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354 Cards in this Set

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Question
Answer
24-year-old male develops testicular cancer. Metastatic spread occurs by what route?
Para-aortic lymph nodes (recall descent of testes during development).
Woman with previous cesarean section has a scar in her lower uterus close to the opening of the os. What is she at ↑ risk for?
Placenta previa.
Obese woman presents with hirsutism and ↑ levels of serum estosterone.
Polycystic ovarian syndrome.
Pregnant woman at 16 weeks of gestation presents with an atypically large abdomen.
High hCG; hydatidiform mole.
55-year-old postmenopausal woman is on tamoxifen therapy. What is she at ↑ risk of acquiring?
Endometrial carcinoma.
Gonadal drainage Venous drainage
Left ovary/testis → left gonadal vein → left renal vein → IVC Right ovary/testis → right gonadal vein → IVC
Gonadal drainage Lymphatic drainage drainage
Ovaries/testes → para-aortic lymph nodes
Ligaments of the uterus/contents Suspensory ligament of ovaries
Contains the ovarian vessels.
Ligaments of the uterus/contents Contains the ovarian vessels.
Suspensory ligament of ovaries
Ligaments of the uterus/contents Contains the uterine vessels.
Transverse cervical (cardinal) ligament
Ligaments of the uterus/contents Transverse cervical (cardinal) ligament
Contains the uterine vessels.
Ligaments of the uterus/contents Round ligament of uterus
Contains no important structures.
Ligaments of the uterus/contents Contains no important structures.
Round ligament of uterus
Ligaments of the uterus/contents Contains the round ligaments of the uterus and ovaries and the uterine tubules and vessels.
Broad ligament
Ligaments of the uterus/contents Broad ligament
Contains the round ligaments of the uterus and ovaries and the uterine tubules and vessels.
innervation of the male sexual response
Point and Shoot. -Erection is mediated by the Parasympathetics -Emission is mediated by the Sympathetis -Ejaculation is mediated by visceral and somatic nerves.
Derivation of sperm parts
-Acrosome is derived from the Golgi apparatus and -flagellum (tail) from one of the centrioles. -Middle piece (neck) has Mitochondria.
Sperm food supply
fructose.
sperm locations from nothing to vagina
SEVEN UP -Seminiferous tubules -Epididimys -Vas deferens -Ejaculatory ducts -(Nothing) -Urethra -Penis
Sperm development what forms blood-testis barrier
Junctional complex (tight junction) between Sertoli cells
Sperm development Spermatogenesis begins at puberty with
spermatogonia (type A and type B)
Sperm development Full development takes
2 months.
Sperm development Spermatogenesis occurs in
Seminiferous tubules
Sperm development Blood-testis barrier what and why
physical barrier in the testis between the tissues responsible for spermatogenesis and the bloodstream -to avoid autoimmune response
Sperm development #N of Primary spermatocyte
4N
Sperm development #N of Secondary spermatocyte
2N
Sperm development #N of Spermatid (N)
1N
progression of cells to sperm and N number
Spermatogonium 1° (diploid, 2N) Mitosis spermatocyte 2° (diploid, 4N) Meiosis I spermatocyte (haploid, 2N) Meiosis II Spermatid (haploid, N)
Male spermatogenesis products/functions of products Androgen-binding protein (ABP)
Ensures that testosterone in seminiferous tubule is high
Male spermatogenesis products/functions of products Ensures that testosterone in seminiferous tubule is high
Androgen-binding protein (ABP)
Male spermatogenesis products/functions of products Inhibits FSH
Inhibin
Male spermatogenesis products/functions of products Inhibin
Inhibits FSH
Male spermatogenesis products/functions of products Testosterone
Differentiates male genitalia, has anabolic effects on protein metabolism, maintains gametogenesis, maintains libido, inhibits GnRH, and fuses epiphyseal plates in bone.
Male spermatogenesis products/functions of products Differentiates male genitalia
Testosterone
Male spermatogenesis products/functions of products has anabolic effects on protein metabolism
Testosterone
Male spermatogenesis products/functions of products maintains gametogenesis
Testosterone
Male spermatogenesis products/functions of products maintains libido
Testosterone
Androgens names
Testosterone, dihydrotestosterone (DHT), androstenedione.
Androgens Source
-DHT and testosterone (testis), -androstenedione (adrenal).
Androgens Targets
Skin, prostate, seminal vesicles, epididymis, liver, muscle, brain.
Androgens Function
1. Differentiation of wolffian duct system into internal gonadal structures 2. 2° sexual characteristics and growth spurt during puberty 3. Required for normal spermatogenesis 4. Anabolic effects–– ↑ muscle size, ↑ RBC production 5. ↑ libido
Androgens potency
DHT > testosterone > androstenedione.
Testosterone is converted to DHT by ?????? and inhibition by ??????
the enzyme 5α-reductase, which is inhibited by finasteride.
??????is converted to DHT by the enzyme 5α-reductase, which is inhibited by finasteride.
Testosterone
Testosterone is converted to ?????? by the enzyme 5α-reductase, which is inhibited by finasteride.
