Vol. 24, No.
2 February 2002
CE Article #1 (1.5 contact hours)
Refereed Peer Review
KEY FACTS
■ Benign prostatic hyperplasia
(BPH) is a spontaneous,
age-related condition that
affects 95% of intact male
dogs by 9 years of age.
■ Treatment of BPH with
antiandrogens has clinical
application in stud dogs.
■ Prostatic malignancy is
uncommon.
99
Comments? Questions?
Email: compendium@medimedia.com
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Noninfectious Prostatic
Diseases in Dogs
National University of La Plata, Argentina
Cristina Gobello, DVM
Yanina Corrada, MV
ABSTRACT: The prostate—the only accessory gland of the genital tract in dogs—is under
androgenic control. Common canine prostatic disorders include benign prostatic hyperplasia
(BPH), prostatitis, cysts, and adenocarcinoma. BPH is a common age-related condition that
occurs in 95% of male dogs by 9 years of age. The exact pathogenesis of canine BPH is not
completely understood, although it is known that dihydrotestosterone is the key factor in stim-
ulating prostate growth. Clinical signs of BPH include sanguineous preputial discharge, consti-
pation, and tenesmus. Clinical signs respond to castration or to antiandrogenic treatment
(e.g., finasteride), which inhibits conversion of testosterone to dihydrotestosterone (resulting
in prostatic involution). A number of studies in stud dogs have demonstrated that certain
antiandrogens may have clinical application without producing clinically adverse effects or
changes in semen quality and fertility. Ultrasonography-guided biopsy facilitates the diagnosis.
Prostatic adenocarcinoma is often difficult to diagnose in the early stages and is even more
difficult to manage. Neither prostatectomy nor castration has been found to improve the qual-
ity of life or to effectively cure the disease. Serum and seminal markers have enhanced the
early, noninvasive diagnosis of prostatic diseases, although further research is necessary to
define their exact role in different disorders.
T
he prostate—the only accessory sex gland in the intact male dog—is an
androgen-dependent, ovoid-shaped, bilobed gland composed of glandu-
lar and stromal elements that encircle the urethra caudal to the neck of
the urinary bladder.1 With increasing volume (as in older dogs), the prostate
tends to move farther into the abdomen; in young dogs and those castrated at an
early age, it resides within the pelvic inlet.2 The prostate contributes fluid to the
first and third fractions of the canine ejaculate.3
Prostate disorders (i.e., benign prostatic hyperplasia [BPH], prostatitis, cysts,
squamous metaplasia, neoplasia, and their combinations) are common in male
dogs. Many therapies are available for the different diseases; therefore, a specific
diagnosis is essential for proper therapy and prognosis.4 This article briefly
reviews noninfectious diseases of the canine prostate gland.
BENIGN PROSTATIC HYPERPLASIA
BPH—the most common disease of the canine prostate—is a spontaneous,
age-related condition in intact male dogs. BPH increases with frequency almost
linearly with age; close to 95% of dogs are affected by 9 years of age.5 BPH
affects the prostate diffusely and causes it to expand dorsally.6 The disease begins
100 Small Animal/Exotics
as glandular hyperplasia in dogs as young as 2.5 years of
age. Dogs older than 4 years of age with BPH tend to
become cystic (cystic hyperplasia) as multiple small
cysts form in the parenchyma.7 BPH occurs in two
phases: glandular and complex. In dogs younger than 5
years of age, BPH is primarily glandular (i.e., mainly
epithelial). In older dogs, the complex form, in which
hyperplasia and areas of atrophic epithelium are pres-
ent, is typically observed.8
Pathogenesis
BPH develops in males with intact testes and is age
related. Its exact pathogenesis is not completely under-
stood. Dihydrotestosterone (DHT), which is irre-
versibly converted from testosterone (T2) by the action
of 5 α -reductase within prostatic epithelial cells, is
accepted as a key hormone in stimulating enlargement
of the canine prostate by enhancing growth in both
stromal and glandular components.9 Dogs experience a
moderate decline in circulating T2 and DHT concen-
trations throughout adult life, while serum estradiol
remains unchanged with age.10,11 Thus the growth of
the prostate with advancing age takes place while there
is a decline in the ratio of circulating androgen to estra-
diol. The role of estrogen in BPH has recently been rec-
ognized.12,13 Estrogens induce nuclear DHT receptors
and thus may increase the sensitivity of the prostate to
DHT. As dogs age, DHT14,15 concentration and recep-
tors increase in prostatic tissue.
There are indications that pituitary hormones may
also affect the development of BPH. Prolactin has been
shown to regulate differentiation and proliferation of
rat and human prostate epithelium,16–18 and prostate
enlargement was observed in young human patients
with untreated acromegaly.19 Growth hormone may
stimulate prostate enlargement through a direct interac-
tion with growth hormone receptors or enhanced
plasma insulin-like growth factor–1 concentrations.20,21
