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335 Cards in this Set

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  • Back
What is the most common cause of Bartholin gland abscess?
N gonnorrhea
What are examples of Non-neoplastic dermatoses of the vulva?
1.Lichen sclerosis
2.Lichen simplex chronicus
Who does lichen sclerosis occur in? What is the appearance of the skin? What is there a risk of developing?
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
What is the main feature of lichen simplex chronicus? What is there a risk of developing?
a.White plaque-like lesion (leukoplakia)
■Due to squamous cell hyperplasia
b.Small risk for developing squamous cell carcinoma
Note: occurs at vulva
What are tumors of the vulva?
1.Papillary hidradenoma
2.Vulvar intraepithelial neoplasia (VIN)
3.Squamous cell carcinoma
4.Extramammary Paget's disease
5.Malignant melanoma
Calymmatobacterium granulomatis is an STD. What type of bacteria is it? What is the pathogenesis? How does it present? How is it treated?
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
What are donovan bodies seen in?
phagocytized Calymmatobacterium granulomatis ( Klebsiella granulomatis)
Describe Candida albicans! What does it cause? What are risk factors? How is it treated?
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)
Chlamydia trachomatis is what type of organism? What is seen on histologic exam? What does it cause in newborns? How is it treated?
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
What does Chlamydia trachomatis cause in males and females?
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
What do C. trachomatis subspecies cause? How are they treated?
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
Describe Gardnerella vaginalis! How does it present? What cell type is present? How is pregnancy effected? How is it treated?
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
What is the most common cause of vaginitis?
Gardnerella vaginalis
What does Haemophilus ducreyi cause? Does it occur more in men or women? What is presentation? How is diagnosed and treated?
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)
school of fish appearance is seen under the microscope. What is the organism? Describe it!
Haemophilus ducreyi is a fastidious gram-negative coccobacillus that causes chancroid
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?
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
What types of HPV are associated with STDs? What happens? What types are associated with cancer?
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
What is the Most common overall STD?
HPV... 80% of sexually active women will have acquired HPV by age 50
What is seen histologically with HPV infection? What can reduce risk of cancer? How HPV treated?
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
What are the features of N gonnorhea? What does it infect? When do symptoms present? How is it diagnosed and treated?
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
What are longterm complications of N gonnorrhea? What is a risk factor for develping it?
1)ectopic pregnancy,
2) male sterility,
3) disseminated gonococcemia (C6-C9 deficiency risk factor),
4) septic arthritis,
5) Fitz-Hugh-Curtis (FHC) syndrome
Disseminated gonococcemia can cause what in the extremities?
1) septic arthritis (knee),
2) tenosynovitis (hands, feet),
3) pustules (hands, feet); more common in women than men
Treponema pallidum has 3 stages of infection what are they? What occurs in each?
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
What type of organism is Treponema pallidum? What are nonspecific and specific screening tests? How is it treated?
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
The Jarisch-Herxheimer reaction occurs in what? And what is it?
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
Trichomonas vaginalis is what? What does it produce? How is it treated?
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)
Which organism causes "ground glass" nuclei with intranuclear inclusions? Pseudohyphae indicate what?
1) HSV2
2) Candida albicans
Someone has numerous palmer plaques and papules and flat, plaque-like lesions (arrows) of condyloma latum. What do they have?
A woman has numerous pear-shaped, flagellated organisms in her vag. What is the organism?
Trichomonas vaginalis
What is Rokitansky-Kuster-Hauser (RKH) syndrome? What results?
1.Absence of the upper vagina and uterus
2.Anatomic cause of primary amenorrhea
What is Gartner's duct cyst? Where is the cyst located?
1) vaginal disorder
2) Remnant of the wolffian (mesonephric) duct
3) Presents as a cyst on the lateral wall of the vagina
Where do Rhabdomyomas occur? Are they benign or malignant?
a.Benign tumor of skeletal muscle
b.Other locations are the tongue and heart
who do Embryonal rhabdomyosarcomas occur in? How are they characterized?
a.Occurs in girls < 5 years old
b.Necrotic, grape-like mass protrudes from the vagina
Clear cell adenocarcinoma of the vagina occurs when?
1) women with intrauterine exposure to diethylstilbestrol (DES)
What was diethylstilbestrol used for? What is inhibited? What structures are remnants? What cancer is the women predisposed to and where may it occur?
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
Besides cancer what does diehtybestrol cause?
1) Abnormally shaped uterus that thwarts implantation
2) Cervical incompetence
■Common cause of recurrent abortions
Vaginal squamous cell carcinoma is the result of what? What are most cancers of the vagina from?
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.
What is the normal anatomy and histology of a the uterus and cervix?
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
What can induce metaplasia at the cervix? What causes nabothian cysts?
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
Are Nabothian cysts a normal finding in adult women?
What percent of women presenting with vaginal discharge have cervicitis? Can cervicitis be found in any sexually active woman?
a.Accounts for 20% to 25%
b. yes
Where does acute cervicitis appear? What are causes?
a. transformation zone.
b. Chlamydia trachomatis, N. gonorrhoeae, Trichomonas vaginalis, Candida, herpes simplex virus (HSV-2), HPV
Clinically how does acute cervicitis present?
