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111 Cards in this Set

  • Front
  • Back
growth hormone's homolog
TSH in same family as? structure?
LH, FSH glycoprotein family
alpha units same, beta units diff
sister products to ACTH
POMC produces
melanocyte stim hormone (MSH), beta lipotropin, beta endorphin
hormones a pit
TSH, LH, FSH, ACTH, GH, prolactin
regulation GH
increased: sleep, stress, puberty H, starvation, exercise, hypoglycemia
decreased: SS, somatomedins, obesity, hyperglycemia, pregnancy
hypothalamic control and negative feedback for GH
hypothal-GHRH, SS inhibit
negative feedback
somatomedins (a pit and hypothal)
GHRH inhibits hypo sxn GHRH
GH stim SS from hypothal which then inhibits
GH excess would do what to glucose levels
glucose intolerance bc GH prevents glu uptake by cells
effects GH
-decrease glu uptake by cells
-incr lipolysis
-increase protein syn and lean body mass
-increase production IGF
how does prolactin inhibit ovulation
inhibits syn and rel of GnRH
regulation prolactin
- DA, + TRH with prolactin inhibiting its own rel at hypo
increase/decrease prolactin sxn
increase: estrogen/preg, breast feeding, sleep, stress, TRH
decrease: DA, SS, prolactin (neg fdbk)
besides serum osmolarity what incr, decr ADH
(incl grps Rx)
incr-volume contraction 50%, pain, nausea** powerful, hypoglycemia, nicotine, opiates, anti neo
decr-EtOH, alpha agonists, ANP (and decr serum osmolarity)
regulation oxytocin
increased by suckling and dilation of cervix and orgasm
(can use to induce labor and decr postpartum bldg)
synthesis of T4--thru oxidation I2
incl Rx
-iodide pump (inhib by thiocyanate, perchlorate, hi level I)
-oxidation of I- to I2 by peroxidase (inhib by PTU)
synthesis T4 from organification on
-Tyr incorporated into thyroglobulin as extruded into lumen Tyr residues react iwth I2 to form MIT, DIT
-coupling to T3 or T4
-iodinated thyroglobulin stored until TSH stim,
how thyroid levels change with hep failure and preg
hep failure: decr TBG, decr total thyroid, free thyroid stays same
preg: incr TBG, incr total thyroid, free thyroid stays same
inhibition in thryoid path
T3 inhibits at a. pituitaru
effects of thyroid thru molecular mech
incr beta 1 R on heart,incr HR, SV
incr Na/K/ATPase incr BMR
cortisol inflamm effects
induce syn lipocortin - plA2
inhibit IL2 syn/sxn
inhib His, Serotonin sxn
up regulate alpha1, incr BP
how insulin protein made
made as single chain peptide proinsulin, w/in storage vesicles proteases cleave the C-peptide. C-peptide is also secreted w insulin (indicated level endogenous insulin)
FSH regulation men
(FSH act on Sertoli maintain spermatogenesis), also makes inhibin which inhib FSH sxn
LH regulation men
(LH act on Leydig-testost syn), testosterone inhib rel GnRH, and LH (at hypothal and a pit)
how puberty created by hormones
start pulsatile GnRH release, which causes pulsatile FSH, LH release. GnRH upregulates its own R
describe theca cell actions
LH stim theca to produce testosterone, goes to granulosa cells for aromatase to convert to 17beta estradiol (2nd stp stim by FSH)
role LH, FSH
-steroid genesis in follicle and corpus luteum
-follicular develop beyond antral stage
action estrogen
prolifer, develop ovarian granulosum
endometrial prolifer
develop genitalae (internal and external), breast, 2 sex, female fat
hepatic syn proteins (upreg estrogen, LH, progesteron R)
inhibit FSH, LH surge
incr myometrial excitability
stim prolactin but then blocks its action on breast?
action progesterone
negative feedback FSH, LH luteal phase,
maintain secretory of uterus during luteal,
maint preg,
myo excitability,
breast develop,
produce thick mucus which inhibits sperm entry,
decr myomet excit so can implant,
develop endometrial sxns and spiral artery develop
incr body temperature
uterine sm m cxn
follicular phase
day 1-14
primordial follicle develops to graafian, estradiol increase causing prolifer uterus, FSH, LH suppressed by estradiol at a pituitary (progest low)
day 15--always 14 d before menses
burst estradiol has positive feedback, causing LH surge, ovulation occurs
cervical mucus increases, less viscous so sperm can penetrate
luteal phase
day 15-28
corpus luteum develops, syn estrogen and progesteron, increase endometrium, if fertilization doesn't occur corpus luteum regresses and estradiol and progesterone levels decrease abruptly
if fertilization occurs what happens
placenta makes HCG rescuing corpus luteum, corpus luteum produces estradiol and progesterone. but 2,3 trimesgter progesterone produced by placenta, estrogen produced by fetal adrenal gland in coordination with placenta
hormones 2-3 trimester?
