2007 First Aid Ch 16 Reproductive

Front 1

24-year-old male develops
testicular cancer. Metastatic spread occurs by what route?

Back 1

Para-aortic lymph nodes (recall
descent of testes during
development).

Front 2

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?

Back 2

Placenta previa.

Front 3

Obese woman presents with
hirsutism and ↑ levels of serum
estosterone.

Back 3

Polycystic ovarian syndrome.

Front 4

Pregnant woman at 16 weeks
of gestation presents with an
atypically large abdomen.

Back 4

High hCG; hydatidiform mole.

Front 5

55-year-old postmenopausal
woman is on tamoxifen therapy. What is she at ↑ risk
of acquiring?

Back 5

Endometrial carcinoma.

Front 6

Gonadal drainage
Venous drainage

Back 6

Left ovary/testis → left gonadal vein → left renal vein → IVC

Right ovary/testis → right gonadal vein → IVC

Front 7

Gonadal drainage
Lymphatic drainage drainage

Back 7

Ovaries/testes → para-aortic lymph nodes

Front 8

Ligaments of the uterus/contents

Suspensory ligament
of ovaries

Back 8

Contains the ovarian vessels.

Front 9

Ligaments of the uterus/contents

Contains the ovarian vessels.

Back 9

Suspensory ligament
of ovaries

Front 10

Ligaments of the uterus/contents

Contains the uterine vessels.

Back 10

Transverse cervical
(cardinal) ligament

Front 11

Ligaments of the uterus/contents

Transverse cervical
(cardinal) ligament

Back 11

Contains the uterine vessels.

Front 12

Ligaments of the uterus/contents

Round ligament
of uterus

Back 12

Contains no important structures.

Front 13

Ligaments of the uterus/contents

Contains no important structures.

Back 13

Round ligament
of uterus

Front 14

Ligaments of the uterus/contents

Contains the round ligaments of the uterus and
ovaries and the uterine tubules and vessels.

Back 14

Broad ligament

Front 15

Ligaments of the uterus/contents

Broad ligament

Back 15

Contains the round ligaments of the uterus and
ovaries and the uterine tubules and vessels.

Front 16

innervation of the
male sexual response

Back 16

Point and Shoot.
-Erection is mediated by the Parasympathetics
-Emission is mediated by the Sympathetis
-Ejaculation is mediated by visceral and somatic
nerves.

Front 17

Derivation of sperm parts

Back 17

-Acrosome is derived from the Golgi apparatus and
-flagellum (tail) from one of the centrioles.
-Middle piece (neck) has Mitochondria.

Front 18

Sperm food supply

Back 18

fructose.

Front 19

sperm locations from nothing to vagina

Back 19

SEVEN UP
-Seminiferous tubules
-Epididimys
-Vas deferens
-Ejaculatory ducts
-(Nothing)
-Urethra
-Penis

Front 20

Sperm development

what forms blood-testis barrier

Back 20

Junctional complex (tight junction) between
Sertoli cells

Front 21

Sperm development

Spermatogenesis begins at puberty with

Back 21

spermatogonia (type A and type B)

Front 22

Sperm development

Full development takes

Back 22

2 months.

Front 23

Sperm development

Spermatogenesis occurs in

Back 23

Seminiferous tubules

Front 24

Sperm development

Blood-testis barrier what and why

Back 24

physical barrier in the testis between the tissues responsible for
spermatogenesis and the bloodstream

-to avoid autoimmune response

Front 25

Sperm development #N of

Primary spermatocyte

Back 25

4N

Front 26

Sperm development #N of

Secondary spermatocyte

Back 26

2N

Front 27

Sperm development #N of

Spermatid (N)

Back 27

1N

Front 28

progression of cells to sperm and N number

Back 28

Spermatogonium 1° (diploid, 2N)
Mitosis
spermatocyte 2° (diploid, 4N)
Meiosis I
spermatocyte (haploid, 2N)
Meiosis II
Spermatid (haploid, N)

Front 29

Male spermatogenesis products/functions of products

Androgen-binding protein (ABP)

Back 29

Ensures that testosterone in seminiferous tubule is high

Front 30

Male spermatogenesis products/functions of products

Ensures that testosterone in seminiferous tubule is high

Back 30

Androgen-binding protein (ABP)

Front 31

Male spermatogenesis products/functions of products

Inhibits FSH

Back 31

Inhibin

Front 32

Male spermatogenesis products/functions of products

Inhibin

Back 32

Inhibits FSH

Front 33

Male spermatogenesis products/functions of products

Testosterone

Back 33

Differentiates male genitalia, has anabolic effects on protein metabolism,
maintains gametogenesis, maintains libido,
inhibits GnRH, and fuses epiphyseal plates
in bone.

Front 34

Male spermatogenesis products/functions of products

Differentiates male genitalia

Back 34

Testosterone

Front 35

Male spermatogenesis products/functions of products

has anabolic effects on protein metabolism

Back 35

Testosterone

Front 36

Male spermatogenesis products/functions of products

maintains gametogenesis

Back 36

Testosterone

Front 37

Male spermatogenesis products/functions of products

maintains libido

Back 37

Testosterone

Front 38

Androgens

names

Back 38

Testosterone,
dihydrotestosterone (DHT), androstenedione.

Front 39

Androgens

Source

Back 39

-DHT and testosterone (testis),

-androstenedione (adrenal).

Front 40

Androgens

Targets

Back 40

Skin, prostate, seminal vesicles, epididymis, liver,
muscle, brain.

Front 41

Androgens

Function

Back 41

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

Front 42

Androgens

potency

Back 42

DHT >
testosterone >
androstenedione.

Front 43

Testosterone is converted to
DHT by ?????? and inhibition by ??????

Back 43

the enzyme 5α-reductase, which is inhibited by finasteride.