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
How is acute cervicitis diagnosed?
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
What causes follicular cervicitis? What is seen histologically?
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.
What is the primary source for conjunctivitis and pneumonia in newborns?
Cervicitis from chlamydia trachomatis
How do you know if a pap was done properly?
There are metaplastic squamous cells or mucus-secreting columnar cells in the sample
What is the purpose of the pap smear?
screen for sqaumous dysplasia/cancer, evaluates hormonal status
Superficial squamous cells indicate on a pap indicate what?
adequate estrogen
Intermediate squamous cells indicate on a pap indicate what?
adequate progesterone
Parabasal cells on a pap smear indicate what?
lack of estrogen and progesterone
A pap smear shows 70% superficial squamous cells, 30% intermediate squamous cells. What is going on?
This is the pap of a normal non-pregnant woman
100% intermediate squamous cells are seen on a pap smear. What is going on?
Woman is pregnant
a. this results from high progesterone
A pap smear is Atrophic with parabasal cells and inflammation. Who could this be from?
elderly woman because they lack both estrogen and progesterone
A woman with continous exposure to estrogen and no progesterone would show what on a pap smear?
100% superficial squamous cells
Cervical (endocervical) polyp occur where? In who? Is it cancerous?
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
What are clinical findings in a woman with cervical polyps?
a.Postcoital bleeding
b.Vaginal discharge
What is Cervical intraepithelial neoplasia associated with?
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
What are risk factors for Cervical intraepithelial neoplasia?
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
When is the peak incidence of cervical intraepithelial neoplasia? How specific is a pap for it?
a. Peak incidence is 35 years of age.
b. False negative rate on detecting dysplasia on a cervical Pap smear is 40%.
How is Cervical intraepithelial neoplasia classified?
■Mild dysplasia involving the lower third of the epithelium
■Moderate dysplasia involving the lower two thirds of the epithelium
■Severe dysplasia to carcinoma in situ involving the full thickness of the epithelium
How does cervical intraepithelial neoplasia progress? Is it reversible?
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
What are clinical and lab findings in cervical intraepithelial neoplasia?
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
What is the Average age for cervical cancer?
Who does cervical cancer occur more in? Why?
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.
What is the least common gynecologic cancer?
How does cervical cancer present clinically?
a. Abnormal vaginal bleeding (most common)
■ Usually postcoital
b. Malodorous discharge
c. Postcoital bleeding
How do cervical cancers progress and extend to other tissues? What is main cause of death? Where it metastisize?
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)
what is the 1 and 5 year survival of cervical cancer?
◦The 1- and 5-year relative survival rates are 88% and 72%, respectively
Histogically a cervical sample shows Koilocytosis where squamous cells have wrinkled pyknotic nuclei surrounded by a clear halo. What is cause?
What is thelarche? What is the sequence of development to menarche?
1.Breast budding
2. breast budding, growth spurt, pubic hair, axillary hair, menarche
What is unique about a girls menarche for the first 1 to 1.5 years?
they are anovulatory
In a fertility work up what day are endometrial biopsies done? How will you know if ovulation occurred?
1) on day 21 to see if ovulation has occurred.
2) Presence of secretory endometrium on day 21 confirms that ovulation has occurred.
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?
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
What day does ovulation occur on? What are indicators? What causes Mittleschmerz?
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
What mediates the secratory phase? What changes occur in the endometrium? How many days until the fertilized egg implants?
■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
What is An exaggerated secretory phase in pregnancy called?
Called the Arias-Stella phenomenon
Why do Newborn baby girls commonly have vaginal bleeding?
sudden drop of maternal hormones with delivery
What are the functions of FSH in female?
a.Prepares the follicle of the month
b.Increases aromatase synthesis in the granulosa cells
c.Increases the synthesis of LH receptors
What are the functions of LH in the proliferative phase? What hormones are increased?
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.
What is the function of LH in the ovulatory phase? What hormone does it help synthesize in secretory phase?
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
Where is HCG synthesized? What is its function? How many weeks is it active?
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
How do oral contraceptives work? What are they composed of?
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
What is the main estrogen in a nonpregnant woman? What makes it?
b.Derived from aromatization of testosterone in granulosa cells
What is the weak estrogen produced during menopause? Where is it made and from what?
b.Derived from adipose cell aromatization of androstenedione
■Androstenedione is synthesized in the adrenal cortex
What is the End-product of estradiol metabolism? When is it elevated?
b.Primary estrogen of pregnancy
■Derives from fetal adrenal, placenta, and maternal liver
Where are Androstenedione, DHEA, DHEA-sulfate, and testosterone synthesized in a woman? What is testosterone converted to?
1. Androstenedione
◦Equal derivation from ovaries and adrenal cortex
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
a.Derived from conversion of androstenedione to testosterone
b.Testosterone is synthesized in the ovaries and adrenal glands.
■Testosterone is peripherally converted to dehydroxytestosterone
What increases liver production of SHBG? What decreases it?
a. Estrogen increases
b. Androgens, obesity, hypothyroidism all decrease synthesis
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?
↑ SHBG, ↓ FT; ↓ SHBG, ↑ FT

■Common cause of hirsutism
What happens to RBC mass and PV in pregnancy? To GFR? To creatinine clearance?