Clinical Signs and Diagnosis
Most cases of BPH are not associated with clinical
signs. Intermittent, hemorrhagic or clear to light yel-
low urethral discharge and intermittent or persistent
hematuria occur in some dogs. Although blood is fre-
quently observed in semen samples and the volume of
ejaculate is decreased,10 total sperm count and fertility
are not affected by BPH. It is only when the prostate
becomes large enough to compress the colon and
interferes with defecation that serious effects result and
rectal tenesmus and constipation may be present.22
Occasionally, ribbonlike stools are observed if the
enlarged prostate compresses the rectum. Although
urethral obstructive disease occurs in men with BPH,
Compendium February 2002
it is extremely rare in dogs.23 The most common com-
plication of BPH in dogs is secondary bacterial infec-
tion of the gland, leading to prostatitis.7 Perineal her-
nias are less common complications.
Diagnosis of BPH is based on the presence of typical
clinical signs and on detecting a uniform prostatic
enlargement by palpation, radiography, and/or ultra-
sonography. The caudal/dorsal aspect of the prostate in
most dogs can be palpated via the rectum, although the
position of the prostate in the caudal abdomen depends
on bladder distention, age, and disease.2 On digital rec-
tal palpation, the hypertrophied prostate is found to be
enlarged but symmetric, soft with a smooth contour,
movable, and painless. Prostatic volume in affected
dogs may be two to 6.5 times greater than that of nor-
mal dogs.24–28
Hematologic and serum biochemical findings are
unaffected by hyperplasia, while urinalysis and semen
samples may be normal or contain blood without
pyuria or bacteriuria. Samples for cytologic analysis and
culture can be obtained by ejaculation, prostatic mas-
sage, or aspiration biopsy. Prostatic massage is per-
formed by removing urine from the bladder, placing
the tip of a urinary catheter in the prostatic urethra
(using rectal palpation as a guide), gently massaging the
prostate via the rectum or abdomen for 1 to 2 minutes,
and aspirating material into the catheter.
The normal gland is not easily seen in survey radi-
ographs but can be identified using retrograde contrast
urethrocystography with bladder distention.29 Hyper-
plastic prostates are usually visible on survey abdominal
radiographs as mild to moderate prostatic enlargements
with dorsal displacement of the colon and cranial dis-
placement of the bladder. The prostate is considered
enlarged when the prostatic diameter, as visualized on
the lateral radiographic view, is greater than 70% of the
distance between the sacral promontory and the pubis.30
Ultrasonography allows for assessment of prostatic
contour as well as parenchymal tissue. Ultrasonography
usually shows an enlarged, uniformly isoechoic to hyper-
echoic prostate4 with occasional small areas of decreased
echogenicity if cystic hyperplasia is present.7 Cavity areas
are typically well defined and smoothly marginated.
Definitive diagnosis is based on histopathologic find-
ings, although collection of prostatic cells by transrectal
fine-needle aspiration, with or without ultrasonogra-
phy-guided placement, has also proved to be a success-
ful and simple method of diagnosis. Depending on the
location of the gland and prostatic size, transabdominal
aspiration is also possible. Needle aspiration should be
avoided in dogs with abscessation since large numbers
of bacteria may be seeded along the needle tract. Com-
plications of aspiration are rare; occasionally, mild tran-
Compendium February 2002
sient hematuria occurs. 7 Needle core biopsy of the
prostate can also be performed by transabdominal
approach. Histologic evidence of mild chronic intersti-
tial inflammation is common in BPH.7 The principal
diagnostic differentials are chronic prostatitis and squa-
mous metaplasia.
Treatment
Treatment of BPH is required only if related abnor-
mal signs are present. The objective of treatment is to
decrease prostatic size, which alleviates related signs.
The most effective and standard treatment is
castration.31 Canine prostatic size decreases by 50%
within 3 weeks of castration and by 70% within 9
weeks.31 Castration is not appropriate for dogs required
for breeding. Furthermore, castration is sometimes
refused by owners and some older dogs may be at a
high risk for surgical complications.
Various medical treatments are available for BPH,
but none is currently recognized to be as effective as
castration. The primary use of drugs is to maintain
breeding soundness for short periods and to lessen pros-
tatic size if obstructive disease exists. Several agents may
be antiandrogenic, and each has a different mechanism
of action. Relapses occur after cessation of therapy in
all cases.
Noninfectious Prostatic Diseases 101
Diethylstilbestrol (0.2 to 1.0 mg PO every 2 to 3
days for 3 to 4 weeks) was reported to be an effective
treatment for BPH in dogs. 6,7 Potential side effects
include bone marrow suppression, pancytopenia, and
squamous metaplasia of the prostate with ductal
obstruction and cyst formation.
