Exam 3 Review Flashcards

1
Q

1) Which is the only finding in fibrocystic condition of the breast that has an increased risk of having carcinoma?

A

*Atypical Epithelial Hyperplasia

  • epithelial hyperplasia becomes multilayered, with atypical nuclear change
  • the more severe and atypical the hyperplasia the greater the risk
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2
Q

2) General features of fibroadenoma?

  • what do they consist of?
  • what age group are you more likely to see a fibroadenoma?

(Remember a woman undergoes her highest amount of estrogenic control after puberty and no longer after menopause)

A
  • MOST common of the BENIGN breast tumors (99%)
  • Typically, the diameter 2-5 cm & are well encapsulated spherical nodules, well-circumscribed from breast parenchyma & freely moveable from surrounding breast substance
  • Compose of 2 components : fibrous stroma & glandular epithelium (dense/rubber like)
  • The fibroblastic component of the tumor resembles normal interlobular stroma enclosing glandular & cystic spaces lined by epithelium
  • Tumors of young women in UPPER OUTER quadrant
  • Easily removed w/out consequences, they DONT undergo malignant change & have excellent prognosis
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3
Q

3) Signs and symptoms of a woman with fibrocystic disease? (remember it is bilateral disease)

A
  • Fibrocystic changes usually affects BOTH breasts, & b/c changes are symmetrical, patients may complain mostly of pain, modularity, & sensitivity on palpation
  • Small lumps may fluctuate, corresponding to the fluid filled cysts, and even areas of calcification
  • Mammography reveals condensed areas, cysts, & calcification -> indistinguishable from those seen in cancer, **BIOPSY examination, only safe way to establish definitive diagnosis

Typically doesn’t require Tx unless premalignant changes from atypical epithelial hyperplasia are found, additional surgical resection is recommended.

-Most surgeons perform an extended lumpectomy, they remove indurated glandular part of breast parenchyma. The prognosis overall is excellent.

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4
Q

4) Most characteristic clinical features of intraductal papilloma

A
  • Neoplastic papillary growth w/in a duct.
  • MOST are solitary & found w/in principle lactiferous ducts or sinuses. Presents clinically as serous or bloody discharge from nipple a small sub-areolar mass & “RARELY nipple retraction.”
  • Complete excision of the duct system should be performed to ovoid local recurrence.
  • “Multiple papillomas” are associated w/ an increased risk of Papillary Carcinomas. Solitary ones = BENIGN.

Note: Bloody/Serous nipple discharge= intraductal papilloma

*Single nodule in a single breast (characteristic of ductal)

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5
Q

5) Which conditions have blue dome cysts?

A
  • Blue dome cysts are only seen in FIBROCYSTIC CHANGE!
    1. Any imbalances of estrogen/progesterone hormones are thought to be the etiology with changes in the ducts, lobules and stroma.
    2. Normal loose intralobular CT is replaced by dense CT, rich in collagen and unresponsive to hormones.
    3. Ductal epithelium continues to proliferate because it retains its responsiveness to hormones. The dilated ducts may become entrapped in the dense connective tissue stroma, leading to a Blue-Domed cyst.
    4. Besides the fibrosis and the cysts, called Blue-Domed Cysts, which are the most common types of alterations, there is also Epithelial Hyperplasia which is always present
    5. When the epithelial hyperplasia becomes multilayered, with atypical nuclear change, this is referred to as Atypical Epithelial Hyperplasia, which is the only change related to the development of carcinoma
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6
Q

5) Which conditions have fibrous tissue?

A
  • **Chronic Mastitis
  • Rare disease of unknown cause
  • produces small lumps in the breast may mimic cancer, biopsy needed.
  • When extensive necrosis occurs from acute matitis, destroyed breast tissue is replaced by fibrous scar & may have nipple retraction–> mistaken for carcinoma
  • **Fibrocystic change of the breast
  • **Fibroadenomas
  • **Gynecomastia/Carcinoma
  • Male breast -enlargement w/ hormonal changes during puberty
  • enlargement is secondary to inordinate proliferation of ducts & surrounds CT
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7
Q

5) Which conditions have encapsulation?

