Reproductive

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Where is FSH produced in males?: F[S]H = [S]ertoli cells -> [S]perm production
Where is LH produced in males?: [L]H = [L]eydig cells
What are the three androgens?: In order of potency:

[1] Dihydrotestosterone (DHT)
[2] Testosterone
[3] Androstenedione

(They make a great band!)
Where are each of the androgens produced?: DHT & Testosterone -> Testis

Androstenedione -> Adrenal
How do you get DHT from Testosterone?: 5alpha-reductase converts DHT to testosterone. It is inhibited by finasteride.
What are the targets for androgens?: [] skin
[] prostate
[] seminal vesicles
[] epididymis
[] liver
[] muscle
[] brain
What is the function of androgens?: [A hairy wolf with a low voice and lots of muscles wants to swim and have sex]

[] Differentiation of wolffian duct system into internal gonadal structure
[] Secondary sexual characteristics & pubertal growth spurt
[] Spermatogenesis
[] Anabolism [+]muscle size [+] RBC production
[] [+] Libido
How do you get estrogens from androgens?: Aromatase found in adipose tissue converts testosterone & androstenedione into estrogen.
What are the different potencies of various estrogens?: Estradiol > Estrone > Estriol
What is the sources of estrogens?: Ovary -> estradiol
Placenta -> Estriol
Blood -> Aromatization
What are the functions of estrogens?: [Things that change with puberty: 'Hair', 'Skin', Genitals, Breast, Fat, Liver, Hormones (FSH&LH), Excitement, Cholesterol]

[] Growth of follicle
[] Endometrial proliferation
[] Development of genitalia
[] Stromal development of breast
[] Female fat distribution
[] Hepatic synthesis of transport proteins
[] Feedback inhibition of FSH
[] LH surge (feedback changes from negative -> positive just before surge)
[] [+] myometrial excitability
[] [+] HDL, [-] LDL
What's the deal with estrogen hormone replacement therapy?: After menopause, estrogen -> [-] hot flashes, [-] bone loss BUT [+]endometrial cancer unless opposed by progesterone
What can lead to increased risk of endometrial cancer?: unopposed estrogen:

[] ERT
[] Early Menarche
[] Late Menopause
What enzyme in which cell does LH act upon?: Desmolase in the Theca cell converts Cholesterol to Androstenedione.
What enzyme in which cell does FSH act upon?: Aromatase in the Granulosa cell converts Androstenedione to Estrogen.
What is the pathway from Cholesterol to Estrogen?: Cholesterol -> Androstenedione (via Desmolase in Theca cell)
...
Androstenedione -> Estrogen (via Aromatase in Granulosa cell)
What is the source of progresterone?: [] Corpus luteum
[] placenta
[] adrenal cortex
[] testes
What is indicated by elevation of progesterone?: ovulation
What are the functions of progesterone?: [What happens when you're pregnant: secretions, varicosities (arteries), less sex (excitability), more mucus, feel hot, don't eat FiSH and then you try to relax)

[] Maintenance of pregnancy
[] Stimulate endometrial glandular secretions
[] Stimulate spiral artery development
[] [-] myometrial excitability
[] Production of thick cervical mucus
[] [+] body temp
[] Inhibits gonadotropins [LH, FSH]
[] Relax uterine smooth muscles
What are the two phases of the menstrual cycle called?: [] Proliferative phase
[] Secretory phase
During what part of the menstrual cycle is follicular growth fastest?: second week of proliferative phase
What stimulates endometrial proliferation?: Estrogen
What maintains endometrium to support implantation?: Progesterone
What happens with decreased progesterone?: decreased fertility
What is Mittelschmerz?: blood from ruptured follicle causes peritoneal irritation ('feeling' ovulation)
What are the steps that cause ovulation?: [1] Estrogen surge day before ovulation
[2] Stimulates LH, inhibits FSH
[3] LH surge causes ovulation
[4] Progesterone induces temp increase
[5] Ferning of cervical mucosa
How do oral contraceptives work?: They prevent estrogen surge so no LH surge so no ovulation.
What stage would you find oocytes during childhood?: Meiosis I is arrested in pr[O]phase until [O]vulation
What stage would you find oocytes in the fallopian tubes?: Meiosis II is arrested in [MET]aphase until the egg [MEETS] a sperm.
What is the source of hCG?: Syncytiotrophoblast of placenta?
What does the syncytiotrophoblast produce?: hCG
What is the function of hCG?: [] Maintains corpus luteum for 1st trimester by acting like LH. Placenta takes over in 2nd trimester
[] Detects pregnancy in urine 8 days after fertilization
[] Elevated hCG also occurs in hydatidiform moles or choriocarcinoma
What hormonal changes occur in menopause?: [-] estrogen
[++] FSH
[+] LH (no surge)
[+] GnRH
What is the average age of onset of menopause?: 51 y/o. Earlier in smokers
What havoc does menopause cause?: [HAVOC]