Progestins may be potent antiandrogenics that
induce a negative feedback effect, inhibit pituitary
gonadotropin secretion, and have a direct effect on the
prostate. Medroxyprogesterone acetate (3 mg/kg SC
given twice at 4-week intervals) has been used to treat
BPH by decreasing prostate size in 4 to 6 weeks with-
out adversely affecting semen quality or libido.32 It has
been shown that doses of medroxyprogesterone acetate
between 3.0 and 4.8 mg/kg SC did not affect semen
quality for 27 weeks after treatment, although there was
a reduction in serum T2 concentrations from weeks 5 to
13 after treatment.33 A similar study showed that nei-
ther megestrol acetate (2 mg/kg PO for 7 days) nor
medroxyprogesterone acetate (10 mg/kg SC) produced
a change in semen quality. However, 20 mg/kg of
medroxyprogesterone acetate produced a rapid and sig-
nificant decrease in spermatozoa motility, morphology,
and output. 34 Other progestins (e.g., cyproterone
acetate [1.25 to 2.5 mg/kg/day PO for 15 days],35 del-
madinone acetate [1 to 2 mg/kg SC every month],36
102 Small Animal/Exotics
chlormadinone acetate [2 mg/kg/day PO for 3 or 4
weeks]) are also indicated for the treatment of BPH.37
Although most of these studies have shown that
progestins are effective and do not have detrimental
reproductive effects when used at low doses, patients
should be monitored for diabetes mellitus and mam-
mary nodules when treatment is prolonged.32,38
Flutamide inhibits androgen uptake and/or nuclear
binding by binding to androgen receptors. 39 The
reported dose is 5 mg/kg/day PO.
Finasteride is a commercially available synthetic
steroid that inhibits type II 5α-reductase, which pre-
vents conversion of T2 into DHT.40 Beagles with BPH
that were treated with finasteride (1 mg/kg/day PO for
16 to 21 weeks) showed prostatic atrophy and a 50%
to 70% reduction in prostatic volume.25,40,41 This dose
of finasteride also decreased serum concentrations of
DHT with no adverse effect on testis histology or
semen quality. There was a decrease in the third frac-
tion of the ejaculate, but fertility was conserved (mat-
ings 20 to 22 weeks after treatment were fertile).41 A
dose–response study of finasteride at 0.1, 0.25, or 0.5
mg/kg/day PO for 7 days in three normal intact male
dogs showed significant decreases in serum concentra-
tions of DHT without changing serum concentrations
of T2; therefore, libido and spermatogenesis remained
normal. This study suggested that these lower doses
may be effective.28 In a recent study to determine the
effect of finasteride at 0.1 to 0.5 mg/kg/day PO in
nine client-owned dogs with spontaneous BPH, treat-
ment decreased prostatic diameter, volume, and serum
concentrations of DHT after 16 weeks. Finasteride
treatment caused a decrease in semen volume but had
no adverse effect on semen quality and no effect on
serum concentration of T2.28,42 Five of nine dogs in this
study were used to breed bitches. They had a normal
libido during copulation and were successfully bred to
bitches that became pregnant.42
Finasteride is indicated at a dose of 0.1 mg/kg/day
PO, and no adverse effects have been noted after pro-
longed treatment.43 Because finasteride does not act
quickly, 2 to 3 months of treatment may be required to
significantly decrease prostatic size. Finasteride can be
combined with a single dose of a long-acting progestin
at the beginning of the treatment.43
Tamoxifen is a synthetic nonsteroidal antiestrogenic
drug with both antagonist and agonist effects. 44 In
dogs, tamoxifen produces an estrogenic response. There
are insufficient data available about the efficacy of
tamoxifen in the treatment of canine BPH.
PROSTATIC CYSTS
Prostatic cysts may be associated with BPH and fluid
Compendium February 2002
retention caused by obstruction of canaliculi. Cysts are
cavitating lesions containing clear to turbid fluid within
(retention) or outside (paraprostatic) the prostatic
parenchyma.45 The remnant of the uterus masculinus
occasionally results in enlarged cysts that are associated
with the prostate by a stalk or adhesions.46 The cysts
can be extremely large and can be palpated from the
abdomen, usually displacing the bladder cranially and
ventrally. Affected dogs may be asymptomatic or may
develop signs referable to concurrent BPH or to physi-
cal displacement of abdominal viscera. Radiography
reveals a circular fluid density in the caudal abdomen,
and ultrasonography can be used to confirm the struc-
ture. Cysts can be secondarily infected; surgical excision
or omentectomy is the treatment of choice.7,47
SQUAMOUS METAPLASIA
Excessive serum estrogen concentrations cause the
epithelial cells of the prostate to undergo squamous
metaplasia and to decrease secretion of prostatic fluids.
The syndrome can occur as a result of exogenous estro-
gen administration or estrogen-secreting Sertoli cell
tumors. Clinical signs are minimal except for potential
hemorrhagic urethral discharge and a hyperestrogenic
skin pattern. Retention cysts may develop as a conse-
quence of the dilation of prostatic acini secondary to
estrogen-induced squamous metaplasia.46
Rectal palpation reveals an enlarged gland without
