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40 Cards in this Set
- Front
- Back
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Teratogens - ACE inhibitors - DES - Lithium - Valproate - Warfarin |
- ACE inhibitors = renal damage - DES = vaginal clear cell adenocarcinoma - Lithium = Ebstein anomaly (atrialized R ventricle) - Valproate = inhibition of maternal folate absorption → neural tube defects - Warfarin = Bone deformities, fetal hemorrhage, abortion, ophtho abnormalities |
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Cytotrophoblast vs. Syncitiotrophoblast |
Cytotrophoblast = inner layer of chorionic villi (on baby side, into mother's placenta) Syncitiotrophoblast = outer layer of chorionic villi, secretes hCG + hPL (on baby's side) |
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Urachus |
Duct between fetal bladder and yolk sac (becomes allantois, for pee) Failure to close: - Patent urachus (urine from umbilicus) - Urachal cyst (infoection, adenoCA) - Vesicourachal diverticulum (outpouching of bladder) |
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Vitelline duct |
Obliterated in the 7th week, connects yolk sac to midgut lumen (for poop) Failure to close: - Vitelline fistula (meconium from umbilicus) - Meckel diverticulum (can have ectopic gastric mucosa/pancreatic tissue) |
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Female genital embryology |
Default Mesonephric duct (Wolffian duct) degenerates Paramesonephric duct (Mullarian duct) develops |
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Male genital embryology |
SRY gene on Y chromosome produces testis-determining factor for testes development - Sertoli cells secrete Mullarian Inhibitory Factor (MIF) → suppresses development of paramesonephric (Mullarian) duct - Leydig cells secrete androgens → stimulate development of mesonephric (Wolffian) duct |
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Paramesonephric duct (Mullarian) |
Female internal structures Fallopian tubes, uterus, upper 1/3 of vagina If Mullarian duct problems in females, will have 2ndary sexual characteristics (ovaries working), but amenorrhea |
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Mesonephric (Wolffian) duct |
Male internal structures (except prostate!) Seminal vesicles, epididymis, ejaculatory duct, ductus deferens |
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Sertoli cells |
Support/nourish sperm Make Mullarian Inhibitory Factor (in utero) Once out of utero: - Secrete inhibin (inhibits FSH) - Secrete androgen-binding protein (maintain local levels of T) - Tight junctions btw sertoli cells = blood-testes barrier - Temperature sensitive! - Convert T and androstenedione to estrogen via aromatase |
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Leydig cells |
Androgens (2ndary male characteristics in utero) Need 5α-reductase to convert T to DHT for secondary characteristics (external genitalia, etc.) Out of utero - Secrete T in the presence of LH - NOT temperature sensitive - (also contain aromatase) |
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Lymphatic drainage of ovaries/testes |
Para-aortic LNs |
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Lymphatic drainage of distal vagina/vulva/scrotum |
Superficial LNs |
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Lymphatic drainage of proximal vagina/uterus |
Obturator, external iliac and hypogastric LNs |
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Autonomic innervation of the male sexual response |
Point, Shoot, Sleep Parasympathetic = erection - NO → ↑cGMP → SM relaxation → vasodilation → proerectile Sympathetic = ejaculation Sympathetic = getting soft |
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Sildenafil, vardenafil |
Inhibit cGMP breakdown (so ↑ SM relaxation, ↑ vasodilation, ↑ erection) |
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Estrogen |
Development of genitalia and breast, female fat distribution Growth of follicle, endometrial proliferation, ↑ myometrial excitability ↑↑↑ of estrogen, LH and progesterone receptors; results in feedback inhibition of FSH and LH; then LH surge; stimulation of prolactin secretion LH activates theca cells (cholesterol to androstenedione); FSH activates granulosa cells (androstenedione to estrogens) |
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Progesterone |
Stimulation of endometrial glandular secretions and spiral arteries; maintenance of pregnancy; ↓ myometrial excitability; thick cervical mucus, ↑ body temperature, inhibition of gonadotropins (LH and FSH), uterine SM relaxation, ↓ estrogen receptor expressivity |
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Menstrual cycle (in short) |
FSH stimulates several follicles to form Dominant follicle produces estrogen (others regress) Estrogen peaks, causing LH and FSH to peak (releases neg inhibition) LH peak responsible for follicle rupture Ovum released Follicle condenses and produces progesterone (maintains thick uterine wall) Corpus luteum degenerates, uterine wall shed |
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Oogenesis |
