Reproductive Flashcards
Venous drainage of Left and Right Ovaries/Testes:
Left Ovary/Testis –> L gonadal vein –> L renal vein –> IVC
R ovary/testis –> R gonadal vein –> IVC
***this is the same as with the adrenals: Left adrenal drains to L renal vein before draining into IVC (but, Right adrenal drains into Right adrenal vein, which drains straight into IVC)
Lymphatic drainage of Ovaries/Testes:
Para-aortic lymph nodes
Lymphatic drainage of distal 1/3 of vagina, vulva, scrotum:
superficial inguinal nodes
Lymphatic drainage of proximal 2/3 of vagina, uterus
Obturator, external iliac, and hypogastric nodes
On which side is a varicocele more common to occur? Why?
Varicoceles are more common on the the left; b/c flow is less continuous on the left (left testis –> left spermatic vein –> left renal vein –> IVC)
Cell type in the Ovaries:
Simple cuboidal epithelium
Cell type in Fallopian Tubes?
Simple columnar epithelium
–> Ciliated!
Cell type in Uterus?
Simple columnar epithelium
–>pseduostratified, tubular glands
Cell type in Endocervix? Ectocervix?
- Endocervix–> Simple columnar epithelium
* Ectocervix –> Stratified squamous epithelium
Cell type in Vagina:
stratified squamous epithelium
–>non-keratinized
Which female reproductive ligament is a derivative of the gubernaculum?
Round ligament of uterus
- ->connects uterine fundus to labia majora
- ->does not contain any structures!
- ->Travels through the round inguinal canal
- ->Gubernaculum involved in descent of ovaries/testes during development
Pathway of sperm during ejaculation:
“SEVEN UP”
*Seminiferous tubules –> Epididymis –> Vas deferens –> Ejaculatory ducts –> (Nothing) –> Urethra –> Penis
Which nerve is involved in male Erection? Emission? Ejaculation?
*First: Point and Shoot (Erection = PSNS; Emission = SNS)
- Nerves involved:
- Erection –> pelvic nerve (PSNS)
- Emission –> hypogastric nerve (SNS)
- Ejaculation –> pudendal nerve (visceral and somatic nerves)
- Emission = sperm and seminal fluid travel from scrotum into prostatic urethra
- Ejaculation = from prostatic urethra to outside world
Sildenafil and Vardenafil mechanism:
–> both inhibit cGMP breakdown. So: increased amounts of cGMP –> smooth muscle relaxation –> vasodilation –> proerectile
*NO also stimulates increased cGMP
*This is in opposed to Norepinephrine:
NE–>increases intracellular Calcium –> smooth muscle contraction –> vasoconstriction –> antierectile
What type of cell produce primary spermatocytes? Where are these cells located?
- ->Spermatogonia = Germ cells –> produce primary spermatocytes
- ->line seminiferous tubules
Sertoli cells:
- Where are they located?
- Functions?
- ->line seminiferous tubules
- ->overall: support sperm synthesis
- Functions:
- secrete inhibin (inhibits FSH)
- secrete ABP (Androgen-Binding Protein)
- produce anti-mullerian hormone (mullerian-inhibiting factor)
- form blood-testis barrier (tight jxns b/w adjacent Sertoli cells)
- support and nourish developing spermatozoa
- regulate spermatogenesis
***note: sertoli cells are temperature sensitive: if increase temperature (like with a varicocele or cryptochordism (undescended testes)) –> get decreased sperm production and decreased inhibin
Leydig cells:
- Where are they located?
- Functions?
- Located in interstitium of seminiferous tubules
- Functions:
- secrete Testosterone!
- -> this is unaffected by temperature! (unlike Sertoli cells, which are affected by temperature)
Where does spermatogenesis occur? When does it occur?
- -> occurs in seminiferous tubules
- -> begins at puberty
Spermiogenesis:
part of spermatogenesis: spermatids loss cytoplasmic contents, gain acrosomal cap to form mature spermatozoon
Testosterone vs DHT (Dihydrotestosterone) vs Androstenedione:
Potency: DHT > Testosterone > Androstenedione
*DHT and Testosterone are produced in testes:
Testosterone –> DHT (by 5-alpha-reductase)
*Androstenedione is produced in adrenals
***both Testosterone and Androstenedione are converted to Estrogen in adipose tissue and Sertoli cells by Aromatase!
Testosterone is involved in the differentiation of all internal genitalia, except?