concomitant signs unless cysts are present.48 Cytology
of prostatic fluids reveals squamous epithelial cells and
possible hemorrhage. Preputial swabs can also show evi-
dence of estrogen-secreting tumors by revealing squa-
mous cells like those of a bitch in estrus.49 Biopsy con-
firms metaplasia, and treatment is focused on the
elimination of the estrogenic source (i.e., castration of
neoplastic testis or interruption of the exogenous estro-
gen administration). After removal of the estrogen
source, the prostate returns to normal.50
PROSTATIC NEOPLASIA
Prostatic malignancy is uncommon; adenocarcinoma
is the most common tumor followed by locally invasive
transitional cell carcinomas. Other prostatic tumors,
representing less than 10% of all neoplasms, include
adenomas, leiomyomas, fibromas, and sarcomas.51 Ade-
nocarcinomas most commonly appear in 8- to 10-year-
old dogs.52,53 The prevalence of adenocarcinoma in dogs
castrated at a young age is at least equal to (and may be
greater than) that in intact dogs. 53,54 Five histologic
grades of adenocarcinoma have been described, and
neutered dogs are most likely to have poorly differenti-
ated ones. Concomitant prostatic hyperplasia usually
occurs with adenocarcinoma in intact dogs.
Compendium February 2002
Clinical Signs and Diagnosis
Anorexia, weight loss, tenesmus, dyschezia, hema-
turia, stranguria, and rear limb weakness are common
signs in dogs with prostatic adenocarcinoma. 52 This
tumor has a great potential for secondary spread to
pelvic lymph nodes, lumbar vertebrae, pelvic bones,
and more distant sites. The initial clinical manifesta-
tions of malignancy include bone metastasis leading to
myelopathy, pain, neurologic deficits of the hind limbs,
and lameness. Rectal examination reveals an irregular,
indurated, immobile, asymmetric, enlarged prostate
that may be painful.46 The prostate may be so enlarged
that it may drop over the pelvic brim and create a pal-
pable mass in the caudal abdomen. It is important to
consider that the prostate gland should not be
detectable in castrated dogs, and the finding of a “nor-
mal prostate” is suggestive of malignancy.
In contrast to prostatic adenocarcinoma in men,
canine prostatic adenocarcinoma does not appear to be
androgen responsive as androgen deprivation has not
been beneficial in its management.55 Tumors do not
respond to hormonal therapy or commonly used cyto-
toxic drugs. Chemotherapy should be used only as a
last resort for diffuse metastatic disease.51 Conversely, a
study found that a high grade of prostate intraepithelial
neoplasia (PIN; a known precursor of human prostate
Noninfectious Prostatic Diseases 103
cancer) is frequently present in the prostates of elderly
intact dogs. Its appearance is influenced by testicular
androgens as it does not appear in castrated animals.56
Canine PIN is similar in its morphology and
immunophenotype to its human counterpart and is,
therefore, suggested to be a precursor to adenocarci-
noma in dogs as well.57
Radiographic findings in dogs with prostatic adeno-
carcinoma include prostatic enlargement and mineral-
ization, sublumbar lymphadenopathy, and lung and
appendicular skeletal metastasis. Ultrasonographic
appearance of the neoplastic canine prostate includes
prostatomegaly, mineralization of the parenchyma, pres-
ence of focal to diffuse hyperechoic areas, and an irregu-
lar/discontinuous prostatic contour.4,53,55 Exfoliative
cytology by transrectal or transabdominal aspiration or
needle core biopsy is a successful method for diagnosing
prostatic adenocarcinoma.55 Retrograde urethrocystogra-
phy reveals periurethral asymmetry as well as narrowing,
distortion, or destruction of the prostatic urethra.30
Treatment
Intact dogs may benefit from surgical or pharmaco-
logic castration as regression of the hyperplasic compo-
nent can result in relief. External beam radiation ther-
apy is reported to shrink some canine prostatic tumors
104 Small Animal/Exotics
with relief of urinary outflow obstruction and obstipa-
tion, but survival times remain short.55 Intraoperative
radiotherapy is also a promising new technique for
treating localized prostatic carcinoma, having low mor-
bidity and a 30% likelihood of tumor control.51 The
prognosis is grave. Total transurethral prostatectomy is
indicated for early-stage lesions; however, this proce-
dure is technically difficult and most dogs become
incontinent after surgery. Surgical resection is not rec-
ommended as the disease is not usually diagnosed at an
early stage.
PROSTATIC MARKERS
Canine prostate-specific arginine esterase (CPSE),
the major secretory product of the canine prostate that
constitutes more than 90% of canine seminal pro-
teins,58 is a known marker for canine prostatic secre-
tion, although its exact role in the various diseases of
the canine prostate is not yet completely understood.59
CPSE is present in similar concentrations in all frac-
tions of the split canine ejaculate.58–60 It is produced
under androgenic control and can be inhibited by
antiandrogen treatment or surgical castration. 61–63
(Unfortunately, a CPSE kit is not currently available in
