Br Patholgy: Female Gu And Breast

Front 1

What is the most common cause of Bartholin gland abscess?

Back 1

N gonnorrhea

Front 2

What are examples of Non-neoplastic dermatoses of the vulva?

Back 2

1.Lichen sclerosis
2.Lichen simplex chronicus

Front 3

Who does lichen sclerosis occur in? What is the appearance of the skin? What is there a risk of developing?

Back 3

a.Usually occurs in postmenopausal women
b.Thinning of the epidermis
■Parchment-like appearance of skin
c.Small risk for developing squamous cell carcinoma
Note: occurs at vuvla

Front 4

What is the main feature of lichen simplex chronicus? What is there a risk of developing?

Back 4

a.White plaque-like lesion (leukoplakia)
■Due to squamous cell hyperplasia
b.Small risk for developing squamous cell carcinoma
Note: occurs at vulva

Front 5

What are tumors of the vulva?

Back 5

1.Papillary hidradenoma
2.Vulvar intraepithelial neoplasia (VIN)
3.Squamous cell carcinoma
4.Extramammary Paget's disease
5.Malignant melanoma

Front 6

Calymmatobacterium granulomatis is an STD. What type of bacteria is it? What is the pathogenesis? How does it present? How is it treated?

Back 6

1. gram-negative coccobacillus that causes granuloma inguinale
2. Organism phagocytized by macrophages (Donovan bodies)
3. Creeping, raised sore that heals by scarring; no lymphadenopathy
4. Treatment: doxycycline or trimethoprim-sulfamethoxazole
Note: now called Klebsiella granulomatis

Front 7

What are donovan bodies seen in?

Back 7

phagocytized Calymmatobacterium granulomatis ( Klebsiella granulomatis)

Front 8

Describe Candida albicans! What does it cause? What are risk factors? How is it treated?

Back 8

1) Yeasts and pseudohyphae (elongated yeasts); part of normal vaginal flora
2) Second most common vaginitis in the United States
3) Risk factors: diabetes, antibiotics, pregnancy, OCP
4) Pruritic vaginitis with a white discharge and fiery red mucosa
5) Treatment: fluconazole (single dose)

Front 9

Chlamydia trachomatis is what type of organism? What is seen on histologic exam? What does it cause in newborns? How is it treated?

Back 9

1) obligate intracellular human pathogen that is gram -
2) Incubation period 7-12 days after exposure; red inclusions (reticulate bodies) in infected metaplastic squamous cells; reticulate bodies divide to form elementary bodies, which are the infective bodies producing infection
3) Infections in newborns: conjunctivitis (ophthalmia neonatorum), pneumonia
4) DNA probe test for quick diagnosis
7) Treatment: azithromycin 1 g (single dose); doxycycline

Front 10

What does Chlamydia trachomatis cause in males and females?

Back 10

1) Infections in males: NSU (sterile pyuria), epididymitis, proctitis
2) Infections in females: urethritis (sterile pyuria), cervicitis, PID, perihepatitis (FHC syndrome-scar tissue between peritoneum and surface of liver from pus from PID), proctitis, Bartholin gland abscess

Front 11

What do C. trachomatis subspecies cause? How are they treated?

Back 11

1) STD; lymphogranuloma venereum
2) Papules with no ulceration; inguinal lymphadenitis with granulomatous microabscesses and draining sinuses
3) Lymphedema of scrotum or vulva; women also may develop rectal strictures
4) Treatment: doxycycline

Front 12

Describe Gardnerella vaginalis! How does it present? What cell type is present? How is pregnancy effected? How is it treated?

Back 12

1) Gram-negative rod that causes bacterial vaginosis
2) Most common vaginitis
3) Malodorous vaginal discharge; vaginal pH > 4.5
4) Organisms adhere to squamous cells producing "clue cells"
5) Increased incidence of preterm delivery and low-birth-weight newborns
6) Treatment: metronidazole; same treatment in pregnancy

Front 13

What is the most common cause of vaginitis?

Back 13

Gardnerella vaginalis

Front 14

What does Haemophilus ducreyi cause? Does it occur more in men or women? What is presentation? How is diagnosed and treated?

Back 14

1) STD; gram-negative rod that causes chancroid
2) Male dominant disease (10:1); high incidence of HIV
3) Incubation 4-7 days
4) Painful genital and perianal ulcers with suppurative inguinal nodes
5) Diagnosis with Gram stain ("school of fish" appearance) and culture
6) Treatment: ceftriaxone or azithromycin 1 g (single dose)

Front 15

school of fish appearance is seen under the microscope. What is the organism? Describe it!

Back 15

Haemophilus ducreyi is a fastidious gram-negative coccobacillus that causes chancroid

Front 16

What does HSV2 cause? What does a smear show? How is delt with during delivery of baby? How is it treated? What are structural features of virus?

Back 16

1) STD; virus remains latent in sensory ganglia
2) Recurrent vesicles that ulcerate; locations-penis, vulva, cervix, perianal area
3) Tzanck preparation: scrapings removed from the base of an ulcer; see multinucleated squamous cells with eosinophilic intranuclear inclusions
4) Pregnancy: if virus is shedding, baby is delivered by cesarean section
5) Treatment: acyclovir (decreases recurrences)
6) double stranded linear DNA icosahedral capsid in envelope

Front 17

What types of HPV are associated with STDs? What happens? What types are associated with cancer?

Back 17

1) STD; types 6 and 11 (90%; low risk types) associated with condyloma acuminata (venereal warts); fernlike or flat lesions in genital area (e.g., penis, vulva, cervix, perianal)
2) Types 16 and 18 (high risk types) associated with dysplasia and squamous cancer

Front 18

What is the Most common overall STD?

Back 18

HPV... 80% of sexually active women will have acquired HPV by age 50

Front 19

What is seen histologically with HPV infection? What can reduce risk of cancer? How HPV treated?

Back 19

1) Virus produces koilocytic change in squamous epithelium
2) Cells have wrinkled pyknotic nuclei surrounded by a clear halo
3) Approximately 90% spontaneously clear within 2 years (most within 8 months); older women will more often have persistent disease
4) Vaccine decreases risk for developing cervical cancer
5) Treatment: topical podophyllin; α-IFN injection; imiquimod cream

Front 20

What are the features of N gonnorhea? What does it infect? When do symptoms present? How is it diagnosed and treated?

Back 20

1) gram-negative diplococcus that infects glandular or transitional epithelium; symptoms appear 2-7 days after sexual exposure
2) Infection sites similar to C. trachomatis
3) DNA probe test for quick diagnosis
4) Treatment: ceftriaxone

Front 21

What are longterm complications of N gonnorrhea? What is a risk factor for develping it?

Back 21

1)ectopic pregnancy,
2) male sterility,
3) disseminated gonococcemia (C6-C9 deficiency risk factor),
4) septic arthritis,
5) Fitz-Hugh-Curtis (FHC) syndrome

Front 22

Disseminated gonococcemia can cause what in the extremities?

Back 22

1) septic arthritis (knee),
2) tenosynovitis (hands, feet),
3) pustules (hands, feet); more common in women than men

Front 23

Treponema pallidum has 3 stages of infection what are they? What occurs in each?

Back 23

1) Primary syphilis: solitary painless, indurated chancre; locations-penis, labia, mouth
2) Secondary syphilis: maculopapular rash on trunk, palms, soles; generalized lymphadenopathy; condylomata lata, which are flat lesions in same area as condylomata acuminata; alopecia
3) Tertiary syphilis: neurosyphilis, aortitis, gummas

Front 24

What type of organism is Treponema pallidum? What are nonspecific and specific screening tests? How is it treated?

Back 24

1) STD; gram-negative spirochete that causes syphilis
2) Nonspecific screening tests: RPR or VDRL; titers decrease after treatment
3) Confirmatory treponemal test: FTA-ABS; positive with or without treatment
4) Treatment: penicillin

Front 25

The Jarisch-Herxheimer reaction occurs in what? And what is it?

Back 25

1) Occurs in syphillis.
2) intensification of rash in primary or secondary syphilis may occur due to proteins released from dead organisms after treatment with penicillin

Front 26

Trichomonas vaginalis is what? What does it produce? How is it treated?

Back 26

1) flagellated protozoan with jerky motility
2) Produces vaginitis, cervicitis, and urethritis; strawberry-colored cervix and fiery red vaginal mucosa; greenish, frothy discharge
3) Treatment: metronidazole (both partners)

Front 27

Which organism causes "ground glass" nuclei with intranuclear inclusions? Pseudohyphae indicate what?

Back 27

1) HSV2
2) Candida albicans

Front 28

Someone has numerous palmer plaques and papules and flat, plaque-like lesions (arrows) of condyloma latum. What do they have?

Back 28

syphillis

Front 29

A woman has numerous pear-shaped, flagellated organisms in her vag. What is the organism?

Back 29

Trichomonas vaginalis

Front 30

What is Rokitansky-Kuster-Hauser (RKH) syndrome? What results?

Back 30

1.Absence of the upper vagina and uterus
2.Anatomic cause of primary amenorrhea

Front 31

What is Gartner's duct cyst? Where is the cyst located?

Back 31

1) vaginal disorder
2) Remnant of the wolffian (mesonephric) duct
3) Presents as a cyst on the lateral wall of the vagina

Front 32

Where do Rhabdomyomas occur? Are they benign or malignant?

Back 32

a.Benign tumor of skeletal muscle
b.Other locations are the tongue and heart

Front 33

who do Embryonal rhabdomyosarcomas occur in? How are they characterized?

Back 33

a.Occurs in girls < 5 years old
b.Necrotic, grape-like mass protrudes from the vagina

Front 34

Clear cell adenocarcinoma of the vagina occurs when?

Back 34

1) women with intrauterine exposure to diethylstilbestrol (DES)

Front 35

What was diethylstilbestrol used for? What is inhibited? What structures are remnants? What cancer is the women predisposed to and where may it occur?

Back 35

1) DES was used to prevent a threatened abortion.
2) DES inhibits müllerian differentiation.
■Müllerian structures: tubes, uterus, cervix, upper third of vagina
3) Vaginal adenosis
a. Remnants of müllerian glands
■Produces red, superficial ulcerations in the upper portion of the vagina
b. Precursor lesion for clear cell adenocarcinoma
4) Small risk for developing the cancer (1:1000)
5) Cancer may involve upper vagina or cervix

Front 36

Besides cancer what does diehtybestrol cause?

Back 36

1) Abnormally shaped uterus that thwarts implantation
2) Cervical incompetence
■Common cause of recurrent abortions

Front 37

Vaginal squamous cell carcinoma is the result of what? What are most cancers of the vagina from?

Back 37

a. Primary squamous cell carcinoma has an HPV type 16 association.
b. Most cancers are an extension of a cervical squamous cancer into the vagina.

Front 38

What is the normal anatomy and histology of a the uterus and cervix?