Front 44

??????is converted to
DHT by the enzyme 5α-reductase, which is inhibited by finasteride.

Back 44

Testosterone

Front 45

Testosterone is converted to
?????? by the enzyme 5α-reductase, which is inhibited by finasteride.

Back 45

DHT

Front 46

Testosterone and androstenedione are converted to estrogen
in ????? by ??????

Back 46

adipose tissue by enzyme aromatase.

Front 47

?????? converted to estrogen
in adipose tissue by enzyme aromatase.

Back 47

Testosterone and androstenedione

Front 48

Testosterone and androstenedione are converted to ???????
in adipose tissue by enzyme aromatase.

Back 48

estrogen

Front 49

Estrogen

Source

Back 49

Ovary (estradiol),
placenta (estriol),
blood (aromatization).

Front 50

Estrogen

Functions (10)

Back 50

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

Front 51

Estrogen

effects on LH

Back 51

LH surge (estrogen feedback on LH secretion switches to positive from negative just before
LH surge)

Front 52

Estrogens

potency

Back 52

Potency––estradiol > estrone
> estriol.

Front 53

Estrogen levels in pregnancy

Back 53

50-fold ↑ in estradiol and estrone

1000-fold ↑ in estriol
(indicator of fetal well being)

Front 54

Estrogen

indicator of fetal well being

Back 54

1000-fold ↑ in estriol

Front 55

Progesterone

Source

Back 55

Corpus luteum,
placenta,
adrenal cortex,
testes.

Front 56

Progesterone

Function (7)

Back 56

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

Front 57

Progesterone mnemonic

Back 57

Progesterone Prepares for
Pregnancy.

Front 58

Elevation of ?????? is
indicative of ovulation.

Back 58

progesterone

Front 59

Follicular growth is fastest
during

Back 59

2nd week of proliferative phase.

Front 60

stimulates endometrial proliferation.

Back 60

Estrogen

Front 61

maintains endometrium to support
implantation.

Back 61

Progesterone

Front 62

?????progesterone leads to ↓ fertility.

Back 62

↓

Front 63

↓ progesterone leads to ??fertility.

Back 63

↓

Front 64

blood from ruptured follicle causes peritoneal irritation that can mimic appendicitis.

Back 64

Mittelschmerz

Front 65

Mittelschmerz

Back 65

blood from ruptured follicle causes peritoneal irritation that can mimic appendicitis.

Front 66

Oral contraceptives mech

Back 66

prevent estrogen surge, LH
surge → ovulation does not occur.

Front 67

Ovulation steps

Back 67

Estrogen surge day before ovulation.
Stimulates LH, inhibits FSH.
LH surge causes ovulation (rupture of follicle).
↑ temperature (progesterone induced). Ferning of cervical mucosa.

Front 68

Meiosis and ovulation

Back 68

-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)

Front 69

hCG

Source

Back 69

Syncytiotrophoblast of placenta.

Front 70

hCG

Function

Back 70

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.

Front 71

Used to detect pregnancy because it appears in the urine 8 days after successful fertilization (blood and urine tests)

Back 71

hCG

Front 72

hCG

wrt testing

Back 72

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.

Front 73

women with hydatidiform moles or choriocarcinoma.

Back 73

Elevated hCG

Front 74

Cessation of estrogen production with age-linked decline in number of ovarian follicles.

Back 74

Menopause

Front 75

Menopause

what

Back 75

Cessation of estrogen production with age-linked
decline in number of ovarian follicles.

Front 76

Menopause

age

Back 76

Average age of onset is 51 years (earlier in smokers).

Front 77

Menopause

hormonal changes

Back 77

↓ estrogen
↑↑ FSH
↑ LH (no surge)
↑ GnRH.

Front 78

Menopause

clinical findings

Back 78

Menopause causes HAVOC:
Hot flashes,
Atrophy of the Vagina, Osteoporosis,
Coronary artery disease.

Front 79

Bicornuate uterus

mech

Back 79

Results from incomplete fusion of the paramesonephric ducts.

Front 80

Results from incomplete fusion of the paramesonephricducts. Associated with urinary tract abnormalities and infertility.

Back 80

Bicornuate uterus

Front 81

Bicornuate uterus

complications

Back 81

Associated with urinary tract abnormalities and infertility.

Front 82

Abnormal opening of penile urethra on inferior (ventral) side of penis due to failure of urethral folds to close.

Back 82

Hypospadias

Front 83

Hypospadias

what and mech

Back 83

Abnormal opening of penile urethra on inferior (ventral) side of penis due to failure of urethral folds to close.

Front 84

Abnormal opening of penile urethra on superior (dorsal) side of penis due to faulty positioning of genital tubercle.

Back 84

Epispadias

Front 85

Hypospadias

Back 85

Abnormal opening of penile urethra on superior (dorsal) side of penis due to faulty positioning of genital tubercle.

Front 86

Congenital penile abnormalities

which is more common

Back 86

Hypospadias is more common
than epispadias.

Front 87

Hypospadias

complications and Tx

Back 87

Fix
hypospadias to prevent UTIs.

Front 88

Exstrophy of the bladder is
associated with ?????

Back 88

epispadias.

Front 89

????? is associated with epispadias.

Back 89

Exstrophy of the bladder

Front 90

Klinefelter’s syndrome


phenotype/genotype

Back 90

[male] (XXY),

Front 91

[male] (XXY),

Back 91

Klinefelter’s syndrome

Front 92

Turner’s syndrome

phenotype/genotype

Back 92

[female] (XO),

Front 93

[female] (XO)

Back 93

Turner’s syndrome

Front 94

Double Y males

phenotype/genotype

Back 94

[male] (XYY),

Front 95

[male] (XYY)

Back 95

Double Y males

Front 96

Klinefelter’s syndrome

appearance

Back 96

Testicular atrophy, eunuchoid body shape, tall, long extremities, gynecomastia, female hair distribution.