- -> Testosterone is NOT involved in differentiation of prostate!
- -> DHT is! (DHT is also involved in differentiation of penis and scrotum –> external genitalia)
Which forms of Androgens are converted to Estrogen?
Testosterone and Androstenedione
17-beta-estradiol
Form of estrogen that is formed in the ovaries
–>predominant form of estrogen during reproductive years
Estriol
- ->form of estrogen that is formed in placenta
- ->predominant type of estrogen in serum during pregnancy
Estrone
- ->form of estrogen formed in blood via aromatization
- -> predominant form of estrogen during menopause
Which form of estrogen is most potent?
Highest potency: Estradiol > Estrione > Estriol
Affect of estrogen on Prolactin?
Estrogen stimulated prolactin secretion, BUT it inhibits prolactin’s action on the breast! (so, don’t give OCPs to breast-feeding women!)
Where on cell are estrogen receptors found?
–>receptors are in nucleus; translocate to nucleus when bound by ligand (cytosolic steroid receptor)
Effect of estrogen on HDL and LDL?
*increased HDL, decreases LDL!
Theca cells:
Stimulated by LH
*convert cholesterol –> Androstenedione, by the enzyme desmolase (17-alpha-hydroxylase!)
Granulosa cells:
- stimulated by FSH
* get Andostenedione from Theca cells and convert: Androstenedione –> Estrogen, via Aromatase!
Desmolase
Enzyme that converts cholesterol –> Androstenedione in Theca cells of ovary
–>Desmolase = 17-alpha-hydorxylase
3 sources of Estrogens:
- Ovaries (Estradiol)
- Blood/Aromatization (Estrone)
- Placenta (Estriol)
Sources of Progesterone:
- Corpus luteum
- Placenta
- Adrenal Cortex
- Testes
Progesterone functions:
- -> it’s “Pro-gestation!”
- stimulates endometrial gland secretions
- maintains pregnancy
- decreases myometrial excitability (vs estrogen, which increases it; but, want to maintain pregnancy, so not excite myometrium!)
- produces thick cervical mucus (so sperm won’t enter)
- increases body temp
- INHIBITS FSH and LH
- relaxes uterine smooth muscle (prevents contractions)
- decreases estrogen receptor expressivity
Which phase of the menstrual cycle is variable length? Which is a constant length and how long?
Follicular phase = Proliferative phase –> phase from menstruation to ovulation = variable
Luteal phase = Secretory phase –> phase between ovulation and menstruation = constant 14 days.
Definition of:
- oligomenorrhea?
- polymenorrhea?
- metrorrhagia?
- menometrorrhagia?
- oligomenorrhea: >35 days
- polymenorrhea <21 days
- metrorrhagia = frequent but irregular menstruation
- menometrorrhagia = heavy, irregular menstruation at irregular intervals
Mittelschmerz
–>ovulation may mimic appendicitis: blood from ruptured follicle causes peritoneal irritation that can mimic appendicitis
What happens during ovulation?
Estrogen surge and increased GnRH receptors on ant pit–> stimulates LH surge/release –> rupture of follicle (ovulation) –> increased progesterone (which causes an increased temperature)
Oogenesis:
- phase at birth?
- phase at ovulation?
- Arrested in Prophase of Meiosis 1 until ovulation
- Arrested in Metaphase of Meiosis 2 until fertilization
***If fertilization does not occur, secondary oocyte degenerates
Where does fertilization usually occur?
- -> Ampulla of fallopian tube
- occurs within 1 day after ovulation
How long after fertilization does implantation within uterus wall occur?
6 days after fertilization
How long after fertilization/conception does hCG appear in blood? in urine?
- ->in blood 1 week after conception/fertilization
- ->in urine (ie home pregnancy test) 2 weeks after conception/fertilization
Source of hCG?
Syncytiotrophoblast of placenta
Function of hCG?
