Prostate

1.

How common is carcinoma of the prostate and what age group

is most affected?
Most common cancer in men. 300,000 new dx in US/year. Older men, 50+,
especially 70+
2.
Most carcinomas of the prostate are of what histologic type?
Adenocarcinoma diffusely infiltrating well-differentiated neoplastic glandular
epithelium
3.

Discuss the clinical significance of occult (Stage A) carcinoma of

the prostate.
Microscopic tumors confined to prostate. ~70% of men over 80. Significant
clinical consequences 10-20% of pts. Good prognosis.
4.

What are the most common stages at diagnosis for prostate

carcinoma and how does this affect prognosis?
Majority of pts. present at Stage C or D (extension beyond prostate or mets)
10-40% ten-year survival
5.

Discuss the clinical importance of digital rectal examination in men

and relate this to the anatomic location of prostatic carcinoma.
Helpful in dx, esp. at early stages. ~70% occur in peripheral zone, posteriorly
palpable through rectal exam
6.

Describe the character of the bone metastases in prostatic

carcinoma.
Hematogenous spread to axial bones osteolytic and esp. osteoblastic bony
mets.
7.

What is the clinical value of prostatic acid phosphatase and

prostatic specific antigen in prostatic carcinoma?
Produced by prostatic epithelium. Not actually that sensitive/specific for detection
of cancer, but PSA is very useful for monitoring post-tx for
recurrence, since levels should be 0 after tx. Free vs. bound PSA:
low relative free PSA is a marker of malignancy.
8.

What three therapies are used to treat prostatic cancer and how are
these related to stage?
Surgery and radiotherapy for tumors confined to prostate Stage A/B. Hormonal
tx for advanced metastatic. Includes orchiectomy, exogenous
estrogens, synthetic LH-releasing hormone agonists. Often induces
remission, but hormone-insensitive clones develop.

9.

Discuss age, race, and environment as risk factors in the

development of prostatic carcinoma.
Risk incr w/age. US blacks>US whites>Asians. Environmental factors suggested
b/c incidence rises in populations who move from low incidence to
high incidence areas.
10.

What age group is most often affected by prostatic nodular

hyperplasia?

Older men
11.
How common is prostatic nodular hyperplasia?
Very common - 70% of men by age 60, 90% by age 80.
12.

What are the most common clinical presentations of prostatic

nodular hyperplasia and how is this related to its anatomic
location?
Urethral obstruction due to location in transitional zone (peri-urethral). Sx
secondary to urethral compression, urinary retention frequency,
nocturia, difficulty starting/stopping, overflow dribbling, dysuria,
UTI.
13. What hormone appears to be related to the development of prostatic
nodular hyperplasia?
DHT mediator of prostatic growth, esp. potent in older men in whom increased
estradiol sensitizes prostate to effects of DHT.
14.

What is the relationship of prostatic nodular hyperplasia to

carcinoma?
No relationship suggested by current evidence.
Testis
1.
What is the cell of origin of most neoplasms of the testis?
Germ cells 95% of testicular neoplasms
2.
How common is testicular cancer?
GCTs low incidence (6/100,000), but most common malignant tumor of men
15-34.
3.
What age group is most often affected by testicular cancer?
Young men 15-34.
4.

What is the most common type of pure testicular germ cell tumor?

Seminoma 30-50% of GCTs. Homogenous gray/white lobulated, w/out

hemorrhage/necrosis. Sheets of uniform, large cells fried egg
appearance, lymphocytic infiltrate.
5.

List three other types of malignant germ cell tumors of the testis
and discuss why they are clinically classified together as nonseminomatous germ cell tumors.
Classified separately b/c clinical behavior is similar, distinct from seminoma.
-Embryonal carcinoma resembles adenocarcinoma. CD30+
-Yolk-sac tumor bubbly stroma, eosinophilic blobs, Schiller-Duval bodies, AFP+
-Choriocarcinoma rare in pure form, very aggressive, hCG+, hemorrhage, large
multinucleated cells
-Teratoma usu benign when pre-pubertal, malignant post-puberty
6.