Front 97

Klinefelter’s syndrome

lab findings

Back 97

Presence of inactivated X chromosome (Barr body).

Front 98

Klinefelter’s syndrome

complications

Back 98

Common cause of hypogonadism
seen in infertility workup.

Front 99

Turner’s syndrome

appearance

Back 99

Short stature, webbing of neck,

Front 100

Turner’s syndrome

lab findings

Back 100

No Barr body.
ovarian dysgenesis (streak ovary)

Front 101

Turner’s syndrome

complications

Back 101

-coarctation of the aorta,
-most common cause of 1° amenorrhea.
-Horseshoe kidney
-cystic hygroma

Front 102

cystic hygroma

Back 102

a lymphatic malformation, is a benign proliferation of lymph vessels, fluid filled sacs that result from blockage of the lymphatic system

Front 103

a lymphatic malformation, is a benign proliferation of lymph vessels, fluid filled sacs that result from blockage of the lymphatic system

Back 103

cystic hygroma

Front 104

Pseudohermaphroditism what is it

Back 104

Disagreement between the phenotypic (external genitalia) and gonadal (testes vs.
ovaries) sex.

Front 105

Female pseudohermaphrodite

genotype/phenotype

Back 105

XX - Ovaries present, but external genitalia are virilized or ambiguous.

Front 106

XX - Ovaries present, but external genitalia are virilized or ambiguous.

Back 106

Female pseudohermaphrodite

Front 107

male pseudohermaphrodite

genotype/phenotype

Back 107

XY - Testes present, but external genitalia are female or ambiguous

Front 108

Female pseudohermaphrodite

mech

Back 108

excessive and inappropriate exposure to androgenic steroids during early gestation

Front 109

Female pseudohermaphrodite

causes

Back 109

congenital adrenal hyperplasia or exogenous administration of androgens during pregnancy).

Front 110

Female pseudohermaphrodite

mech

Back 110

Most common form is androgen insensitivity syndrome (testicular feminization).

Front 111

true hermaphrodite

genotype/phenotype

Back 111

(46,XX or 47,XXY) Both ovary and testicular tissue present; ambiguous genitalia. Very rare.

Front 112

Androgen insensitivity syndrome

genotype/phenotype

Back 112

(46,XY)

normal-appearing female; female external genitalia with rudimentary vagina; uterus and uterine tubes generally absent; develops testes

Front 113

Androgen insensitivity syndrome

complications

Back 113

testes (often found in labia majora; surgically removed to prevent malignancy

Front 114

Androgen insensitivity syndrome

Lab findings

Back 114

of testosterone, estrogen, and LH are all high.

Front 115

5α-reductase deficiency

mech and clinical findings

Back 115

Unable to convert testosterone to DHT. Ambiguous genitalia until puberty, when
↑ testosterone causes masculinization of genitalia.

Front 116

5α-reductase deficiency

lab findings

Back 116

Testosterone/estrogen levels
are normal; LH is normal or ↑.

Front 117

Hydatidiform mole

what is it

Back 117

A pathologic ovum (“empty egg”––ovum with no DNA) resulting in cystic swelling of chorionic villi and proliferation of chorionic epithelium (trophoblast).

Front 118

Hydatidiform mole

lab findings

Back 118

High HCG

Front 119

Hydatidiform mole

gross

Back 119

“Honeycombed uterus,” “cluster of grapes” appearance. Enlarged uterus.

Front 120

Most common precursor of choriocarcinoma.

Back 120

complete Hydatidiform mole

Front 121

complete mole wrt
genotype
origin
fetus
cancer

Back 121

Genotype of a complete mole is 46,XX and is completely paternal in origin (no maternal chromosomes); no associated fetus. increased risk of choriocarcinoma

Front 122

partial mole wrt
genotype
origin
fetus
cancer

Back 122

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

Front 123

Preeclampsia

what

Back 123

triad of hypertension, proteinuria, and edema

Front 124

Eclampsia

what

Back 124

eclampsia is the addition
of seizures

Front 125

Preeclampsia

%'s and when

Back 125

7% of pregnant women from 20 weeks’ gestation to 6
weeks postpartum.

Front 126

Preeclampsia

who is at increased risk

Back 126

↑ incidence in patients with preexisting hypertension, diabetes, chronic renal disease, and autoimmune disorders.

Front 127

Preeclampsia

mech and associations

Back 127

-Etiology involves placental ischemia.

-Can be associated with HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets).

Front 128

Preeclampsia

clinical findings

Back 128

Headache, blurred vision, abdominal pain, edema of face and extremities, altered
mentation, hyperreflexia;

Front 129

Preeclampsia

Tx

Back 129

Delivery of fetus as soon as viable. Otherwise bed rest, salt restriction, and monitoring
and treatment of hypertension.

Front 130

Preeclampsia

lab findings

Back 130

thrombocytopenia, hyperuricemia.
elevated Liver enzymes

Front 131

Eclampsia

Tx

Back 131

a medical emergency, IV magnesium
sulfate and diazepam.

Front 132

Abruptio placentae

what

Back 132

premature detachment of placenta from implantation site.

Front 133

Abruptio placentae

clinical findings

Back 133

Painful uterine bleeding (usually during 3rd trimester). Fetal death.

Front 134

Abruptio placentae

associations and risk factors

Back 134

May be associated with DIC. ↑ risk with smoking, hypertension, cocaine use.

Front 135

premature detachment of placenta from implantation site.

Back 135

Abruptio placentae

Front 136

Placenta accreta

what

Back 136

defective decidual layer allows placenta to attach directly to myometrium.

