repro Flashcards
ACE inhibitor teratogen
REnal damage
alkylating agens teratogen
absence of digits, multiple anomalies
Aminoglycosides teratogen
CN VIII
carbamazepine teratogen
NTDs, craniofacial defects, fingernail hypoplasia, developmental delay, IUGR
DES teratogen
persistence of glandular epithelium in upper 1/3 of vagina –> vaginal clear cell adenocarcinoma, congenital mullerian anomalies
folate antagonists teratogen
NTDs
Lithium teratogen
Ebstein’s (atrialized RV)
Phenytoin teratogen
Fetal hydantoin syndrome: microcephaly, dysmorphic craniofacial features, hypoplastic nails and distal phalanges, cardiac defects, IUGR, MR
Tetracyclines teratogen
discolored teeth
thalidomide teratogen
limb defects (“flipper”)
Valproate teratogen
inhibition of maternal folate absorption –> NTDs
Warfarin teratogen
bone deformities, fetal hemorrhage, abortion, ophthalmologic
heparin doesn’t cross placenta
maternal diabetse teratogen
caudal regression syndrome, congenital heart defects, NTDs
vitamin A excess teratogen
SABs, cleft palate, cardiac anomalies
XRT teratogen
microcephaly, MR
breast epithelium
two layers!
luminal cell (epithelium) – protect duct and make milk in lobules
myoepithelial – contractile
periductal mastitits
smokers –> relative vitamin A deficiency –> squamous metaplasia of lactiferous ducts –> inflammation behind blockage –> subareolar mass with granulation tissue –> nipple retraction
fat necrosis
trauma –> disruption –> saponification –> calcifications, giant cells.
fibrocystic change
hormone mediated, cystic change of lobules and terminal ducts.
hormone mediated.
“vague irregularity”
“blue dome cysts,” fibrosis, cysts, apocrine metaplasia–> No increased risk for Ca!
Ductal hyperplasia (excess layers of epithelium) and sclerosing adenosis (too many glands, can be calcified) –> 2X risk
Atypical hyperplasia (ductal or lobular) –> 5X
NB incr risk of Ca is bilateral!
apocrine metaplasia
only metaplasia that doesn’t incr risk for Ca
intraductal papilloma
small tumor that grows in lactiferous ducts, beneath areola
Serous or bloody d/c
slight inc in Ca risk
must distinguish from papillary carcinoma (will lose myoepithelial cells)
fibroadenoma
small, mobile, firm mass with sharp edges
mot common tumor in pre-menopausal women
incr size and pain with incr estrogen
Not pre-malignant
Phyllodes tissue
Large bulky mass of connective tissue and cysts with “leaf like projections” (similar to fibroadenoma, but overgrowth of fibrous component)
POST-menopausal women
CAN be malignant
DCIS
Ductal hyperplasia –> DCIS. Fills ductal lumen
Early malignancy w/o BM penetration
Comedo type has high grade cells with caseous necrosis and dystrophic calcification at center of ducts (detected on mammo)
Paget dz of nipple
excematous patches on nipple, ulceration.
Paget cells = large cells in epidermis with clear halo
Suggests underlying DCIS! (not true for Paget’s of vulva
Invasive ductal Ca
most common type of invasive
p/w mass (“rock hard”), “stellate”
small, glandular, duct-like cells in desmoplastic stroma (connective tissue)
NB single cell type in epithelium = Ca
Inflammatory carcinoma
subtype of ductal Ca
looks like mastitis that doesn’t resolve with Abx. peau d’orange
cancer present in dermal lymphatics –> blocks drainage
poor prognosis
Medullary Ca
high grade malignant cells with inflammatory infiltrate
incr in BRCA1
good prognosis
LCIS
malignant proliferation from lobule cells
no mass or calcifications (incidental finding)
lack of E-cadherin (CAM)
often multifocal and bilateral
Risk factor for carcinoma, moreso than true cancer
Tx: Tamoxifen and close follow up.
invasive lobular Ca
single-file pattern of invasion due to loss of E-cadherin.
staging of breast Ca
sentinel node Bx
HER2/neu
cell surface growth factor R
(vs Estrogen and progesterone, which are nuclear)
Gene amplification –> excess
trastuzumab = blocker
triple negative Ca
poor prognosis
afr am women
triple negative Ca
poor prognosis
afr am women
BRCA1
incr risk of medullary breast Ca
serous ovarian Ca (also fallopian tube)
BRCA2
breast carcinoma in males
epispadias
more rare than hypospadias
abnormal positioning of genital tubercle
associated with bladder exstrophy
Management of testicular mass
DONT biopsy (seeding of scrotum) Vast majority are germ cell and malignant
seminoma
Germ cell tumor
large cells, clear cytoplasm, central nuclei “fried egg”
homogenous mass with no hemorrhage or necrosis
incr PLAP. radiosensitive, late mets = good prognosis
embryonal carcinoma
malignant, painful. primitive “embryo-like” cells. hemorrhage, early hematogenous spread
incr AFP or bhCG
CTX can cause to mature
yolk sac tumor
most common testicular tumor in children analogous to yolk sac ovarian tumor
“schiller-duval body” = glomeruloid.
elevated AFP
choriocarcinoma
synctiotrophoblasts (hCG) and cytotrophoblasts.
hCG –> hyperthyroidism or gynecomastia
mets to lungs (tiny mass in testicle, massive mets)
Teratoma
mature fetal tissue
2-3 embryonic layers
benign in females, malignant in males
AFP or hCG
Sertoli cell tumor
sex cord stromal tumor
tubules
clinically silen
leydig cell tumor
sex cord stromal tumor
androgen (precocious puberty or gynecomastia)
Reinke crystals
testicular lymphoma
most common testicular mass in male >60, often b/l
often DLBCL