DHT
Testosterone and androstenedione are converted to estrogen in ????? by ??????
adipose tissue by enzyme aromatase.
?????? converted to estrogen in adipose tissue by enzyme aromatase.
Testosterone and androstenedione
Testosterone and androstenedione are converted to ??????? in adipose tissue by enzyme aromatase.
estrogen
Estrogen Source
Ovary (estradiol), placenta (estriol), blood (aromatization).
Estrogen Functions (10)
1. Growth of follicle 2. Endometrial proliferation, 3. Development of genitalia 4. Stromal of breast 5. Female fat distribution 6. Hepatic synthesis of transport proteins 7. Feedback inhibition of FSH 8. LH surge 9. ↑ myometrial excitability 10. ↑ HDL, ↓ LDL
Estrogen effects on LH
LH surge (estrogen feedback on LH secretion switches to positive from negative just before LH surge)
Estrogens potency
Potency––estradiol > estrone > estriol.
Estrogen levels in pregnancy
50-fold ↑ in estradiol and estrone 1000-fold ↑ in estriol (indicator of fetal well being)
Estrogen indicator of fetal well being
1000-fold ↑ in estriol
Progesterone Source
Corpus luteum, placenta, adrenal cortex, testes.
Progesterone Function (7)
1. Stimulation of endometrial glandular secretions and spiral artery development 2. Maintenance of pregnancy 3. ↓ myometrial excitability 4. Production of thick cervical mucus, which inhibits sperm entry into the uterus 5. ↑ body temperature 6. Inhibition of gonadotropins (LH, FSH) 7. Uterine smooth muscle relaxation
Progesterone mnemonic
Progesterone Prepares for Pregnancy.
Elevation of ?????? is indicative of ovulation.
progesterone
Follicular growth is fastest during
2nd week of proliferative phase.
stimulates endometrial proliferation.
Estrogen
maintains endometrium to support implantation.
Progesterone
?????progesterone leads to ↓ fertility.
↓ progesterone leads to ??fertility.
blood from ruptured follicle causes peritoneal irritation that can mimic appendicitis.
Mittelschmerz
Mittelschmerz
blood from ruptured follicle causes peritoneal irritation that can mimic appendicitis.
Oral contraceptives mech
prevent estrogen surge, LH surge → ovulation does not occur.
Ovulation steps
Estrogen surge day before ovulation. Stimulates LH, inhibits FSH. LH surge causes ovulation (rupture of follicle). ↑ temperature (progesterone induced). Ferning of cervical mucosa.
Meiosis and ovulation
-1° oocytes begin meiosis I during fetal life and complete meiosis I just prior to ovulation -Meiosis I is arrested in prOphase for years until Ovulation. -Meiosis II is arrested in METaphase until fertilization. (An egg MET a sperm)
hCG Source
Syncytiotrophoblast of placenta.
hCG Function
1. Maintains the corpus luteum for the 1st trimester by acting like LH. In the 2nd and 3rd trimester, the placenta synthesizes its own estrogen and progesterone and the corpus luteum degenerates.
Used to detect pregnancy because it appears in the urine 8 days after successful fertilization (blood and urine tests)
hCG
hCG wrt testing
Used to detect pregnancy because it appears in the urine 8 days after successful fertilization (blood and urine tests) Elevated hCG in women with hydatidiform moles or choriocarcinoma.
women with hydatidiform moles or choriocarcinoma.
Elevated hCG
Cessation of estrogen production with age-linked decline in number of ovarian follicles.
Menopause
Menopause what
Cessation of estrogen production with age-linked decline in number of ovarian follicles.
Menopause age
Average age of onset is 51 years (earlier in smokers).
Menopause hormonal changes
↓ estrogen ↑↑ FSH ↑ LH (no surge) ↑ GnRH.
Menopause clinical findings
Menopause causes HAVOC: Hot flashes, Atrophy of the Vagina, Osteoporosis, Coronary artery disease.
Bicornuate uterus mech
Results from incomplete fusion of the paramesonephric ducts.
Results from incomplete fusion of the paramesonephricducts. Associated with urinary tract abnormalities and infertility.
Bicornuate uterus
Bicornuate uterus complications
Associated with urinary tract abnormalities and infertility.
Abnormal opening of penile urethra on inferior (ventral) side of penis due to failure of urethral folds to close.
Hypospadias
Hypospadias what and mech
Abnormal opening of penile urethra on inferior (ventral) side of penis due to failure of urethral folds to close.
Abnormal opening of penile urethra on superior (dorsal) side of penis due to faulty positioning of genital tubercle.
Epispadias
Hypospadias
Abnormal opening of penile urethra on superior (dorsal) side of penis due to faulty positioning of genital tubercle.
Congenital penile abnormalities which is more common
Hypospadias is more common than epispadias.
Hypospadias complications and Tx
Fix hypospadias to prevent UTIs.
Exstrophy of the bladder is associated with ?????
epispadias.
????? is associated with epispadias.