Front 137

Placenta accreta

clinical findings

Back 137

Massive hemorrhage after delivery.

Front 138

Placenta accreta

risk factors

Back 138

Predisposed by prior C-section or inflammation.

Front 139

defective decidual layer allows placenta to attach directly to myometrium.

Back 139

Placenta accreta

Front 140

Placenta previa

what and findings

Back 140

attachment of placenta to lower uterine segment. May occlude
cervical os. Painless bleeding in any trimester.

Front 141

Painless bleeding in any trimester.

Back 141

Placenta previa

Front 142

Ectopic pregnancy

locations

Back 142

most often in fallopian tubes,
confirm with ultrasound.

Front 143

Ectopic pregnancy

clinical/Lab findings

Back 143

↑ hCG and sudden lower abdominal pain; Often clinically mistaken for appendicitis.

Front 144

Ectopic pregnancy

risk factors

Back 144

predisposed by salpingitis (PID).

Front 145

Ectopic pregnancy

confromation

Back 145

confirm with ultrasound.

Front 146

Polyhydramnios

definition

Back 146

> 1.5–2 L of amniotic fluid;

Front 147

Polyhydramnios

associations and complications

Back 147

associated with esophageal or duodenal atresia, causing inability to swallow amniotic fluid, and with anencephaly.

Front 148

Oligohydramnios

associations and complications

Back 148

associated with bilateral renal agenesis or posterior urethral
valves (in males) and resultant inability to excrete urine.

Front 149

oligohydramnios

definition

Back 149

< 0.5 L of amniotic fluid;

Front 150

< 0.5 L of amniotic fluid;

Back 150

oligohydramnios

Front 151

> 1.5–2 L of amniotic fluid;

Back 151

Polyhydramnios

Front 152

Cervical pathology

Dysplasia and carcinoma in situ
describe and classification

Back 152

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.

Front 153

Cervical pathology

Dysplasia and carcinoma in situ
associations and progression

Back 153

HPV 16, 18. May progress slowly to invasive carcinoma.

Front 154

Cervical pathology

Invasive carcinoma
what type

Back 154

Often squamous cell carcinom

Front 155

Cervical pathology

Dysplasia and carcinoma in situ
wrt testing

Back 155

Pap smear can catch cervical dysplasia (koilocytes) before
it progresses to invasive carcinoma

Front 156

Cervical pathology

Invasive carcinoma
wrt specific invasion

Back 156

Lateral invasion can block ureters, causing renal
failure.

Front 157

Endometriosis

Back 157

Non-neoplastic endometrial glands/stroma in abnormal locations outside the uterus.

Front 158

Non-neoplastic endometrial glands/stroma in abnormal locations outside the uterus.

Back 158

Endometriosis

Front 159

Endometriosis

clinical findings

Back 159

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.

Front 160

“chocolate cysts.”

Back 160

Endometriosis

Front 161

Endometriosis

complications

Back 161

Often results in infertility

Front 162

Adenomyosis

Back 162

Endometriosis within the myometrium.

Front 163

Endometriosis within the myometrium.

Back 163

Adenomyosis

Front 164

Endometrial hyperplasia

Back 164

Abnormal endometrial gland proliferation usually caused by excess estrogen stimulation.

Front 165

Abnormal endometrial gland proliferation usually caused by excess estrogen stimulation.

Back 165

Endometrial hyperplasia

Front 166

Endometrial hyperplasia

wrt complications

Back 166

↑ risk for endometrial carcinoma

Front 167

Endometrial hyperplasia

clinical findings

Back 167

Most commonly manifests linically as vaginal
bleeding.

Front 168

Endometrial carcinoma

how common and who

Back 168

Most common gynecologic malignancy. Peak age 55–65 years old

Front 169

Most common gynecologic malignancy

Back 169

Endometrial carcinoma

Front 170

Endometrial carcinoma

clinical findings

Back 170

Clinically presents with vaginal bleeding.

Front 171

Endometrial carcinoma

Risk factors

Back 171

prolonged use of estrogen without progestins, obesity, diabetes, hypertension, nulliparity,
and late menopause.

Front 172

Endometrial carcinoma

Typically preceded by

Back 172

endometrial hyperplasia.

Front 173

Most common of all tumors in females

Back 173

Leiomyoma

Front 174

Leiomyoma

how common and who

Back 174

Most common of all tumors in females. ↑ incidence in blacks

Front 175

Leiomyoma

gross findings

Back 175

multiple tumors with well
demarcated borders.

Front 176

Leiomyoma

prognosis

Back 176

Benign smooth muscle tumor; malignant transformation is rare. Does not progress to leiomyosarcoma

Front 177

Leiomyoma

wrt estrogen

Back 177

Estrogen sensitive––tumor size ↑ with pregnancy and ↓ with
menopause.

Front 178

Leiomyosarcoma

gross

Back 178

Bulky irregularly shaped tumor with areas of necrosis and hemorrhage

Front 179

Leiomyosarcoma

cause and who

Back 179

typically arising de novo (not from leiomyoma). ↑ incidence in blacks.

Front 180

Leiomyosarcoma

Prognosis

Back 180

Highly aggressive tumor with
tendency to recur.

Front 181

Leiomyosarcoma

clinical findings

Back 181

May protrude from cervix and bleed.

Front 182

Polycystic ovarian syndrome

lab findings

Back 182

↑ LH, ↓ FSH, ↑ testosterone.

Front 183

Polycystic ovarian syndrome

clinical findings

Back 183

amenorrhea, infertility, obesity, and hirsutism.

Front 184

Polycystic ovarian syndrome

mech

Back 184

↑ LH production leads to anovulation, hyperandrogenism
due to deranged steroid synthesis

Front 185

Polycystic ovarian syndrome

Tx

Back 185

Treat with weight loss, OCPs, gonadotropin analogs, or surgery.