- know the definition of desmoplasia

A

Benign Tumors of the Breast Fibroadenomas:

  1. The most common of the benign tumors
  2. Typically, diameter 2-5 cm & are well-encapsulated spherical nodules, well-circumscribed from breast parenchyma & are freely moveable from surrounding breast substance
  3. Tumor is composed of 2 components: fibrous stroma and glandular epithelium

**Desmoplasia - Where the tumor cells infiltrating the tissue are surrounded by dense connective tissue that is produced by the host in response to the tumor (appears firm & gritty when sectioned)

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8
Q

6) What is the common etiology of fat necrosis of breast and likewise what breast conditions can mimic a carcinoma because of the fibrous scarring?

A
  • # 1 cause of fat necrosis of the breast is TRAUMA
  • Tends to occur as a solitary, sharply localized process in one breast, & almost all patients give a history of previous trauma, prior surgical intervention, or radiation therapy.

-Grossly, there is hemorrhage w/ CENTRAL FAT NECROSIS, later forms a nodule of gray-white firm tissue w/ foci of chalk-white debris
Possible confusion w/ cancer when fibrotic

Conditions that can mimic carcinoma: 
a) Chronic Mastitis
-produces small lumps, w/ necrosis tissue replaced by fibrous scar & "nipple retraction"
b) Central Fat necrosis of the breast 
(white firm tissue w/ foci is fibrotic)
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9
Q

7) What are the major features of gynecomastia?

  • What does the male breast not have?
  • What are some of the causes of gynecomastia?
A
  • Gynecomastia is male breast enlargement associated w/ hormonal changes in puberty
  • Enlargement is caused by proliferation of excretory ducts that surround connective tissue
  • Occurs in adulthood owing to an EXCESS of ESTROGEN, as from cirrhosis or tumors
  • Fibrous cap of tissue directly under the areola
  • ductal(no lobules) in origin & invades more rapidly because of less adipose tissue
  • Male breast has NO lobules but does still have DUCTS
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10
Q

8) Directly and indirectly related to risk factors for breast cancers (two questions)

  • Sex?
  • Age?
  • Race?
A
  • The most important risk factor points to hormonal & genetic etiologies which may act concomitantly, they are paired w/ some additional unidentified carcinogenic substances in environment, or w/ carcinogenic viruses.
    1. Sex: Females are affected 100 times more
    2. Age: RARE BEFORE puberty and quite unusual in young women. Incidence slowly rises after age of 35 years & peaks in postmenopausal women who are 60 yrs old.
    3. Race: Uncommon in Japanese, and Chinese, and MOST common in Caucasians, spec. Jews.
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11
Q

8) Directly and indirectly related to risk factors for breast cancers (two questions)

  • Genetics?
  • Hormonal factors ?
A
  1. Genetics: If a mother had/ has breast cancer all daughters have increased risk. (Also for sisters of a patient with breast cancer.) A history of familial cancer increases the risk for relatives be 5-10 fold & possibly higher in some.
  2. Hormonal Factors: Women exposed to estrogens for prolonged periods tend to develop breast cancer. More common in early menarche & late menopause (influence of ovarian sex hormones).
    Nulliparous women @ greater risk, than those who have multiple children, b/c pregnancy interrupts the cyclic secretion of ovarian estrogens.

-Breast cancers have estrogen receptors, & growth of these cells can be inhibited/slowed down by synthetic anti-estrogen drugs—> important role of hormones in breast cancer.

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12
Q

8) Directly and indirectly related to risk factors for breast cancers (two questions)

  • Presence of other cancers?
  • Premaligant Fibrocystic Changes & Multiple intraductal papillomatosis ?
  • Other causes?
A
  1. Presence of other cancers: Incidence increased in women who have cancer in other breast, as well as those who have ovarian or endometrial cancer, b/c these tumors are hormonally induced, occurring in women in whom there is hyperestrinism.
  2. Premalignant Fibrocystic Changes and Multiple Intraductal Papillomatosis:
    * *Atypical Epithelial Hyperplasia, along w/ multiple intraductal papillomas can progress to invasive carcinoma, if not removed.
  3. Other causes:
    Obesity, high fat diets, & moderate alcohol consumption can all increase the risk.

-The more severe & atypical hyperplasia, greater the risk.

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13
Q

9) What is the most common location for breast cancer to occur?

A

-Upper outer quadrant (45%), central under the areola (25%)

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14
Q

10) The main difference from invasive and in situ is preachment of?