Exstrophy of the bladder
Klinefelter’s syndrome phenotype/genotype
[male] (XXY),
[male] (XXY),
Klinefelter’s syndrome
Turner’s syndrome phenotype/genotype
[female] (XO),
[female] (XO)
Turner’s syndrome
Double Y males phenotype/genotype
[male] (XYY),
[male] (XYY)
Double Y males
Klinefelter’s syndrome appearance
Testicular atrophy, eunuchoid body shape, tall, long extremities, gynecomastia, female hair distribution.
Klinefelter’s syndrome lab findings
Presence of inactivated X chromosome (Barr body).
Klinefelter’s syndrome complications
Common cause of hypogonadism seen in infertility workup.
Turner’s syndrome appearance
Short stature, webbing of neck,
Turner’s syndrome lab findings
No Barr body. ovarian dysgenesis (streak ovary)
Turner’s syndrome complications
-coarctation of the aorta, -most common cause of 1° amenorrhea. -Horseshoe kidney -cystic hygroma
cystic hygroma
a lymphatic malformation, is a benign proliferation of lymph vessels, fluid filled sacs that result from blockage of the lymphatic system
a lymphatic malformation, is a benign proliferation of lymph vessels, fluid filled sacs that result from blockage of the lymphatic system
cystic hygroma
Pseudohermaphroditism what is it
Disagreement between the phenotypic (external genitalia) and gonadal (testes vs. ovaries) sex.
Female pseudohermaphrodite genotype/phenotype
XX - Ovaries present, but external genitalia are virilized or ambiguous.
XX - Ovaries present, but external genitalia are virilized or ambiguous.
Female pseudohermaphrodite
male pseudohermaphrodite genotype/phenotype
XY - Testes present, but external genitalia are female or ambiguous
Female pseudohermaphrodite mech
excessive and inappropriate exposure to androgenic steroids during early gestation
Female pseudohermaphrodite causes
congenital adrenal hyperplasia or exogenous administration of androgens during pregnancy).
Female pseudohermaphrodite mech
Most common form is androgen insensitivity syndrome (testicular feminization).
true hermaphrodite genotype/phenotype
(46,XX or 47,XXY) Both ovary and testicular tissue present; ambiguous genitalia. Very rare.
Androgen insensitivity syndrome genotype/phenotype
(46,XY) normal-appearing female; female external genitalia with rudimentary vagina; uterus and uterine tubes generally absent; develops testes
Androgen insensitivity syndrome complications
testes (often found in labia majora; surgically removed to prevent malignancy
Androgen insensitivity syndrome Lab findings
of testosterone, estrogen, and LH are all high.
5α-reductase deficiency mech and clinical findings
Unable to convert testosterone to DHT. Ambiguous genitalia until puberty, when ↑ testosterone causes masculinization of genitalia.
5α-reductase deficiency lab findings
Testosterone/estrogen levels are normal; LH is normal or ↑.
Hydatidiform mole what is it
A pathologic ovum (“empty egg”––ovum with no DNA) resulting in cystic swelling of chorionic villi and proliferation of chorionic epithelium (trophoblast).
Hydatidiform mole lab findings
High HCG
Hydatidiform mole gross
“Honeycombed uterus,” “cluster of grapes” appearance. Enlarged uterus.
Most common precursor of choriocarcinoma.
complete Hydatidiform mole
complete mole wrt genotype origin fetus cancer
Genotype of a complete mole is 46,XX and is completely paternal in origin (no maternal chromosomes); no associated fetus. increased risk of choriocarcinoma
partial mole wrt genotype origin fetus cancer
PARTial mole is made up of 3 or more PARTS (triploid 69XXY egg 23X and 2 sperm; may contain fetal PARTS. NO increased risk of cancer
Preeclampsia what
triad of hypertension, proteinuria, and edema
Eclampsia what
eclampsia is the addition of seizures
Preeclampsia %'s and when
7% of pregnant women from 20 weeks’ gestation to 6 weeks postpartum.
Preeclampsia who is at increased risk
↑ incidence in patients with preexisting hypertension, diabetes, chronic renal disease, and autoimmune disorders.
Preeclampsia mech and associations
-Etiology involves placental ischemia. -Can be associated with HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets).
Preeclampsia clinical findings
Headache, blurred vision, abdominal pain, edema of face and extremities, altered mentation, hyperreflexia;
Preeclampsia Tx
Delivery of fetus as soon as viable. Otherwise bed rest, salt restriction, and monitoring and treatment of hypertension.
Preeclampsia lab findings
thrombocytopenia, hyperuricemia. elevated Liver enzymes
Eclampsia Tx
a medical emergency, IV magnesium sulfate and diazepam.
Abruptio placentae what
premature detachment of placenta from implantation site.
Abruptio placentae clinical findings
Painful uterine bleeding (usually during 3rd trimester). Fetal death.
Abruptio placentae associations and risk factors
May be associated with DIC. ↑ risk with smoking, hypertension, cocaine use.
premature detachment of placenta from implantation site.
Abruptio placentae
Placenta accreta what
defective decidual layer allows placenta to attach directly to myometrium.
Placenta accreta clinical findings
Massive hemorrhage after delivery.