Front 186

Ovarian cysts

Follicular cyst

Back 186

distention of unruptured graafian follicle. May be associated with
hyperestrinism and endometrial hyperplasia.

Front 187

Ovarian cysts

Corpus luteum cyst

Back 187

hemorrhage into persistent corpus luteum. Menstrual irregularity.

Front 188

Ovarian cysts

Theca-lutein cyst

Back 188

often bilateral/multiple. Due to gonadotropin stimulation.
Associated with choriocarcinoma and moles.

Front 189

Ovarian cysts

“Chocolate cyst”

Back 189

blood-containing cyst from ovarian endometriosis. Varies with menstrual cycle.

Front 190

Ovarian cysts

distention of unruptured graafian follicle. May be associated with
hyperestrinism and endometrial hyperplasia.

Back 190

Follicular cyst

Front 191

Ovarian cysts

hemorrhage into persistent corpus luteum. Menstrual irregularity.

Back 191

Corpus luteum cyst

Front 192

Ovarian cysts

often bilateral/multiple.

Back 192

Theca-lutein cyst

Front 193

Ovarian cysts

Due to gonadotropin stimulation.
Associated with choriocarcinoma and moles.

Back 193

Theca-lutein cyst

Front 194

Ovarian cysts

blood-containing cyst from ovarian endometriosis.

Back 194

“Chocolate cyst”

Front 195

Ovarian cysts

Varies with menstrual cycle.

Back 195

“Chocolate cyst”

Front 196

Dysgerminoma

what type of tumor

Back 196

Ovarian germ cell tumor

Front 197

Ovarian germ cell tumors

name them

Back 197

Dysgerminoma
Yolk sac (endodermal sinus tumor)
Choriocarcinoma
Teratoma

Front 198

Ovarian non–germ cell tumors

name them

Back 198

1. Serous cystadenoma
2. Serous cystadenocarcinoma
3. Mucinous cystadenoma
4. Mucinous cystadenocarcinoma
5. Brenner tumor
6. Ovarian fibroma
7. Granulosa cell tumor

Front 199

Yolk sac (endodermal sinus tumor)

what type of tumor

Back 199

Ovarian germ cell tumor

Front 200

Choriocarcinoma

what type of tumor

Back 200

Ovarian germ cell tumor

Front 201

Teratoma

what type of tumor

Back 201

Ovarian germ cell tumor

Front 202

Serous cystadenoma


what type of tumor

Back 202

Ovarian non–germ cell tumors

Front 203

Serous cystadenocarcinoma

what type of tumor

Back 203

Ovarian non–germ cell tumors

Front 204

Mucinous cystadenoma

what type of tumor

Back 204

Ovarian non–germ cell tumors

Front 205

Mucinous cystadenocarcinoma

what type of tumor

Back 205

Ovarian non–germ cell tumors

Front 206

Brenner tumor

what type of tumor

Back 206

Ovarian non–germ cell tumors

Front 207

Ovarian fibroma

what type of tumor

Back 207

Ovarian non–germ cell tumors

Front 208

Granulosa cell tumor

what type of tumor

Back 208

Ovarian non–germ cell tumors

Front 209

descrptions of Ovarian germ cell tumors

Dysgerminoma

Back 209

Malignant, equivalent to male seminoma. Sheets of uniform cells. ↑ hCG.

Front 210

descrptions of Ovarian germ cell tumors

Yolk sac (endodermal
sinus tumor)

Back 210

Aggressive malignancy in ovaries (testes in boys) and sacrococcygeal area of young
children. ↑ AFP.

Front 211

descrptions of Ovarian germ cell tumors

Choriocarcinoma

Back 211

Rare but malignant; can develop during pregnancy in mother or baby. Large,
hyperchromatic hyncytiotrophoblastic cells. ↑ hCG.

Front 212

descrptions of Ovarian germ cell tumors

Teratoma types

Back 212

Mature teratoma (“dermoid cyst”)––most frequent benign ovarian tumor.
Immature teratoma– –aggressively malignant.
Struma ovarii--contains functional thyroid tissue

Front 213

Ovarian germ cell tumors

↑ hCG.

Back 213

Choriocarcinoma

and

Dysgerminoma

Front 214

Ovarian germ cell tumors

↑ AFP.

Back 214

Yolk sac (endodermal sinus tumor)

Front 215

90% of ovarian germ cell tumors

Back 215

Teratoma

Front 216

Struma ovarii

Back 216

Teratoma contains functional thyroid tissue

Front 217

Ovarian germ cell tumors

Teratoma contains functional thyroid tissue

Back 217

Struma ovarii

Front 218

Ovarian non–germ cell tumors

Frequently bilateral, lined with fallopian tube–like epithelium. Benign.

Back 218

Serous cystadenoma

Front 219

Ovarian non–germ cell tumors

malignant and frequently bilateral.

Back 219

Serous cystadenocarcinoma

Front 220

Ovarian non–germ cell tumors

multilocular cyst lined by mucus-secreting epithelium. Benign.

Back 220

Mucinous cystadenoma

Front 221

Ovarian non–germ cell tumors

malignant. Pseudomyxoma peritonei

Back 221

Mucinous cystadenocarcinoma

Front 222

Ovarian non–germ cell tumors

benign tumor that resembles Bladder epithelium.

Back 222

Brenner tumor

Front 223

Brenner tumor

Back 223

tumors that are part of the surface epithelial-stromal tumor group of ovarian neoplasms.
benign tumor that resembles Bladder epithelium.

Front 224

Meigs’ syndrome

Back 224

triad of ovarian fibroma, ascites, and hydrothorax.

Front 225

triad of ovarian fibroma, ascites, and hydrothorax.