A

**When it reaches the BASEMENT MEMBRANE

-Noninvasive/ in situ – a malignant population of cells that lack the capacity to invade through the basement membrane and therefore no distant spread

-Invasive/ infiltrating – tumors that infiltrate the tissue are surrounding with CT which is produced by the host in response to the tumor
o This dense CT pulls on the adjacent tissue, causing puckering of the skin and retraction of the nipple

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15
Q

11) What is the difference between FNA vs a surgical biopsy or incisional biopsy?

A
  • *FNA (fine needle aspiration)
  • sample may be too small to establish definitive diagnosis & procedure must be repeated
  • done @ initial screening
  • *Surgical biopsy requires incision of skin & is performed under general anesthesia
  • confirms diagnosis of cancer
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16
Q

12) What does the mammogram look for?

A
  • Specialized X-ray technique, allows detailed examination of breast w/ low density radiographs
  • Tumor masses can be detected in early stages of development even before they are palpable seen as increased density w/ frequent calcification
  • Smallest tumor can be less than 0.5 cm
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17
Q

13) Know the difference from modified radical mastectomy and lumpectomy

A
  • Lumpectomy: most conservative surgical procedure as it is limited to resection of the tumor with surrounding fat tissue
  • Modified radical MASTECTOMY: removal of breast tissue, skin, areola, nipple, pectoralis(except), and most of underarm lymph nodes (EVERYTHING)

Modified means that the pectoralis is not remove

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18
Q

14) What route do breast cancers metastasize via?

A

Lymphatics- b/c most lymph ducts drain into axillary lymph nodes, most metastases are found in the axillary area.

  • As focal lesions, cancer extends in all directions & adhere to deep fascia of chest wall–> become fixed
  • Medially or centrally located tumors spread into internal mammary lymph nodes
  • **Distant metastases: in lungs, liver, bones, brain, and adrenals
  • **Local: Internal mammary lymph nodes & axillary lymph nodes
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19
Q

15) What is the function and other name for Sertoli (Sustenticular) cells?

A
  • For support & nutrition of the spermatozoa, located between the germ cells
  • “inside” seminal vesicles while the Leydig cells are “outside”
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20
Q

16) Which of the following 3 accessory male glands produces the largest amount of seminal fluid?

A

1) Seminal Vesicles 60%
2) Prostate 13-33%
3) Cowpers (Bulbourethral) Gland 7-10%

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21
Q

17) What is the lining epithelium of the Vas deferens (Ductus deferens) and Epididymis?

A
  • Epididymis: Lined w/ Ciliated Pseudo-stratified Columnar Epithelium & walls contain smooth muscle
  • Vas Deferens: lined by Pseudo-stratified Epithelium w/ a heavy coat of 3 muscle layers that propel sperm towards urethra by peristalsis
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22
Q

18) What is the definition of cryptorchidism and what is the most common malignant and nonmalignant complications?

A
  • A congenital malpositioning of the testes outside of their nomal scrotal location-it is the MOST important of the congenital abnormalities.
  • The descent of the testes may be arrested at any point from the abdomen to the upper scrotum.
  • Mostly commonly unilateral, one quarter it is bilateral, and the cause for the maldescent is unknown.
  • Adult men with untreated bilateral cryptorchidism are ***INFERTILE, but orchiopexy before the age of 2 years generally prevents this complication
  • The RISK of developing germ cell tumors in untreated Crytorchidism, most commonly ***Seminomas and Embryonal Carcinomas (BOTH malignant), is increased 10-35 times.
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23
Q

19) When do the testes descend down into the scrotum. At what week?

A

-Fetal testes are originally located in the abdominal cavity

-During intrauterine life- the testes slowly descend towards the inguinal canal and
through it, reaching the scrotum by “33 weeks “

-They lie in the pelvic cavity and at about 2 months prior to birth they descend into the scrotum

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24
Q

20) What testicular tumor is commonly seen in Crytorchidism?