What is the difference in the biologic behavior of teratoma of the

ovary and testis?
Benign in ovary, malignant in testis???
7.

What is the most common clinical presentation of germ cell

tumors of the testis?
Painless testicular enlargement
8.

Discuss the distinction of seminoma and non-seminomatous

germ cell tumors of the testis with respect to stage,
radiosensitivity, prognosis, and the secretion of polypeptide
hormones and enzymes.
Seminomas best prognosis, present at low stage, very radiosensitive, dont
secrete markers
Non-seminomatous present w/tumors spread beyond testes (Stage 2/3),
radioresistant, more aggressive, but complete remission in 90%
with aggressive tx. Secrete markers like hCG (choriocarcinoma)
and AFP (yolk-sac tumor).
9.
Define cryptorchidism and testicular torsion.
Cryptorchidism undescended testes 0.5% of adult male population. Infertility,
predisposes to testicular cancer.
Torsion twisting of spermatic cord, obstruction of venous (not usu arterial)
vascular beds result of violent movt or trauma
10.
List five significant causes of testicular atrophy.
Atherosclerotic vascular disease, inflammatory orchitis (esp. mumps),
cryptorchidism, hypopituitarism, malnutrition, semen outflow obstruction,
irradiation, prolonged exposure to female sex hormones, Klinefelters syndrome
Uterus

1.
Name the three major histologic types of endometrial hyperplasia.
Simple vs. complex, with/without atypia.
2.

What is the relationship of endometrial hyperplasia to

endometrial carcinoma?
Simple w/out atypia uncommon to progress (1%)
Complex w/out atypia 3% progress
Simple w/atypia 8%
Complex w/atypia 29%
3.

What clinical symptom is most common in both endometrial

hyperplasia and endometrial carcinoma?
Abnormal bleeding
4.
How common is endometrial carcinoma?
Most common gynecologic malignancy in US 40,100 new dx/year.
Whites>non-whites.
5.

What are the peak ages for endometrial carcinoma and

hyperplasia?
Post-menopausal (?)
6.

The pathogenesis of endometrial carcinoma and hyperplasia is

strongly related to what hormone?
Estrogen (prolonged exposure to unopposed estrogen). Also, PTEN tumor
suppressor gene.
7.

Differentiate between grade and stage in endometrial carcinoma,

tell how they affect prognosis and why the prognosis of endometrial
carcinoma is fairly good?
Grade degree of differentiation. Stage degree of spread. Worse grade or
stage = worse prognosis, but clinical stage more important
8.
What cells make up leiomyomas (fibroids)?
Smooth muscle cells. Can be intramural (w/in myometrium), submucosal
(beneath endometrium), subserosal (beneath serosa)
9.

Are leiomyomas benign or malignant?

Benign
10.
How common are leiomyomas?
Most common tumor in humans. 75% of reproductive-age women; each uterus
has average of 6.5 tumors
11.

What are two common symptoms with leiomyomas?

Asx or abnormal uterine bleeding, impaired fertility, compression of bladder

(frequency of urination)
Cervix
1.
Why is the transformation zone important?
Site of most dysplasias and malignancies
2.
Most carcinomas of the cervix are of what type?
Squamous cell carcinoma 70%
3.

What is the most likely cause of the decline in death rate for
cervical cancers over the past fifty years?
Increased Pap screening detection of premalignant lesions (particularly of
squamous cell origin)
4. Describe the concept of preinvasive neoplasia and the
nomenclature used to describe it in the cervix.
Preinvasive hasnt gone beyond epithelium
Cervical Intraepithelial Neoplasia (CIN). Koilocytosis, enlarged nuclei, incr N:C
ratio, nuclear hyperchormasia, loss of polarity, mitoses.
CIN 1 lower 1/3 of epithelial layer. Not truly precancerous. 60% regress
CIN 2 lower 2/3. 40% regress
CIN 3 whole thickness. Decreased koilocytes. 1-7% - early invasive disease.
10-20% progress to carcinoma if untx.
5.

What is the peak age for invasive squamous cell carcinoma of the
cervix and how does this compare to the peak age for CIN?
Mean age for invasive cervical cancer 47 years (bimodal peak). CIN3 30
years. Precancerous lesions exist in noninvasive stage for 15-20
years before progressing.
6.