Placenta accreta risk factors
Predisposed by prior C-section or inflammation.
defective decidual layer allows placenta to attach directly to myometrium.
Placenta accreta
Placenta previa what and findings
attachment of placenta to lower uterine segment. May occlude cervical os. Painless bleeding in any trimester.
Painless bleeding in any trimester.
Placenta previa
Ectopic pregnancy locations
most often in fallopian tubes, confirm with ultrasound.
Ectopic pregnancy clinical/Lab findings
↑ hCG and sudden lower abdominal pain; Often clinically mistaken for appendicitis.
Ectopic pregnancy risk factors
predisposed by salpingitis (PID).
Ectopic pregnancy confromation
confirm with ultrasound.
Polyhydramnios definition
> 1.5–2 L of amniotic fluid;
Polyhydramnios associations and complications
associated with esophageal or duodenal atresia, causing inability to swallow amniotic fluid, and with anencephaly.
Oligohydramnios associations and complications
associated with bilateral renal agenesis or posterior urethral valves (in males) and resultant inability to excrete urine.
oligohydramnios definition
< 0.5 L of amniotic fluid;
< 0.5 L of amniotic fluid;
oligohydramnios
> 1.5–2 L of amniotic fluid;
Polyhydramnios
Cervical pathology Dysplasia and carcinoma in situ describe and classification
Disordered epithelial growth; begins at basal layer and extends outward. Classified as CIN 1, CIN 2, or CIN 3 (carcinoma in situ), depending on extent of dysplasia.
Cervical pathology Dysplasia and carcinoma in situ associations and progression
HPV 16, 18. May progress slowly to invasive carcinoma.
Cervical pathology Invasive carcinoma what type
Often squamous cell carcinom
Cervical pathology Dysplasia and carcinoma in situ wrt testing
Pap smear can catch cervical dysplasia (koilocytes) before it progresses to invasive carcinoma
Cervical pathology Invasive carcinoma wrt specific invasion
Lateral invasion can block ureters, causing renal failure.
Endometriosis
Non-neoplastic endometrial glands/stroma in abnormal locations outside the uterus.
Non-neoplastic endometrial glands/stroma in abnormal locations outside the uterus.
Endometriosis
Endometriosis clinical findings
Characterized by cyclic bleeding (menstrual type) from ectopic endometrial tissu resulting in blood-filled “chocolate cysts.” In ovary or on peritoneum. Manifests clinically as severe menstrual-related pain.
“chocolate cysts.”
Endometriosis
Endometriosis complications
Often results in infertility
Adenomyosis
Endometriosis within the myometrium.
Endometriosis within the myometrium.
Adenomyosis
Endometrial hyperplasia
Abnormal endometrial gland proliferation usually caused by excess estrogen stimulation.
Abnormal endometrial gland proliferation usually caused by excess estrogen stimulation.
Endometrial hyperplasia
Endometrial hyperplasia wrt complications
↑ risk for endometrial carcinoma
Endometrial hyperplasia clinical findings
Most commonly manifests linically as vaginal bleeding.
Endometrial carcinoma how common and who
Most common gynecologic malignancy. Peak age 55–65 years old
Most common gynecologic malignancy
Endometrial carcinoma
Endometrial carcinoma clinical findings
Clinically presents with vaginal bleeding.
Endometrial carcinoma Risk factors
prolonged use of estrogen without progestins, obesity, diabetes, hypertension, nulliparity, and late menopause.
Endometrial carcinoma Typically preceded by
endometrial hyperplasia.
Most common of all tumors in females
Leiomyoma
Leiomyoma how common and who
Most common of all tumors in females. ↑ incidence in blacks
Leiomyoma gross findings
multiple tumors with well demarcated borders.
Leiomyoma prognosis
Benign smooth muscle tumor; malignant transformation is rare. Does not progress to leiomyosarcoma
Leiomyoma wrt estrogen
Estrogen sensitive––tumor size ↑ with pregnancy and ↓ with menopause.
Leiomyosarcoma gross
Bulky irregularly shaped tumor with areas of necrosis and hemorrhage
Leiomyosarcoma cause and who
typically arising de novo (not from leiomyoma). ↑ incidence in blacks.
Leiomyosarcoma Prognosis
Highly aggressive tumor with tendency to recur.
Leiomyosarcoma clinical findings
May protrude from cervix and bleed.
Polycystic ovarian syndrome lab findings
↑ LH, ↓ FSH, ↑ testosterone.
Polycystic ovarian syndrome clinical findings
amenorrhea, infertility, obesity, and hirsutism.
Polycystic ovarian syndrome mech
↑ LH production leads to anovulation, hyperandrogenism due to deranged steroid synthesis
Polycystic ovarian syndrome Tx
Treat with weight loss, OCPs, gonadotropin analogs, or surgery.
Ovarian cysts Follicular cyst
distention of unruptured graafian follicle. May be associated with hyperestrinism and endometrial hyperplasia.
Ovarian cysts Corpus luteum cyst
hemorrhage into persistent corpus luteum. Menstrual irregularity.