A
  • The risk of developing germ cell tumors in untreated cryptorchidism, most commonly Seminomas and Embryonal Carcinomas, is increased 10-35 times
  • Germ cell tumors aren’t reported in patients who had an orchiopexy before age 5 – it’s crucial to treat this disorder early
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25
Q

21) What are the general features of Klinefelter’s syndrome?
- What is the karyotype and some of the clinical features of

A
  • Male HYPOGONADISM (one of the most common causes) Occurs when there are 2 or more X chromosomes & 1 or more Y chromosome = XXY
  • 1 in 850 live male births.
  • Rarely diagnosed before puberty b/c testicular abnormality does not develop until early teens
  • Eunuchoid body habitus w/ long legs, creates appearance of elongated body w/ small atrophic testes, a small penis, & lack of secondary sex characteristics (deep voice, beard voice & male distribution of pubic hair.

-The HYPOGONADISM is MOST consistent finding.
Plasma FSH levels consistently ELEVATED & TESTOSTERONE levels REDUCED.

  • The pathology relates to reduced spermatogenesis & infertility. Testicular tubules are totally atrophied, & replaced by pink, hyaline, collagenous.
  • The leydig cells appear larger, owing to the diffuse atrophy of the tubules.
  • The classic pattern is associated with a 47 XXY karyotype, & comprises 85% of cases. Pattern results from both maternal & paternal nondisjunction (about 50/50) during meiotic division.

***ALL other NON-DISJUNCTIONAL Conditions are a result of MATERNAL never paternal.

26
Q

22) What is the definition of a hydrocele vs spermatocele? Know general characteristics of both

A

-Hydrocele: (MOST COMMON) Collection of serous fluid in the scrotal sac between the 2 layers of the tunica vaginalis.

  • It is a benign condition that disappears when underlying disease has been eliminated.
  • Long-standing hydroceles may cause testicular atrophy or compression of epididymis.

-Diagnosis is made either by ultrasound or transillumination of the fluid in scrotum, w/ the opaque testis outlined within the fluid-filled space.

Congenital- Most common cause of scrotal swelling in infants & is often associated w/ an inguinal hernia. 

Acquired- Occurs in adults & in secondary to some other disease affecting scrotum, as an infection, tumor, or trauma. Cause of fluid accumulation unknown.
27
Q

22) What is the definition of a hydrocele vs spermatocele? Know general characteristics of both

A

Spermatocele:

  • A cystic mass formed from protrusions of widened efferent ducts of the epididymis or rete testis.
    - Manifests as a paratesticular nodule or soft mass filled w/ milky fluid
    - Histologically, cyst is lined by cuboidal epithelium that contains spermatozoa in various stages of development.
28
Q

23) What is the most common etiology of torsion of the testes? (Where the testes become dead and black devoid of oxygen)

A

Torsion of the spermatic cord, if complete, produces severe pain and infarction of the testicular germ cells within a few hours.

MOST commonly presents shortly after “vigorous physical exercise”
-An abrupt onset of scrotal pain followed by swelling heralds the diagnosis. The swollen, firm testis shows both gross and microscopic features of hemorrhagic infarction

29
Q

24) What type of cancer is cancer of the penis and what are the risk factors for carcinoma of penis?

A
  • Squamous Cell Carcinoma of the Penis presents as an ULCERATED and HEMORRHAGIC MASS on the glans or prepuce.
  • It may be ulcerated or exophytic-fungating grossly.
  • Microscopically, well-differentiated, focally keratinizing, squamous cell carcinomas, that may or may not be invasive into dermis.
  • Spread locally to inguinal & iliac lymph nodes before spreading rarely to distant organs
  • Risk Factors*
    1. Middle or Older-aged men over 60yrs”
    2. Uncircumcised men”
    3. Smegma (product of penile coronal glands desquamated cells & keratin debris)
  • Material accumulates under prepuce, & plays role as a prolonged contact carcinogen for mucosal cells.
    4. “HPV” types 16 and 18 factors for pathogenesis.
30
Q

25) What is the most common male condition of the male reproductive system related to a herpes infection?