Back 38

1. Cervix includes the endocervix + exocervix
◦The exocervix begins at the cervical os.
2. Exocervix is normally lined by squamous epithelium.
3. Endocervical glands are normally lined by mucus-secreting columnar cells.
4. Endocervical epithelium normally migrates down to the exocervix

Front 39

What can induce metaplasia at the cervix? What causes nabothian cysts?

Back 39

1. Exposure to the acid pH of the vagina produces squamous metaplasia.
2. The area undergoing metaplasia is called the transformation zone.
a) This zone is where squamous dysplasia and cancer develop.
b) It must be sampled when performing a cervical Papanicolaou (Pap) smear.
c) Metaplastic squamous cells block endocervical gland orifices.
3. Obstruction of outflow of mucus produces nabothian cysts

Front 40

Are Nabothian cysts a normal finding in adult women?

Back 40

yes

Front 41

What percent of women presenting with vaginal discharge have cervicitis? Can cervicitis be found in any sexually active woman?

Back 41

a.Accounts for 20% to 25%
b. yes

Front 42

Where does acute cervicitis appear? What are causes?

Back 42

a. transformation zone.
b. Chlamydia trachomatis, N. gonorrhoeae, Trichomonas vaginalis, Candida, herpes simplex virus (HSV-2), HPV

Front 43

Clinically how does acute cervicitis present?

Back 43

1) Vaginal discharge (most common)
2) Pelvic pain
3) Dyspareunia
4) Painful on palpation
5) Bleeds easily when obtaining cultures
6) Cervical os is erythematous and may be covered by an exudate

Front 44

How is acute cervicitis diagnosed?

Back 44

1) DNA probe for Chlamydia and Neisseria gonorrhoeae
■These organisms account for >50% of acute cervicitis.
2) Wet mount for Trichomonas
3) Obtain a cervical Pap smear

Front 45

What causes follicular cervicitis? What is seen histologically?

Back 45

a. C. trachomatis
b. Pronounced lymphoid infiltrate with germinal centers
c. Chlamydia infects metaplastic squamous cells.
(1) Cells contain vacuoles with red inclusions (reticulate bodies).
(2) Reticulate bodies develop into elementary bodies, which are infective particles.

Front 46

What is the primary source for conjunctivitis and pneumonia in newborns?

Back 46

Cervicitis from chlamydia trachomatis

Front 47

How do you know if a pap was done properly?

Back 47

There are metaplastic squamous cells or mucus-secreting columnar cells in the sample

Front 48

What is the purpose of the pap smear?

Back 48

screen for sqaumous dysplasia/cancer, evaluates hormonal status

Front 49

Superficial squamous cells indicate on a pap indicate what?

Back 49

adequate estrogen

Front 50

Intermediate squamous cells indicate on a pap indicate what?

Back 50

adequate progesterone

Front 51

Parabasal cells on a pap smear indicate what?

Back 51

lack of estrogen and progesterone

Front 52

A pap smear shows 70% superficial squamous cells, 30% intermediate squamous cells. What is going on?

Back 52

This is the pap of a normal non-pregnant woman

Front 53

100% intermediate squamous cells are seen on a pap smear. What is going on?

Back 53

Woman is pregnant
a. this results from high progesterone

Front 54

A pap smear is Atrophic with parabasal cells and inflammation. Who could this be from?

Back 54

elderly woman because they lack both estrogen and progesterone

Front 55

A woman with continous exposure to estrogen and no progesterone would show what on a pap smear?

Back 55

100% superficial squamous cells

Front 56

Cervical (endocervical) polyp occur where? In who? Is it cancerous?

Back 56

a.Non-neoplastic polyp that protrudes from the cervical os
b.Arises from the endocervix
c.Most commonly present in perimenopausal women and multigravida women
d.Most commonly occur between 30 and 50 years of age
e.Not precancerous

Front 57

What are clinical findings in a woman with cervical polyps?

Back 57

a.Postcoital bleeding
b.Vaginal discharge

Front 58

What is Cervical intraepithelial neoplasia associated with?

Back 58

1. HPV
a) Low risk-types 6, 11
b) High risk-types 16, 18
c) HPV produces koilocytosis in squamous cells
■Clear halo containing a wrinkled, pyknotic nucleus

Front 59

What are risk factors for Cervical intraepithelial neoplasia?

Back 59

1) Early age of onset of sexual intercourse
2) Multiple, high-risk partners
3) High-risk types of HPV in a biopsy
4) Smoking, oral contraceptive pills (OCPs)
5) Immunodeficiency

Front 60

When is the peak incidence of cervical intraepithelial neoplasia? How specific is a pap for it?

Back 60

a. Peak incidence is 35 years of age.
b. False negative rate on detecting dysplasia on a cervical Pap smear is 40%.

Front 61

How is Cervical intraepithelial neoplasia classified?

Back 61

a.CIN I
■Mild dysplasia involving the lower third of the epithelium
b.CIN II
■Moderate dysplasia involving the lower two thirds of the epithelium
c.CIN III
■Severe dysplasia to carcinoma in situ involving the full thickness of the epithelium

Front 62

How does cervical intraepithelial neoplasia progress? Is it reversible?

Back 62

a.Reversal to normal is more likely in CIN I.
b.Requires 10 years to progress from CIN I to CIN III
c.Requires 10 years to progress from CIN III to invasive cancer

Front 63

What are clinical and lab findings in cervical intraepithelial neoplasia?

Back 63

a. Dysplasia is not usually visible to naked eye; colposcopy is required.
■Occasionally, flat to warty appearing condyloma acuminata are visible.
b.Colposcopy findings, after application of acetic acid:
■Acetowhite areas with punctation, mosaic pattern, or abnormal vascularity

Front 64

What is the Average age for cervical cancer?

Back 64

45

Front 65

Who does cervical cancer occur more in? Why?

Back 65

a.Least common gynecologic cancer
■Due to early detection of CIN with Pap smears
b.Higher incidence in developing countries
c.In U.S. population incidence in descending order:
■Hispanic, black, white
d.Majority are squamous cell carcinoma (75-80% of cases).
■Small cell cancer and adenocarcinoma are less common types.

Front 66

What is the least common gynecologic cancer?

Back 66

cervical

Front 67

How does cervical cancer present clinically?

Back 67

a. Abnormal vaginal bleeding (most common)
■ Usually postcoital
b. Malodorous discharge
c. Postcoital bleeding

Front 68

How do cervical cancers progress and extend to other tissues? What is main cause of death? Where it metastisize?

Back 68

a. Extends down into the vagina
b. Extends out into the lateral wall of the cervix and vagina
c. Infiltrates the bladder wall and obstructs the ureters
■ Postrenal azotemia leading to renal failure is a common cause of death.
d.Distant metastases (e.g., lungs)

Front 69

what is the 1 and 5 year survival of cervical cancer?

Back 69

◦The 1- and 5-year relative survival rates are 88% and 72%, respectively

Front 70

Histogically a cervical sample shows Koilocytosis where squamous cells have wrinkled pyknotic nuclei surrounded by a clear halo. What is cause?

Back 70

HPV

Front 71

What is thelarche? What is the sequence of development to menarche?

Back 71

1.Breast budding
2. breast budding, growth spurt, pubic hair, axillary hair, menarche

Front 72

What is unique about a girls menarche for the first 1 to 1.5 years?

Back 72

they are anovulatory

Front 73

In a fertility work up what day are endometrial biopsies done? How will you know if ovulation occurred?

Back 73

1) on day 21 to see if ovulation has occurred.
2) Presence of secretory endometrium on day 21 confirms that ovulation has occurred.

Front 74

What occurs during the follicular (proliferative) phase of the menstrual cycle? When does estrogen surge occur? What is relationship of estrogen to FSH and LH?

Back 74

a.Estrogen-mediated proliferation of endometrial glands
■Most variable phase of the cycle
b.Estrogen surge occurs 24 to 36 hours prior to ovulation.
(1) Stimulates luteinizing hormone (LH) release
■Positive feedback
(2) Stimulates follicle-stimulating hormone (FSH) release
(a) Positive feedback on FSH and LH
(b) Serum LH > FSH; greatest positive feedback on LH
(3) LH surge initiates ovulation

Front 75

What day does ovulation occur on? What are indicators? What causes Mittleschmerz?

Back 75

a.Occurs between days 14 and 16
b.Ovulation indicators
(1) Increase in body temperature
■Effect of progesterone
(2) Subnuclear vacuoles in endometrial cells
(3) Mittelschmerz
■Peritoneal irritation from blood from the ruptured follicle

Front 76

What mediates the secratory phase? What changes occur in the endometrium? How many days until the fertilized egg implants?

Back 76

a.Progesterone-mediated
■Least variable phase of the cycle
b.Increased gland tortuosity and secretion
c.Edema of stromal cells
d.Changes occurring after fertilization
(1) Fertilization usually occurs in the ampulla
(2) Fertilized egg spends 3 days in the fallopian tube.
(3) Fertilized egg spends 2 days in the uterine cavity.
■Implants in the endometrial mucosa on day 21

Front 77

What is An exaggerated secretory phase in pregnancy called?

Back 77

Called the Arias-Stella phenomenon

Front 78

Why do Newborn baby girls commonly have vaginal bleeding?

Back 78

sudden drop of maternal hormones with delivery

Front 79

What are the functions of FSH in female?

Back 79

a.Prepares the follicle of the month
b.Increases aromatase synthesis in the granulosa cells
c.Increases the synthesis of LH receptors

Front 80

What are the functions of LH in the proliferative phase? What hormones are increased?

Back 80

a.LH in the proliferative phase
(1) Increases the synthesis of 17-ketosteroids in the theca interna
■17-KS are dehydroepiandrosterone (DHEA) and androstenedione.
(2) DHEA is converted to androstenedione.
(3) An oxidoreductase converts androstenedione to testosterone.
(4) Testosterone enters granulosa cells and is aromatized to estradiol.

Front 81

What is the function of LH in the ovulatory phase? What hormone does it help synthesize in secretory phase?

Back 81

b.LH surge is induced by a sudden increase in estrogen.
■Ovulation occurs when LH > FSH.
c.LH in the secretory phase
■Theca interna primarily synthesizes 17-hydroxyprogesterone

Front 82

Where is HCG synthesized? What is its function? How many weeks is it active?

Back 82

1) Synthesized in the syncytiotrophoblast lining the chorionic villus
2) Acts as an LH analogue by maintaining the corpus luteum of pregnancy.
3) Corpus luteum synthesizes progesterone for 8 to 10 weeks

Front 83

How do oral contraceptives work? What are they composed of?

Back 83

a.Baseline levels of estrogen prevent the midcycle estrogen surge.
■Prevents the LH surge and ovulation
b.Progestins arrest the proliferative phase and cause gland atrophy.
c.Progestins inhibit LH, which also prevents the LH surge.
d. render the cervical mucus hostile to sperm.
e. alter fallopian tube motility

Front 84

What is the main estrogen in a nonpregnant woman? What makes it?