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
Does a pregnant woman have repiratory alkalosis or acidosis during pregnancy? Why?
1) alkalosis
a.Effect of estrogen and progesterone stimulating respiratory center
b.Decrease in Paco2 causes a corresponding increase in Pao2
Why during pregnancy are free T4 and cortisol increased?
a.Estrogen stimulates synthesis of thyroid-binding globulin and transcortin.
b.Increased binding proteins increases total thyroxine and cortisol.
■No clinical signs of overactivity
How is menopause defined?
no menses for 1 year after age 40
What are causes of menopause?
(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
What are clinical findings in menopause?
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
■Increased risk for vertebral and Colles fractures
Analysis of hormone levels in menopause show what?
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
How is menopause treated? What can be prevented if uterus is still present?
a.Estrogen replacement if symptomatic
b.Progestin added if uterus is still present
■Prevent endometrial adenocarcinoma
What are risks of longterm therapy with estrogen/progestin?
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
What is virilization?
hirsutism + male secondary sex characteristics
In hirsutisim and virilization what is increased? What is the origin of the hormones?
(1) Ovarian origin-testosterone (free testosterone; sometimes total) is primarily increased
(2) Adrenal origin-DHEA-sulfate and testosterone increased
What are causes of hirsutism and virilization? What drugs can cause?
(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
hirsutism caused by ovary has elevated? but hirsutism caused by adrenals has elevated?
1) testosterone
2) ↑ DHEA-S, testosterone
When do the symptom of PCOD begin? What are women at increased risk for?
1) Symptoms begin around menarche.
2) Increased risk of endometrial cancer
Note: Hirsutism occurs more often than virilization.
Hormonal what is occuring that leads to the development of cysts in PCOD?
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
What are clinical findings in PCOD?
(1) Menstrual irregularities
■Oligomenorrhea is the most common complaint.
(2) Hirsutism, infertility, obesity (40-50%)
Blood work in PCOD shows what?
1) ↑ LH, ↓ FSH; LH:FSH ratio > 2
2) Increased serum testosterone (free and total) and androstenedione
3) Increased serum estrogen
How can hirsutism and virilization be treated?
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
How much blood is lost for someone to have menorrhagia? What is a sign in the blood?
a. Loss of blood > 80 mL per period
b. Excessive passage of clots
■ Indicates plasmin does not have enough time to dissolve clot
What is dysmenorrhea?
(1) Painful menses
(2) Approximately 50% of women have dysmenorrhea.
■Approximately 10% are incapacitated for 1 to 3 days
What does primary dysmenorrhea occur? what causes it?
a) Only occurs in ovulatory cycles
b) Due to increased prostaglandin F2α (PGF2α)
c) Increases uterine contractions
What does secondary dysmenorrhea occur with?
a) Endometriosis (most common)
b) Adenomyosis
c) Leiomyomas
d) Cervical stenosis
How is primary dysmenorrhea treated?
Nonsteroidals; OCP; nifedipine; magnesium sulfate
What is dysfunctional uterine bleeding?
Abnormal uterine bleeding unrelated to an anatomic cause
What are the types of dysfunctional uterine bleeding?
(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
When does anovulatory dysfunctional uterine bleeding occur? What causes it? how is it treated?
(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
A woman with Inadequate luteal phase has the ovulatory type of dysfunctional uterine bleeding. What is wrong? What is the treatment?
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
Irregular shedding of the endometrium is an ovulatory type of dysfunctional uterine bleeding. What causes it and how is it treated?
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
How is primary amenorrhea defined? What is a contributing factor?
(1) Absence of menses by 16 years of age
(2) Most cases are due to constitutional delay.
■Family history of delayed onset of menses
How is secondary amenorrhea defined? What are most cases due to?
(1) Absence of menses for 3 months
(2) Most cases are due to pregnancy
What is occuring in amenorrhea caused by a problem in the hypothalamic/pituitary axis? What are examples?
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
ovarian problems that cause amenorrhea are consistent with what blood findings? What is a cause? What happens when estrogen and progesterone are administered?
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
What are hormone levels in amennorhea caused by end-organ resistance? What are causes?
(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
What happens in Rokitansky-Kuster-Hauser syndrome? what is another name for the condition?
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
What enzyme takes androstenidione to testosterone? What is the function of 17-hydroxylase?
1) oxidoreductase
2) take progesterone to 17-hydroxyprogesterone
What are causes of uterine bleeding in a prepubertal female?
1) Vulvovaginitis: poor hygiene, infection (e.g., gonorrhea), sexual abuse, foreign bodies
2) Embryonal rhabdomyosarcoma
What are the most common causes of uterine bleeding between mearche to 20?
1) Anovulatory DUB
2) Von Willebrand's disease
What are the most common causes of uterine bleeding between 20 and 40?
1) Pregnancy and its complications (most common cause)
2) Ovulatory types of DUB
3) PID, hypothyroidism, submucosal leiomyomas, adenomyosis, endometrial polyp, endometriosis
What is are causes of uterine bleeding in a woman over 40?
1) Anovulatory DUB (most common cause in perimenopausal period)
2) Endometrial hyperplasia/cancer (most common cause in menopause)
when is endometritis most common?