A

CMV- cytopathic effect on cells which becomes multinucleate giant cells with intranuclear inclusion cells will be BLUE

HSV-2- intranuclear inclusions have RED color

31
Q

26) What is peyronie’s disease and know characteristics about it (coat hanger weiner)

A

-A malady of unknown etiology, characterized by focal, asymmetric, fibrous induration of penis shaft resulting in curvature & pain during erection

  • Presents as an ill-defined fibrous nodule in a young or middle-aged male without any change in the overlying skin
  • Dense dermal fibrosis w/ a non-specific chronic inflammatory infiltrate & collagen slowly replaces muscles
  • Is a Chronic Inflammation of the Tunica Albuginea (CITA)
32
Q

27) What are the characteristics of primary syphilis as a sexually transmitted disease

A

Primary -> At the site of inoculation, the spirochetes multiply and a local, non-tender ulcer called a Chancre usually forms in 2-10 weeks
The ulcer heals spontaneously but spirochetes spread widely in tissues and 1-3 months later…

33
Q

27) What are the characteristics of secondary/tertiary syphilis as a sexually transmitted disease

A

SECONDARY -> Maculopapular rash, on palms & soles, or as moist papules on the skin & mucous membranes. Moist lesions on genitals are called “condylomata lata” (ONLY SEEN in SECONDARY)

  • Resulting in meningitis, nephritis or a hepatitis, organ lesions rich w/ spirochetes & highly infectious. Will spontaneously heal
  • Also lymphadenopathy, arthritis, & fever

TERTIARY syphilis -> occurs years after initial infection & most frequently involves AORTA (80-85%) w/ aneurysm formation or aortic regurgitation.

-Involves CNS (5-10%) resulting in Neurosyphilis, from a chronic meningitis to TABES DORSALIS (spirochetal damage to sens. nerves of dorsal root= ataxia, NO pain sensation & deep tendon reflex)

  • General Paresis caused by invasion of BRAIN by spirochetes & manifested by loss of physical & mental functions w/ mood alterations, terminating in severe DEMENTIA
  • May also show granulomas called GUMMAS in skin, bones, & liver ( grossly are gray-white & rubbery that heal by scarring)
34
Q

28) What are general characteristics of Gonorrhea and the difference between MALE and female

A

aka: Gonococcus (GC)
Causes 3rd most common STD (behind venereal warts & Chlamydia)
(only in humans)

-Symptomatic in MALES & Asymptomatic in FEMALES

-Infections of anorectal area & pharynx act as sources of infection
-Virulence factors:
Pili - allows adherence to host cells & prevents phagocytosis
IgA Protease - hydrolyzes host secretory IgA

Gonococcal Disease in Men
-Organism penetrates mucous membranes of the urethra causing inflammation (urethritis)
Some will be asymptomatic, but most will complain of painful urination w/ PURULENT urethral DISCHARGE
-BOTH types can PASS infection to another sexual partner

***Complications include: epididymitis, prostatitis, & urethral strictures

35
Q

28) What is Gonorrhea and the difference between male and FEMALE

A

Gonococcal Disease in Women
Like men, women develop a GC urethritis w/ painful burning on urination & purulent discharge from urethra

Urethritis is ASYMPTOMATIC w/ minimal urethral discharge
Infects columnar epithelium of cervix → becomes reddened & friable w/ a purulent exudate
-Asymptomatic & symptomatic women can transmit the infection

  • Symptomatic women complain of:
    1. lower abdominal discomfort
    2. pain w/ sexual intercourse (dyspareunia)
    3. purulent vaginal discharge

GC infection of cervix can progress to PID, an infection of uterus (endometritis), fallopian tubes (salpingitis), and/or ovaries (oophoritis)
Chlamydia trachomatis is other major cause of PID

36
Q

29) General characteristics of trichomonad vaginalis in both males and females

A
  • Sexually transmitted protozoan
    -Found in female vagina & male urethra
    -Pear-shaped organism w/ a central nucleus & 4 anterior flagella
    **Exists only as a trophozoite w/ no cyst form
    -MOST common infections worldwide
    25-50% of women in U.S can harbor organism
    -Frequency of symptomatic disease is highest among sexually active women & lowest in postmenopausal women

CAUSES: watery, foul-smelling greenish discharge w/ itching & burning
Infection in MEN ASYMPTOMATIC, but 10% have a urethritis

***Diagnosis is by WET MOUNT prep of vaginal/prostatic secretions for moving trophozoites

37
Q

30) What is HSV1 and is there cross reactivity? -What is the other name for HSV1?