[H]ot flashes
[A]trophy of the [V]agina
[O]steoporosis
[C]AD
What is a bicornuate uterus?: "Two horned" uterus.

Results from incomplete fusion of the paramesonephric ducts.

Associated with urinary tract abnormalities and infertility.
What are the two types of congenital penile abnormalities?: Hypo[s]padias (pee on your [s]hoes; ventral side; more common)

[E]pispadias (pee on in your [e]ye; dorsal side)
What causes hypospadias?: failure of urethral folds ot close. Associated with UTIs.
What causes epispadias?: Faulty positioning of genital tubercle. Associated with exstrophy of bladder.
What are the different kinds of sex chromosome disorders?: [XXY] Klinefelter Syndrome (male) 1:850

[XO] Turner Syndrome (female) 1:3000

[XYY] Double Y males (male) 1:1000
What are the clinical findings associated with Klinefelter Syndrome?: [] Testicular atrophy
[] eunuchoid body shape
[] long extremities
[] gynecomastia
[] female hair distribution
[] barr body
[] hypogonadism and infertility
<Male with Barr body>: Klinefelter Syndrome
What are the clinical findings associated with Turner Syndrome?: [] Short stature
[] Menopause before menarche (streak ovary)
[] Webbing of neck
[] Coarctation of aorta
[] common cause of primary amenorrhea
[] no barr body
[] "nuckle, nuckle, dimple, nuckle"
<Female with no barr body>: Turner syndrome
What is the clinical findings of Double Y males?: [Why] are so many seen as inmates of penal institutions?

[] Phenotypically normal
[] Very Tall
[] Severe Acne
[] Antisocial behavior
What is pseudohermaphroditism?: Disagreement between the phenotypic (external genitalia) and gonadal (testes vs. ovaries) sex.
What are the clinical findings in female pseudohermaphroditism?: Ovaries present but external genitalia are virilized or ambiguous. 46, XX
What causes female pseudohermaphroditism?: Excessive or inappropriate exposure to androgenic steroids during early gestation:

[] Congenital adrenal hyperplasia
[] Exogenous administration of androgens during pregnancy
What is the clinical presentation of male pseudohermaphroditism?: Testes present, but external genitalia are female or ambiguous.

Most common form is androgen insensitivity syndrome. 46, XY
What is the clinical presentation of a true hermaphrodite?: Both ovary and testicular tissue is present; ambiguous genitalia. Very rare. (46,XX or 47,XXY)
What is the clinical presentation of a person with Androgen insensitivity syndrome?: [] Normal appearing female with defect in androgen receptor.
[] Female external genitalia with rudimentary vagina
[] Uterus and uterine tubes absent
[] Develops testes (often found in labia majora)
[] High levels of testosterone, estrogen & LH
[] 46,XY
What is the clinical presentation of a person with 5alpha-reductase deficiency?: Unable to convert testosterone to DHT.