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
What is acute endometritis most often due to?
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
How does acute endometritis present? How is it treated?
(1) Fever
(2) Uterine tenderness
(3) Purulent or foul vaginal discharge (lochia)
(4) Abdominal pain
(5) Cefoxitin; ticarcillin-clavulanate; ampicillin-sulbactam
What are causes of chronic endometritis? How is it treated?
(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
What happens to the endometrium in Adenomyosis? Who does it primarily occur in?
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
clinically how does a woman present with adenomyosis? How is it diagnosed? Treated?
1) Menorrhagia, dysmenorrhea, pelvic pain
2) Definitive diagnosis with myometrial biopsy
3) Treatment is hysterectomy
Where is the pouch of Douglas located? Can it be felt? What is it a common site for?
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).
What is endometriosus? What is the prevalence? Average age of onset?
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
What is the pathogenesis of endometriosus? How can it spread?
a. Reverse menses through fallopian tubes (most common)
■ Implantation of viable endometrial cells
b. Coelomic metaplasia
c. Vascular or lymphatic spread
What are common sites where endometriosus occurs?
Ovaries (most common), rectal pouch, fallopian tubes, intestine
Clinically how will a woman with endometriosus present?
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
What is the endometriosus triad?
dysmenorrhea, dyspareunia, infertility
what is a useful serum diagnostic marker for endometriosus? Is it sensitive or specific?
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
How is endometriosus treated?
a. Combination oral contraceptives
b. Progestins (e.g., medroxyprogesterone acetate)
c. Gonadotropin-releasing hormone agonists
d. Laparoscopic removal of implants
What is an endometrial polyp? Is there a high or low risk of cancer?
a. Benign polyp that enlarges with estrogen stimulation
b. Does not progress to endometrial carcinoma
c. Can protrude through the cervix into the vagina
A woman with endometrial polyps presents how? What age group is affected?
a. Common cause of menorrhagia in 20- to 40-year-old age bracket
b. Spotting between menstrual periods or after menopause
How is an endometrial polyp treated?
a. Dilation and curettage
b. Hysteroscopy
Endometrial hyperplasia is the result of what?
prolonged estrogen stimulation
What are risk factors for endometrial hyperplasia?
(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)
What are the types of endometrial cancer? The characteristics of each? Which have high risk of cancer?
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
Clinically how will a woman with endometrial hyperplasia present? How do you treat her?
a.Menorrhagia, metrorrhagia, menometrorrhagia
b.Postmenopausal bleeding
c. OCPs, Medroxyprogesterone acetate, Hysterectomy if atypia is present
What is metrorraghia? What is menometrorrhagia?
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
The Most common gynecologic tumor is?
a. Endometrial carcinoma
b. Median age at onset, 60 years old
What are risk factors for endometrial carcinoma? What decreases risk? What other type of cancer are they at risk of getting?
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
What are the types of endometrial carcinomas? Which has worst prognosis?
(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
How and to where does endometrial carcinoma srpead?
a. Spreads down into the endocervix
b. Spreads out into the uterine wall
c. Lungs are the most common site of metastasis
How does endometrial cancer present? What drug is used to treat it?
1) Postmenopausal bleeding (90%)
2) tamoxifen
What is a Leiomyoma ("fibroids")? Who does it occur in? When will the tumor become larger?
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
How do leiomyomas progress or change? What can they become?
(1) Degeneration
(2) Dystrophic calcification
(3) Hyalinization
■ Reason for the term "fibroids"
b. They rarely transform into leiomyosarcomas
What are clinical findings in Leiomyoma?
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
How is a leiomyoma diagnosed and treated?
4. Diagnosis
a. Transabdominal or transvaginal ultrasound
b. MRI
5. Treatment
a. Myotomy if women want to preserve fertility
b. Hysterectomy
What is the Most common sarcoma of the uterus? What is seen on histologic exam? What is treatment?
1) Leiomyosarcoma
2) Numerous atypical mitoses and foci of necrosis
3) Treatment is surgery
What is another name for Malignant mixed müllerian tumors? What is it composed of? What occurs?
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
In Carcinosarcoma what is seen from the mesenchymal component? What is there a strong association with? What is prognosis?
1) muscle, cartilage, and bone
2) Strong association with previous irradiation
3) Poor prognosis
4) Treatment is surgery
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?
1) endometriosus
2) leiomyomas
Where do Hydatid cysts of Morgagni occur? What are they? What part of structure are they near? What can they cause?
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).
What is the Most common cause of female infertility and ectopic pregnancy? What are risk factors?
1) PID
Risk factors:
(1) Multiple sexual partners
(2) Vaginal douching
(3) Previous episodes of PID
(4) Unprotected sex
What are causes of PID? Both STD and non-STD!
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)
What are gross findings in PID?
a. Fallopian tubes are filled with pus
b. Most common cause of hydrosalpinx
■ Pus resorbs, leaving a clear fluid distending the tube
Clinically how do women with PID present?