Back 225

Meigs’ syndrome

Front 226

Ovarian non–germ cell tumors

bundles of spindle-shaped fibroblasts

Back 226

Ovarian fibroma

Front 227

Ovarian non–germ cell tumors

secretes estrogen →precocious puberty (kids).

Back 227

Granulosa cell tumor

Front 228

Call-Exner bodies

Back 228

granulosa cells arranged haphazardly around a space containing eosinophilic fluid

Front 229

Pseudomyxoma peritonei

Back 229

intraperitonealaccumulation of mucinous material from ovarian (Mucinous cystadenocarcinoma) or appendiceal tumor.

Front 230

"jelly belly" aka

Back 230

Pseudomyxoma peritonei

Front 231

Pseudomyxoma peritonei aka

Back 231

"jelly belly"

Front 232

granulosa cells arranged haphazardly around a space containing eosinophilic fluid

Back 232

Call-Exner bodies

Front 233

Ovarian non–germ cell tumors

endometrial hyperplasia or carcinoma in adults. Call-Exner bodies

Back 233

Granulosa cell tumor

Front 234

Breast tumors

benign types

Back 234

1. Fibroadenoma–
2. Intraductal papilloma
3. Cystosarcoma phyllodes

Front 235

Breast tumors

malignant types

Back 235

1. Ductal carcinoma in situ
2. Invasive ductal,
3. Comedocarcinoma
4. Inflammatory
5. Invasive lobular
6. Medullary
7. Paget’s disease of the breast

Front 236

Breast tumors

most common tumor < 25 years

Back 236

Fibroadenoma

Front 237

Breast tumors

Small, mobile, firm mass with
sharp edges. ↑ size and tenderness with pregnancy. Not a precursor to breast cancer.

Back 237

Fibroadenoma

Front 238

Breast tumors

benign tumor of lactiferous ducts; presents with serous or bloody
nipple discharge.

Back 238

Intraductal papilloma

Front 239

Breast tumors

large, bulky mass of connective tissue and cysts. Tumor may have “leaflike” projections. Some may be malignant.

Back 239

Cystosarcoma phyllodes

Front 240

Breast tumors
Malignant tumors

in general

Back 240

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;

Front 241

Breast tumors

the single most important prognostic factor.

Back 241

Lymph node involvement

Front 242

Breast tumors

early malignancy without basement
membrane penetration.

Back 242

Ductal carcinoma in situ (DCIS)––

Front 243

Breast tumors

The worst and most invasive.

Back 243

Invasive ductal, no specific type

Front 244

Breast tumors

ductal, with cheesy consistency due to central necrosis.

Back 244

Comedocarcinoma

Front 245

Breast tumors

lymphatic involvement; poor prognosis.

Back 245

Inflammatory

Front 246

Breast tumors

often multiple, bilateral.

Back 246

Invasive lobular

Front 247

Breast tumors

fleshy, cellular, lymphocytic infiltrate. Good prognosis.

Back 247

Medullary

Front 248

Breast tumors

eczematous patches on nipple.

Back 248

Paget’s disease of the breast

Front 249

Paget’s disease of the breast

description, cells, what it means, where is it also seen

Back 249

––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.

Front 250

Breast tumors

risk factors

Back 250

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.

Front 251

Breast tumors

Risk is NOT increased by

Back 251

fibroadenoma or nonhyperplastic cysts.

Front 252

Common breast conditions

Fibrocystic disease
how common, and who

Back 252

Most common cause of “breast lumps” age 25–menopause.

Front 253

Common breast conditions

Fibrocystic disease
presentation and risk

Back 253

Presents with diffuse breast
pain and multiple lesions, often bilateral. Usually does not indicate ↑ risk of
carcinoma.

Front 254

Fibrocystic disease

types

Back 254

1. Fibrosis–
2. Cystic–
3. Sclerosing–
4. Epithelial hyperplasia–

Front 255

Fibrocystic disease types

hyperplasia of breast stroma.

Back 255

Fibrosis

Front 256

Fibrocystic disease types

fluid filled.

Back 256

Cystic

Front 257

Fibrocystic disease types

↑ acini and intralobular fibrosis.

Back 257

Sclerosing

Front 258

Fibrocystic disease types

–↑ in number of epithelial cell layers in terminal duct
lobule.

Back 258

Epithelial hyperplasia

Front 259

Fibrocystic disease types

↑ risk of carcinoma with atypical cells. Occurs > 30 years.

Back 259

Epithelial hyperplasia

Front 260

Acute mastitis

what/ mech

Back 260

Breast abscess; during breast-feeding ↑ risk of bacterial infection through cracks in the nipple; Staphylococcus aureus is the most common pathogen.

Front 261

Fat necrosis of breast

Back 261

A benign painless lump; forms due to injury to breast tissue.

Front 262

A benign painless lump; forms due to injury to breast tissue

Back 262

Fat necrosis of breast

Front 263

Gynecomastia

mech and causes

Back 263

Results from hyperestrogenism (cirrhosis, testicular tumor, puberty, old age),
Klinefelter’s syndrome, or drug induced (cimetidine, alcohol abuse, marijuana,
heroin, psychoactive drugs, digitalis).

Front 264

Prostatitis

clinical findings and causes

Back 264

Dysuria, frequency, urgency, low back pain. Acute: bacterial; chronic: bacterial or
abacterial (most common).

Front 265

Benign prostatic hyperplasia

mech

Back 265

May be due to an age-related increase in estradiol with
possible sensitization of the prostate to the growth promoting effects of DHT.

Front 266

Benign prostatic hyperplasia

prostate gross changes

Back 266

Characterized by a nodular enlargement of the periurethral (lateral and middle) lobes of the prostate gland, compressing the urethra into a vertical slit.

Front 267

Benign prostatic hyperplasia

clinical findings

Back 267

↑ frequency of urination, nocturia, difficulty starting and stopping the stream of urine, and dysuria.