–>maintains corpus luteum (and progesterone) during 1st trimester by secreting LH. During 2nd and 3rd trimesters, placenta synthesizes its own estriol and progesterone, so corpus luteum degenerates
Pathologic states with increased hCG?
- hydatidiform mole
- choriocarcinoma (ovarian germ cell tumor)
Hormonal changes in menopause (estrogen, FSH, LH, GnRH):
- decreased estrogen (primary source of estrogen = peripheral conversion of androgens –> estrone)
- increased FSH
- increased LH (but not as much as FSH)
- increased GnRH
Hormone findings in Klinefelter’s: (LH, FSH, Testosterone, Estrogen)
- decreased inhibin (d/t testicular atrophy, dysgenesis of seminiferous tubules) –> increased FSH
- decreased testosterone (d/t abnormal Leydig cell fxn) –> increased LH –> increased Estrogen
- So:
- increased FSH
- increased LH
- decreased testosterone
- increased estrogen
- decreased sperm
Hormonal and other findings in Turner’s:
- Atrophy of ovaries = “streak ovaries” –> infertility
- horseshoe kidding
- webbing of neck
- short stature
- preductal coarctation of aorta
- bicuspid aortic valve
- hormones:
- decreased estrogen
- increased LH and FSH
-No Barr body in neutrophils (b/c only have 1 X, so all X’s are active!)
Causes of female pseudohermaphroditism (XX, ovaries, but virilized or ambiguous external genitalia):
- ->d/t excessive androgen exposure early in gestation:
- Congenital Adrenal Hyperplasia (21-hydroxylase or 11-beta-hydroxylase deficiency)
- Exogenous steroids during pregnancy
Causes of male pseduohermaphroditism (XY, tests, but female or ambiguous external genitalia):
–>Androgen Insensitivity Syndrome = Testes feminization
Androgen Insensitivity Syndrome:
- Genotype
- Defect
- Presentation
- Hormones (Testosterone, Estrogen, LH, FSH)
- XY
- Defect in androgen receptor
- Presentation:
- normal appearing female (b/c no response to androgens)
- female external genitalia with rudimentary vagina (b/c still have lower 2/3rds of vagina, b/c lower 2/3rds develop from urogenital sinus; whereas upper 1/3rd develops from mullerian duct, but no mullerian duct in this case)
- no uterus or uterine tubes
- no sexual hair
- develops testes (see 2 lumps in labia majora; must be removed to prevent cancer)
- Hormones:
- Elevated Testosterone
- Elevated Estrogen
- Elevated LH
- Normal FSH
5-alpha-reductase deficiency:
- presentation?
- Hormones?
- autosomal recessive, in XY males:
- ->can’t convert testosterone to DHT
- ambiguous genitalia until puberty, then masculinization/male external genitalia at puberty, b/c of increased testosterone secretion –> “penis at 12”
- Normal internal genitalia
- Hormones:
- Normal testosterone, Estrogen
- Normal or elevated LH
Anosmia, lack of secondary sex characteristics –> ?
-hormones in this condition (GnRH, FSH, LH, Testosterone…)?
- ->Kallman syndrome
- defective development of GnRH cells and olfactory –> so, decreased synthesis of GnRH in hypothalamus
- autosomal dominant condition
- Hormones:
- decreased GnRH
- decreased FSH and LH
- decreased testosterone
- decreased sperm count
“honeycombed uterus” or “cluster of grapes” appearance of uterus?
–>hydatidiform mole
“snowstorm” appearance at 1st sonogram?
–>Hydatidiform mole
Most common precursor of choriocarcinoma?
–>Hydatidiform mole
Treatment for hydatidiform mole?
–>D and C, and Methotrexate
Karyotype of Complete vs Partial Hydatidiform mole:
- Complete: 46XX or 46XY
* Partial: 69XXX, 69XXY, 69XYY
Components (sperm, egg) of Complete vs Partial moles?
- Complete: 2 sperm, no/empty egg
* Partial: 2 sperm + 1 egg
What is preeclampsia? eclampsia?
- Preeclampsia = HTN + Proteinuria (and commonly edema too)
* Eclampsia = Preeclampsia + seizures
Preeclampsia timing? if before 20 weeks?