Back 84

a.estradiol
b.Derived from aromatization of testosterone in granulosa cells

Front 85

What is the weak estrogen produced during menopause? Where is it made and from what?

Back 85

a.estrone
b.Derived from adipose cell aromatization of androstenedione
■Androstenedione is synthesized in the adrenal cortex

Front 86

What is the End-product of estradiol metabolism? When is it elevated?

Back 86

a.estriol
b.Primary estrogen of pregnancy
■Derives from fetal adrenal, placenta, and maternal liver

Front 87

Where are Androstenedione, DHEA, DHEA-sulfate, and testosterone synthesized in a woman? What is testosterone converted to?

Back 87

1. Androstenedione
◦Equal derivation from ovaries and adrenal cortex
2. DHEA
a. Mainly synthesized in the adrenal cortex (80%)
b. Remainder is synthesized in the ovaries.
3. DHEA-sulfate
◦Almost exclusively synthesized in the adrenal cortex
4.Testosterone
a.Derived from conversion of androstenedione to testosterone
b.Testosterone is synthesized in the ovaries and adrenal glands.
■Testosterone is peripherally converted to dehydroxytestosterone

Front 88

What increases liver production of SHBG? What decreases it?

Back 88

a. Estrogen increases
b. Androgens, obesity, hypothyroidism all decrease synthesis

Front 89

SHBG has a greater binding affinity for testosterone than estrogen. What is the relationship of SHBG to free testosterone? What does increased SHBG do in women?

Back 89

↑ SHBG, ↓ FT; ↓ SHBG, ↑ FT

■Common cause of hirsutism

Front 90

What happens to RBC mass and PV in pregnancy? To GFR? To creatinine clearance?

Back 90

a. both are increased
■Increase in plasma volume > increase in RBC mass.
b.Causes a 1-g/dL drop in hemoglobin (Hb) (dilutional effect)
c.Increases glomerular filtration rate (GFR)
(1) Creatinine clearance (CCr) is increased.
(2) Increased clearance of urea and creatinine
■Serum levels are at the lower limit of normal.
(3) Increases pressure to pump blood into the maternal lake in the placenta

Front 91

Does a pregnant woman have repiratory alkalosis or acidosis during pregnancy? Why?

Back 91

1) alkalosis
a.Effect of estrogen and progesterone stimulating respiratory center
b.Decrease in Paco2 causes a corresponding increase in Pao2

Front 92

Why during pregnancy are free T4 and cortisol increased?

Back 92

a.Estrogen stimulates synthesis of thyroid-binding globulin and transcortin.
b.Increased binding proteins increases total thyroxine and cortisol.
■No clinical signs of overactivity

Front 93

How is menopause defined?

Back 93

no menses for 1 year after age 40

Front 94

What are causes of menopause?

Back 94

(1) Physiologic
(a) Waxing and waning of estrogen levels
■Due to decreased ovarian function
(b) Depletion of granulosa and thecal cells
(c) Lack of response to gonadotropins
(d) Increased LH stimulates androgen production in stromal cells
(2) Surgical removal/radiation of ovaries
(3) Turner's syndrome
(4) Family history of early menopause
(5) Left-handedness

Front 95

What are clinical findings in menopause?

Back 95

a. Secondary amenorrhea
b. Hot flushes, night sweats
c.Atrophic vaginitis
■ Pruritus, burning, bleeding, dyspareunia
d. Mood swings, anxiety, depression, insomnia
e. Decreased libido
f. Urinary incontinence
g. Headaches, tiredness, lethargy
h.Osteoporosis
■Increased risk for vertebral and Colles fractures

Front 96

Analysis of hormone levels in menopause show what?

Back 96

a.Increase in FSH and LH
(1) Due to drop in estrogen and progesterone, respectively
(2) Serum FSH is the best marker.
b.Decreased serum estradiol

Front 97

How is menopause treated? What can be prevented if uterus is still present?

Back 97

a.Estrogen replacement if symptomatic
b.Progestin added if uterus is still present
■Prevent endometrial adenocarcinoma

Front 98

What are risks of longterm therapy with estrogen/progestin?

Back 98

1) Thromboembolism
2) Coronary heart disease, stroke
3) Slight risk for breast cancer
4) Increased risk for dementia in women ≥ 65 years old
■Applies also if only taking estrogen

Front 99

What is virilization?

Back 99

hirsutism + male secondary sex characteristics

Front 100

In hirsutisim and virilization what is increased? What is the origin of the hormones?

Back 100

(1) Ovarian origin-testosterone (free testosterone; sometimes total) is primarily increased
(2) Adrenal origin-DHEA-sulfate and testosterone increased

Front 101

What are causes of hirsutism and virilization? What drugs can cause?

Back 101

(1) Polycystic ovary syndrome most common cause
(2) Idiopathic (5-15%)
(3) Adrenogenital syndrome
(4) Insulin resistance syndrome
(5) Drugs (<1%)
■Examples-androgenic progestins, phenytoin, cyclosporin, minoxidil
(6) Ovarian tumor
■Leydig cell tumor, Sertoli-Leydig cell tumor
(7) Adrenal tumor (<1%)
■Adenoma/carcinoma producing Cushing's syndrome
(8) Obesity
■Decreased SHBG causes an increase in free testosterone.
(9) Hypothyroidism

Front 102

hirsutism caused by ovary has elevated? but hirsutism caused by adrenals has elevated?

Back 102

1) testosterone
2) ↑ DHEA-S, testosterone

Front 103

When do the symptom of PCOD begin? What are women at increased risk for?

Back 103

1) Symptoms begin around menarche.
2) Increased risk of endometrial cancer
Note: Hirsutism occurs more often than virilization.

Front 104

Hormonal what is occuring that leads to the development of cysts in PCOD?

Back 104

1) Increased pituitary synthesis of LH and decreased synthesis of FSH
(a) Increased LH increases androgen synthesis.
(b) Androgens are aromatized to estrogen in the adipose cells.
■Increased estrogen increases risk for endometrial carcinoma.
(c) Increased estrogen has a positive feedback on LH and negative feedback on FSH.
(d) Suppression of FSH causes follicle degeneration.
(e) Fluid accumulation produces subcortical cysts that enlarge the ovaries

Front 105

What are clinical findings in PCOD?

Back 105

(1) Menstrual irregularities
■Oligomenorrhea is the most common complaint.
(2) Hirsutism, infertility, obesity (40-50%)

Front 106

Blood work in PCOD shows what?

Back 106

1) ↑ LH, ↓ FSH; LH:FSH ratio > 2
2) Increased serum testosterone (free and total) and androstenedione
3) Increased serum estrogen

Front 107

How can hirsutism and virilization be treated?

Back 107

1) Low-dose OCPs or medroxyprogesterone
■Suppress ovarian steroidogenesis and LH
2) Spironolactone if OCPs unacceptable
■Block androgen receptors on hair follicle
3) LH-releasing hormone analogues
■Inhibit ovarian androgen production

Front 108

How much blood is lost for someone to have menorrhagia? What is a sign in the blood?

Back 108

a. Loss of blood > 80 mL per period
b. Excessive passage of clots
■ Indicates plasmin does not have enough time to dissolve clot

Front 109

What is dysmenorrhea?

Back 109

(1) Painful menses
(2) Approximately 50% of women have dysmenorrhea.
■Approximately 10% are incapacitated for 1 to 3 days

Front 110

What does primary dysmenorrhea occur? what causes it?

Back 110

a) Only occurs in ovulatory cycles
b) Due to increased prostaglandin F2α (PGF2α)
c) Increases uterine contractions

Front 111

What does secondary dysmenorrhea occur with?

Back 111

a) Endometriosis (most common)
b) Adenomyosis
c) Leiomyomas
d) Cervical stenosis

Front 112

How is primary dysmenorrhea treated?

Back 112

Nonsteroidals; OCP; nifedipine; magnesium sulfate

Front 113

What is dysfunctional uterine bleeding?

Back 113

Abnormal uterine bleeding unrelated to an anatomic cause

Front 114

What are the types of dysfunctional uterine bleeding?

Back 114

(a) Menorrhagia
(b) Hypomenorrhea
■Decreased amount of bleeding during normal cycle
(c) Metrorrhagia
■Excessive flow and duration at irregular intervals
(d) Menometrorrhagia
■Combination of menorrhagia and metrorrhagia
(e) Oligomenorrhea
■Intervals > 35 days
(f) Polymenorrhea
■Intervals < 21 days

Front 115

When does anovulatory dysfunctional uterine bleeding occur? What causes it? how is it treated?

Back 115

(1) Occurs at the extremes of reproductive life
(a) Menarche to age 20 years
(b) Perimenopausal period
(2) Excessive estrogen stimulation relative to progesterone
(a) Absent secretory phase of the cycle
(b) Produces endometrial hyperplasia and excessive bleeding
(3) Treatment: OCPs; progestational agents

Front 116

A woman with Inadequate luteal phase has the ovulatory type of dysfunctional uterine bleeding. What is wrong? What is the treatment?

Back 116

1) Inadequate maturation of the corpus luteum
(a) Inadequate synthesis of progesterone
■Delay in development of the secretory phase
(b) Decreased serum 17-hydroxyprogesterone
■Blood drawn 7 days after
(c) Implicated in infertility and recurrent pregnancy loss
3) Treatment
(a) If follicle size is normal, progesterone supplementation
(b) If follicle size is inadequate, clomiphene sulfate is recommended

Front 117

Irregular shedding of the endometrium is an ovulatory type of dysfunctional uterine bleeding. What causes it and how is it treated?

Back 117

1) Persistent luteal phase with continued secretion of progesterone
2) Mixture of proliferative and secretory glands in the menstrual effluent
3) Treatment: OCP; medroxyprogesterone acetate

Front 118

How is primary amenorrhea defined? What is a contributing factor?

Back 118

(1) Absence of menses by 16 years of age
(2) Most cases are due to constitutional delay.
■Family history of delayed onset of menses

Front 119

How is secondary amenorrhea defined? What are most cases due to?

Back 119

(1) Absence of menses for 3 months
(2) Most cases are due to pregnancy

Front 120

What is occuring in amenorrhea caused by a problem in the hypothalamic/pituitary axis? What are examples?

Back 120

1) Decreased synthesis of FSH and LH
a) Decreased synthesis of estrogen and progesterone
b) Hypogonadotropic (↓ FSH and LH) hypogonadism
2) No withdrawal bleeding after receiving progesterone
■Endometrial mucosa is not estrogen-stimulated.
(3) Examples
a) Hypopituitarism, prolactinoma
b) Anorexia nervosa

Front 121

ovarian problems that cause amenorrhea are consistent with what blood findings? What is a cause? What happens when estrogen and progesterone are administered?