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)
ziehen (zog)
to move, pull
How is PID diagnosed?
a. cervical motion tenderness and adnexal tenderness
b. Culture of cervical discharge
c. Laparoscopy
d. Transvaginal ultrasound; MRI (best sensitivity and specificity)
How is PID treated?
a. Empiric treatment with uterine, adnexal, and cervical motion tenderness
b. Ceftriaxone + doxycycline (covers both N. gonorrhoeae and C. trachomatis)
What is Salpingitis isthmica nodosa?
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)
What are complications of Salpingitis isthmica nodosa? How is it diagnosed?
2. Infertility, ectopic pregnancy
3. Diagnose with hysterosalpingography
◦ Beading appearance in areas of constriction
What are risk factors for ectopic pregnancy?
1) Scarring from previous PID (most common cause)
2) Endometriosis
3) Altered tubal motility, Salpingitis isthmica nodosa
4) Progestin-only pill; previous tubal ligation
Where are sites of implantation of ectopic pregnancy's?
(1) Majority occur within the tubes
■ Most are in the broad ampullary portion below the fimbriae.
(2) Ovaries, abdominal cavity
Clinically how does a woman with an ectopic pregnancy present?
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%)
What are complications of an ectopic pregnancy?
a. Rupture with intra-abdominal bleed
■ Most common cause of death in early pregnancy
b. Most common cause of hematosalpinx
■ Blood in the tube
How are ectopic pregnancy's diagnosed?
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
How is an ectopic pregnancy treated?
a. Methotrexate if stable and no hemorrhage
b. Conservative surgery; salpingectomy
What is the most common cause of an ovarian mass? are they neoplastic? How are they treated?
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
What is the Most common ovarian mass in pregnancy? Are they neoplastic? What can they be confused with?
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
What is oophoritis a complication of?
complication of mumps or PID
Stromal hyperthecosis occurs in who? what happens?
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
How does Stromal hyperthecosis present?
a. Hirsutism or virilization
b. Association with acanthosis nigricans and insulin resistance
c. Hypertension
d. Treatment is oophorectomy
Are ovarian tumors benign or malignant before 45? When is median age of presentation? Do they usually present early or as advanced?
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
What are risk factors for ovarian cancer?
(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
What are the classifications of ovarian tumors?
a.Surface-derived tumors
b.Germ cell tumors
c.Sex cord stromal tumors
What percent do Surface-derived ovarian tumors account for? Where do they derive from? Are they benign or malignant?
(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
What are germ cell ovarian tumors similiar to? A they malignant?
(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
Are Sex cord stromal ovarian tumors benign or malignant?
(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
Where do tumors come from that metastisize to the ovary?
(1) Accounts for 5% of ovarian tumors
(2) Common primary cancers metastasizing to ovaries
■Breast, stomach (e.g., Krukenberg tumors)
What are clinical findings with an ovarian tumor?
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
What are Signs of hyperestrinism from estrogen-secreting ovarian tumors?
(1) Bleeding from endometrial hyperplasia/cancer
(2) 100% superficial squamous cells in a cervical Pap smear
What antigen is increased in the serum of a woman with a surface derived ovarian tumor?
What is the prognosis of ovarian cancer?
a. Better prognosis if <65 years old
b. Overall 1- and 5-year relative survival rates for ovarian cancer are 75% and 45%, respectively
What are the examples of surface-derived ovarian tumors?
1) Serous tumors
2) Mucinous tumors
3) Endometrioid
4) Brenner tumor
What are serous ovarian tumors the most common of? What is seen histologically? What are the 2 types?
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
Histologically how do mucinous ovarian tumors present? What does seeding produce? What are the two types?
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
Endometroid is a surface-derived ovarian tumor. Is it benign or malignant? B/L or U/L?
1) Malignant tumors associated with endometrial carcinoma (15-30% of cases); tumor resembles endometrial carcinoma
2) Commonly bilateral
Brenner tumor is a surface derived ovarian tumor. Are the benign or malignant? What do they contain?
1) Usually benign
2) Contain Walthard's rests (transitional-like epithelium)
What are examples of germ-cell ovarian tumors?
1) Cystic teratoma
2) Dysgerminoma
3) Yolk sac tumor
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?
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
What does the struma ovarii type of germ cell tumor have?
functioning thyroid tissue
Dysgerminoma is a germ cell ovarian tumor. What blood enzyme is increased? What is it similar to in men? What is it associated with?
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
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?
1) Malignant tumor; most common ovarian cancer in girls < 4 years old
2) Contain Schiller-Duval bodies (resemble yolk sac)
3) Increased α-fetoprotein
What are examples of Sex-Cord Stromal ovarian Tumors?
1) Thecoma-fibroma
2) Granulosa-theca cell tumor
3) Sertoli-Leydig cell
4) Gonadoblastoma
Thecoma-fibroma is a sex-cord stromal ovarian tumor. Is it benign or malignant? What is it associated with? Ovarian time what happens?
1) Benign tumor associated with Meigs' syndrome (ascites, right-sided pleural effusion); regression of effusions follows removal of tumor
2) Commonly calcify
Granulosa-theca cell tumor is a sex-cord stromal ovarian tumor. Is it benign or malignant? What does it contain and do?
1) Low-grade malignant tumor
2) Feminizing tumor (produces estrogen) that contains Call-Exner bodies
Sertoli-Leydig cell tumor is a sex-cord stromal ovarian tumor. Are they benign or malignant? What do they contain?