Preeclampsia: from 20 weeks gestation to 6 weeks postpartum
*If preeclampsia before 20 weeks –> Molar pregnancy
HELLP syndrome:
- ->associated with preeclampsia/eclampsia:
- Hemolysis
- Elevated LFTs
- Low Platelets
–>anemia + bruising/gum bleeding + jaundice + elevated BP
Treatment of Preeclampsia/Eclampsia?
- ->Deliver fetus if possible, safe
- ->Monitor, supportive, bed rest, salt restriction
- -> IV magnesium sulfate (1st choice) or Diazepam for seizures in eclampsia
Placental abruption:
- what is it?
- presentation?
- risk factors?
- ->premature detachment of placenta from implantation site
- ->PAINFUL bleeding during 3rd trimester, fetal death; if abrupt, can be fatal
- ->may lead to DIC
- Risk factors: (anything that causes vasoconstriction)
- smoking
- HTN
- cocaine use
Placenta accreta:
- what is it?
- presentation?
- risk factors?
–>placenta attaches to myometrium (instead of endometrium) so no separation of placenta after birth
–>Massive bleeding AFTER delivery
- Risk factors:
- prior C-section
- inflammation
- placenta previa
Placenta previa:
- what is it?
- presentation?
- risk factors?
–>attachment of placenta to lower uterine segment; placenta may cover/block the internal os (so don’t stick finger in to check/dx, b/c may tear and bleed)
–>PAINLESS bleeding in ANY trimester
- Risk factors:
- multiparity
- prior C-section
Endometrial biopsy of an ectopic pregnancy:
–>Decidualized endometrium, but no chorionic villi
Ectopic Pregnancy:
- most common location?
- Presentation?
- Risk factors?
–>usually in fallopian tubes
- Presentation:
- elevated hCG (to normal pregnancy levels)
- sudden abdominal pain (may look like appendicitis)
- may or may not have bleeding
- decidualized endometrium, but no chorionic villi on biopsy
- Risk factors: (anything that causes tubal scarring)
- hx of PID
- ruptured appendix
- prior tubal surgery
Painless bleeding any trimester of pregnancy?
–>Placenta previa (placenta attaching to lower part of uterine, ie cover the internal os)
Painful bleeding during 3rd trimester?
–> placenta accreta (detachment of placenta from implantation site)
bleeding after birth/delivery?
- ->Placenta accreta (placenta doesn’t separate after birth)
- ->can also get postpartum hemorrhage from any retained placental tissue
Polyhdramnios - conditions?
- Esophageal/Duodenal atresia (can’t swallow fluid)
- Anencephaly (can’t swallow fluid…)
Oligohydramnios - conditions?
- placental insufficiency
- bilateral renal agenesis (can’t pee) (Potter’s)
- posterior urethral valves in males (can’t pee)
Cervical Carcinoma in situs (CIN):
- what is it? where does it start?
- cause?
- risk factors?
- ->begins at squamo-columnar jxn of cervix and extends out
- Associated with HPV 16 and 18
- may progress (slowly) to invasive carcinoma if untreated
- Main risk factors:
- ->multiple sex partners
- ->smoking
Which HPV strains are associated with cervical cancer? And, what is the MECHANISM?
- ->HPV 16 and 18
- HPV 16:
- E6 gene inhibits p53 suppressor gene
- HPV 18:
- E7 gene inhibits Rb suppressor gene
Koilocytes:
- ->cells look kind of like fried eggs (wrinkled nuceli with perinuclear halo)
- ->associated with cervical dysplasia; HPV
Endometritis:
- cause/what is it?
- trtmnt?
–>inflammation of endometrium d/t retained products in the uterus (like after delivery, miscarriage, abortion, IUD/foreign body)
- Treat:
- cefoxitin (2nd gen cephalosporin)
- ticarcillin-clavulanate (anti-pseudomonal + beta-lactamase inhibitor)
- ampicillin-sulbactam (aminopenicillin + beta-lactamase inhibitor)
Endometriosis:
- what is it?
- presentation?
- treatment?
–>endometrial glands outside the uterus (in ovaries, peritoneum…)
- Presentation:
- cyclic bleeding from ectopic endometrial tissue
- “chocolate cysts” = blood-filled areas from ectopic endometrial tissue bleeding
- severe menstrual related pain
- dyspareunia
- menorrhagia
- infertility
- normal-sized uterus!