progesterone produced by placenta, estrogen produced by fetal adrenal gland DHEA-S, then hydrolyzed in fetal liver, transgered to placenta where aromatized to estrogen
initiation event in partuition
lactation mech
why not during preg?
why no ovulation?
prolactin lvls incr in preg but lactation doesn't occur bc estrogen and progesterone block action prolactin on breast. after partuition decr estrogen and profesterone
suckling-stim oxytocin and prolactin
the prolactin inhibits HCG preventing ovulation
hormones in menopause
large incr FSH, decr estrogen, incr LH, incr GnRH
menopause causes
HAVOC Hot flashes, atrophy vagina, osteoporosis, CAD
what indication fertility
progesterone (low infertility), hi progesterone also indicates ovulation
types estrogens, strengths, where from
estradiol (ovary)>estrone > estriol (placenta)
effect of testosterone
-difftn wolffian duct system
-2 sex and grwth spurt
-anabolic (incr mscl, RBC production)
-inhibits GnRH
-fuses epiphyseal plate
potency of testost
FSH stim what hormone production of Sertoli
Sertoli to produce ABP, inhibin
role ABP
androgen-binding protein, ensures testosterone in seminiferous tubules is hi
feedback in spermatogenesis
testosterone inhibits hypo and inhibin inhibits A. pituit
sperm development
spermatogonia A, B (diploid 2N)
(A forms both A, B)
spermatocyte (diploid, 4N)
2 spermatocyte (haploid 2N)
spermatid (haploid, N)
how long does spermatogenesis take
what forms blood testis barrier
tight junctions bw Sertoli
derivation sperm part
middle has mitochondria
**uses fructose
when meiosis I complete
meosis I begun in fetal life, completed just prior to ovulation
what phase is meosis I stopped in
when meosis II happen
at ovulation,? arrested at metaphase until fertilization
name neoplastic germ cell of ovary
-benign cystic teratoma (dermoid cyst)
(struma ocarii composed thyroid), can be immature
-yolk sac
acute pain day 21-26
think corpus luteum cyst (confused w ruptured tubal preg)
presentation of dermoid cyst
(aka benign cystic teratoma)
asx, all maternal (opp molar preg), 3 layers
dysgerminoma presents?
13-30y, but dx early respond to XRT
analog of seminoma in female
two markers for ovarian cancer
histology of choriocarcinoma
no chorionic villi, trophoblast invading myomet, usu after complete mole
call-exner body
rosette arrang cells around fluid=granulosa sex cord tumor ovary
how granulosa ovarian tumor present
usu precocious puberty bc it secretes estrogen
brenner tumor
benign tumor of ovary resembles bladder
pseudomyxoma peritonei
when cystadenocarcinoma leads to intraperitoneal collection of mucinous
name non-germ cell ovarian tumors
-cystadenoma (benign)
-fibroma (benign)
MC s/p partum residual placenta, Staph or Strep
endometrial carcinoma presentation
usu preceeded by endometrial hyperplasia, present post menopause vaginal bleeding, peak older age 55-65. types include endometroid (>50%) better px, papillary, clear
name uterine tumors
-fibroma (uterine leiomyomata)
how do uterine fibroids present
heavy menstrual bldg (bc stimulated bby estrogen)
origin of uterine fibroids
sm mscl myometrium
presentation leiomyosarcoma
bulky tumor w necrosis, hemorrhage, arises de novo more often in blacks. may protrude from os.