Back 121

1) Decreased synthesis of estrogen and progesterone
(a) Increase in serum FSH and LH, respectively
(b) Hypergonadotropic (FSH and LH) hypogonadism
(2) No withdrawal bleeding after receiving progesterone
■Endometrial mucosa is not estrogen-stimulated.
(3) Examples
(a) Turner's syndrome

Front 122

What are hormone levels in amennorhea caused by end-organ resistance? What are causes?

Back 122

(1) Prevents the normal egress of blood
■More likely cause of primary amenorrhea
(2) Normal levels of FSH, LH, estrogen, and progesterone
(3) No withdrawal bleeding after receiving progesterone
(4) Examples
(a) Imperforate hymen, Rokitansky-Kuster-Hauser syndrome
(b) Asherman syndrome
■Removal of stratum basalis owing to repeated curettage

Front 123

What happens in Rokitansky-Kuster-Hauser syndrome? what is another name for the condition?

Back 123

Müllerian agenesis is a congenital malformation in women characterised by a failure of the müllerian ducts to develop, resulting in a missing uterus and fallopian tubes and variable malformations of the upper portion of the vagina
Note: second most common cause of primary amennorhea

Front 124

What enzyme takes androstenidione to testosterone? What is the function of 17-hydroxylase?

Back 124

1) oxidoreductase
2) take progesterone to 17-hydroxyprogesterone

Front 125

What are causes of uterine bleeding in a prepubertal female?

Back 125

1) Vulvovaginitis: poor hygiene, infection (e.g., gonorrhea), sexual abuse, foreign bodies
2) Embryonal rhabdomyosarcoma

Front 126

What are the most common causes of uterine bleeding between mearche to 20?

Back 126

1) Anovulatory DUB
2) Von Willebrand's disease

Front 127

What are the most common causes of uterine bleeding between 20 and 40?

Back 127

1) Pregnancy and its complications (most common cause)
2) Ovulatory types of DUB
3) PID, hypothyroidism, submucosal leiomyomas, adenomyosis, endometrial polyp, endometriosis

Front 128

What is are causes of uterine bleeding in a woman over 40?

Back 128

1) Anovulatory DUB (most common cause in perimenopausal period)
2) Endometrial hyperplasia/cancer (most common cause in menopause)

Front 129

when is endometritis most common?

Back 129

a. Uterine infection following delivery (vaginal/cesarean section) or abortion
b. Rate of postpartum endometritis is 1% to 8%.
c. Most common genital tract infection following delivery
d. More common in preterm deliveries

Front 130

What is acute endometritis most often due to?

Back 130

a. Most often due to bacterial infection following delivery or miscarriage
b. Group B streptococcus (Streptococcus agalactiae) is a common pathogen.
c. Other pathogens-group A streptococcus, Staphylococcus aureus, Bacteroides fragilis, C. trachomatis, N. gonorrhoeae, Escherichia coli

Front 131

How does acute endometritis present? How is it treated?

Back 131

(1) Fever
(2) Uterine tenderness
(3) Purulent or foul vaginal discharge (lochia)
(4) Abdominal pain
(5) Cefoxitin; ticarcillin-clavulanate; ampicillin-sulbactam

Front 132

What are causes of chronic endometritis? How is it treated?

Back 132

(1) Retained placenta
(2) Gonorrhea, intrauterine device (Actinomyces israelii)
(3) Key histologic finding is the presence of plasma cells
4) Cefoxitin; ticarcillin-clavulanate; ampicillin-sulbactam

Front 133

What happens to the endometrium in Adenomyosis? Who does it primarily occur in?

Back 133

a. Invagination of the stratum basalis into the myometrium
1) Glands and stroma thicken myometrial tissue.
2) Produces uterine enlargement
b.Highest incidence in women in mid- to late 40s
c.Common finding in hysterectomy specimens

Front 134

clinically how does a woman present with adenomyosis? How is it diagnosed? Treated?

Back 134

1) Menorrhagia, dysmenorrhea, pelvic pain
2) Definitive diagnosis with myometrial biopsy
3) Treatment is hysterectomy

Front 135

Where is the pouch of Douglas located? Can it be felt? What is it a common site for?

Back 135

1) anterior to the rectum and posterior to the uterus
2) palpated by digital rectal examination
3) common site to collect blood (e.g., ruptured tubal pregnancy), malignant cells (e.g., seeding by ovarian cancer), endometrial implants, and pus (e.g., pelvic inflammatory disease).

Front 136

What is endometriosus? What is the prevalence? Average age of onset?

Back 136

1. Functioning glands and stroma are located outside the uterus
■Cyclic bleeding of gland and stromal implants
2. Prevalence is highest in women with dysmenorrhea (40-60%)
3. Average age at time of diagnosis is 25 to 29 years old.
4. Multifactorial inheritance has been implicated

Front 137

What is the pathogenesis of endometriosus? How can it spread?

Back 137

a. Reverse menses through fallopian tubes (most common)
■ Implantation of viable endometrial cells
b. Coelomic metaplasia
c. Vascular or lymphatic spread

Front 138

What are common sites where endometriosus occurs?

Back 138

Ovaries (most common), rectal pouch, fallopian tubes, intestine

Front 139

Clinically how will a woman with endometriosus present?

Back 139

a. Dysmenorrhea (most common)
b. Abnormal bleeding
■Premenstrual spotting, menorrhagia
c. Painful stooling during menses
■ Implants located in rectal pouch
d. Intestinal obstruction and bleeding during menses
e. Increased risk for ectopic pregnancy
f. Infertility, dyspareunia
g. Enlargement of ovaries
■ Blood-filled cysts

Front 140

What is the endometriosus triad?

Back 140

dysmenorrhea, dyspareunia, infertility

Front 141

what is a useful serum diagnostic marker for endometriosus? Is it sensitive or specific?

Back 141

1.Increased serum cancer antigen 125 (CA125)
b) Excellent sensitivity but poor specificity (increased false positive results)
■ It is a cancer antigen that is also increased in surface derived ovarian cancers and other gynecologic disorders.
2) More useful in excluding endometriosis when it returns negative

Front 142

How is endometriosus treated?

Back 142

a. Combination oral contraceptives
b. Progestins (e.g., medroxyprogesterone acetate)
c. Gonadotropin-releasing hormone agonists
d. Laparoscopic removal of implants

Front 143

What is an endometrial polyp? Is there a high or low risk of cancer?

Back 143

a. Benign polyp that enlarges with estrogen stimulation
b. Does not progress to endometrial carcinoma
c. Can protrude through the cervix into the vagina

Front 144

A woman with endometrial polyps presents how? What age group is affected?

Back 144

a. Common cause of menorrhagia in 20- to 40-year-old age bracket
b. Spotting between menstrual periods or after menopause

Front 145

How is an endometrial polyp treated?

Back 145

a. Dilation and curettage
b. Hysteroscopy

Front 146

Endometrial hyperplasia is the result of what?

Back 146

prolonged estrogen stimulation

Front 147

What are risk factors for endometrial hyperplasia?

Back 147

(1) Early menarche or late menopause
(2) Nulliparity
(3) Obesity
■Increased aromatization of androgens to estrogen
(4) Polycystic ovary syndrome
(5) Taking estrogen without progesterone
(6) Anovulatory menstrual cycles
(7) Hereditary nonpolyposis colon cancer (Lynch syndrome)

Front 148

What are the types of endometrial cancer? The characteristics of each? Which have high risk of cancer?

Back 148

1) Simple hyperplasia
a) Increased number of cystically dilated glands
b) No glandular crowding
(2) Complex hyperplasia
a) Increased number of dilated glands with branching
b) Glandular crowding
(3) Atypical hyperplasia
a) Glandular crowding and dysplastic epithelium
b) Greatest risk for endometrial cancer

Front 149

Clinically how will a woman with endometrial hyperplasia present? How do you treat her?

Back 149

a.Menorrhagia, metrorrhagia, menometrorrhagia
b.Postmenopausal bleeding
c. OCPs, Medroxyprogesterone acetate, Hysterectomy if atypia is present

Front 150

What is metrorraghia? What is menometrorrhagia?

Back 150

1) uterine bleeding at irregular intervals, particularly between the expected menstrual periods
2) prolonged or excessive uterine bleeding occurs irregularly and more frequently than normal

Front 151

The Most common gynecologic tumor is?

Back 151

a. Endometrial carcinoma
b. Median age at onset, 60 years old

Front 152

What are risk factors for endometrial carcinoma? What decreases risk? What other type of cancer are they at risk of getting?

Back 152

a. Prolonged estrogen stimulation
■ Same risk factors as endometrial hyperplasia
b. OCPs decrease risk.
■ Due to antiestrogen effect of progestins
c. Increased risk for breast cancer

Front 153

What are the types of endometrial carcinomas? Which has worst prognosis?

Back 153

(1) Well-differentiated adenocarcinoma
a) Most common type
b) Adenoacanthoma
■ Contains foci of benign squamous tissue (no prognostic significance)
c) Adenosquamous carcinoma
■ Contain foci of malignant squamous cancer (worse prognosis)
(2) Papillary adenocarcinoma
■ Highly aggressive cancer

Front 154

How and to where does endometrial carcinoma srpead?

Back 154

a. Spreads down into the endocervix
b. Spreads out into the uterine wall
c. Lungs are the most common site of metastasis

Front 155

How does endometrial cancer present? What drug is used to treat it?

Back 155

1) Postmenopausal bleeding (90%)
2) tamoxifen

Front 156

What is a Leiomyoma ("fibroids")? Who does it occur in? When will the tumor become larger?

Back 156

a. Benign smooth muscle tumor
b. Most frequently diagnosed gynecologic tumor
c. Occurs in 20% to 50% of women > 30 years old
d. More common in blacks than whites
e. Estrogen-sensitive tumors
■May become larger during pregnancy

Front 157

How do leiomyomas progress or change? What can they become?

Back 157

(1) Degeneration
(2) Dystrophic calcification
(3) Hyalinization
■ Reason for the term "fibroids"
b. They rarely transform into leiomyosarcomas

Front 158

What are clinical findings in Leiomyoma?

Back 158

a. Menorrhagia (when located in submucosa)
b. Obstructive delivery
c. Cramping during menses
d. Pressure on colon (constipation)
e. Pressure on bladder
■ Increased frequency, urgency, incontinence

Front 159

How is a leiomyoma diagnosed and treated?

Back 159

4. Diagnosis
a. Transabdominal or transvaginal ultrasound
b. MRI
5. Treatment
a. Myotomy if women want to preserve fertility
b. Hysterectomy

Front 160

What is the Most common sarcoma of the uterus? What is seen on histologic exam? What is treatment?

Back 160

1) Leiomyosarcoma
2) Numerous atypical mitoses and foci of necrosis
3) Treatment is surgery

Front 161

What is another name for Malignant mixed müllerian tumors? What is it composed of? What occurs?

Back 161

1) carcinosarcomas
2) Endometrial adenocarcinoma + malignant mesenchymal (stromal) tumor
a. Primarily occur in postmenopausal women
b. Bulky, necrotic tumors that often protrude through the cervical os

Front 162

In Carcinosarcoma what is seen from the mesenchymal component? What is there a strong association with? What is prognosis?