*Treatment = Danazol (synthetic androgen that acts as partial agonist at androgen receptors)
Adenomyosis:
- what is it?
- presentation?
- treatment?
–>endometrial tissue within myometrium (so, like endometriosis, but still within uterus - in the myometrium)
- Presentation:
- menorrhagia (heavy bleeding)
- dysmenorrhea
- pelvic pain
- Enlarged uterus (vs normal uterus in endometriosis)
*Treatment = hysterectomy
Most common gynecological malignancy?
- ->Endometrial carcinoma
- vaginal bleeding, post-menopause; usually preceded by endometrial hyperplasia (from elevated estrogens…)
Most common tumor in females?
–>Leiomyoma = fibroid
=benign, smooth muscle tumor in uterus, well-demarcated, rare malignant transformation (does not progress to leiomyosarcoma)
-tumors are estrogen-sensitive (bigger during pregnancy; smaller during menopause)
-may cause uterine bleeding (leading to anemia)
-whorled pattern of smooth muscle bundles
Gynecological tumors:
- 3 highest incidence:
- 3 with worst prognosis:
Incidence: Endometrial > Ovarian > Cervical
(Cervical is most common worldwide, but not in US)
Worst prognosis: Ovarian > Cervical > Endometrial
*so, ovarian has worst prognosis…
Age of menopause in premature ovarian failure:
–>before 40 yo
Hormone levels in PCOS: (LH, FSH, Testosterone, Estrogen):
-what is the primary cause?
- elevated LH (primary cause)
- decreased FSH
- elevated testosterone
- elevated estrogen (from testosterone aromatization)
Increased risk of what cancer in PCOS pts?
–>increased risk of endometrial cancer (d/t elevated estrogens, from aromatization of androgens in fat cells)
Treatment for PCOS:
- Weight loss
- OCPs
- Medroxyprogesterone (decreases LH and adrogenesis)
- Spirinolactone (treats acne and hirsutism; think: spirinolactone causes gynecomastia! so, has anti-androgen side effects)
- Clomiphene (SERM; for women who want to get pregnant)
most common ovarian mass in young women?
Follicular cyst = unrupture graafian follicle (so, fails to become corpus luteum); follicle distends…
corpus luteum cyst:
–>ovarian cyst that arises d/t hemorrhage into a persistent corpus luteum; resolves spontaneously
Dermoid cyst:
–>an ovarian cyst - a mature teratoma (benign)
Endometroid cyst:
=”chocolate cyst” –> an ovarian cyst from endometriosis within ovary
–>varies with menstrual cycle (when filled with blood = chocolate cyst)
ovarian germ cell tumor with elevated hCG and LDH?
- ->Dysgerminoma (malignant, equivalent to male seminoma, but rarer)
- ->associated with Turner’s
ovarian germ cell tumor with elevated hCG?
- ->Choriocarcinoma
- NO chorionic villi
- develop during pregnancy in baby or mother
- may spread hematogenously to lungs
ovarian germ cell tumor with elevated AFP (alpha-feto-protein)?
- ->Yok sac/Endometrial sinus tumor
- aggressive malignancy
- yellow solid mass
- 50% have Schiller-Duval bodies (look like glomeruli)
Most common ovarian germ cell tumor (90% of them)?
- ->Teratomas (most of which are benign, mature dematoid cysts)
- Teratomas = contain cells from 2 or 3 germ cell layers
- immature teratoma= malignant
- struma ovarri = contains thyroid cells; may present as hyperthyroidism
Schiller-Duval bodies:
- -> look like glomeruli
- -> found in 50% of yolk sac tumors (both male and female)
Struma Ovarii:
- -> ovarian teratoma that contains thyroid tissue
- may present as hyperthyroidism
CA-125:
- ->tumor marker for ovarian cancer
- not very specific; so, good for monitoring progression, but not for screening
Most important risk factor for ovarian non-germ cell tumors?