Squamous cell carcinoma of the cervix correlates with factors

that suggest what mode of transmission?
Risk factors related to sexual activity transmission of HPV via sexual contact
7.
Name a possible viral vector in squamous cell carcinoma.
Human papilloma virus esp. HPV 16 and 18 (6, 11 genital warts)
8.

How is tumor stage related to prognosis in invasive cervical

carcinoma?
Stage related to degree of spread. Impt for prognosis. Grade does not correlate
w/prognosis.

9.

Discuss the definition, incidence, locations, pathogenesis and

clinical significance of endometriosis.
Of cervix mean age 37 years, range 20-51. Abnormal uterine bleeding, postcoital bleeding.
General Endometrial tissue outside of uterus. Ages 20-30, 10% of women.
Functional tissue, responds to hormonal menstrual changes. Consists of glands,
stroma, and old hemorrhage. Pain, infertility.
Pathogenesis: retrograde
menstruation, angiolymphatic dissemination, metaplastic change of secondary
mullerian system. Ovaries>uterine ligaments>rectovaginal septum>pelvic
peritoneum. Can occur anywhere, but usu in pelvis. Can undergo malignant
transformation.
Breast:
1.
How common is carcinoma of the breast?
Most common malignancy in women ~200,000 new dx/year in US. 1/9 US
women.
2.
What age group is most often affected by breast cancer?
Peak incidence in 4th-6th decades. Rare before 25.
3.
List three important risk factors in developing breast cancer.
Older age, early menarche or late menopause (more years of estrogen
exposure), first pregnancy >35 or nulliparity, affected 1 st degree
relatives
4.
Estrogen

What hormone is probably important in the pathogenesis of breast

cancer?

5.

Discuss the role of genetic factors in the development of breast

cancer.
13% of women have family hx in 1 st-degree relative. Incr risk of other cancers.
BRCA1/2 mutations
6.
Distinguish between ductal and lobular carcinoma.
Ductal 80-90%. Nests and cords of malignant duct cells throughout
parenchyma. Special good prognosis subtypes: medullary,
colloid/mucinous, tubular, papillary
Lobular from lobular epithelium. Usu hard, stellate. Invade single-file through
stroma.
7.
Which type of breast cancer is most likely to be multifocal?
Lobular - ~20% bilateral
8.

Distinguish between noninfiltrating and infiltrating carcinoma

of the breast.

Noninfiltrating = in situ. Not invasive. 8-10X relative risk of invasive carcinoma

(30%)
9.
What is Paget's disease of the breast?
In situ carcinoma of lactiferous ducts w/extension to epidermis. Involves nipple
and areola crusting, discharge. 95% assoc w/underlying
carcinoma (DCIS)
10.
What is inflammatory carcinoma of the breast?
Invasion involves breast lymphatics edema, peau dorange. Can mimic
mastitis.
11.

Why is identification of the subtypes of infiltrating duct carcinoma of

the breast important?
Special subtypes (see #6) have better prognosis
12.
Describe the relationship of stage to prognosis in breast cancer.
Stage is most important prognostic factor, particularly axillary lymph node status.
Five-year survival for Stages 1-4: 80%, 65%, 40%, 10%
13.
Describe the clinical value of mammography.
Impt for detection of lesions, can be detected earlier than by breast exam (?)
14.

Describe the clinical value of estrogen receptor determination in

breast cancer.
ER-positive tumors much more likely to respond to hormonal tx: 70% regress
compared to 5% of ER-negative. Best rates of response
estrogen and progesterone receptors present.
15.
Describe the treatment options in breast carcinoma.
Surgery total or segmental mastectomy w/axillary LN dissection, irradiation,
adjuvant hormonal and chemotherapy.
16.
What is the clinical significance of a fibroadenoma?
Most common benign breast tumor, young women. Produce masses must be
differentiated from cancer
17.