Back 162

1) muscle, cartilage, and bone
2) Strong association with previous irradiation
3) Poor prognosis
4) Treatment is surgery

Front 163

At autopsy a womans rectum is powder burned. What did she have? She also had multiple well-circumscribed, gray-white nodules in her uterus. What is this from?

Back 163

1) endometriosus
2) leiomyomas

Front 164

Where do Hydatid cysts of Morgagni occur? What are they? What part of structure are they near? What can they cause?

Back 164

1) fallopian tubes
2) Cystic müllerian remnants
3) Most often located around the fimbriated end of the tube
4) May undergo torsion (>25%), causing abdominal pain
5) Treatment is surgical removal (laparoscope).

Front 165

What is the Most common cause of female infertility and ectopic pregnancy? What are risk factors?

Back 165

1) PID
Risk factors:
(1) Multiple sexual partners
(2) Vaginal douching
(3) Previous episodes of PID
(4) Unprotected sex

Front 166

What are causes of PID? Both STD and non-STD!

Back 166

1) Most often due to N. gonorrhoeae or C. trachomatis
■Coexisting infection in 45% of cases
(2) Other pathogens (not STD)
B. fragilis, streptococci, Clostridium perfringens, Mycobacteria tuberculosis, cytomegalovirus (CMV)

Front 167

What are gross findings in PID?

Back 167

a. Fallopian tubes are filled with pus
b. Most common cause of hydrosalpinx
■ Pus resorbs, leaving a clear fluid distending the tube

Front 168

Clinically how do women with PID present?

Back 168

a. Fever usually >38.3°C (101°F)
b. Lower abdominal pain
c. Cervical motion, adnexal, uterine tenderness on pelvic examination
d. Abnormal uterine bleeding; vaginal discharge
e. Mucopurulent discharge in cervical os
f. Right upper quadrant pain (5%)
■ Perihepatitis (Fitz-Hughes-Curtis syndrome)

Front 169

ziehen (zog)

Back 169

to move, pull

Front 170

How is PID diagnosed?

Back 170

a. cervical motion tenderness and adnexal tenderness
b. Culture of cervical discharge
c. Laparoscopy
d. Transvaginal ultrasound; MRI (best sensitivity and specificity)

Front 171

How is PID treated?

Back 171

a. Empiric treatment with uterine, adnexal, and cervical motion tenderness
b. Ceftriaxone + doxycycline (covers both N. gonorrhoeae and C. trachomatis)

Front 172

What is Salpingitis isthmica nodosa?

Back 172

1. Invagination of the mucosa into the muscle ("tubal diverticulosis")
a. Produces nodules in the tube that narrow the lumen
b. Probably a postinfectious reaction (e.g., previous C. trachomatis infection)

Front 173

What are complications of Salpingitis isthmica nodosa? How is it diagnosed?

Back 173

2. Infertility, ectopic pregnancy
3. Diagnose with hysterosalpingography
◦ Beading appearance in areas of constriction

Front 174

What are risk factors for ectopic pregnancy?

Back 174

1) Scarring from previous PID (most common cause)
2) Endometriosis
3) Altered tubal motility, Salpingitis isthmica nodosa
4) Progestin-only pill; previous tubal ligation

Front 175

Where are sites of implantation of ectopic pregnancy's?

Back 175

(1) Majority occur within the tubes
■ Most are in the broad ampullary portion below the fimbriae.
(2) Ovaries, abdominal cavity

Front 176

Clinically how does a woman with an ectopic pregnancy present?

Back 176

a. Sudden onset of lower abdominal pain and tenderness (95%)
■ Usually 6 weeks after a previous normal menstrual period
b. Adnexal tenderness (87-99%)
c. Peritoneal signs (rebound tenderness; >70%)
d. Abnormal uterine bleeding (75%)
e. Hypovolemic shock (intraperitoneal bleeding; 2-17%)

Front 177

What are complications of an ectopic pregnancy?

Back 177

a. Rupture with intra-abdominal bleed
■ Most common cause of death in early pregnancy
b. Most common cause of hematosalpinx
■ Blood in the tube

Front 178

How are ectopic pregnancy's diagnosed?

Back 178

a. β-hCG is the best screening test.
(1) Urine screen is usually sensitive enough.
(2) Serum test is used if the urine screen is negative.
(3) Positive test does not prove that an ectopic pregnancy is present.
b. Vaginal ultrasound is the confirmatory test.
■ Check for an amniotic sac.
c. Laparoscopy is used in equivocal cases

Front 179

How is an ectopic pregnancy treated?

Back 179

a. Methotrexate if stable and no hemorrhage
b. Conservative surgery; salpingectomy

Front 180

What is the most common cause of an ovarian mass? are they neoplastic? How are they treated?

Back 180

1. follicular cyst
2. Non-neoplastic cyst
◦ Accumulation of fluid in a follicle or previously ruptured follicle
3. Rupture produces sterile peritonitis with pain.
4. Most regress spontaneously.
5. Ultrasound is the best screening test.
6.Surgical removal if symptomatic

Front 181

What is the Most common ovarian mass in pregnancy? Are they neoplastic? What can they be confused with?

Back 181

1) Corpus luteum cyst
2) Non-neoplastic cyst
a. Accumulation of fluid in the corpus luteum during pregnancy
b. May be confused with an amniotic sac
c. Most regress spontaneously.
3. Surgical removal if symptomatic

Front 182

What is oophoritis a complication of?

Back 182

complication of mumps or PID

Front 183

Stromal hyperthecosis occurs in who? what happens?

Back 183

a. Occurs primarily in obese postmenopausal women
■ Causes bilateral ovarian enlargement
b. Hypercellular ovarian stroma
(1) Vacuolated (luteinized) stromal hilar cells are present
■ Synthesize excess androgens
(2) May cause hirsutism or virilization

Front 184

How does Stromal hyperthecosis present?

Back 184

a. Hirsutism or virilization
b. Association with acanthosis nigricans and insulin resistance
c. Hypertension
d. Treatment is oophorectomy

Front 185

Are ovarian tumors benign or malignant before 45? When is median age of presentation? Do they usually present early or as advanced?

Back 185

a. Tumors are more likely benign in women < 45 years of age.
(1) Risk increases with age.
(2) Median age of presentation is 61 years of age.
(3) Peaks in the late 70s
(4) Approximately 60% present with advanced disease

Front 186

What are risk factors for ovarian cancer?

Back 186

(1) Nulliparity
a) Increased number of ovulatory cycles increases risk.
b) Increased risk for surface-derived ovarian tumors
(2) Genetic factors
a) Mutations of BRCA1 and BRCA2 suppressor genes
b) Lynch syndrome
c) Turner's syndrome
■Increased risk for dysgerminoma
d) Peutz-Jeghers syndrome
■Increased incidence of sex cord tumors with annular tubules
(3) History of breast cancer
(4) Postmenopausal estrogen therapy; obesity (increased estrogen)
(5) OCPs/pregnancy decrease risk for surface-derived ovarian cancers.
■Decreased number of ovulatory cycles

Front 187

What are the classifications of ovarian tumors?

Back 187

a.Surface-derived tumors
b.Germ cell tumors
c.Sex cord stromal tumors
d.Metastasis

Front 188

What percent do Surface-derived ovarian tumors account for? Where do they derive from? Are they benign or malignant?

Back 188

(1) Account for 65% to 70% of ovarian tumors
(2) Derive from coelomic epithelium
(3) Account for the greatest number of malignant ovarian tumors
(4) Malignant tumors commonly seed the omentum

Front 189

What are germ cell ovarian tumors similiar to? A they malignant?

Back 189

(1) Account for 15% to 20% of ovarian tumors
(2) Cancers are similar to those seen in the testicle
(3) A relatively small number of tumors are malignant

Front 190

Are Sex cord stromal ovarian tumors benign or malignant?

Back 190

(1) Account for 3% to 5% of ovarian tumors
(2) Derive from stromal cells
(3) May be hormone-producing
(4) Majority of tumors are benign

Front 191

Where do tumors come from that metastisize to the ovary?

Back 191

(1) Accounts for 5% of ovarian tumors
(2) Common primary cancers metastasizing to ovaries
■Breast, stomach (e.g., Krukenberg tumors)

Front 192

What are clinical findings with an ovarian tumor?

Back 192

a. Abdominal enlargement due to fluid (most common sign)
(1) Malignant ascites most often due to seeding
(2) Signs of malignant ascites due to seeding
(a) Induration in the rectal pouch on digital rectal examination
(b) Intestinal obstruction with colicky pain
b. Palpable ovarian mass in a postmenopausal woman
■ Ovaries should not be palpable in menopausal women.
c. Malignant pleural effusion
■ Common site for ovarian cancer metastasis
d. Cystic teratomas undergo torsion leading to infarction.
■ Radiographs show calcification from bone or teeth
e. Hirsutism or virilization from androgen-secreting tumors

Front 193

What are Signs of hyperestrinism from estrogen-secreting ovarian tumors?

Back 193

(1) Bleeding from endometrial hyperplasia/cancer
(2) 100% superficial squamous cells in a cervical Pap smear

Front 194

What antigen is increased in the serum of a woman with a surface derived ovarian tumor?

Back 194

CA125

Front 195

What is the prognosis of ovarian cancer?

Back 195

a. Better prognosis if <65 years old
b. Overall 1- and 5-year relative survival rates for ovarian cancer are 75% and 45%, respectively

Front 196

What are the examples of surface-derived ovarian tumors?

Back 196

1) Serous tumors
2) Mucinous tumors
3) Endometrioid
4) Brenner tumor

Front 197

What are serous ovarian tumors the most common of? What is seen histologically? What are the 2 types?

Back 197

1) Most common group of primary benign and malignant tumors
2) Most common group of tumors that can be bilateral
3) Cysts are lined by ciliated cells (similar to fallopian tube)
4) Serous cystadenoma (benign; most common benign ovarian tumor);
5) serous cystadenocarcinoma has psammoma bodies (dystrophically calcified tumor cells); most common malignant tumor that is bilateral

Front 198

Histologically how do mucinous ovarian tumors present? What does seeding produce? What are the two types?

Back 198

1) Cysts lined by mucus-secreting cells (similar to endocervix)
2) Large, multiloculated tumors
3) Seeding produces pseudomyxoma peritonei
4) Mucinous cystadenoma (benign); may be associated with Brenner tumors; mucinous cystadenocarcinoma

Front 199

Endometroid is a surface-derived ovarian tumor. Is it benign or malignant? B/L or U/L?

Back 199

1) Malignant tumors associated with endometrial carcinoma (15-30% of cases); tumor resembles endometrial carcinoma
2) Commonly bilateral

Front 200

Brenner tumor is a surface derived ovarian tumor. Are the benign or malignant? What do they contain?