1) Benign masculinizing tumor (produces androgens)
2) Pure Leydig cell tumors contain cells with crystals of Reinke
Gonadoblastoma is a Sex-Cord Stromal ovarian Tumor. is it benign or malignant? What is it associated with? What do they do longterm?
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
Where does a Krukenberg tumor come from? What cell type is in the ovary? What is the mode of metastisis?
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
What covers the fetal surface? What covers the chorion? What does the maternal surface contain?
1) chorionic plate
2) amnion
3) cotyledons covered by a layer of decidua basalis
Which cell layer lines the chorionic villi? When divided what forms the inner layer and the outer layer of the chorionic villi?
1) trophoblastic
2) cytotrophoblastic
3) syncytotrophoblastic
What does the syncytotrophoblastic layer produce?
(a) Synthesizes hCG
(b) Synthesizes human placental lactogen (HPL)
human placental lactogen corresponds to what? What type of activity does it have?
Directly correlates with placental mass and has anti-insulin activity
What vessels does the umbilical cord contain?
1) 2 arteries, 1 vein; umbilical vein has most O2
What is there an increased incidence of with a single umbilical artery?
cardiovascular defects; trisomy 18; esophageal atresia
If placental culture is negative for group B streptococcus how should the infection be treated?
treat prophylactically with IV ampicillin + IV erythromycin followed by amoxicillin + erythromycin
What is the most common placental infection? How should it be treated? What are other infections?
1) group B streptococcus
2) penicillin G or ampicillin IV
3) -B. fragilis, Prevotella bivius, group A streptococcus
What is funisitis?
Infection of the umbilical cord
What is chormioamnionitis? What is the danger? How is it treated?
1) Infection of the fetal membranes
2) Danger of neonatal sepsis and meningitis
3) Cefoxitin; ticarcillin-clavulanate
What is placenta previa? what is a risk factor?
(1) Implantation over cervical os
(2) Previous cesarean section is a risk factor (approaches 10%)
How does a woman present with placenta previa?
(1) Presents with painless vaginal bleeding
a. Usually in second or third trimester
(2) Uterus soft and nontender
(3) Fetal distress usually not present
How is placenta previa diagnosed? Which technique should be avoided? How is she treated?
(1) Pelvic examination should not be performed.
(2) Transabdominal ultrasound localizes placenta.
(3) Transvaginal ultrasound confirms placenta previa
(4) Delivery by cesarean section
What occurs in Abruptio placentae? What is it the most common cause of?
(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
What are risk factors for abruptio placentae?
(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
Clinically how will a woman present with abruptio placentae?
Abruptio placentae triad: painful vaginal bleeding, tetanic uterine contractions, fetal compromise
What occurs in placenta accreta?
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
what occurs in a Velamentous insertion?
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
What causes an enlarged placenta?
1) Diabetes mellitus
2) Rh hemolytic disease of newborn (HDN)
3) Congenital syphilis
Can monochorionic twin placentas be diamniotic? In general what results from this type of placenta?
(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
Dichorionic placentas produce what?
(1) Can be identical or fraternal twins
a. Fraternal twins occur when separate eggs are fertilized.
(2) Placentas can be diamniotic or separated
When does preecamplsia occur during pregnancy?
third trimester (24th to 25th weeks)
What are risk factors for preeclampsia?
(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
What can preeclampsia be associated with?
hydatidiform moles
(1) Complete mole, 2%
(2) Partial mole, 5%
Pathologically what is going on at the placenta in preeclampsia?
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.
What are pathologic findings that occur in preeclampsia?
1) Premature aging of the placenta
2) Multiple placental infarctions
3) Spiral arteries show intimal atherosclerosis
What are clinical findings in preeclampsia?
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
What is ecclamplsia? How is it treated?
1) Preeclampsia + seizures is called eclampsia.
(2) Magnesium sulfate is used for treatment.
How is preecclampsia treated?
1) Delivery is the treatment of choice and the only cure for the disease.
2) Magnesium sulfate is given for seizures
What are hydatidiform moles? What are the types? In who and in what countries do they occur most?
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
How are complete moles characterized? What occurs genetically to make one?
(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
What is there an Increased risk of developing with a complete mole?
choriocarcinoma (20% chance)
What are clinical findings with a complete mole?
(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
How is woman with a complete mole treated? How is success followed?
(a) Dilation and curettage
Must remove all material
(b) Follow patient with hCG levels
Should go down to zero
What is a partial mole? What is there a low risk of developing?
(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
What is a choriocarcinoma?
1) Malignant tumor composed of syncytiotrophoblast and cytotrophoblast
2) Chorionic villi are NOT present.
Risk factors for developing a choriocarcinoma are?
(1) Complete mole (50% of cases)
(2) Spontaneous abortion (25% of cases)
(3) Normal pregnancy (25% of cases)
Where do choriocarcinomas metasitisize? How are they characterized?
(1) Lungs and vagina
(2) Lesions are hemorrhagic
How is a choriocarcinoma treated?
1) Excellent response to chemotherapy (methotrexate); low mortality rate
2) Good response does not apply to non-gestationally derived cancer
What is amniotic fluid? What does a high salt content do? What is amniotic fluid a sign of?