Ovarian cysts Theca-lutein cyst
often bilateral/multiple. Due to gonadotropin stimulation. Associated with choriocarcinoma and moles.
Ovarian cysts “Chocolate cyst”
blood-containing cyst from ovarian endometriosis. Varies with menstrual cycle.
Ovarian cysts distention of unruptured graafian follicle. May be associated with hyperestrinism and endometrial hyperplasia.
Follicular cyst
Ovarian cysts hemorrhage into persistent corpus luteum. Menstrual irregularity.
Corpus luteum cyst
Ovarian cysts often bilateral/multiple.
Theca-lutein cyst
Ovarian cysts Due to gonadotropin stimulation. Associated with choriocarcinoma and moles.
Theca-lutein cyst
Ovarian cysts blood-containing cyst from ovarian endometriosis.
“Chocolate cyst”
Ovarian cysts Varies with menstrual cycle.
“Chocolate cyst”
Dysgerminoma what type of tumor
Ovarian germ cell tumor
Ovarian germ cell tumors name them
Dysgerminoma Yolk sac (endodermal sinus tumor) Choriocarcinoma Teratoma
Ovarian non–germ cell tumors name them
1. Serous cystadenoma 2. Serous cystadenocarcinoma 3. Mucinous cystadenoma 4. Mucinous cystadenocarcinoma 5. Brenner tumor 6. Ovarian fibroma 7. Granulosa cell tumor
Yolk sac (endodermal sinus tumor) what type of tumor
Ovarian germ cell tumor
Choriocarcinoma what type of tumor
Ovarian germ cell tumor
Teratoma what type of tumor
Ovarian germ cell tumor
Serous cystadenoma what type of tumor
Ovarian non–germ cell tumors
Serous cystadenocarcinoma what type of tumor
Ovarian non–germ cell tumors
Mucinous cystadenoma what type of tumor
Ovarian non–germ cell tumors
Mucinous cystadenocarcinoma what type of tumor
Ovarian non–germ cell tumors
Brenner tumor what type of tumor
Ovarian non–germ cell tumors
Ovarian fibroma what type of tumor
Ovarian non–germ cell tumors
Granulosa cell tumor what type of tumor
Ovarian non–germ cell tumors
descrptions of Ovarian germ cell tumors Dysgerminoma
Malignant, equivalent to male seminoma. Sheets of uniform cells. ↑ hCG.
descrptions of Ovarian germ cell tumors Yolk sac (endodermal sinus tumor)
Aggressive malignancy in ovaries (testes in boys) and sacrococcygeal area of young children. ↑ AFP.
descrptions of Ovarian germ cell tumors Choriocarcinoma
Rare but malignant; can develop during pregnancy in mother or baby. Large, hyperchromatic hyncytiotrophoblastic cells. ↑ hCG.
descrptions of Ovarian germ cell tumors Teratoma types
Mature teratoma (“dermoid cyst”)––most frequent benign ovarian tumor. Immature teratoma– –aggressively malignant. Struma ovarii--contains functional thyroid tissue
Ovarian germ cell tumors ↑ hCG.
Choriocarcinoma and Dysgerminoma
Ovarian germ cell tumors ↑ AFP.
Yolk sac (endodermal sinus tumor)
90% of ovarian germ cell tumors
Teratoma
Struma ovarii
Teratoma contains functional thyroid tissue
Ovarian germ cell tumors Teratoma contains functional thyroid tissue
Struma ovarii
Ovarian non–germ cell tumors Frequently bilateral, lined with fallopian tube–like epithelium. Benign.
Serous cystadenoma
Ovarian non–germ cell tumors malignant and frequently bilateral.
Serous cystadenocarcinoma
Ovarian non–germ cell tumors multilocular cyst lined by mucus-secreting epithelium. Benign.
Mucinous cystadenoma
Ovarian non–germ cell tumors malignant. Pseudomyxoma peritonei
Mucinous cystadenocarcinoma
Ovarian non–germ cell tumors benign tumor that resembles Bladder epithelium.
Brenner tumor
Brenner tumor
tumors that are part of the surface epithelial-stromal tumor group of ovarian neoplasms. benign tumor that resembles Bladder epithelium.
Meigs’ syndrome
triad of ovarian fibroma, ascites, and hydrothorax.
triad of ovarian fibroma, ascites, and hydrothorax.
Meigs’ syndrome
Ovarian non–germ cell tumors bundles of spindle-shaped fibroblasts
Ovarian fibroma
Ovarian non–germ cell tumors secretes estrogen →precocious puberty (kids).
Granulosa cell tumor
Call-Exner bodies
granulosa cells arranged haphazardly around a space containing eosinophilic fluid
Pseudomyxoma peritonei
intraperitonealaccumulation of mucinous material from ovarian (Mucinous cystadenocarcinoma) or appendiceal tumor.