Back 200

1) Usually benign
2) Contain Walthard's rests (transitional-like epithelium)

Front 201

What are examples of germ-cell ovarian tumors?

Back 201

1) Cystic teratoma
2) Dysgerminoma
3) Yolk sac tumor

Front 202

Cystic teratoma are ovarian germ cell tumors. Are they benign or malignant? Where does differentation stem from? What structures form? What do immature tumors have?

Back 202

1) Usually benign; less than 1% become malignant (usually squamous cancer)
2) Most common benign germ cell tumor
3) Ectodermal differentiation (hair, sebaceous glands, teeth) most prominent
4) Most of these derivatives are found in a nipple-like structure in the cyst wall called Rokitansky tubercle
5) Immature malignant types contain mature and immature components (e.g., muscle, neuroepithelium)
6) Struma ovarii type has functioning thyroid tissue

Front 203

What does the struma ovarii type of germ cell tumor have?

Back 203

functioning thyroid tissue

Front 204

Dysgerminoma is a germ cell ovarian tumor. What blood enzyme is increased? What is it similar to in men? What is it associated with?

Back 204

1) Most common malignant germ cell tumor;
2) characteristic increase in serum LDH; same histologic picture as seminoma of testis
3) Associated with streak gonads of Turner syndrome

Front 205

A yolk sac tumor is a germ cell ovarian tumor. Is it benign or malignant? Who does it occur in? What does it contain? What blood marker is increased?

Back 205

1) Malignant tumor; most common ovarian cancer in girls < 4 years old
2) Contain Schiller-Duval bodies (resemble yolk sac)
3) Increased α-fetoprotein

Front 206

What are examples of Sex-Cord Stromal ovarian Tumors?

Back 206

1) Thecoma-fibroma
2) Granulosa-theca cell tumor
3) Sertoli-Leydig cell
4) Gonadoblastoma

Front 207

Thecoma-fibroma is a sex-cord stromal ovarian tumor. Is it benign or malignant? What is it associated with? Ovarian time what happens?

Back 207

1) Benign tumor associated with Meigs' syndrome (ascites, right-sided pleural effusion); regression of effusions follows removal of tumor
2) Commonly calcify

Front 208

Granulosa-theca cell tumor is a sex-cord stromal ovarian tumor. Is it benign or malignant? What does it contain and do?

Back 208

1) Low-grade malignant tumor
2) Feminizing tumor (produces estrogen) that contains Call-Exner bodies

Front 209

Sertoli-Leydig cell tumor is a sex-cord stromal ovarian tumor. Are they benign or malignant? What do they contain?

Back 209

1) Benign masculinizing tumor (produces androgens)
2) Pure Leydig cell tumors contain cells with crystals of Reinke

Front 210

Gonadoblastoma is a Sex-Cord Stromal ovarian Tumor. is it benign or malignant? What is it associated with? What do they do longterm?

Back 210

1) Malignant tumor with mixture of germ cell tumor (dysgerminoma) and sex-cord stromal tumor;
2) associated with abnormal sexual development in 80% of cases
3) Commonly calcify

Front 211

Where does a Krukenberg tumor come from? What cell type is in the ovary? What is the mode of metastisis?

Back 211

1) primary site arose in the gastrointestinal tract or breast
2) May affect both ovaries
3) contains signet-ring cells from hematogenous spread of a gastric cancer

Front 212

What covers the fetal surface? What covers the chorion? What does the maternal surface contain?

Back 212

1) chorionic plate
2) amnion
3) cotyledons covered by a layer of decidua basalis

Front 213

Which cell layer lines the chorionic villi? When divided what forms the inner layer and the outer layer of the chorionic villi?

Back 213

1) trophoblastic
2) cytotrophoblastic
3) syncytotrophoblastic

Front 214

What does the syncytotrophoblastic layer produce?

Back 214

(a) Synthesizes hCG
(b) Synthesizes human placental lactogen (HPL)

Front 215

human placental lactogen corresponds to what? What type of activity does it have?

Back 215

Directly correlates with placental mass and has anti-insulin activity

Front 216

What vessels does the umbilical cord contain?

Back 216

1) 2 arteries, 1 vein; umbilical vein has most O2

Front 217

What is there an increased incidence of with a single umbilical artery?

Back 217

cardiovascular defects; trisomy 18; esophageal atresia

Front 218

If placental culture is negative for group B streptococcus how should the infection be treated?

Back 218

treat prophylactically with IV ampicillin + IV erythromycin followed by amoxicillin + erythromycin

Front 219

What is the most common placental infection? How should it be treated? What are other infections?

Back 219

1) group B streptococcus
2) penicillin G or ampicillin IV
3) -B. fragilis, Prevotella bivius, group A streptococcus

Front 220

What is funisitis?

Back 220

Infection of the umbilical cord

Front 221

What is chormioamnionitis? What is the danger? How is it treated?

Back 221

1) Infection of the fetal membranes
2) Danger of neonatal sepsis and meningitis
3) Cefoxitin; ticarcillin-clavulanate

Front 222

What is placenta previa? what is a risk factor?

Back 222

(1) Implantation over cervical os
(2) Previous cesarean section is a risk factor (approaches 10%)

Front 223

How does a woman present with placenta previa?

Back 223

(1) Presents with painless vaginal bleeding
a. Usually in second or third trimester
(2) Uterus soft and nontender
(3) Fetal distress usually not present

Front 224

How is placenta previa diagnosed? Which technique should be avoided? How is she treated?

Back 224

(1) Pelvic examination should not be performed.
(2) Transabdominal ultrasound localizes placenta.
(3) Transvaginal ultrasound confirms placenta previa
(4) Delivery by cesarean section

Front 225

What occurs in Abruptio placentae? What is it the most common cause of?

Back 225

(1) Premature separation of placenta due to formation of a retroplacental clot
(a) Separates the placenta from the implantation site
(b) Most common cause of late pregnancy bleeding
(c) Occurs in 1:830 pregnancies

Front 226

What are risk factors for abruptio placentae?

Back 226

(a) Hypertension (greatest risk factor; 40-50% of cases)
(b) Smoking cigarettes
(c) Cocaine addiction; advanced maternal age
(d) Trauma; chorioamnionitis
(e) Premature rupture of membranes
(f) Previous abruptio placentae

Front 227

Clinically how will a woman present with abruptio placentae?

Back 227

Abruptio placentae triad: painful vaginal bleeding, tetanic uterine contractions, fetal compromise

Front 228

What occurs in placenta accreta?

Back 228

1) Direct implantation into muscle without intervening decidua
2) Occurs in 1:2500 pregnancies
3) Great risk for hemorrhage during delivery
4) Commonly requires surgery to control bleeding
5) Hysterectomy is often necessary

Front 229

what occurs in a Velamentous insertion?

Back 229

1) Umbilical cord inserts away from the placental edge.
2) Vessels pass to the placenta through the membranes between the amnion and the chorion.
3) Can be diagnosed by ultrasound
4) Often delivered by cesarean section to avoid vessel tear

Front 230

What causes an enlarged placenta?

Back 230

1) Diabetes mellitus
2) Rh hemolytic disease of newborn (HDN)
3) Congenital syphilis

Front 231

Can monochorionic twin placentas be diamniotic? In general what results from this type of placenta?

Back 231

Yes
(1) Identical twins derive from a single fertilized egg.
(2) Monoamniotic with a single amniotic sac
a. Type for Siamese twins or tangling of umbilical cords
(3) Diamniotic with separate amniotic sacs
(4) Fetal-to-fetal transfusion can occur in either type

Front 232

Dichorionic placentas produce what?

Back 232

(1) Can be identical or fraternal twins
a. Fraternal twins occur when separate eggs are fertilized.
(2) Placentas can be diamniotic or separated

Front 233

When does preecamplsia occur during pregnancy?

Back 233

third trimester (24th to 25th weeks)

Front 234

What are risk factors for preeclampsia?

Back 234

(1) More common in women < 20 years of age and >35 years of age
(2) History of previous preeclampsia
(3) Positive family history
(4) Multiple gestations
(5) Blacks
(6) Thrombocytosis; obesity

Front 235

What can preeclampsia be associated with?

Back 235

hydatidiform moles
(1) Complete mole, 2%
(2) Partial mole, 5%

Front 236

Pathologically what is going on at the placenta in preeclampsia?

Back 236

Abnormal placentation
(1) Causes mechanical or functional obstruction of the spiral arteries
(2) Abnormal trophoblastic tissue invades the spiral arteries.
(1) Normal vasodilators are decreased.
Examples-PGE2, nitric oxide
(2) Vasoconstrictors are increased.
(a) Examples-thromboxane A2, angiotensin II
(b) Increased sensitivity to the effect of angiotensin II
(3) Increase in various growth factors (e.g., vascular growth factor)
c. Net effect is placental hypoperfusion.

Front 237

What are pathologic findings that occur in preeclampsia?

Back 237

1) Premature aging of the placenta
2) Multiple placental infarctions
3) Spiral arteries show intimal atherosclerosis

Front 238

What are clinical findings in preeclampsia?

Back 238

1) Hypertension (increased vasoconstrictors)
a. Ranges from just below 140/90 mm Hg to >160/110 mm Hg
2) Proteinuria in nephrotic
a. range (>3.5 g/24 hours)
b. Usually >5 g/24 hour urine collection
3) Dependent pitting edema
a. Due to loss of albumin in the urine
4) Weight gain > 4 pounds/week
a. Due to retention of sodium
6) Renal disease
a) Swollen endothelial cells in the glomerular capillaries
b) Produces oliguria
Liver disease
(1) Right upper quadrant pain and hepatomegaly
(2) Periportal necrosis with increased transaminases
HELLP syndrome
Hemolytic anemia and disseminated intravascular coagulation

Front 239

What is ecclamplsia? How is it treated?

Back 239

1) Preeclampsia + seizures is called eclampsia.
(2) Magnesium sulfate is used for treatment.

Front 240

How is preecclampsia treated?

Back 240

1) Delivery is the treatment of choice and the only cure for the disease.
2) Magnesium sulfate is given for seizures

Front 241

What are hydatidiform moles? What are the types? In who and in what countries do they occur most?

Back 241

1) Benign tumors of the chorionic villus
2) Complete and partial moles
3) More common at the extremes of age
4) Occurs in 1:1200 pregnancies in the United States
5) Occurs in 1:200 pregnancies in Indonesia

Front 242

How are complete moles characterized? What occurs genetically to make one?

Back 242

(1) The entire placenta is neoplastic.
(2) Dilated, swollen villi without fetal blood vessels
(3) No embryo is present.
(4) 46,XX (90% of cases)
(a) Both chromosomes are of male origin.
(b) Egg is fertilized by two haploid spermatozoa with X chromosomes

Front 243

What is there an Increased risk of developing with a complete mole?

Back 243

choriocarcinoma (20% chance)

Front 244

What are clinical findings with a complete mole?