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
What is polyhydraminos? What causes it?
(1) Excessive amniotic fluid
(2) Causes
(a) Tracheoesophageal (TE) fistula
(b) Duodenal atresia
(c) Maternal diabetes (20%)
**Maternal hyperglycemia → fetal hyperglycemia → fetal polyuria
What are causes of oligohydraminos?
(a) Juvenile polycystic kidney disease
(b) Fetal genitourinary obstruction
(c) Uteroplacental insufficiency
(d) Premature rupture of membranes
What causes increased maternal AFP? What about decreased?
(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
Where is lecithin produced? What is its function?
(1) Synthesized by type II pneumocytes
(2) Decreases alveolar surface tension to prevent atelectasis
Lecithin/sphingomyelin ratio > 2 means what?
adequate surfactant
What increases surfactant synthesis? what decreases it?
1) cortisol, thyroxine
2) insulin
Where is estriol made during pregnancy? Where is it degraded?
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.
What is the down syndrome triad?
↓ urine estriol, serum AFP; ↑ serum hCG
Where are high density areas of the breast?
1) Upper outer quadrant
a. Underscores why cancer is most commonly located in this quadrant
2) Beneath the nipple
What are the effects of estrogen and progesterone on the breast?
1) Estrogen--Stimulates ductal and alveolar growth
2) Progesterone--Stimulates alveolar differentiation
Where does the outer quadrant of the breast drain to? What about inner quadrant?
1) Drain to the axillary lymph nodes
2) Drain to the internal mammary nodes
What is the Most common nonpituitary endocrine disease causing galactorrhea?
primary hypothyroidism
a. Decreased serum thyroxine increases thyrotropin-releasing factor (TRF).
b. TRF stimulates prolactin
Which drugs can cause galactorrhea?
OCPs, phenothiazines, methyldopa, H2-receptor blockers, anxiolytics
What are 2 main causes of bloody nipple discharge?
Intraductal papilloma, ductal cancer
What is the primary cause of mastitis? How is it treated?
a. Acute mastitis due to Staphylococcus aureus
b. Usually occurs during lactation or breast-feeding
(1) If not methicillin resistant, dicloxacillin or cephalexin
(2) If methicillin resistant, trimethoprim-sulfamethoxazole
What causes a greenish-brown nipple discharge?
Mammary duct ectasia (plasma cell mastitis)
What is the most common cause of breast pain in woman <50?
fibrocystic change
What is Mondors disease? how does it present?
1) Superficial thrombophlebitis of veins overlying the breast
2) Presents as a palpable, painful cord
How are fibrocysts characterized? Does their size change with menstrual cycle? Are they malignant?
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
How is sclerosing adenosis characterized? What is it confused with?
1) Proliferation of small ductules/acini in the lobule
2) Pattern is often confused with infiltrating ductal cancer.
3) Often contain microcalcifications
What are pathologic findings in ductal hyperplasia of the breast? What is there an increased risk of developing?
(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
Who is affected by Mammary duct ectasia? What occurs? What does it resemble?
(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
How is plasma cell mastitis treated? What is another name for it?
1) Antibiotics if infection is present
(2) Surgical removal of blocked duct
3) Mammary duct ectasia
What are microscopic findings in traumatic fat necrosis? Is it painful or painless? What does it resemble?
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
What happens when silicone leaks from an implant? Is it associated with autoimmunity?
(1) Produces foreign body giant cells and chronic inflammation
(2) Association with autoimmune disease is not proved.
What is the most common breast tumor? Women taking what drug will develop?
(1) fibroadenoma
(2) Most commonly diagnosed breast tumor
(3) Develop in 50% of women who receive cyclosporine after renal transplantation
How does a fibroadenoma present?
1) Discrete movable, painless or painful mass
2) Multiple lesions may be present (10-15%
In a fibroadenoma what proliferates? Is it neoplastic?
(a) Stroma proliferates and compresses the ducts
(b) Duct epithelium is not neoplastic
Does the size of a fibroadenoma change with period? When will they go away?
1) Increases in size during pregnancy
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%)
Is a phyllodes tumor benign or malignant? is it small or large? Where does it derive from?
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
Most common cause of bloody nipple discharge in women < 50 years old is? Does become cancer? Where do they develop?
1) Intraductal papilloma
2) Develop in the lactiferous ducts or sinuses
3) No increased risk for cancer
4) Surgically remove the duct or sinus.
what nerve is damaged when someone has a winged scapula?
long thoracic nerve (C5,6,7)
What is the most common cancer of adult women? What is the average age?
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).
A family history of breast cancer includes what? What genes?
(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
increased estrogen is associated with breast cancer. Who is at risk as a result?
(1) Early menarche/late menopause
(2) Nulliparity
(3) Postmenopausal obesity
a. Aromatization of androstenedione to estrone
(4) Hormone replacement therapy
What are some random risk associated with breast cancer?
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)
What factors reduce the risk of breast cancer?
breast-feeding; exercise; healthy body weight
Clinically how does breast cancer present?
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
What is mamography used for? What are its limitations? When does screening begin?