A

HSV-1 = Herpes Simplex Virus Type 1

-causes: Herpes Labialis (fever blisters/cold sores), keratitis, encephalitis
transmission is by saliva or direct contact w/ the virus from vesicles
initial vesicular lesions occur in the mouth and on the face– virus then travels up the axon and becomes latent in sensory (trigeminal) ganglia
recurrence occurs when induced by fever, sunlight, stress, ect.

-HSV-1 can also cause a genital herpes

38
Q

30) What is HSV2 and the cross reactivity?

A

HSV-2 = Herpes Simplex Virus Type 2
Antigenically distinct from HSV-1

-CAUSES: Herpes Genitalis, oral/skin/eye disease, aseptic meningitis and a congential infection (TORCH) that is acquired during passage through an infected birth canal
it is sexually transmitted

  • Yes, there is cross-reactivity and HSV-1 can cause gentital herpes & HSV-2 can cause cold sores.
  • Diagnosed by the Tzanck smear
39
Q

31) What is the Tzanck smear used for?

A

-Test for presence of Chickenpox(VZV) or herpes simplex
brings out characteristic changes of herpes & what it does either to corners of mouth or on vulva, vagina, shaft of penis
-Take scrapings from area, put on slide, Tzanck stain, used for molding of nuclei w/ characteristic intranuclear inclusions

-Positive result only indicates presence of herpes simplex (which causes fever blisters) or herpes zoster (which causes chickenpox & shingles), but does not distinguish between the two.

40
Q

32) What is the ovarian homologue to seminoma?

A

Dysgerminoma:

-tumor is large, firm w/ a fleshy cut surface
it is an uncommon tumor, but makes up ½ of all malignant germ cell tumors
treatment is surgical

-Occurs in CHILDHOOD

-ALL are malignant, but only ⅓ are aggressive
highly RADIOSENSITIVE like Seminomas

41
Q

33) What are general characteristics of seminoma since it is the most common testicular tumor. Are there tumor markers associated?

A
  • Stromal invasion of germ cells that gives rise to undifferentiated germ cell tumor

-Present as firm intratesticular poorly demarcated mass, bulges from cut surface of testes
ENTIRE testes replaced by tumor; Yellow-white w/ rare focal areas of hemorrhage & necrosis
display solid nests of proliferating tumor cells btwn fibrovascular trabeculae & lymphocytes
Cells have well-defined borders w/ glycogen rich clear cytoplasm & normal appearing nuclei w/ coarse granular chromatin
½ of all germ cell tumors

-Most common ages 25 to 55 (not seen before puberty)
90% are “classic” type
Rare types: anaplastic & spermatocytic seminomas
Sensitive to radiation (85-95% 5 yr survival rate)
Chemo can be curative (90%)
Cryptorchidism increased risk of developing seminomas 10-35x

***No serological tumor markers

42
Q

34) What tumor marker does the yolk sac tumor of infancy produce? (same as endodermal sinus tumor)

A

AFP- alpha fetoprotein

43
Q

35) Differentiate the severity of seminoma carcinoma

A

Seminoma (more benign):

Most common testicular tumor
Accounts for half of all germ cell tumors.

  • The tumor is not found before puberty & most patients are between ages of 25 & 55
  • 90% of ALL seminomas are classic type, w/ anaplastic & spermatocytic seminomas presenting as much rare variants.
  • Presents as a firm intratesticular poorly demarcated mass, bulges from cut surface of testes
  • Sensitive to radiation treatment
44
Q

35) Differentiate the severity of embryonal carcinoma

A

-Second most common germ cell tumor, accounting for 15-35% of these neoplasms

  • DON’T occur before puberty, & found between ages of 20 & 35
  • More AGGRESSIVE & lethal than Seminomas

-Grossly tumor is SMALL, & does replace entire testis. On sectioning, it’s gray-white, poorly demarcated, & bulging, w/ varying degrees of hemorrhage & necrosis

45
Q

36) What tissues can be found in testicular teratoma? (teratoma is homologous to dermoid cyst of ovaries)

A
  • Germ cell tumors characterized by tissue from ALL 3 germ layers
  • Comprise almost half of germ cell tumors in infants & children but less than 5% of tumors in adults.