"jelly belly" aka
Pseudomyxoma peritonei
Pseudomyxoma peritonei aka
"jelly belly"
granulosa cells arranged haphazardly around a space containing eosinophilic fluid
Call-Exner bodies
Ovarian non–germ cell tumors endometrial hyperplasia or carcinoma in adults. Call-Exner bodies
Granulosa cell tumor
Breast tumors benign types
1. Fibroadenoma– 2. Intraductal papilloma 3. Cystosarcoma phyllodes
Breast tumors malignant types
1. Ductal carcinoma in situ 2. Invasive ductal, 3. Comedocarcinoma 4. Inflammatory 5. Invasive lobular 6. Medullary 7. Paget’s disease of the breast
Breast tumors most common tumor < 25 years
Fibroadenoma
Breast tumors Small, mobile, firm mass with sharp edges. ↑ size and tenderness with pregnancy. Not a precursor to breast cancer.
Fibroadenoma
Breast tumors benign tumor of lactiferous ducts; presents with serous or bloody nipple discharge.
Intraductal papilloma
Breast tumors large, bulky mass of connective tissue and cysts. Tumor may have “leaflike” projections. Some may be malignant.
Cystosarcoma phyllodes
Breast tumors Malignant tumors in general
Common postmenopause. Arise from mammary duct epithelium or lobular glands. Overexpression of estrogen/progesterone receptors or erb-B2 (HER-2, an EGF receptor) is common;
Breast tumors the single most important prognostic factor.
Lymph node involvement
Breast tumors early malignancy without basement membrane penetration.
Ductal carcinoma in situ (DCIS)––
Breast tumors The worst and most invasive.
Invasive ductal, no specific type
Breast tumors ductal, with cheesy consistency due to central necrosis.
Comedocarcinoma
Breast tumors lymphatic involvement; poor prognosis.
Inflammatory
Breast tumors often multiple, bilateral.
Invasive lobular
Breast tumors fleshy, cellular, lymphocytic infiltrate. Good prognosis.
Medullary
Breast tumors eczematous patches on nipple.
Paget’s disease of the breast
Paget’s disease of the breast description, cells, what it means, where is it also seen
––eczematous patches on nipple. Paget cells––large cells with clear halo; suggest underlying carcinoma. 7. Paget’s disease of the breast––eczematous patches on nipple. Paget cells––large cells with clear halo; suggest underlying carcinoma. Also seen on vulva.
Breast tumors risk factors
Risk factors: gender, age, early 1st menarche (< 12 years old), delayed 1st pregnancy (> 30 years old), late menopause (> 50 years old), family history of 1st-degree relative with breast cancer at a young age.
Breast tumors Risk is NOT increased by
fibroadenoma or nonhyperplastic cysts.
Common breast conditions Fibrocystic disease how common, and who
Most common cause of “breast lumps” age 25–menopause.
Common breast conditions Fibrocystic disease presentation and risk
Presents with diffuse breast pain and multiple lesions, often bilateral. Usually does not indicate ↑ risk of carcinoma.
Fibrocystic disease types
1. Fibrosis– 2. Cystic– 3. Sclerosing– 4. Epithelial hyperplasia–
Fibrocystic disease types hyperplasia of breast stroma.
Fibrosis
Fibrocystic disease types fluid filled.
Cystic
Fibrocystic disease types ↑ acini and intralobular fibrosis.
Sclerosing
Fibrocystic disease types –↑ in number of epithelial cell layers in terminal duct lobule.
Epithelial hyperplasia
Fibrocystic disease types ↑ risk of carcinoma with atypical cells. Occurs > 30 years.
Epithelial hyperplasia
Acute mastitis what/ mech
Breast abscess; during breast-feeding ↑ risk of bacterial infection through cracks in the nipple; Staphylococcus aureus is the most common pathogen.
Fat necrosis of breast
A benign painless lump; forms due to injury to breast tissue.
A benign painless lump; forms due to injury to breast tissue
Fat necrosis of breast
Gynecomastia mech and causes
Results from hyperestrogenism (cirrhosis, testicular tumor, puberty, old age), Klinefelter’s syndrome, or drug induced (cimetidine, alcohol abuse, marijuana, heroin, psychoactive drugs, digitalis).
Prostatitis clinical findings and causes
Dysuria, frequency, urgency, low back pain. Acute: bacterial; chronic: bacterial or abacterial (most common).
Benign prostatic hyperplasia mech
May be due to an age-related increase in estradiol with possible sensitization of the prostate to the growth promoting effects of DHT.
Benign prostatic hyperplasia prostate gross changes
Characterized by a nodular enlargement of the periurethral (lateral and middle) lobes of the prostate gland, compressing the urethra into a vertical slit.
Benign prostatic hyperplasia clinical findings
↑ frequency of urination, nocturia, difficulty starting and stopping the stream of urine, and dysuria.
Benign prostatic hyperplasia complications
May lead to distention and hypertrophy of the bladder, hydronephrosis, and UTIs. Not considered a premalignant lesion.
Benign prostatic hyperplasia labs
↑ free prostate-specific antigen (PSA).
Prostatic adenocarcinoma where and Dx
Arises most often from the posterior lobe (peripheral zone) of the prostate gland and is most frequently diagnosed by digital rectal examination (hard nodule) and prostate biopsy.