the veterinary market.) In one study, serum CPSE was
elevated in dogs with BPH (mean concentration, 189.7
ng/ml; n = 25) compared with normal intact dogs
(mean concentration, 41.8 ng/ml; n = 20).64 Further-
more, CPSE ranged from 20 to 300 µg/ml in urine
samples of normal dogs, and dogs with acute (1000 to
2000 µg/ml) or necrotizing (5 to 10 µg/ml) prostatitis
could be differentiated.65
Serum concentrations of prostatic acid phosphatase
(AcP) and prostate-specific antigen (PSA) are tumor
markers routinely used to monitor recurrence of pros-
tatic carcinoma in men. Information about the useful-
ness of these markers in dogs is still controversial.
According to some studies, prostatic AcP does not seem
to be specific and PSA does not increase in dogs with
prostatic carcinoma.64,66 Although quite similar bio-
chemically to the human enzyme, canine prostatic AcP
is approximately 100 times less concentrated in prostatic
tissue and plasma than its counterpart in humans.67,68
In one study, serum and seminal plasma concentra-
tions or activities of AcP, PSA, and CPSE were meas-
ured in normal dogs, dogs with BPH, dogs with bacter-
ial prostatitis, and dogs with prostatic carcinoma to
determine whether these assays would be valuable in
differentiating dogs with prostatic carcinoma from nor-
mal dogs and those with other prostatic disorders.64
PSA was not detected in canine serum or seminal
plasma. Serum and seminal AcP activities did not differ
significantly between normal dogs and those with pros-
Compendium February 2002
tatic diseases or among dogs with different prostatic
disorders. However, serum CPSE activities were signifi-
cantly higher in dogs with BPH than in normal dogs;
mean serum activity in dogs with BPH, bacterial pros-
tatitis, and prostatic carcinoma did not differ signifi-
cantly.64 Canine prostatic adenocarcinoma does not
appear to be associated with significant increases in
CPSE, AcP, or PSA activities, possibly because of
down-regulation of these enzymes by prostatic carci-
noma cells.64,66 Conversely, another study concluded
that low serum total AcP and prostatic AcP do not rule
out prostatic adenocarcinoma but an elevated concen-
tration can be a useful criterion for diagnosing canine
prostatic cancer.69
DISCUSSION
Diagnosing each prostatic disease is difficult because
similar signs are observed in dogs with different types of
disease. The etiopathology of BPH, the most common
prostatic disease in dogs, appears to be associated with a
complex mechanism of hormonal imbalances that is not
completely understood. BPH is found in a few species
(e.g., humans, dogs, chimpanzees).68 Considerable infor-
mation about canine BPH has been learned because
dogs are the most practical and reliable model for study-
ing the disease in men.70 When interpreting reports,
however, anatomic, histologic, and pathologic differ-
ences between species should be considered. A complete
understanding of the hormonal background of BPH
will greatly improve treatment of this disorder. Although
it is known that signs of BPH respond to castration or
finasteride treatment, more information about 5 α-
reductase inhibitors is necessary before they can be
widely recommended for treating BPH.
Prostatic carcinoma in dogs is often difficult to diag-
nose in the early stages of the disease and is even more
difficult to manage after a diagnosis is made. A high
grade of PIN seems to be an intermediate stage
between benign epithelium and invasive carcinoma.
Neither prostatectomy nor castration has been found to
provide a good quality of life or effectively cure the dis-
ease. The lack of hormone dependency may be due to
the fact that most carcinomas are diagnosed as end-
stage cancer in dogs.
Ultrasonography provides an accurate, noninvasive,
diagnostic technique for evaluating the internal archi-
tecture of the different diseases of the prostate,
although definitive diagnosis should be based on histo-
logic findings.
Serum and seminal prostatic-specific markers could
enhance early noninvasive diagnosis of prostatic disease
and assessment of treatment response. 71 CPSE, the
major secretory product of the prostate, is regulated by
Compendium February 2002
T2 control and therefore may also serve as a functional
marker of the androgenic state and response to antian-
drogenic therapy.63 Results show that proteins of pros-
tatic origin appear in the serum of dogs as a result of
prostatic pathology, especially BPH. More studies are
needed to confirm the status of AcP as a marker of
prostatic cancer in dogs. Canine prostatic adenocarci-
noma does not appear to be associated with significant
increases in CPSE or AcP activities.
Although further research is necessary to define the
exact role of CPSE, it seems to be a promising diagnos-
tic tool for nonneoplastic canine prostatic disorders.
Future studies should also address the quantitative rela-
tionship among serum and prostatic androgen levels,
prostatic androgen-dependent problems, and how these
are affected by antiandrogen treatment.
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108 Small Animal/Exotics Compendium February 2002