-Classified as:
Mature Teratomas
Immature Teratomas
Malignant Teratomas

-The most important predictor of the biological behavior of a testicular teratomas is the age of the patient:
Adults: malignancy
Children/infants: benign

46
Q

37) What are the two hormone producing tumors of the testes

A
  • Leydig Cell Tumor (Interstitial Cell Tumor): androgens, estrogens or both
  • Sertoli Cell Tumor: Androgens and estrogens or both

TUMOR MARKERS:
1. Embryonal Carcinomas: Beta-HCG and AFP

  1. Yolk Sac Tumor: AFP
  2. Choriocarcinoma: HCG
  3. Leydig cell tumors: Androgens, estrogens, or both
  4. Sertoli cell tumor: Androgens, estrogens, or both
47
Q

38) What are the general features about testicular choriocarcinoma (same one that is in ovary, endometrium and seen after hydatidiform mole)

A
  • Highly malignant testicular tumor, represents germ cell extraembryonic differentiation to components of placenta namely, cyto & syncytiotrophoblast
  • Causes NO testicular enlargement & detected ONLY as small painless nodule
  • Cut surface contains marked hemorrhage & necrosis
  • Microscopically, trophoblastic tissues found in areas of hemorrhage

-syncytiotrophoblasts are large multinucleated giant cells w/ abundant vacuolated cytoplasm, ( contains HCG).
Cytotrophoblasts are polygonal cells, with round, hyperchromatic nuclei and sparse cytoplasm

-Pure tumors are rare and this is mostly observed as a component of a mixed germ cell tumor

48
Q

39) What cancer represents the most common urinary tract neoplasm?

A

Bladder cancer (transitional cell)

  • 52,000 new cases each year in the US and 10,000 deaths
  • Peak incidence in men ages 60-80 (rare under 50)
  • 2x more common than renal cell cancer but same amount of deaths
49
Q

40) What parasite is involved in causing bladder cancer that is endemic to Egypt?

A

In Egypt, Schistosoma haematobium (parasite) can lead to cancer of the urinary bladder

  • lays eggs inside of urinary bladder wall
  • causes squamous cell carcinoma
50
Q

41) Differentiate the different tumor markers in prostate cancer.
What is PSA?
-What does the tumor release?
-What is PSA used for?

A

PSA: Prostate Specific Antigen
-Both malignant & normal prostatic cells express specific antigen called Prostate Specific Antigen (PSA).

  • Tumor cells release this antigen into circulation, & detected immunochemically in blood (& tissue) of patients w/ prostatic cancer. A positive result should be interpreted in context of other clinical findings.
  • Can PSA be used as a tumor marker? Detectable levels after prostatectomy suggest persistent local or metastatic disease.

“If the serum PSA is elevated, diagnosis is confirmed by needle biopsies of prostate, usually done transrectally.
PSA levels in the serum usually correlate w/ the CANCER VOLUME”

51
Q

41) Differentiate the different tumor markers in prostate cancer. What is Bone alkaline phosphatase?

A
  • Alkaline Phosphatase is another blood enzyme, in contrast to PAP & PSA, it’s NOT expressed or produced by prostatic cells, but is abundant in Osteoblasts.
  • When prostatic carcinoma cells mets to bone & evoke an osteoblastic rx., the proliferation of osteoblasts results in an increase in Alkaline Phosphatase in blood
52
Q

42) What type of cancer is prostate cancer (adenocarcinom

A

-98% adenocarcinomas
multicentric lesions located in peripheral zones of prostate (posterior lobe)

-Limited to glands bound by BM but can later give rise to cellocally invasive lesions into surrounding fibromuscular stroma & seminal vesicles

-Perineural invasion common
spreads to lymph → pelvic → iliac → retroperitoneal lymph nodes

53
Q

43) What is BPH? Who is more likely to get BPH? What is the theory or pathophysiology of BPH and does it progress to cancer (no)

-

A
  • BPH: (Benign Prostatic Hyperplasia) Nodular Hyperplasia of the Prostate
  • What is it? Common, reactive, benign hyperplastic lesion that may obstruct flow of urine, related to male hormonal changes (occurs w/ AGING)

Most likely to get it: Western European & US people, higher prevalence in US Blacks, peaks at age 70 (RARE if younger than 40)

-Pathophysiology theory: NOT fully understood. Proposed theories invoke a hormonal mechanism, implying testosterone plays a crucial role. Development of prostate at puberty occurs ONLY in presence of male sex hormones

**Does NOT progress to cancer

54
Q

44) What does a TURP stand for and why is it done to males that can’t pee anymore?