Arrested in Prophase I until Ovulation Arrested in Metaphase II until fertilization |
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Lactation |
After labour, ↓ in progesterone and estrogen disinhibits lactation Prolactin = induces/maintains lactation, ↓ repro function Oxytocin = assists in milk letdown, promotes uterine contractions |
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hCG |
From syncytiotrophoblasts of placenta Maintains corpus luteum (and therefore progesterone) for 1st trimester (2nd and 3rd trimesters, placenta makes P and E itself) α subunit identical to that if TSH, FSH and LH; β subunit different |
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Hydatitiform mole |
Abnormal conception w/swollen and oedematous villi w/proliferation of trophoblasts Uterus larger than expected, β-hCG ↑↑↑ Presents in second trimester w/grape-like pass through vaginal canal "Snowstorm" on US Rx: suction curettage. Monitor β-hCG to ensure adequate removal and screen for chorioCA (CA of trophoblasts, no villi) |
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Partial mole |
Normal ovum fertilized by 2 sperm (or one sperm that duplicates, 69 chromosomes) Fetal tissue present Villous edema patchy Focal trophoblastic proliferation (around villi) Minimal risk for chorioCA |
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Complete mole |
Empty ovum fertilized by 2 sperm or one sperm that duplicates (46 chromosomes) No fetal tissue Villous deem everywhere Lots of trophoblastic proliferation 2-3% risk for chorioCA |
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Placental abruption |
Placenta pulls off before delivery Abrupt, painful bleeding in 3rd trimester Life-threatening for mother and fetus **cocaine use (+ trauma, HTN, smoking, etc.) |
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Placenta accreta/increta/percreta |
DEfective decidual layer Accreta = attaches to myometrium Increta = attaches into myometrium Percreta = attaches through myometrium |
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Placenta previa |
Attachment of placenta to lower uterine segment (partially or fully covers internal cervical os) Bleeding during delivery |
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Gene products of HPV (for CA) |
E6 = inhibits tumor suppressor gene p53 E7 = inhibits tumor suppressor gene RB |
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Surface epithelial tumors |
Most common type of ovarian tumor CA-125 to track treatment response Cystadenocarcinoma (serous [watery] and mucinous [mucus]; can be benign, borderline or malignant) Endometrioid (endometrial-like glands, often malignant) Brenner (urothelial cells "Bladder", usually benign) |
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Fibroadenoma |
Small, mobile, firm mass w/sharp edges Most common tumour in ppl < 35 YO ↑ size and tenderness w/↑ estrogen NO ↑ risk of cancer |
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Intraductal papilloma |
Small tumour in lactiferous ducts (often beneath areola) Serous or bloody nipple discharge (also papillary CA can cause) Slight risk (1.5-2X) for CA |
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Phyllodes tumour
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Large bulky mass of CT and cysts, "leaf-like" projections Some may become malignant |
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Ductal carcinoma (in situ and malignant) |
Fills ductal lumen Microcalcifications on mammography Early malignancy w/o BM penetration (subtype = comedocarinoma) When invasive: - "rock-hard" mass w/sharp margins - retraction of nipple, dimpling of skin - worst, most invasive, and most common - (subtype = medullary and inflammatory [peau d'orange]) |
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Lobular carcinoma (in situ and malignant) |
Fills lobules Discohesive (not stuck together) b/c no E-cadherin adhesion protein Tx: tamoxifen When invasive: Orderly row of cells But NO mass formation because no E-cadherin! |
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BPH |
Hyperplasia of prostate gland Compresses urethra ↑ PSA Rx: α1-antagonists (to relax sphincter), Finasteride aka 5α-reductase inhibitors (block conversion of T to DHT) |
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Leuprolide
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GnRH analog Agonist when pulsatile (infertility) Antagonist when continuous (prostate cancer, precocious puberty, fibroids) |
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SERMs |
Clomiphene - PCOS (antagonist at E receptors in hypothalamus) Tamoxifen - ER+ breast cancer (antagonist on breast tissue, agonist at uterus, bone) Raloxifene - osteoporosis (agonist on bone, antagonist at uterus) |
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Finasteride |
5α reductase inhibitor ↓ T to DHT For BPH and promotes hair growth |
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Flutamide |
Nonsteroidal competitive inhibitor of androgens at the T receptor For prostate carcinoma |
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Tamulosin |
α1-antagonist to treat BPH Inhibits SM contraction |