–> Family hx (genetics –> BRCA-1, BRCA-2, HNPCC)
Krukenberg tumor:
- -> Ovarian tumor that is d/t metastasis from GI (gastric adenocarcinoma)
- ->have mucin-secreting signet cells
Call-Exner bodies:
- ->found in Granulosa cell tumors (ovarian tumor)
- ->fluid-filled spaces b/w granulosa cells
Ovarian tumor that looks like bladder?
- ->Brenner tumor
- benign and unilateral
- “coffee bean” nuclei
Ovarian tumor that secretes estrogen?
- ->Granulosa cell tumor
- may have uterine bleeding (from elevated estrogen)
- have Call-Exner bodies (small follicles filled with eosinophilic secretions; fluid-filled spaces b/w granulosa cells)
Benign ovarian tumor with intestine-like tissue/mucus-secreting epithelium?
–>Mucinous cystadenoma (On histology, looks like intestines!)
Ovarian tumor with psammoma bodies:
- Serous Cystadenocarcinoma
- malignant, often bilateral
- accounts for 45% of ovarian tumors
(PSMM:
- Papillary thyroid
- Serous ovary
- Meningioma
- Mesothelioma)
Benign tumor that accounts for 20% of non-germ cell ovarian tumors?
–>serous cystadenoma
***note: serous cystadenocarcinoma (malignant version) accounts for 45% of non-germ cell ovarian tumors
Meig’s syndrome:
Triad:
Ovarian fibroma + Ascites + Hydrothorax
–>pulling sensation in groin
Clear Cell Adenocarcinoma of Vagina: Main risk factor?
–> DES exposure to women when they were in-utero
Sarcoma Botyroides:
- ->a type of rhabdomyosarcoma
- affects girls under 4 yo!
- desmin positive tumor cells (desmin stains muscle…)
Fibroadenoma:
- ->most common breast tumor in women <35 yo
- small, mobile, firm mass; benign
- NOT precursor to breast cancer
Intraductal Papilloma:
- BENIGN breast tumor
- tumor is in lactiferous ducts, so secretes serous of bloody nipple discharge
- very slight risk for carcinoma
Phyllodes tumor:
- Benign breast tumor; may become malignant
- Large bulky mass of connective tissue and cystys; usually in women in their 60’s
Most important prognostic factor in breast cancer?
–>Axillary lymph node involvement
Noninvasive (ie no BM involvement) ductal breast cancer (type of ductal carcinoma in situ) with casesous necrosis (central necrosis surrounded by cancer cells)?
–>Comedocarcinoma
Most common type of malignant breast cancer? Prognosis?
- ->Invasive ductal breast cancer
- ->most invasive; poorest prognosis
- ->Precursor = DCIS (ductal carcinoma in situ)
- firm, fibrous, rock-hard mass; classic “stellate” morphology
Breast cancer in which breast skin looks like orange peel (“peau d’orange”)?
- ->Inflammatory invasive breast cancer
- neoplastic cells block lymph drainage, so get edema, and the orange-peel-like breast skin.
Paget’s disease of breast:
- ->eczema-like patches on the nipple
- Paget cells are large cells in epidermis with clear halo
- may see on vulva too
Acute Mastitis:
- ->breast abscess associated with breast feeding
- results b/c get increased cracks in nipple from breast feeding, so increased risk of bacterial infection through cracks
- ->usually caused by S. aureus
Gynecomastia: Causes?
- Causes:
- hyperestrogenism
- Klinefelter’s
- Drugs: “Some Drugs Create Awesome Knockers”
- ->Spirinolactone
- ->Digitalis
- ->Cimetidine
- ->Alcohol
- ->Ketoconazole
- Other drugs: marijuana, estrogen, heroin, psychoactive drugs
BPH:
- what is it?
- serum marker?
- treatment?
Benign Prostatic Hyperplasia (NOT hypertrophy!) –> Hyperplasia of prostate gland
-associated with elevated PSA (free Prostate-Specific Antigen)
- Treatment:
- Finasteride (anti-androgen; decreases size of prostate)
- Tamsulosin or Terazosin (alpha-1-blockers) –> relax smooth muscle
Elevated PSA (Prostate-Specific Antigen)?
- Prostitis
- BPH
- Prostatic adenocarcinoma (have increased total PSA, but DECREASED fraction of Free PSA)
Prostatic adenocarcinoma: May metastasize to?