A

TURP = Transurethral Resection of the Prostate

-Done as tx w/ Nodular Hyperplasia (BPH) obstructive uropathy

  • Increased pressure of urine in bladder, reflux of urine into ureters, dilation of ureters (hydroureters), dilation of renal collecting system
  • Hydronephrosis–> end-stage RENAL Disease
  • Essentially creates new urethra opening
  • use electrocautery & stent
55
Q

45) Which ethnic group has highest incidence of BPH vs prostate cancer?

A

BPH: MOST frequent in Western Europe & U.S (least common in Orient)
-Higher prevalence in U.S. blacks
disease peaks around age 70, rare younger than 40

PROSTATE cancer:
MOST common cancer in men
3rd most common cause of cancer related to death in males
tumor of older men (60-80 yo)

-HIGH frequency in US & Scandinavian countries (low in Mexico, Japan, Greece)
higher rates in U.S blacks (2x more than whites)

-Familial risk: increased risk in persons whose 1st degree relatives affected

  • INCREASED risk w/ high dietary fat consumption
  • Green/yellow vegetables DECREASED RISK
  • Increased risk w/ exposure to Cadmium, rubble, textiles
56
Q

46) What are general characteristics about the prostate gland (a question about the normal make up)

A
  • Doughnut-shaped gland, inferior to urinary bladder, surrounds upper urethra
  • Size of chestnut
  • Secretes alkaline fluid (makes up 13-33% of semen)
  • Has 30 to 50 individual compound tubuloalveolar glands
  • Each gland has a duct, delivers secretory product to prostatic urethra
  • Development of prostate at puberty occurs only in presence of male sex hormones
  • Come from urethral epithelium (urogenital sinus), distal to the neck of the bladder
  • “Transitional epithelium”
  • Prostate is homologous to female Skeen’s gland
  • Prostate glands lined by simple to pseudostratified columnar epi.

-Lumen of glands house round to oval prostatic concentrations (corpora amylacea) composed of calcified glycoproteins

57
Q

47) What is difference between acute & chronic prostatitis

  • What organisms are involved in each?
  • Which organism is more likely to cause granulomatous prostatitis with granulomas?
A
  • Definition: inflammation of prostate gland
  • Causes: Gram negative uropathogens, E. coli, Chlamydia, Mycoplasma, Trichomonas

–Mycobacterium Tuberculosis & Histoplasma capsulatum BOTH produce GRANULOMAS

Acute:
S/S: intense discomfort w/ urination, fever, chills, perineal pain
Causes: Gram negative bacteria, E. coli, previous UTI b/c reflux of infected urine into prostate
Dx: urine culture, presence of PMNs
Tx: antibiotics

Chronic:
S/S: suprapubic, perineal & low back pain, dysuria, nocturia
Causes: preceded by episodes of acute prostatitis
Dx: urine contains bacteria, lymphocytes, plasma cells & macrophages seen
Tx: prolonged antibiotic therapy

**Granulomatous prostatitis caused by Mycobacterium tuberculosis and Histoplasma capsulatum

58
Q

48) What is the gleason score? What is a good vs bad score in prognosis of patient with adenocarcinoma of the prostate? (two questions on it)

A

-Classification of prostate cancers based on five histologic patterns of tumor gland formation & infiltration, used in prognosis

2 scores given: MOST PROMIENT & MINORITY pattern

-Numbered 1 to 5: 1 = best/well differentiated, 5 = poorest differentiated

  • Gleason score is the sum of the grades
  • *Best differentiated tumors have score 2
  • *Poorly differentiated cancers have score 10
  • *Most prostate cancers have Gleason scores between 4 and 7
59
Q

49) Give general characteristics of tumor marker PSA

A

PSA = Prostate Specific Antigen
marker for prostate cancer

  • Exhibited by BOTH malignant & normal prostatic cells
  • Tumor cells release antigen into serum (& tissue)
  • PSA levels correlate w/ cancer volume
  • PSA levels after prostatectomy suggest persistent local & metastatic disease
  • PSA levels in blood should be 0 in non cancerous men
60
Q

–Acute prostatis has _________ whereas Chronic prostatitis has_________

A
  • Neutrophils

- Macrophages, plasma cells, and lymphocytes