Prostatic adenocarcinoma Lab findings
Prostatic acid phosphatase and PSA are useful tumor markers (↑ total PSA, with ↓ fraction of free PSA). Osteoblastic metastases in bone may develop in late stages, as indicated by an ↑ in serum alkaline phosphatase and PSA.
↑ in serum alkaline phosphatase and PSA.
Osteoblastic metastases from Prostatic adenocarcinoma
Cryptorchidism what and complications
Undescended testis (one or both); lack of spermatogenesis due to ↑ body temperature; associated with ↑ risk of germ cell tumors.
Testicular germ cell tumors names
-Seminoma -Embryonal carcinoma -Yolk sac (endodermal sinus) tumor -Choriocarcinoma -Teratoma
Testicular non–germ cell tumors names
-Leydig cell -Sertoli cell -Testicular lymphoma
~95% of all testicular tumors
Testicular germ cell tumors
Seminoma how common and who
most common testicular tumor, mostly affecting males age 15–35.
Testicular germ cell tumors Malignant; painless testicular enlargement;
Seminoma
Testicular germ cell tumors Malignant; painful;
Embryonal carcinoma
Testicular germ cell tumors ↑ AFP
Yolk sac (endodermal sinus) tumor
Testicular germ cell tumors Malignant, ↑ hCG.
all Choriocarcinoma 10% of Seminoma
Testicular germ cell tumors Unlike in females, in males this tumor is most often malignant.
mature teratoma
Testicular non–germ cell tumors Benign, contains Reinke crystals
Leydig cell
Testicular non–germ cell tumors usually androgen producing, gynecomastia in men, precocious puberty in boys.
Leydig cell
Leydig cell tumor findings
Benign, contains Reinke crystals; usually androgen producing, gynecomastia in men, precocious puberty in boys.
Testicular non–germ cell tumors Benign, androblastoma from sex cord stroma.
Sertoli cell
Most common testicular cancer in older men.
Testicular lymphoma
Reinke crystals
crystal-like inclusions in the interstitial cells of the testis (Leydig cells) and hilus cells in the ovary
crystal-like inclusions in the interstitial cells of the testis (Leydig cells) and hilus cells in the ovary
Reinke crystals
Penile pathology Carcinoma in situ: names
-Bowen disease -Erythroplasia of Queyrat -Bowenoid papulosis
Bowen disease clinical findings, when and progression
Solitary crusty plaque, usually on the shaft of the penis or on the scrotum; peak incidence in fifth decade of life; becomes invasive SCC in <10% of cases.
Solitary crusty plaque, usually on the shaft of the penis or on the scrotum; peak incidence in fifth decade of life; becomes invasive SCC in <10% of cases.
Bowen disease
Erythroplasia of Queyrat
Red velvety plaques, usually involving the glans; otherwise similar to Bowen disease
Red velvety plaques, usually involving the glans; otherwise similar to Bowen disease
Erythroplasia of Queyrat
Bowenoid papulosis clinical findings, when and progression
Multiple papular lesions; affects younger age group than the other two; usually does not become invasive.
Multiple papular lesions; affects younger age group than the other two; usually does not become invasive.
Bowenoid papulosis
Penile pathology Squamous cell carcinoma (SCC) who
Rare in circumcised men; uncommon in US and Europe, more common in Asia, Africa, and South America.
Penile pathology Squamous cell carcinoma (SCC) associations
Commonly associated with HPV.
Rare in circumcised men; uncommon in US and Europe, more common in Asia, Africa, and South America. Commonly associated with HPV.
Penile Squamous cell carcinoma (SCC)
Antiandrogens names
Finasteride Flutamide Ketoconazole, spironolactone
Finasteride mech and clinical uses
A 5α-reductase inhibitor (↓ conversion of testosterone to dihydrotestosterone). Useful in BPH. Also promotes hair growth––used to treat male-pattern baldness.
Finasteride aka
propecia
propecia aka
Finasteride
Flutamide mech and clinical uses
A nonsteroidal competitive inhibitor of androgens at the testosterone receptor. Used in prostate carcinoma.
A nonsteroidal competitive inhibitor of androgens at the testosterone receptor. Used in prostate carcinoma.
Flutamide
A 5α-reductase inhibitor (↓ conversion of testosterone to dihydrotestosterone). Useful in BPH. Also promotes hair growth––used to treat male-pattern baldness.
Finasteride (propcia)
Antiandrogens mech/clinical use of Ketoconazole
Inhibit steroid synthesis; used in the treatment of polycystic ovarian syndrome to prevent hirsutism.
Inhibit steroid synthesis; used in the treatment of polycystic ovarian syndrome to prevent hirsutism.
Ketoconazole as an Antiandrogen
Antiandrogens mech/clinical use of spironolactone
Inhibit steroid binding; used in the treatment of polycystic ovarian syndrome to prevent hirsutism.
Inhibit steroid binding; used in the treatment of polycystic ovarian syndrome to prevent hirsutism.
spironolactone as an Antiandrogen
Leuprolide Mechanism
GnRH analog with agonist properties when used in pulsatile fashion; antagonist properties when used in continuous fashion.