[] Ambiguous genitalia until puberty
[] At puberty, [+] testosterone causes masculinization of genitalia
[] Testosterone/Estrogen levels normal
[] LH may be high.
What causes benign prostatic hyperplasia?: Men > 50 years of age.
Age-related increase in estradiol sensitizes prostate to growth-promoting effects of DHT.
What are the clinical findings associated with benign prostatic hyperplasia?: [] Men > 50 years of age.
[] Nodular enlargement of periurethral (lateral & middle) lobess of prostate
[] Compression of urethra into a verticla slit
[] [+] frequency of urination, nocturia, dysuria & difficulty stopping & starting stream of urine.
What are the complications associated with benign prostatic hyperplasia?: [] distention and hypertrophy of the bladder
[] hydronephrosis
[] UTI
What are the clinical presentations of prostatic adenocarcinoma?: [] Men > 50 y/o
[] Posterior lobe of prostate gland
[] diagnosed as hard nodule on digital rectal exam
[] elevated prostatic acid phosphate and PSA
What tumor markers are available for prostatic adenocarcinoma?: PSA & Prostatic acid phosphatase
<Elevated serum alkaline phosphatase & PSA>: Osteoblastic metastases on prostatic adenocarcinoma
<Honeycombed uterus>: Hydatidiform mole
What is a Hydatidiform mole?: A pathologic ovum ("empty egg") resulting in cystic swelling of chorionic villi and proliferation of chorionic epithelium (trophoblast).
What is the clinical findings of a Hydatidiform mole?: [] "Honeycombed uterus" or "cluster of grapes" appearance.
[] High Beta-hCG
[] Common precursor of choriocarcinoma
What is a common precursor of choriocarcinoma?: hydatidiform mole
What is the difference between a complete and a partial hydatidiform mole?: Genotype of [complete] mole is 46,XX and is [completely] paternal in origin with no associated fetus.

[Part]ial mole is made up of 3 or more [Parts] (triploid/tetraploid) with fetal [Parts]
What is the difference between preeclampsia and eclampsia?: preeclampsia is a triad of findings:

[] hypertension
[] proteinuria
[] edema

eclampsia adds:
[] seizures
When does preeclampsia/eclampsia manifest itself?: 7% of pregnant women from 20 weeks' gestation to 6 weeks postpartum.
What factors increase the risk of preeclampsia/eclampsia?: [] preexisting hypertension
[] diabetes
[] chronic renal disease
[] autoimmune disorders
What is teh HELLP syndrome?: Associated with preeclampsia/eclampsia:

[H]emolysis
[E]levated [L]FTs
[L]ow [P]latelets
What are the clinical features of preeclampsia/eclampsia?: [] Headache
[] Blurred vision
[] abdominal pain
[] edema of face and extremities
[] altered mentation
[] hyperrelexia
[] thrombocytopenia
[] hyperuricemia
What is the treatment for preeclampsia?: Delivery of fetus as soon as viable. Otherwise bed rest, salt restriction and monitering and treatment of hypertension.

For eclampsia, a medical emergency, IV magnesium sulfate & diazepam.
What is abruptio placentae?: Premature separation of placenta. PAINFUL uterine bleeding (3rd trimester). Fetal death.
What factors increase the risk of abruptio placentae?: [] DIC
[] smoking
[] hypertension
[] cocaine use
What is placenta accreta?: Defective decidual layer allows placenta to attach directly to myometrium. Massive hemorrhage after delivery.
What factors increase the risk of placenta accreta?: [] prior C-section
[] inflammation
What is placenta previa?: Attachment of placenta to lower uterine segment. May occluse cervical os.
What are the clinical findings assocaited with placenta previa?: PAINLESS bleeding in any trimester
What is an ectopic pregnancy?: A fertalized egg outside the uterus. Most often in fallopian tubes.
What are the clinical findings associated with ectopic pregnancy?: [] Salpingitis (PID)
[] [+] hCG w/ lower abdominal pain
What are the two types of amniotic fluid abnormalities?: Polyhydramnios > 1.5-2 L amniotic fluid