Primarily a screening test
1) Detects nonpalpable breast masses (detects 80-90%)
2) Does not distinguish benign from malignant
3) annually at age 40; earlier if patient is high risk
Mammography can identify what when cancer is present? I
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
How does breast cancer spread?
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.
Where are the most common sites of breast cancer metastisis? When will metastisis occur?
1) Lungs, bone, liver, brain, ovaries
2) May metastasize 10 to 15 years after treatment
3) Pain in bone metastasis is relieved with radiation.
With breast cancer does nodal or extranodal have a greater significance?
extranodal spread has greater significance than nodal metastasis alone
What is a sentinel node in breast cancer?
initial node draining the tumor
What does it mean if the sentinel node is negative? Positive?
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.
Who are Estrogen and progesterone receptor assay usually positive in? What is the clinical significance?
(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
What are tests performed in breast cancer cases?
(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
What is the Treatment for high-risk patients without breast cancer?
Treatment with tamoxifen or raloxifene reduces risk
What are level I, II, III nodes in breast cancer?
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.
What is breast conservation therapy?
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
What is the prognosis of breast cancer?
(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%
How does gynecomastia present?
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)
What is the source of estrogen in gynecomastia?
(1) Peripheral aromatization (85%)
(a) Testosterone to estradiol
(b) Androstenedione to estrone
(2) Leydig cells (15%)
When does normal physiologic gynecomastia occur in men?
(1) Newborn (60-90%)
(2) Puberty (peaks at ages 13-14 years)
(3) Elderly (occurs between 50-80 years of age)
What is breast conservation therapy?
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
What is the prognosis of breast cancer?
(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%
How does gynecomastia present?
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)
What is the source of estrogen in gynecomastia?
(1) Peripheral aromatization (85%)
(a) Testosterone to estradiol
(b) Androstenedione to estrone
(2) Leydig cells (15%)
When does normal physiologic gynecomastia occur in men?
(1) Newborn (60-90%)
(2) Puberty (peaks at ages 13-14 years)
(3) Elderly (occurs between 50-80 years of age)
How does the liver contribute to gynecomastia?
(1) Inability to metabolize estrogen
(2) Inability to metabolize 17-ketosteroids
a. Peripherally aromatized to estrone
What genetic conditions lead to gynecomastia?
(1) Klinefelter's syndrome
a. Increased aromatization of androgens to estrogens in Leydig cells
(2) Testicular feminization
a. Decreased androgen receptor synthesis
What are drugs that can lead to gynecomastia?
(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
Which cancer can lead to gynecomastia? Why?
Choriocarcinoma of testis producing hCG
which endocrine disorders can lead to gynecomastia?
(1) Primary hypogonadism
Leydig cell dysfunction
(2) Secondary hypogonadism
a. Pituitary/hypothalamic dysfunction
What are risk factors in men for developing breast cancer?
1) Inactivation of BRCA2 suppressor gene
2) Klinefelter's syndrome
3) Usually have a poor prognosis
Is Ductal carcinoma in situ palpable? What are its patterns? What do they contain? are they invasive? How are they treated?
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"
How does a Lobular carcinoma in situ present? Histologically what is seen? Are they unilateral or bilateral?
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
histologically how does Infiltrating ductal carcinoma look? What do 1/3 have?
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)
how does pagets of the breast present?
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%
What is medullary carcinoma of the breast associated with? How is the tumor characterized? Are they estrogen/progesterone positive?
1) Associated with BRCA1 mutations
2) Bulky, soft tumor with large cells and lymphoid infiltrate
3) Majority are estrogen and progesterone receptor negative
How does inflammatory breast carcinoma present? What is the prognosis?
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
Histologically how does invasive lobular carcinoma present?
Neoplastic cells arranged in linear fashion or form concentric circles (bull's-eye appearance)
Where does tubular breast carcinoma develop? is it unilateral or bilateral?
1) Develops in terminal ductules
2) Increased incidence of cancer in opposite breast (10-40%)
who does colloid (mucinous) breast carcinoma occur in? How are they characterized histologically?
1) Usually occurs in elderly women
2) Neoplastic cells are surrounded by extracellular mucin
Which breast disorders occur at the lactiferous sinus?
1) intraductal papilloma
2) plasma mastitis
3) breast abcess
Which breast disorders occur at the major duct?
1) fibrocystic change
2) ductal cancer
Which breast disorders occur at the terminal duct?
1) tubular carcinoma
Which breast disorders occur at the lobule?
1) lobular carcinoma
2) sclerosing adenosis
Which breast disorders occur in the stroma?
1) phyllodes tumor
2) fibroadenoma
Tumor cells fill ducts and tumor cell necrosis is a cheesy consistency?
intraductal carcinoma in situ
tumor cells arranged in cords, islands and glands embedded in dense fibrous stroma with firm consistency?
invasive ductal carcinoma
How are pagets cells characterized? what other cancer is usually present
1) large surrounded by a clear halo and invade epidermis
2) ductal carcinoma almost always present
clusters of neoplastic cells fill intralobular ductules and acini and can lead to invasive carcinoma, also may be bilateral
lobular carcinoma
often multicentric or bilateral with cells in linear fashion (indian-file)
invasive lobular carcinoma