highly aggressive, tend recur
presentation uterine leiomyoma
MC tumor in females, often present w mltpl and incr in blacks. estrogen sensitive so incr with preg decr w menopause. does not transform into malignancy
what is the MC gyn malig
endometrial carcnioma (and incr in freq unlike cervical cancer)
adenomyosis, describe, presentation
endomet glands burrow into mscl>3mm. present dysmen, uterine bldg, enlarged tender uterus
endometriosus, describe, present
endomet tissue outside uterus usu ovaries
cyclic bldg w choc cysts
placenta previa, describe, present
placenta att to lower uterine seg soplacenta covers os, if total do C-sxn
presents: painless bleeding
abruptio placenta
premature sep of placenta
present: painful bldg usu in 3rd trimester, assoc w DIC
how might preclampse present clinically
HA, blurred vision, abd pain, edema, AMS, hyperreflexia (decr plt, incr uric)
who at risk for preclampsia
DM, HTN, CRF, autoimmune
placenta accreta
abnormally deep implant of placenta bc defect of decidua layer (usu s/p C-sxn).
onto myomet=acreta
pain, 6wk LMP
ectopic preg
how ectopic preg present
pain 6 wk LMP
fibrocystic brst d
diffuse, bilateral mltpl lesions w green/brown d/c. no increase of cancer unless atypia
what presents bloody d/c (breast dz)
intraductal papilloma, tumor of lactiferous ducts
fibroadenoma of brst
<30 small, mobile, sharp borders-COMMON benign
cystosarcoma phyllodes
older, large bulky tumor of CT and cysts "leaf like" must completely excise. benign
ductal invasive carcinoma
firm, fibrous mass, COMMON
worst is comedo, also cribiform, solid, papill
name the benign brst tumors
-intraductal papilloma
-cystosarcoma phyllodes
comedocarcinoma breast
ductal w cheesy consistency due to central necrosis, worst px of ductals
ductal in situ v lobular in situ
ductal=risk same breast
lobular=risk both breasts
invasive lobular brst ca
often mltpl, bilateral
medullary brst ca
fleshy, cellular, lymphocytic infiltrate
good px
paget's dz, histology, related dz
ecz patches on nipple suggesting underlying cancer.
paget cells=large cells with clear halo
also seen on vulva
inflammatory brst ca
lymphatic involvement-poor px
brst cancer-lymph infiltrate
brst cancer-"indian file"
invasive lobular
risks breast cancer
-family hx
-hx of brst cancer yourself
-early menarche, late meno, nulliparty, first preg>30
-high fat diet
-fibrocystic dz w atypia
Meigs syndrome
ovarian fibroma, ascites, hydrothorax
condyloma acuminatum
veneral wart, usu HPV6, 11
how difft BPH from prostate adeno?
increased total PSA with decreased fraction free PSA suggests malignancy
male-most testicular tumors are benign or malign? what class?
malignant, >90germ cell
name testicular germ cell tumors
yolk sac
name non germ cell testicular carc
leydig, sertoli
present of seminoma
mid 30's painless mass in testis, may have incr HCG.
present of embryonal
2nd MC present w pain or met, usu incr HCG. hemorr, necrosis, worse px
present yolk sac testicular ca
in infancy/early childhoon, with incr AFP
testicular teratoma
in males the mature one is also MALIGNANT! (as well as immature)
present choriocarcinoma, morph
20-30's can be seen in combo, incr HCG, invasion vasculature w/o LN.
cells resemble cytotropho and syncytiotropho
leydig testicular tumor, px, morph
often benign, see intracytoplasm Reinke crystals
present sertoli testicular cancer
usu benign, no endocrine manifest
describe progression of gamete formation
primary gametocyte (46, 4N)
2 gametocyte (23, 2N)
Gamete (23, 1N)
describe timeline of gamete development in female
the primordial germ cell arrives in the ovary at 4wk and difft into oogonia (46,2N)
enter meiosis I to form 1 oocytes (46, 4N) by 5mo and stuck in prophase until puberty
during cycle a 1 oocyte completes meoI to form 2 oocyte (23, 2N) and first polar body. then it enter meioII and is stopped in meta until fertilization
describe timeline of gamete develop in male
primordial germ cell (46, 2N) arrive at testis at wk4 and are dormant until puberty.\
At puberty they difft into type A spermatogonia (46,2N) and some of those turn into B.
the B spermatagonia (46, 2N) enter meosis I and form 1 spermatocytes (46,4N). these then complete meoI and form 2 2spermatocytes (23,1N)
then they undergo spermiogenesis (formation acrosome, condensation nu...)
once sperm are out they most undergo capacitation in the female tract (unmasking glycosyltxrs, removal protein)
when sperm binds zona pellucida undergo acrosome rxn, that helps sperm get thru zona pellucida.
penetration zona pellucida elicits cortical rxn so a 2nd sperm can't fertilize
2nd oocyte completes meoII before the nuclei fuse
then zona pellucida must be degraded before it can implant