Oligohydramnios < 0.5 L amniotic fluid
What causes polyhydramnios?: An inability to swallow amniotic fluid due to esophageal/dudoenal atresia. Also associated with anencephaly.
What causes oligohydramnios?: An inability to exrete urine due to bilateral renal agenesis or posterior urethral valves in males.
What different kinds of cervical pathology are found?: [] Dysplasia & CIS = Disordered epithelial growth associated with HPV 16,18. May progress to invasive carcinoma.
[] Invasive carcinoma = Often squamous cell carcinoma.
How can you prevent invasive cervical carcinoma?: Pap smear can catch cervical dysplasia before it progresses to invasive carcinoma.
What complications can arise from invasive cervical carcinoma?: Lateral invasion can block uereters casuing renal failure.
What are six different types of uterine pathology?: [1] Endometriosis
[2] Adenomyosis
[3] Endometrial hyperplasia
[4] Endometrial carcinoma
[5] Leiomyoma
[6] Leiomyosarcoma
What is endometriosis?: Non-neoplastic endometrial glands/stroma in abnormal locations OUTSIDE the uterus.
<"Chocolate cysts">: blood-filled ovarian cysts indicative of endometriosis of ovaries.
What are the clinical manifestations of endometriosis?: [] cyclic bleeding from ectopic endometrial tissue.
[] found in ovary & on peritoneum
[] severe menstrual-related pain
[] results in infertility
What is adenomyosis?: endometriosis within the myometrium
What causes endometrial hyperplasia?: Excess estrogen stimulation causes endometrial gland proliferation.
What are the clinical presentations of endometrial hyperplasia?: [] vaginal bleeding
[] [+] risk of endometrial carcinoma
What is the most common gynecological malignancy?: endometrial carcinoma
What is the peak age for endometrial carcinoma?: 55-65 years old
What are the clinical manifestations of endometrial carcinoma?: [] vaginal bleeding
[] often preceeded by endometrial hyperplasia
What risk factors contribute to a greater risk of endometrial carcinoma?: [] prolonged estrogen use
[] obesity
[] hypertension
What is the most common of all tumors in females?: Leiomyoma = fibroid of myometrium.
Does leiomyoma progress to leiomyosarcoma?: Nope. Separate processes.
What factors increase or decrease the size of a leiomyoma?: Estrogen size -> [+] pregnancy, [-] menopause
Who is at an increased risk for developing leiomyoma and leiomyosarcoma?: [+] African americans
What are the clinical findings of a leiomyosarcoma?: [] Bulky tumor with areas of necrosis & hemorrhage.
[] Agressive (recurs)
[] May protrude from cervix and bleed
<a single recurrant leiomyoma>: It's probably not a leiomyoma, but rather a leiomyosarcoma
What causes polycystic ovarian syndrome?: [+] LH production leads to anovulation and hyperandrogenism due to deranged steroid synthesis. (aka high estrogens & high androgens)
What are the clinical features of polycystic ovarian syndrome?: [] amenorrhea
[] infertility
[] obesity
[] hirsutism
What is the treatment for polycystic ovarian syndrome?: [] Weight loss
[] OCPs
[] Gonadotropin analogs
[] Surgery
What are four different types of ovarian cysts?: [1] Follicular cyst
[2] Corpus luteum cyst
[3] Theca-lutein cyst
[4] Chocolate cyst
What is a follicular cyst?: Distention of unruptured graafian follicle. Associated with hyperestrinism & endometrial hyperplasia.
What is a corpus luteum cyst?: Hemorrhage into persistent corpus luteum. Presents with menstrual irregularity.
What is a theca-lutein cyst?: Often bilateral/multiple. Due to gonadotropin stimulation. Associated with choriocarcinoma and moles.
What is a "chocolate cyst"?: blood containing cyst from ovarian endometriosis. Varies with menstrual cycle.
What kind of ovarian cyst is associated with hyperestrinism and endometrial hyperplasia?: Follicular cyst
What kind of ovarian cyst is associated with choriocarcinoma and moles?: Theca-lutein cyst
What kind of ovarian cyst varies with menstrual cycle?: "Chocolate cyst"
What kind of ovarian cyst is associated with menstrual irregularity?: Corpus luteum cyst
What are the five types of germ cell tumors?: [1] Germinomas
[2] Yolk sac tumors
[3] Choriocarcinoma
[4] Embryonal carcinoma
[5] Teratomoa
What is the most common malignant germ cell tumor of the ovaries and testes?: Germinomoa. Dysgerminoma in ovaries, Seminoma in testes
What is the clinical presentation of a dysgerminoma?: Common malignant germ cell tumor of the ovary. Sheets of uniform cells with [+] hCG
What is the clinical presentation of a seminoma?: Common malignant germ cell tumor of the testes. Presents with painless testicular enlargement. Increased risk with cryptorchidism.
What factors increase the risk for seminoma?: cryptorchidism
Where are yolk sac tumors found?: Aggressive malignancy in ovaries, testes & sacrococcygeal area of young children.
What are the clinical findings associated with yolk sac tumors?: Schiller-Duval bodies with primitive glomeruli and [+] AFP.
<Schiller-Duval bodies>: yolk-sac tumor
What is a choriocarcinoma?: [] rare but malignant
[] large hyperchromatic syncytiotrophoblastic cells.
[] develops during pregnancy in mother or baby.
[] [+] hCG
<hyperchromatic syncytiotrophoblastic cells>: choriocarcinoma
What is the second most common testicular germ cell tumor?: embryonal carcinoma
What is the clinical presentation of an embryonal carcinoma?: [] painful testicular mass
[] glandular with papillary convolutions
How do teratomas present in females?: [] contain cells from 3 germ layers.
[] mature teratoma is benign while immature form is aggressively malignant
How do teratomas present in males?: [M]en, [M]ature teratomas are [M]alignant and painful. Can present with gynecomastia.
What is struma ovarii?: ovarian teratoma containing thyroid tissue
What are the seven types of ovarian non-germ cell tumors?: [1] Serous cystadenoma
[2] Serous cystadenocarcinoma
[3] Mucinous cystadenoma
[4] Mucinous cystadenocarcinoma
[5] Brenner tumor
[6] Ovarian fibroma
[7] Granulosa cell tumor
What are the two most common non-germ cell tumors of the ovary? (Hint: They often present bilaterally): [1] Serous cystadenoma (20%) Benign.
[2] Serous cystadenocarcinoma (50%) Malignant.
What two types of non-germ cell ovarian tumors are lined by mucous-secreting epithelium?: [1] Mucinous cystadenoma
[2] Mucinous cystadenocarcinoma
What is pseudomyxoma peritonei?: Intraperitoneal accumulation of mucinous material from ovarian or appendiceal tumor
What is a Brenner tumor?: benign non-germ cell tumor of the ovary that resembles [B]ladder epithelium
What is Meigs' syndrome?: Triad of: Ovarian fibroma, ascites & hydrothorax
<Ovarian fibroma, ascites & hydrothorax>: Meigs' syndrome
What are Call-Exner bodies?: small follicles filled with eosinophilic secretions
What does granulosa cell tumors secrete?: Estrogen (Granulosa cell!) -> precocious puberty in kids.
What are the three types of testicular non-germ cell tumors?: [1] Leydig cell
[2] Sertoli cell
[3] Testicular lymphoma
What is a Leydig cell tumor?: Benign non-germ cell testicular tumor containing Reinke crystals. Produces androgens -> gynecomastia / precocious puberty in boys
What tumors are associated with precocious puberty?: Girls: Granulosa cell tumors -> Estrogen