ARTICLE #1 CE TEST

CE
The article you have read qualifies for 1.5 con-
tact hours of Continuing Education Credit from
the Auburn University College of Veterinary Med-
icine. Choose the best answer to each of the follow-
ing questions; then mark your answers on the
postage-paid envelope inserted in Compendium.

1. The prostate is physiologically ____________ organ.

a. an estrogen-dependent c. a progesterone-dependent
b. an androgen-dependent d. a hormone-independent

2. The most common prostatic disease is

a. squamous metaplasia. c. adenocarcinoma.
b. BPH. d. prostatic cysts.

3. As male dogs age,

a. estrogen and androgen tend to increase.
b. androgen tends to increase and estrogen tends to decrease.
c. androgen tends to decrease and estrogen tends to stay the same.
d. estrogen decreases and androgen remains the same.

4. A common sign of BPH is

a. dysuria. c. bloody prepuce discharge.
b. purulent prepuce discharge. d. hematochezia.

5. The best treatment for BPH is

a. estrogen. c. prostatectomy.
b. castration. d. detailed follow-up.

6. Finasteride is
a. an androgen-receptor blocker. c. a 5α-reductase inhibitor.
b. an antiestrogen. d. an aromatase inhibitor.

7. Squamous metaplasia is related to

a. excessive androgens. c. excessive estrogens.
b. exogenous progestins. d. diminished estrogens.

8. The most common prostatic neoplasia is

a. adenocarcinoma. c. adenoma.
b. transitional cell carcinoma. d. leiomyoma.

9. The major secretory product of the canine prostate is

a. CPSE. c. PSA.
b. prostatic AcP. d. alkaline phosphatase.

10. Definitive diagnosis of prostatic diseases is obtained by means of

a. radiography. c. exfoliative cytology.
b. ultrasonography. d. needle core biopsy.