Front 268

Benign prostatic hyperplasia

complications

Back 268

May lead to distention and hypertrophy of the bladder, hydronephrosis,
and UTIs. Not considered a premalignant lesion.

Front 269

Benign prostatic hyperplasia

labs

Back 269

↑ free prostate-specific antigen (PSA).

Front 270

Prostatic adenocarcinoma

where and Dx

Back 270

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.

Front 271

Prostatic adenocarcinoma

Lab findings

Back 271

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.

Front 272

↑ in serum alkaline
phosphatase and PSA.

Back 272

Osteoblastic metastases from Prostatic adenocarcinoma

Front 273

Cryptorchidism

what and complications

Back 273

Undescended testis (one or both); lack of spermatogenesis due to ↑ body temperature; associated with ↑ risk of germ cell tumors.

Front 274

Testicular germ cell tumors

names

Back 274

-Seminoma
-Embryonal carcinoma
-Yolk sac (endodermal sinus) tumor
-Choriocarcinoma
-Teratoma

Front 275

Testicular non–germ cell tumors

names

Back 275

-Leydig cell
-Sertoli cell
-Testicular lymphoma

Front 276

~95% of all testicular tumors

Back 276

Testicular germ cell tumors

Front 277

Seminoma

how common and who

Back 277

most common testicular tumor, mostly affecting males age 15–35.

Front 278

Testicular germ cell tumors

Malignant; painless testicular enlargement;

Back 278

Seminoma

Front 279

Testicular germ cell tumors

Malignant; painful;

Back 279

Embryonal carcinoma

Front 280

Testicular germ cell tumors

↑ AFP

Back 280

Yolk sac (endodermal sinus) tumor

Front 281

Testicular germ cell tumors

Malignant, ↑ hCG.

Back 281

all Choriocarcinoma

10% of Seminoma

Front 282

Testicular germ cell tumors

Unlike in females, in males this tumor is most often malignant.

Back 282

mature teratoma

Front 283

Testicular non–germ cell tumors

Benign, contains Reinke crystals

Back 283

Leydig cell

Front 284

Testicular non–germ cell tumors

usually androgen producing, gynecomastia in men, precocious puberty in boys.

Back 284

Leydig cell

Front 285

Leydig cell tumor findings

Back 285

Benign, contains Reinke crystals; usually androgen producing, gynecomastia in men,
precocious puberty in boys.

Front 286

Testicular non–germ cell tumors

Benign, androblastoma from sex cord stroma.

Back 286

Sertoli cell

Front 287

Most common testicular cancer in older men.

Back 287

Testicular lymphoma

Front 288

Reinke crystals

Back 288

crystal-like inclusions in the interstitial cells of the testis (Leydig cells) and hilus cells in the ovary

Front 289

crystal-like inclusions in the interstitial cells of the testis (Leydig cells) and hilus cells in the ovary

Back 289

Reinke crystals

Front 290

Penile pathology
Carcinoma in situ: names

Back 290

-Bowen disease

-Erythroplasia of Queyrat

-Bowenoid papulosis

Front 291

Bowen disease

clinical findings, when and progression

Back 291

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.

Front 292

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.

Back 292

Bowen disease

Front 293

Erythroplasia of Queyrat

Back 293

Red velvety plaques, usually involving the glans; otherwise similar to Bowen disease

Front 294

Red velvety plaques, usually involving the glans; otherwise similar to Bowen disease

Back 294

Erythroplasia of Queyrat

Front 295

Bowenoid papulosis

clinical findings, when and progression

Back 295

Multiple papular lesions; affects younger age group than the other two; usually does not
become invasive.

Front 296

Multiple papular lesions; affects younger age group than the other two; usually does not
become invasive.

Back 296

Bowenoid papulosis

Front 297

Penile pathology Squamous cell
carcinoma (SCC)

who

Back 297

Rare in circumcised men; uncommon in US and Europe, more common in Asia, Africa, and South America.

Front 298

Penile pathology Squamous cell
carcinoma (SCC)

associations

Back 298

Commonly associated with HPV.

Front 299

Rare in circumcised men; uncommon in US and Europe, more common in Asia, Africa, and South America. Commonly associated with HPV.

Back 299

Penile Squamous cell carcinoma (SCC)

Front 300

Antiandrogens

names

Back 300

Finasteride
Flutamide
Ketoconazole,
spironolactone

Front 301

Finasteride

mech and clinical uses

Back 301

A 5α-reductase inhibitor (↓ conversion of testosterone to dihydrotestosterone). Useful
in BPH. Also promotes hair growth––used to treat male-pattern baldness.

Front 302

Finasteride aka

Back 302

propecia

Front 303

propecia aka

Back 303

Finasteride

Front 304

Flutamide

mech and clinical uses

Back 304

A nonsteroidal competitive inhibitor of androgens at the testosterone receptor. Used in
prostate carcinoma.

Front 305

A nonsteroidal competitive inhibitor of androgens at the testosterone receptor. Used in
prostate carcinoma.

Back 305

Flutamide

Front 306

A 5α-reductase inhibitor (↓ conversion of testosterone to dihydrotestosterone). Useful
in BPH. Also promotes hair growth––used to treat male-pattern baldness.

Back 306

Finasteride (propcia)

Front 307

Antiandrogens mech/clinical use of

Ketoconazole

Back 307

Inhibit steroid synthesis; used in the treatment of polycystic ovarian syndrome to prevent
hirsutism.

Front 308

Inhibit steroid synthesis; used in the treatment of polycystic ovarian syndrome to prevent
hirsutism.

Back 308

Ketoconazole as an Antiandrogen

Front 309

Antiandrogens mech/clinical use of

spironolactone

Back 309

Inhibit steroid binding; used in the treatment of polycystic ovarian syndrome to prevent
hirsutism.