- ->may get osteoblastic metastases in bone, in late stages:
- have lower back pain + elevated serum alkaline phosphatase + elevated PSA
Cryptochordism:
- what is it?
- Presentation?
- Hormones: (FSH, LH, Testosterone)
- increasd risk of what cancer?
- -> undescended testes
- ->decreased spermatogenesis (b/c testes are too warm; must be lower/cooler for spermatogenesis to occur)
- Hormones:
- Normal testosterone (b/c Leydig cells are unaffected by temperature; even though they’re in the testes)
- Decreased inhibin (b/c secreted from Sertoli cells) –> Increased FSH
- Normal LH
*Increased risk of germ cell tumors
–>increased risk of cryptochordism in preemies
Varicocele:
- what is it?
- most common side?
- ->dilated veins in pampiniform plexus d/t increased venous pressure
- ->causes scrotal enlargement
- ->usually on Left; because increased resistance to venous flow, b/c longer path than right side
- ->may cause infertility
- ->”bag of worms” appearance
Testicular germ cell tumor with “fried egg” appearing cells?
- ->Seminoma
- malignant, painless tumor; testicular enlargement
- most common testicular tumor
- affects males 15-35
- good prognosis (b/c late mestastasis)
Malignant, PAINFUL testicular germ cell tumor with elevated hCG and elevated or normal AFP:
–>Embryonal carcinoma
testicular germ cell tumor with elevated AFP?
- ->yolk sac tumor (Schiller-duval bodies)
- ->also may see elevated (or normal) AFP in embryonal carcinoma and teratomas
testicular germ cell tumor with elevated hCG:
- ->Choriocarcinoma
- ->Embryonal carcinoma (may also have normal or elevated AFP)
- ->Teratoma (may also have normal/elevated AFP)
Reinke crystals:
–>seen in Leydig cell tumors (non-germ cell testicular tumor; benign)
Most common testicular cancer in older men? cause?
- ->Testicular lymphoma
- d/t metastasis from lymphoma to testes
Testicular Masses that can Transilluminate vs those that cannot transilluminate:
- No transillumination–> think testicular cancer
* Transillumination –> think tunica vaginalis lesions (Hydrocele, Spermatocele)
Hydrocele:
- ->increased fluid in the tunica vaginalis; d/t incomplete fusion of the processus vaginalis (tunica vaginalis stays in communication with the peritoneum)
- ->usually seen in newborns; resolves on own
Most common cause of penile squamous cell carcinoma?
–> HPV (usally in Asia, Africa, S. America)
Peyronie’s disease:
–>Bent penis (from fibrous tissue formation)
Causes of Priapism:
- Spinal cord trauma
- Sickle cell disease (sickled RBCs get trapped i vascular channels)
- Meds:
- ->Trazadone
- ->Cocaine
- ->prostaglandin inhibitors
- ->etc…
Leuprolide:
- what is it?
- clinical uses?
- GnRH analog:
- ->agonist when pulsatile (increases LH/FSH)
- ->antagonist when constant (decreased GnRH receptor in pituitary –> decreased FSH/LH)
- Uses:
- infertility (when pulsatile)
- prostate cancer (when continuous); use together with Flutamide (anti-androgen) to treat prostate cancer
- uterine fibroids
Exemestane:
–>Testosterone drug that can be used to treat estrogen-responsive breast cancer (b/c inhibits aromatase –> decreased estrogen)
Finasteride:
- mechanism?
- uses?
-antiandrogen: inhibits 5-alpha-reductase (so can’t convert testosterone –> DHT)
- Treats:
- BPH
- Male baldness
Flutamide:
- mechanism?
- use?
–>anti-androgen: non-steroid, competitively inhibits androgens at testosterone receptor
-treatment of prostate cancer (can give it with leuprolide (GnRH agonist, given continuously to treat prostate cancer)
Ketoconazole:
- mechanism?
- use?
–>anti-fungal drug! But, can be used for non-fungal treatments: inhibits desmolase (17-alpha-hydroxylase) –> so inhibits steroid synthesis
- Prevents hirsutism in PCOS
- side effects = gynecomastia and amenorrhea
Spirinolactone:
- mechanism?