Boys: Leydig cell tumors -> Androgens
What is a sertoli cell tumor?: Benign non-germ cell testicular tumor from sex cord stroma.
What is a the most common testicular cancer in older men?: testicular lymphoma
What type of breast disease is often bilateral?: Fibrocystic disease
What are the four histologic types of fibrocystic disease?: [1] Fibrosis = stromal hyperplasia
[2] Cystic = fluid filled
[3] Sclerosing = [+]acini
[4] Epithelial hyperplasia = [+] # epithelial cell layers in terminal duct lobule. [+] carcinoma risk with atypical cells. > 30y/o
What are the three types of benign breast tumors?: [1] Fibroadenoma
[2] Cystosarcoma phyllodes
[3] Intraductal papilloma
What is the most common breast tumor in women under 25?: Fibroadenoma
What is the clinical presentation of a fibroadenoma of the breast?: Benign. Small, mobile, firm mass with sharp edges. [+] size and tenderness with period/pregnancy. <25 y/o
What is the clinical presentation of cystosarcoma phyllodes?: Benign tumor of the breast. Large, bulky mass of connective tissue and cysts. Tumor may have "leaflike" projections.
<Tumor with "leaflike" projections>: Cystosarcoma phyllodes of the breast
What is the clinical presentation of an intraductal papilloma?: Benign breast tumor of lactiferous ducts. Presents with nipple discharge.
<Bleeding from single hole when pressing on nipple>: Intraductal papilloma
Where does breast carcinoma arise from?: mammary duct epithelium or lobular glands
What receptors are frequently overexpressed in breast carcinoma?: estrogen/progesterone receptors or erb-B2 / HER-2
What are the seven histologic types of breast carcinomas?: [1] Ductal carcinoma in situ (DCIS)
[2] Invasive ductal
[3] Comedocarcinoma
[4] Inflammatory
[5] Invasive lubular
[6] Medullary
[7] Paget's disease of the breast
<breast tumor with cheesy consistency>: Comedocarcinoma (think popping a zit)
<bilateral breast carcinoma>: Invasive lobular
<Large cells with clear halo>: Paget cells suggestive of underlying carcinoma
What is DCIS?: Ductal carcinoma in situ an early malignancy without basement membrane penetration.
What does DCIS grow up to become?: Invasive ductal carcinoma (that's why you need to catch DCIS fast)
What is the breast carcinoma with the worst prognosis?: Inflammatory = lymphatic involvement.
What is unique about the presentation of invasive lobular carcinoma?: It is often multiple and bilateral
<Eczematous patches on nipple>: Paget's disease
What are the risk factors for breast disease?: [] Gender
[] Age
[] Early menarche <12 y/o
[] Late menopause >50 y/o
[] delayed 1st pregnancy > 30 y/o
[] family history of 1st-degree relative with breast cancer at a young age