What is the most probable pathogenesis of fibrocystic disease of

the breast?
Excess estrogen or deficiency of progesterone
18.
List three histologic (microscopic) patterns of fibrocystic disease.
Cystic blue dome cysts. Focal or multifocal. Epithelial cells can become large,
eosinophilic = apocrine metaplasia
Sclerosing adenosis intralobular fibrosis, proliferation of small ductules and
acini
Epithelial hyperplasia proliferations of epithelial cells lining ducts, lobules, or
both. With or w/out cellular/architectural atypia.
19.

How common is fibrocystic disease?

Clinical incidence 40-50%. Pathologic incidence 60-80%. Found on 60-90%

of autopsies.
20.
What is a blue dome cyst?
Cysts in fibrocystic disease up to 5 cm, unopened, blue appearance.
21.

What is the relationship of fibrocystic disease and breast cancer

and how is this related to the three patterns of fibrocystic disease?
Unclear relationship, but risk proportional to degree of epithelial hyperplasia.
Other two subtypes have only minor associations with devt of
cancer
22.
What are the clinical significances of fibrocystic disease?
? Need to be differentiated from cancer. Mild risk of devt of cancer depending on
subtype. Relevance of responsiveness to sex steroid hormones???
Ovary
1.
What are the three major divisions of primary ovarian neoplasia?
Epithelial, germ cell, stromal
2.
Which is the most common ovarian malignancy?
Surface epithelial tumors 70% of primary ovarian neoplasms
3.

Name two major histologic subtypes of surface epithelial tumors of

the ovary and describe their macroscopic and microscopic
appearances.
Serous mostly benign. Often bilateral. Unilocular cyst, may have papillary-type
projection, thickening or mass, or necrosis. Micro cystic lesions,
epithelial thickening, papillary projections. Benign: non-complex
columnar epithelium +/- cilia; malignant: more complex,
Psammoma bodies
Mucinous mostly benign. Multilocular, unilateral. Thick mucin, usu. large. Tall
columnar mucinous epithelium. Pseudomyxoma peritonei
mucinous tumor associated with mucinous ascites, implants,
adhesions, etc.
4.
What are cystadenomas of the ovary?
Benign cystic tumors with simple epithelial lining. Present as adnexal masses.
5.

Explain the concept of borderline tumor of the ovary and state its
clinical importance.
Borderline like malignant, tend to by cystic with epithelial atypia and
proliferation. Distinguished by lack of destructive invasion. Survival
for borderline much higher (10-yr 75%) than malignant (10-30%).
Require less extensive surgery.
6.

What age group is most often affected by epithelial malignancies of

the ovary?

5th-7th decades
7.

Why is the prognosis of ovarian epithelial malignancies so

often poor?
Usually not detected until high stage (over half spread beyond pelvis)
8.
What is the most common germ cell tumor of the ovary?
Mature/benign cystic teratomas younger women, unilocular w/hair, teeth,
sebaceous material, components of 3 germ cell layers, squamous
epithelium w/hair and adnexal structures predominate
9.

What is the most common malignant germ cell neoplasm of the

ovary?
Dysgerminoma 50% of malignant germ cell tumors counterpart to male
seminoma. 2nd-3rd decade, unilateral, radiosensitive, good
prognosis. Only 1/3 are clinically aggressive
10.

List the three major types of sex cord-stromal tumors of the ovary
and discuss their malignant potential.
Granulosa cell tumors Associated w/incr estrogen. Coffee-bean nuclei, CallExner bodies, inhibin+. 10-15% develop endometrial carcinoma. 525% malignant. 5% recur or metastasize (numbers vary based on
part of syllabus?)
Fibrothecoma associated with Meigs Syndrome, Basal Cell Nevus Syndrome
Sertoli-Leydig Cell tumor (androblastoma) Associated w/ androgenic
manifestations. ~5% recur of metastasize
11.

What is the relationship of sex steroid production to sex cordstromal tumors of the ovary?
Granulosa cell tumors and fibrothecomas estrogen. Sertoli-Leydig - androgens
11. List two common sources of metastatic disease to the ovary.
Other pelvic organs (fallopian tube, opposite ovary), GI tract (Krukenberg tumor
signet ring tumor of stomach mets to ovaries), appendix, breast