Back 244

(a) Painless vaginal bleeding in fourth or fifth month of pregnancy
(b) Severe vomiting
(c) Preeclampsia is present in 2% of patients.
(d) Uterus is too large for gestational age.
(e) Increased hCG for the gestational age
(f) "Snowstorm appearance" with ultrasound

Front 245

How is woman with a complete mole treated? How is success followed?

Back 245

(a) Dilation and curettage
Must remove all material
(b) Follow patient with hCG levels
Should go down to zero

Front 246

What is a partial mole? What is there a low risk of developing?

Back 246

(1) Not all villi are neoplastic or dilated.
(2) Normal embryo is present (no chromosome abnormality).
(a) Triploid (69,XY)
(b) Egg with 23,X is fertilized by a 23,X and a 23,Y sperm.
(3) Preeclampsia in 5% of patients
(4) Low risk (2-3%) risk for developing a choriocarcinoma

Front 247

What is a choriocarcinoma?

Back 247

1) Malignant tumor composed of syncytiotrophoblast and cytotrophoblast
2) Chorionic villi are NOT present.

Front 248

Risk factors for developing a choriocarcinoma are?

Back 248

(1) Complete mole (50% of cases)
(2) Spontaneous abortion (25% of cases)
(3) Normal pregnancy (25% of cases)

Front 249

Where do choriocarcinomas metasitisize? How are they characterized?

Back 249

(1) Lungs and vagina
(2) Lesions are hemorrhagic

Front 250

How is a choriocarcinoma treated?

Back 250

1) Excellent response to chemotherapy (methotrexate); low mortality rate
2) Good response does not apply to non-gestationally derived cancer

Front 251

What is amniotic fluid? What does a high salt content do? What is amniotic fluid a sign of?

Back 251

1) Predominantly fetal urine
2) High salt content causes ferning when dried on a slide.
3) Excellent sign of premature rupture of the amniotic sac
4) Swallowed and recycled by the fetus

Front 252

What is polyhydraminos? What causes it?

Back 252

(1) Excessive amniotic fluid
(2) Causes
(a) Tracheoesophageal (TE) fistula
(b) Duodenal atresia
(c) Maternal diabetes (20%)
**Maternal hyperglycemia → fetal hyperglycemia → fetal polyuria

Front 253

What are causes of oligohydraminos?

Back 253

(a) Juvenile polycystic kidney disease
(b) Fetal genitourinary obstruction
(c) Uteroplacental insufficiency
(d) Premature rupture of membranes

Front 254

What causes increased maternal AFP? What about decreased?

Back 254

(1) Open neural tube defect
(2) Related to folate deficiency
(3) Folate stores should be adequate before pregnancy.
4) Neural tube is already developed by the end of the first month of gestation.
5) Decreased maternal AFP
Down syndrome

Front 255

Where is lecithin produced? What is its function?

Back 255

(1) Synthesized by type II pneumocytes
(2) Decreases alveolar surface tension to prevent atelectasis

Front 256

Lecithin/sphingomyelin ratio > 2 means what?

Back 256

adequate surfactant

Front 257

What increases surfactant synthesis? what decreases it?

Back 257

1) cortisol, thyroxine
2) insulin

Front 258

Where is estriol made during pregnancy? Where is it degraded?

Back 258

a. Fetal zone of the adrenal cortex
(1) Converts pregnenolone synthesized in the placenta to DHEA-sulfate
(2) Fetal zone is absent in anencephaly (absent brain).
b. Fetal liver
DHEA-sulfate is 16-hydroxylated to 16-OH-DHEA-sulfate.
c. Maternal placenta
(1) Placental sulfatase cleaves off the sulfate from 16-OH-DHEA-sulfate.
(2) 16-OH-DHEA is converted by aromatase to free unbound estriol.
d. Maternal liver
(1) Free estriol is conjugated to estriol sulfate and estriol glucosiduronate.
(2) Both compounds are excreted in maternal urine and bile.

Front 259

What is the down syndrome triad?

Back 259

↓ urine estriol, serum AFP; ↑ serum hCG

Front 260

Where are high density areas of the breast?

Back 260

1) Upper outer quadrant
a. Underscores why cancer is most commonly located in this quadrant
2) Beneath the nipple

Front 261

What are the effects of estrogen and progesterone on the breast?

Back 261

1) Estrogen--Stimulates ductal and alveolar growth
2) Progesterone--Stimulates alveolar differentiation

Front 262

Where does the outer quadrant of the breast drain to? What about inner quadrant?

Back 262

1) Drain to the axillary lymph nodes
2) Drain to the internal mammary nodes

Front 263

What is the Most common nonpituitary endocrine disease causing galactorrhea?

Back 263

primary hypothyroidism
a. Decreased serum thyroxine increases thyrotropin-releasing factor (TRF).
b. TRF stimulates prolactin

Front 264

Which drugs can cause galactorrhea?

Back 264

OCPs, phenothiazines, methyldopa, H2-receptor blockers, anxiolytics

Front 265

What are 2 main causes of bloody nipple discharge?

Back 265

Intraductal papilloma, ductal cancer

Front 266

What is the primary cause of mastitis? How is it treated?

Back 266

a. Acute mastitis due to Staphylococcus aureus
b. Usually occurs during lactation or breast-feeding
Treatment:
(1) If not methicillin resistant, dicloxacillin or cephalexin
(2) If methicillin resistant, trimethoprim-sulfamethoxazole

Front 267

What causes a greenish-brown nipple discharge?

Back 267

Mammary duct ectasia (plasma cell mastitis)

Front 268

What is the most common cause of breast pain in woman <50?

Back 268

fibrocystic change

Front 269

What is Mondors disease? how does it present?

Back 269

1) Superficial thrombophlebitis of veins overlying the breast
2) Presents as a palpable, painful cord

Front 270

How are fibrocysts characterized? Does their size change with menstrual cycle? Are they malignant?

Back 270

1) Some cysts have hemorrhage into the cyst fluid.
a. Called "blue-domed" cysts
2) Vary in size with the menstrual cycle
3) No malignant potential
4) May have to surgically remove if recurrent

Front 271

How is sclerosing adenosis characterized? What is it confused with?

Back 271

1) Proliferation of small ductules/acini in the lobule
2) Pattern is often confused with infiltrating ductal cancer.
3) Often contain microcalcifications

Front 272

What are pathologic findings in ductal hyperplasia of the breast? What is there an increased risk of developing?

Back 272

(1) Papillary proliferation is called papillomatosis.
(2) Apocrine metaplasia refers to the presence of large, pink-staining cells.
(3) Atypical ductal hyperplasia
a. Increased risk for developing cancer, because it is due to excess estrogen stimulation

Front 273

Who is affected by Mammary duct ectasia? What occurs? What does it resemble?

Back 273

(1) Affects 25% of women in menopause
(2) Main ducts fill up with debris.
(a) Causes dilation, rupture, and inflammation
(b) Greenish brown nipple discharge
(3) May produce skin and nipple retraction simulating cancer
(4) No increased risk for breast cancer

Front 274

How is plasma cell mastitis treated? What is another name for it?

Back 274

1) Antibiotics if infection is present
(2) Surgical removal of blocked duct
3) Mammary duct ectasia

Front 275

What are microscopic findings in traumatic fat necrosis? Is it painful or painless? What does it resemble?

Back 275

a. Trauma to breast tissue
Microscopic findings
(1) Lipid-laden macrophages with foreign body giant cells
(2) Fibrosis, dystrophic calcification
b. Painless, indurated mass
c. Painful in acute stage
d. May produce skin retraction simulating cancer

Front 276

What happens when silicone leaks from an implant? Is it associated with autoimmunity?

Back 276

(1) Produces foreign body giant cells and chronic inflammation
(2) Association with autoimmune disease is not proved.

Front 277

What is the most common breast tumor? Women taking what drug will develop?

Back 277

(1) fibroadenoma
(2) Most commonly diagnosed breast tumor
(3) Develop in 50% of women who receive cyclosporine after renal transplantation

Front 278

How does a fibroadenoma present?

Back 278

1) Discrete movable, painless or painful mass
2) Multiple lesions may be present (10-15%

Front 279

In a fibroadenoma what proliferates? Is it neoplastic?

Back 279

(a) Stroma proliferates and compresses the ducts
(b) Duct epithelium is not neoplastic

Front 280

Does the size of a fibroadenoma change with period? When will they go away?

Back 280

1) Increases in size during pregnancy
Estrogen-sensitive
2) May spontaneously disappear or involute during menopause
3) Do not progress into cancer; however, breast cancer may secondarily develop within duct epithelial cells as a separate event (3%)

Front 281

Is a phyllodes tumor benign or malignant? is it small or large? Where does it derive from?

Back 281

1) Bulky tumor derived from stromal cells
2) Most often benign but can be malignant in some cases
3) Hypercellular stroma with mitoses are signs of malignancy.
4) Lobulated tumor with cystic spaces containing leaf-like extensions
5) Often reach massive size
6) Treat by wide excision

Front 282

Most common cause of bloody nipple discharge in women < 50 years old is? Does become cancer? Where do they develop?

Back 282

1) Intraductal papilloma
2) Develop in the lactiferous ducts or sinuses
3) No increased risk for cancer
4) Surgically remove the duct or sinus.

Front 283

what nerve is damaged when someone has a winged scapula?

Back 283

long thoracic nerve (C5,6,7)

Front 284

What is the most common cancer of adult women? What is the average age?

Back 284

1) breast (1:8 lifetime risk)
2) Mean age is 64 years old.
3) Second most common cancer-producing death in women
4) It is also the second most common cancer producing death in adults (includes men and women as a group).

Front 285

A family history of breast cancer includes what? What genes?

Back 285

(1) involves first-generation relatives like Mother, sister
(2) Genetic basis is involved in <10% of cases
(a) Autosomal dominant BRCA1 and BRCA2 association
b) Breasts or ovaries are frequently prophylactically removed.
3) Li-Fraumeni multicancer syndrome
a) Inactivation of TP53 suppressor gene
(3) Other gene relationships
RAS oncogene, ERBB2, RB suppressor gene

Front 286

increased estrogen is associated with breast cancer. Who is at risk as a result?

Back 286

(1) Early menarche/late menopause
(2) Nulliparity
(3) Postmenopausal obesity
a. Aromatization of androstenedione to estrone
(4) Hormone replacement therapy

Front 287

What are some random risk associated with breast cancer?

Back 287

1) Endometrial cancer, ionizing radiation, smoking cigarettes
2) High breast density (determined by mammogram)
3) Recent use of OCPs; obesity after menopause
4) Use of postmenopausal hormone therapy (estrogen and progestin therapy)

Front 288

What factors reduce the risk of breast cancer?

Back 288

breast-feeding; exercise; healthy body weight

Front 289

Clinically how does breast cancer present?

Back 289

1) Painless mass in the breast
2) Usually in the upper outer quadrant
3) Skin or nipple retraction
4) Painless axillary lymphadenopathy
5) Hepatomegaly; bone pain if metastasis has occurred

Front 290

What is mamography used for? What are its limitations? When does screening begin?