Front 310

Inhibit steroid binding; used in the treatment of polycystic ovarian syndrome to prevent
hirsutism.

Back 310

spironolactone as an Antiandrogen

Front 311

Leuprolide

Mechanism

Back 311

GnRH analog with agonist properties when used in
pulsatile fashion; antagonist properties when used
in continuous fashion.

Front 312

Leuprolide

Clinical use

Back 312

Infertility (pulsatile), prostate cancer (continuous–use with flutamide), uterine fibroids.

Front 313

Leuprolide

Toxicity

Back 313

Antiandrogen, nausea, vomiting.

Front 314

GnRH analog with agonist properties when used in
pulsatile fashion; antagonist properties when used
in continuous fashion.

Back 314

Leuprolide

Front 315

Sildenafil, vardenafil

Mechanism

Back 315

Inhibit cGMP phosphodiesterase, causing ↑ cGMP smooth muscle relaxation in the corpus cavernosum, ↑ blood flow, and penile erection.

Front 316

Sildenafil, vardenafil

Clinical use

Back 316

Treatment of erectile dysfunction.

Front 317

Sildenafil, vardenafil

Toxicity

Back 317

Headache, flushing, dyspepsia, blue-green color vision.
Risk of life-threatening hypotension in patients
taking nitrates.

Front 318

Headache, flushing, dyspepsia, blue-green color vision.

Back 318

Sildenafil, vardenafil

Toxicity

Front 319

Inhibit cGMP phosphodiesterase, causing ↑ cGMP, smooth muscle relaxation in the corpus cavernosum

Back 319

Sildenafil, vardenafil

Front 320

Clomiphene

Mechanism

Back 320

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.

Front 321

Clomiphene

Clinical use

Back 321

Treatment of infertility.

Front 322

Clomiphene

Toxicity

Back 322

Hot flashes, ovarian enlargement, multiple simultaneous pregnancies, visual disturbances.

Front 323

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.

Back 323

Clomiphene

Front 324

Mifepristone aka

Back 324

RU-486

Front 325

RU-486 aka

Back 325

Mifepristone

Front 326

Mifepristone

Mechanism

Back 326

Competitive inhibitor of progestins at progesterone receptors.

Front 327

Mifepristone

Clinical use

Back 327

Postcoital abortifacient (prevents implantation).

Front 328

Mifepristone

Toxicity

Back 328

Heavy bleeding, GI effects (nausea, vomiting, anorexia), abdominal pain.

Front 329

Competitive inhibitor of progestins at progesterone receptors. Postcoital abortifacient (prevents implantation).

Back 329

Mifepristone (RU-486)

Front 330

dinoprostine

Back 330

PGE2 analog causing cervical dilation and uterine contraction, inducing labor

Front 331

PGE2 analog causing cervical dilation and uterine contraction, inducing labor

Back 331

dinoprostine

Front 332

ritodrine/terbutaline

Back 332

beta2-agonists that relax the uterus

Front 333

beta2-agonists that relax the uterus

Back 333

ritodrine/terbutaline

Front 334

Anastrazole

Back 334

aromatase inhibitor used in postmenopausal womaen with breats cancer

Front 335

aromatase inhibitor used in postmenopausal womaen with breats cancer

Back 335

Anastrazole

Front 336

Testosterone (methyltestosterone)

Mechanism

Back 336

Agonist at androgen receptors.

Front 337

Testosterone (methyltestosterone)

Clinical use

Back 337

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).

Front 338

Testosterone (methyltestosterone)

Toxicity

Back 338

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.

Front 339

Estrogens

names

Back 339

ethinyl estradiol, DES, mestrano

Front 340

Estrogens

Mechanism

Back 340

Bind estrogen receptors.

Front 341

Estrogens

Clinical use

Back 341

Hypogonadism or ovarian failure, menstrual abnormalities, HRT in postmenopausal women; use in men with androgen-dependent prostate cancer.

Front 342

Estrogens

Toxicity

Back 342

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.

Front 343

Estrogens

Contraindications

Back 343

-ER-positive breast cancer.

Front 344

Progestins

Mechanism

Back 344

Bind progesterone receptors, reduce growth, and increase vascularization of endometrium.

Front 345

Progestins

Clinical use

Back 345

Used in oral contraceptives and in the treatment of endometrial cancer and abnormal uterine bleeding.

Front 346

Tamoxifen

Back 346

Antagonist on breast tissue; used to treat and prevent recurrence of ER-positive breast
cancer.

Front 347

Antagonist on breast tissue; used to treat and prevent recurrence of ER-positive breast
cancer.

Back 347

Tamoxifen

Front 348

Agonist on bone; reduces reabsorption of bone; used to treat osteoporosis.

Back 348

Raloxifene

Front 349

Raloxifene

Back 349

Agonist on bone; reduces reabsorption of bone; used to treat osteoporosis.

Front 350

Oral contraception

Advantages

Back 350

-Reliable (< 1% failure)
-↓ risk of endometrial and ovarian cancer
-↓ incidence of ectopic pregnancy
-↓ pelvic infections
-Regulation of menses

Front 351

Oral contraception

disadvantages

Back 351

-Taken daily
-No protection against STDs
-↑ triglycerides
-Depression, weight gain, -nausea, hypertension
Hypercoagulable state

Front 352

Hormone replacement
therapy (HRT)

used for

Back 352

Used for relief or prevention of menopausal symptoms (hot flashes, vaginal atrophy, etc.)
and osteoporosis (due to diminished estrogen levels).

Front 353

Hormone replacement
therapy (HRT)

toxicity

Back 353

Unopposed estrogen replacement therapy (ERT) increases the risk of endometrial
cancer, so progesterone is added.