- uses?
- ->aldosterone-antagonist; K-sparing diuretic
- by blocking aldosterone = inhibits steroid synthesis
- prevents hirsutism in PCOS
- side effects = gynecomastia and amenorrhea
Clomiphene:
- mechanism?
- uses?
- SERM (Selective Estrogen Receptor Modulator)
- ->partial agonist at estrogen receptors in hypothalamus => prevents normal feedback inhibition; so increases LH and FSH release from pituitary –> stimulates ovulation
- Treats:
- Infertility
- PCOS
*side effects: hot flashes, multiple simultaneous pregnancies, ovarian enlargement…
Tamoxifen:
- mechanism?
- use>
- SERM
- ->breast-tissue antagonist (though, endometrial-agonist)
-treats Estrogen-positive breast cancer
Raloxifene:
- mechanism?
- use?
- ->SERM
- agonist on bone; reduces bone resorption
-treats osteoporosis
Anastrozole:
- Aromatase inhibitor
- ->treats postmenopausal women with breast cancer (b/c inhibits estrogen production)
Mifepristone (RU-486):
- mechanism?
- use?
–>competitive inhibitor of progestins at progesterone receptors
- Uses:
- abortions/termination of pregnancy
- ->administor with Misopristol (PGE1) to induce contractions
Ritodrine:
- mechanism?
- use?
- ->Beta-2-agonist –> relaxes the uterus
- ->used to reduce premature uterine contractions (prevents early delivery)
(beta-2 –> decreases uterine tone)
Terbutaline:
- mechanism?
- use?
- ->Beta-2-agonist
- ->Relaxes uterus; prevents premature contractions (prevents early delivery)
Tamsulosin:
- mechanism?
- use?
–>alpha-1-blocker, selective for receptors on prostate (so does not lower BP, etc…; only affects prostate)
–>inhibits smooth muscle contraction, so used to treat BPH
Danazol:
- mechanism?
- use?
–>synthetic androgen; acts as partial agonist at androgen receptors
- Uses:
- endometriosis
- hereditary angioedema
Sildenafil, Vardenafil:
- ->mechanism?
- ->Toxicity?
- ->Contraindicated with what other drug?
-Inhibits cGMP phosphodiesterase (so increase cGMP –> smooth muscle relaxation –> vasodilation –> penile erection)
- Toxicities:
- impaired blue-green vision (it’s also a little blue pill!)
- headache and flushing (d/t vasodilation)
- dyspepsia (heartburn)
- life-threatening hypotension if given with NITRATES!
Anastrozole:
- Aromatase inhibitor
- ->treats postmenopausal women with breast cancer (b/c inhibits estrogen production)
Mifepristone (RU-486):
- mechanism?
- use?
–>competitive inhibitor of progestins at progesterone receptors
- Uses:
- abortions/termination of pregnancy
- ->administor with Misopristol (PGE1) to induce contractions
Ritodrine:
- mechanism?
- use?
- ->Beta-2-agonist –> relaxes the uterus
- ->used to reduce premature uterine contractions (prevents early delivery)
(beta-2 –> decreases uterine tone)
Terbutaline:
- mechanism?
- use?
- ->Beta-2-agonist
- ->Relaxes uterus; prevents premature contractions (prevents early delivery)
Tamsulosin:
- mechanism?
- use?
–>alpha-1-blocker, selective for receptors on prostate (so does not lower BP, etc…; only affects prostate)
–>inhibits smooth muscle contraction, so used to treat BPH
Danazol:
- mechanism?
- use?
–>synthetic androgen; acts as partial agonist at androgen receptors
- Uses:
- endometriosis
- hereditary angioedema
Sildenafil, Vardenafil:
- ->mechanism?
- ->Toxicity?
- ->Contraindicated with what other drug?
-Inhibits cGMP phosphodiesterase (so increase cGMP –> smooth muscle relaxation –> vasodilation –> penile erection)
- Toxicities:
- impaired blue-green vision (it’s also a little blue pill!)
- headache and flushing (d/t vasodilation)
- dyspepsia (heartburn)
- life-threatening hypotension if given with NITRATES!