[] NOT fibroadenoma or nonhyperplastic cysts
What is the clinical use of Finasteride?: [Fin]asteride = [Five]alpha reductase inhibitor
[-] conversion of testosterone to DHT
[] treat BPH
[] treat Male pattern baldness
What is the clinical use of Flutamide?: Nonsteroidal competitive inhibitor of androgens at the testosterone receptor. Used in prostate carcinoma
What is the clinical use of Ketoconazole & spironolactone?: [] Inhibit steroid synthesis
[] Treat polycystic ovarian syndrome
What is the clinical use for sildenafil/vardenafil?: [Fill] the penis (Erectile dysfunction)
What is the mechanism of sildenafil/vardenafil action?: [1] Inhibit cGMP phosphodiesterase,
[2] [+] cGMP
[3] smooth muscle relaxation in the corpus cavernosum
[4] [+] blood flow & penile erection
What is the toxicity of sildenafil/vardenafil?: [!] Life threatening hypotension if takin nitrates.

[] Headache
[] flushing
[] dyspepsia
[] blue-green color vision
What is the clinical use of Leuprolide?: Pulsatile - Infertility
Continuous w/ flutamide - prostate cancer / uterine fibroids
What is the mechanism of action of Leuprolide?: GnRH analog acts as agonist when used pulsatile, but antagonist when used continuously.
What is the toxicity of Leuprolide?: [] antiandrogen
[] nausea
[] vomiting
{BPH or Male Pattern Baldness}: Finasteride
{Prostate carcinoma}: Flutamide + continuous Leuprolide
{Polycystic ovarian syndrome}: Ketoconazole + Spironolactone
{Erectile Dysfunction}: Sildenafil / Vardenafil (Fill the penis)
{Infertility}: Pulsatile use of Leuprolide
-or-
Clomiphene
{Uterine fibroids}: continuous Leuprolide
{Abortifacient}: Mifepristone (RU-486)
What is the clinical use of Clomiphene?: Treatment of infertility
What is the mechanism of action for Clomiphene?: [+] LH/FSH via partial agonist at estrogen receptors in the pituitary gland. Prevents normal feedback inhibition.
What are the toxicities associated with Clomiphene?: Think estrogen toxicity:

[] Hot flashes
[] Ovarian enlargement
[] multiple pregnancies
[] visual disturbances
What is the clinical use for Mifepristone?: aka RU-486

[] Abortifacient (prevents implantation)
What is the mechanism of action for Mifepristone?: Competitive inhibitor of progestins at progesterone receptors.
What is the toxicities associated with Mifepristone?: [] Heavy bleeding
[] GI effects (nausea, vomiting, anorexia)
[] abdominal pain
What are the advantages & disadvantages of oral contreception use?: Advantages:
[] Reliable
[-] endometrial/ovarian cancer risk
[-] ectopic pregnancy risk
[-] pelvic infections
[] regulation of menses

Disadvantages:
[] Taken daily
[] No STD protection
[+] triglycerides
[] Depression, weight gain, nausea, hypertension
[] hypercoagulable state

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Number of cards 185