Leuprolide Clinical use
Infertility (pulsatile), prostate cancer (continuous–use with flutamide), uterine fibroids.
Leuprolide Toxicity
Antiandrogen, nausea, vomiting.
GnRH analog with agonist properties when used in pulsatile fashion; antagonist properties when used in continuous fashion.
Leuprolide
Sildenafil, vardenafil Mechanism
Inhibit cGMP phosphodiesterase, causing ↑ cGMP smooth muscle relaxation in the corpus cavernosum, ↑ blood flow, and penile erection.
Sildenafil, vardenafil Clinical use
Treatment of erectile dysfunction.
Sildenafil, vardenafil Toxicity
Headache, flushing, dyspepsia, blue-green color vision. Risk of life-threatening hypotension in patients taking nitrates.
Headache, flushing, dyspepsia, blue-green color vision.
Sildenafil, vardenafil Toxicity
Inhibit cGMP phosphodiesterase, causing ↑ cGMP, smooth muscle relaxation in the corpus cavernosum
Sildenafil, vardenafil
Clomiphene Mechanism
A partial agonist at estrogen receptors in the pituitary gland. Prevents normal feedback inhibition and ↑ release of LH and FSH from the pituitary, which stimulates ovulation.
Clomiphene Clinical use
Treatment of infertility.
Clomiphene Toxicity
Hot flashes, ovarian enlargement, multiple simultaneous pregnancies, visual disturbances.
A partial agonist at estrogen receptors in the pituitary gland. Prevents normal feedback inhibition and ↑ release of LH and FSH from the pituitary, which stimulates ovulation.
Clomiphene
Mifepristone aka
RU-486
RU-486 aka
Mifepristone
Mifepristone Mechanism
Competitive inhibitor of progestins at progesterone receptors.
Mifepristone Clinical use
Postcoital abortifacient (prevents implantation).
Mifepristone Toxicity
Heavy bleeding, GI effects (nausea, vomiting, anorexia), abdominal pain.
Competitive inhibitor of progestins at progesterone receptors. Postcoital abortifacient (prevents implantation).
Mifepristone (RU-486)
dinoprostine
PGE2 analog causing cervical dilation and uterine contraction, inducing labor
PGE2 analog causing cervical dilation and uterine contraction, inducing labor
dinoprostine
ritodrine/terbutaline
beta2-agonists that relax the uterus
beta2-agonists that relax the uterus
ritodrine/terbutaline
Anastrazole
aromatase inhibitor used in postmenopausal womaen with breats cancer
aromatase inhibitor used in postmenopausal womaen with breats cancer
Anastrazole
Testosterone (methyltestosterone) Mechanism
Agonist at androgen receptors.
Testosterone (methyltestosterone) Clinical use
Treat hypogonadism and promote development of 2" sex characteristics; stimulation of -anabolism to promote recovery after burn or injury; treat ER-positive breast cancer (exemestane).
Testosterone (methyltestosterone) Toxicity
Causes masculinization in females; reduces intratestic~~lar testosterone in males by inhibiting Leydig cells; leads to gonadal atrophy. Premature closure of epiphyseal plates. increase LDL, decrease HDL.
Estrogens names
ethinyl estradiol, DES, mestrano
Estrogens Mechanism
Bind estrogen receptors.
Estrogens Clinical use
Hypogonadism or ovarian failure, menstrual abnormalities, HRT in postmenopausal women; use in men with androgen-dependent prostate cancer.
Estrogens Toxicity
increase risk of endometrial cancer, bleeding in postmenopausal women, clear cell adenocarcinoma of vagina in females exposed to DES in utero, 1' risk of thrombi.
Estrogens Contraindications
-ER-positive breast cancer.
Progestins Mechanism
Bind progesterone receptors, reduce growth, and increase vascularization of endometrium.
Progestins Clinical use
Used in oral contraceptives and in the treatment of endometrial cancer and abnormal uterine bleeding.
Tamoxifen
Antagonist on breast tissue; used to treat and prevent recurrence of ER-positive breast cancer.
Antagonist on breast tissue; used to treat and prevent recurrence of ER-positive breast cancer.
Tamoxifen
Agonist on bone; reduces reabsorption of bone; used to treat osteoporosis.
Raloxifene
Raloxifene
Agonist on bone; reduces reabsorption of bone; used to treat osteoporosis.
Oral contraception Advantages
-Reliable (< 1% failure) -↓ risk of endometrial and ovarian cancer -↓ incidence of ectopic pregnancy -↓ pelvic infections -Regulation of menses
Oral contraception disadvantages
-Taken daily -No protection against STDs -↑ triglycerides -Depression, weight gain, -nausea, hypertension Hypercoagulable state
Hormone replacement therapy (HRT) used for
Used for relief or prevention of menopausal symptoms (hot flashes, vaginal atrophy, etc.) and osteoporosis (due to diminished estrogen levels).
Hormone replacement therapy (HRT) toxicity
Unopposed estrogen replacement therapy (ERT) increases the risk of endometrial cancer, so progesterone is added.