for endometrial hyperplasia?
Anovulatory cycles, HRT, PCOS, granulosa cell tumor.
Peak occurrence of leiomyomas?
Age 20-40
Most common causes of an ovulation?
Pregnancy, PCOS, obesity, HPO axis, premature ovarian failure, hyperprolactinemia, thyroid, eating
PCOS labs?
High androgens, High LH, low FSH. High androgens decrease SHBG -> increased FREE testosterone (active portion).
Mechanism for OCP treatment for PCOS?
Estrogens increase SHBG -> decreased free testosterone
Complications of PCOS?
Increased risk of endometrial cancer b/c of increased estrogens and absence of progesterone. (Therefore, tx with progesterones)
Most common ovarian mass in young women?
Follicular cyst
Cyst associated with choriocarcinoma and moles?
Theca-lutein cyst
“Chocolate cyst”
Endometriosis. Blood gives it the color.
Dermoid cyst
Mature teratoma with all sorts of tissue.
Corpus luteum cyst
2/2 hemorrhage into a persistent corpus luteum. Self-resolves.
Follicular cyst
Distention of unruptured graafian follicle. Often associated with hyperestrogenism and endometrial hyperplasia.
Most common ovarian neoplasm?
Serous cystadenoma - benign. Thin0walled. Fallopian-like epithelium.
Immature vs. mature teratoma?
Immature teratoma is malignant. More likely to contain thyroid tissue +/- embryonic-like neural tissue.
Psammomma bodied malignant ovarian neoplasm?
Serous cystadenocarcinoma
Granulosa cell tumor
Most common sex-cord tumor. Often produce estrogen/progesterone, so pt’s present with abnormal uterine bleeding or sexual precocity. Call-Exner bodies.
Vaginal clear cell adenocarcinoma?
Women who had DES exposure in utero
Small, mobile firm breast mass that increases in size and tenderness right before menstruation?
Fibroadenoma - found in stroma
Serous or bloody nipple discharge?
Intraductal papilloma. Typically grows beneath areola (lactiferous sinus) and has a slight 1.5-2x risk of carcinoma.
Phyllodes tumor?
LARGE bulky mass of connective tissue (stroma). “Leaf-like” 6th decade
Non-invasive breast neoplasms?
DCIS (doesn’t penetrate BM; in major duct), Comedocarcinoma (caseous necrosis; type of DCIS), Paget disease of breast (results from underlying DCIS extending up to lactiferous ducts).
Invasive ductal vs. invasive lobular breast cancer?
Ductal is worst, most invasive. Firm, “rock-hard” with sharp margins. Stellate infiltration. Invasive lobular is an ORDELRY row (“Indian file”)
Acute mastitis?
An abscess. Staph aureus is most common. Tx = dicloxacillin + continued breast feeding
Drugs that can cause gynecomastia?
Spironolactone, marijuana, digitalis, estrogen, cimetidine, alcohol, heroin, dopamine D2 antagonists, ketoconazole
What lobes enlarge in BPH?
Lateral and middle
What lobes enlarge in prostatic adenocarcinoma?
Posterior lobe
Treatment of BPH?
alpha-1-antagonists (tamsulosin, terazosin). Finasteride (5-alpha reductase inhibitor)
Etiology of variocele?
Poor gonadal venous drainage. Usu. left b/c -> L renal vein.
Presentation of variocele?
Scrotal enlargement, bag of worms, dx w/ US. Decreases fertility b/c of increased temperature (Sertoli cell sensitive)
Non-tranilluminating testicular mass
Cancer
Seminoma
Painless homogenous testicular enlargement in 3rd decade. “Fried egg” on histo. Increased placental alkaline phosphate. Good prognosis. Tx = radiation (sensitive)
Most common testicular tumor of boys < 3 y/o
Yolk sac (endodermal sinus) tumor. “Schiller-Duval bodies’
GnRH analog?
Leuprolide
Clinical uses of leuprolide?
Pulsatile dosages used for infertility. Continuous uses used for uterine fibroids, precocious puberty, and prostate ca (with flutamide).
Names of estrogen drugs
Ethinyl estradiol, DES, mestranol
Clinical use of estrogens
Hypogonadism/ovarian failure, menstrual abnormalities, HRT, men with androgen-dependent prostate cancer
Clomiphene
Antagonist of estrogen receptors in hypothalamus preventing normal feedback inhibition -> increased LH and FSH. Used to treat infertility due to anovulation. SE’s - hot flashes, ovarian enlargement, multiple simultaneous pregnancies, visual disturbances
Tamoxifen vs. raloxifene
Tamoxifen is antagonist on breast, agonist for uterus and bone. Raloxifene is agonist to bone, antagonist for uterus. Both associated with DVTs. Tamoxifen for breast cancer, raloxifene for osteoporosis.
Aromatase inhibitors?
Used for breast cancer. Anastrozole/exemestane
Mifepristone
Competetive inhibitor of progestins. Used with misoprostol (PGE1) for abortion.
Mechanisms of estrogen/progestin vs progestin-only OCPS?
Progestin only causes thickening of cervical mucus and inhibits endometrial proliferation. E/P’s inhibit LH/FSH to prevent ovulation.
Terbutaline
A beta-2 agonist used as a tocolytic in labor.
Danazol
Partial agonist for androgen receptors. Used for endometriosis and hereditary angioedema.
Finasteride
5 alpha-reductase inhibitor. Used for BPH and male pattern baldness.
Flutamide
Competetive inhibitor of androgens at testosterone receptor used for prostate carcinoma.
17,20 desmolase inhibitors
Ketoconazole and spironolactone (also inhibits 17-alpha hydroxylase). Both used for PCOS to prevent hirsuitism. Side effects of gynecomastia and amenorrhea.
Side effects of PDE5 inhibitors?
HA, flushing, dyspepsia, color-vision. Hypotension if used with nitrates = life-threatening
Role of menotropin in fertility treatment?
Menotropin acts like FSH –> formation of dominant follicle. hCG is then used for LH surge to ovulate.
Primary energy source for sperm?
Fructose. Therefore relies on aldose reductase (glucose to sorbitol) and sorbitol dehydrogenase (sorbitol to fructose). High sorbitol dehydrognease activity.