Back 290

Primarily a screening test
1) Detects nonpalpable breast masses (detects 80-90%)
2) Does not distinguish benign from malignant
lesions
3) annually at age 40; earlier if patient is high risk

Front 291

Mammography can identify what when cancer is present? I

Back 291

1) Identifies microcalcifications and spiculated masses with or without microcalcifications (30-50%)
a. Most often occur in ductal carcinoma in situ (DCIS) and sclerosing adenosis
b. Microcalcification pattern suggesting malignancy
c. Five or more tightly clustered microcalcifications that are punctate, microlinear, or branching

Front 292

How does breast cancer spread?

Back 292

a. Spread first by lymphatics and then hematogenously
(1) Outer quadrant cancer spreads to axillary nodes.
(2) Inner quadrant cancers spread to internal mammary nodes.

Front 293

Where are the most common sites of breast cancer metastisis? When will metastisis occur?

Back 293

1) Lungs, bone, liver, brain, ovaries
2) May metastasize 10 to 15 years after treatment
3) Pain in bone metastasis is relieved with radiation.

Front 294

With breast cancer does nodal or extranodal have a greater significance?

Back 294

extranodal spread has greater significance than nodal metastasis alone

Front 295

What is a sentinel node in breast cancer?

Back 295

initial node draining the tumor

Front 296

What does it mean if the sentinel node is negative? Positive?

Back 296

a) If negative for metastasis, the other nodes in that group are usually negative.
b) If positive for metastasis, there is a one-third chance that other nodes in that group have metastases.

Front 297

Who are Estrogen and progesterone receptor assay usually positive in? What is the clinical significance?

Back 297

(1) Most often positive in postmenopausal women
(2) Clinical significance
(a) Confers an overall better prognosis
(b) Candidate for antiestrogen therapy with tamoxifen or raloxifene

Front 298

What are tests performed in breast cancer cases?

Back 298

(1) S phase fraction
a. Above 5% is poor prognosis.
(2) DNA ploidy
a. Diploid tumor is better than an aneuploid tumor.
(3) ERBB2 oncogene status
a. Poor prognosis if amplification (multiple copies) is present
4) estrogen and progesterone assays
a. positive = better prognosis

Front 299

What is the Treatment for high-risk patients without breast cancer?

Back 299

Treatment with tamoxifen or raloxifene reduces risk

Front 300

What are level I, II, III nodes in breast cancer?

Back 300

1) Level I and II axillary lymph nodes in continuity
a. Level I nodes are inferior to the pectoralis minor muscle; level II nodes are beneath the pectoralis minor.
2) Level III nodes if level I and II nodes are grossly involved
a. Level III nodes are medial and superior to the pectoralis minor.

Front 301

What is breast conservation therapy?

Back 301

1) Breast conservation therapy has similar survival rate as modified radical mastectomy
(a) Lumpectomy with microscopically free margins
(b) Sentinel node biopsy (preferable) or removal of level I and II axillary nodes
(c) Breast irradiation

Front 302

What is the prognosis of breast cancer?

Back 302

(1) The 5-year relative survival rate for localized breast cancer (no node involvement) is 98%.
(2) The 5-year relative survival rate for breast cancer with nodal involvement is 84%.
(3) The 5-year relative survival rate for breast cancer with distant spread is 27%.
(4) Survival rate at 5 years for all stages combined is 89%.
(5) Survival rate at 10 years for all stages combined is 80%

Front 303

How does gynecomastia present?

Back 303

1) Subareolar mass
2) more often unilateral than bilateral
3) Due to increased estrogen stimulation
a. Increase in estrogen
b. Decrease in androgens (leaves estrogen unopposed)
c. Defect in androgen receptors (leaves estrogen unopposed)

Front 304

What is the source of estrogen in gynecomastia?

Back 304

(1) Peripheral aromatization (85%)
(a) Testosterone to estradiol
(b) Androstenedione to estrone
(2) Leydig cells (15%)

Front 305

When does normal physiologic gynecomastia occur in men?

Back 305

(1) Newborn (60-90%)
(2) Puberty (peaks at ages 13-14 years)
(3) Elderly (occurs between 50-80 years of age)

Front 306

What is breast conservation therapy?

Back 306

1) Breast conservation therapy has similar survival rate as modified radical mastectomy
(a) Lumpectomy with microscopically free margins
(b) Sentinel node biopsy (preferable) or removal of level I and II axillary nodes
(c) Breast irradiation

Front 307

What is the prognosis of breast cancer?

Back 307

(1) The 5-year relative survival rate for localized breast cancer (no node involvement) is 98%.
(2) The 5-year relative survival rate for breast cancer with nodal involvement is 84%.
(3) The 5-year relative survival rate for breast cancer with distant spread is 27%.
(4) Survival rate at 5 years for all stages combined is 89%.
(5) Survival rate at 10 years for all stages combined is 80%

Front 308

How does gynecomastia present?

Back 308

1) Subareolar mass
2) more often unilateral than bilateral
3) Due to increased estrogen stimulation
a. Increase in estrogen
b. Decrease in androgens (leaves estrogen unopposed)
c. Defect in androgen receptors (leaves estrogen unopposed)

Front 309

What is the source of estrogen in gynecomastia?

Back 309

(1) Peripheral aromatization (85%)
(a) Testosterone to estradiol
(b) Androstenedione to estrone
(2) Leydig cells (15%)

Front 310

When does normal physiologic gynecomastia occur in men?

Back 310

(1) Newborn (60-90%)
(2) Puberty (peaks at ages 13-14 years)
(3) Elderly (occurs between 50-80 years of age)

Front 311

How does the liver contribute to gynecomastia?

Back 311

Cirrhosis
(1) Inability to metabolize estrogen
(2) Inability to metabolize 17-ketosteroids
a. Peripherally aromatized to estrone

Front 312

What genetic conditions lead to gynecomastia?

Back 312

(1) Klinefelter's syndrome
a. Increased aromatization of androgens to estrogens in Leydig cells
(2) Testicular feminization
a. Decreased androgen receptor synthesis

Front 313

What are drugs that can lead to gynecomastia?

Back 313

(1) Drug displacement of estrogen from SHBG
a. Spironolactone, ketoconazole
(2) Drugs with estrogen activity
a. Diethylstilbestrol, digoxin (activates estrogen receptors)
(3) Drugs that block androgen receptors
a. Spironolactone, flutamide
(4) Drugs that decrease androgen production
a. Leuprolide

Front 314

Which cancer can lead to gynecomastia? Why?

Back 314

Choriocarcinoma of testis producing hCG

Front 315

which endocrine disorders can lead to gynecomastia?

Back 315

(1) Primary hypogonadism
Leydig cell dysfunction
(2) Secondary hypogonadism
a. Pituitary/hypothalamic dysfunction

Front 316

What are risk factors in men for developing breast cancer?

Back 316

1) Inactivation of BRCA2 suppressor gene
2) Klinefelter's syndrome
3) Usually have a poor prognosis

Front 317

Is Ductal carcinoma in situ palpable? What are its patterns? What do they contain? are they invasive? How are they treated?

Back 317

1) Nonpalpable
2) Patterns: cribriform (sieve-like), comedo (necrotic center)
3) Commonly contain microcalcifications; cannot be detected by mammogram unless microcalcifications are present
4) One third eventually invade
5) Treated with "lumpectomy"

Front 318

How does a Lobular carcinoma in situ present? Histologically what is seen? Are they unilateral or bilateral?

Back 318

1) Nonpalpable; virtually always an incidental finding in a breast biopsy for other reasons; cannot be identified by mammography
2) Lobules distended with bland neoplastic cells; one third eventually invade;
3) usually estrogen and progesterone receptor positive
4) Increased incidence of cancer in the opposite breast (50-75%); does not have to be a lobular cancer

Front 319

histologically how does Infiltrating ductal carcinoma look? What do 1/3 have?

Back 319

1) Stellate morphology, indurated, gray-white tumor
2) One third have amplification of ERBB2 oncogene
3) Gritty on cut section
4) Induration caused by reactive fibroplasia (desmoplasia)

Front 320

how does pagets of the breast present?

Back 320

1) Extension of DCIS into lactiferous ducts and skin of nipple producing a rash with or without nipple retraction
2) Paget's cells are present
3) Palpable mass present in 50-60%

Front 321

What is medullary carcinoma of the breast associated with? How is the tumor characterized? Are they estrogen/progesterone positive?

Back 321

1) Associated with BRCA1 mutations
2) Bulky, soft tumor with large cells and lymphoid infiltrate
3) Majority are estrogen and progesterone receptor negative

Front 322

How does inflammatory breast carcinoma present? What is the prognosis?

Back 322

1) Erythematous breast with dimpling like an orange (peau d'orange) due to fixed opening of the sweat glands, which cannot expand with lymphedema
2) Plugs of tumor blocking lumen of dermal lymphatics cause localized lymphedema
3) Very poor prognosis
4) Combination chemotherapy followed by surgery and irradiation

Front 323

Histologically how does invasive lobular carcinoma present?

Back 323

Neoplastic cells arranged in linear fashion or form concentric circles (bull's-eye appearance)

Front 324

Where does tubular breast carcinoma develop? is it unilateral or bilateral?

Back 324

1) Develops in terminal ductules
2) Increased incidence of cancer in opposite breast (10-40%)

Front 325

who does colloid (mucinous) breast carcinoma occur in? How are they characterized histologically?

Back 325

1) Usually occurs in elderly women
2) Neoplastic cells are surrounded by extracellular mucin

Front 326

Which breast disorders occur at the lactiferous sinus?

Back 326

1) intraductal papilloma
2) plasma mastitis
3) breast abcess

Front 327

Which breast disorders occur at the major duct?

Back 327

1) fibrocystic change
2) ductal cancer

Front 328

Which breast disorders occur at the terminal duct?

Back 328

1) tubular carcinoma

Front 329

Which breast disorders occur at the lobule?

Back 329

1) lobular carcinoma
2) sclerosing adenosis

Front 330

Which breast disorders occur in the stroma?

Back 330

1) phyllodes tumor
2) fibroadenoma

Front 331

Tumor cells fill ducts and tumor cell necrosis is a cheesy consistency?

Back 331

intraductal carcinoma in situ

Front 332

tumor cells arranged in cords, islands and glands embedded in dense fibrous stroma with firm consistency?

Back 332

invasive ductal carcinoma

Front 333

How are pagets cells characterized? what other cancer is usually present

Back 333

1) large surrounded by a clear halo and invade epidermis
2) ductal carcinoma almost always present

Front 334

clusters of neoplastic cells fill intralobular ductules and acini and can lead to invasive carcinoma, also may be bilateral

Back 334

lobular carcinoma

Front 335

often multicentric or bilateral with cells in linear fashion (indian-file)

Back 335

invasive lobular carcinoma