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PATHOLOGY OF
THE MALE REPRODUCTIVE SYSTEM
BY
CHAPIMA F.
MSc. PTH - Clinical Pathology (UNZA), B.Sc. (UNZA)
Introduction
 Reproduction is the complex set of biological
processes that result in the formation of a new
organism.
 Pathologies and diseases of the reproductive
system are quite common and can not only lead
to sickness but also to a loss in production and
death.
Introduction…………………….
 In this lecture we will cover common Pathologies
and diseases of the male reproductive system.
 The male reproductive system comprises of the
penis, testis and the prostate grand.
Lecture outline
 Diseases of the penis
 Diseases of the testis and epididymis
 Prostate Disorders
DISEASES OF THE PENIS
Congenital Anomalies
Phimosis
 Phimosis is a condition in which the prepuce is
too small to allow normal retraction behind the
glans penis.
 It may be congenital or acquired.
Phimosis…………..
 Congenital phimosis
is a developmental
anomaly
 Acquired phimosis
may result from
inflammation or trauma
which results narrowing
of the prepuce.
Paraphimosis
 Paraphimosis is an abnormally
tight foreskin that is difficult or
impossible to retract back over
the glans penis.
 This condition may be
congenital or result from
inflammation or trauma.
Hypospadias
 Hypospadiasis is a
developmental defect of the
urethra in which the urethral
meatus fails to reach the
end of the penis, but
instead, opens on the
ventral surface of the penis.
Epispadias
 Epispadias is a congenital
anomaly in which the
urethral meatus opens on
the dorsal surface of the
penis.
 It is less common than
hypospadias.
Priapism
 Priapism is a persistent painful erection.
 Common in sickle cell disease and can be due to
penile trauma.
Peyronie's disease
 Peyronie's disease; these are
painful contractures of the
penis leading to lateral
curvature of the penis (in it’s
erect status)
 It makes sexual intercourse
difficult.
 Common in the middle aged
men.
 About 1% of men are affected.
Etiology
 Caused by scar tissue within the corpora
cavernosa.
 The cause of scar is unknown but research
suggests that the condition could have been due
to trauma such as bending or hitting to the
penis which causes bleeding in the corpora
cavernosa and subsequent scar tissue
formation.
Inflammatory disorders
Balanitis
 Balanitis is inflammation of
the glans penis.
 This condition is often
associated with poor hygiene,
allergies and STIs.
 It is rare in circumcised
individuals
NEOPLASMS
Benign tumours
Condyloma Acuminatum
 AKA anogenital warts are
benign tumours caused by
human papilloma virus
especially types 6 and 11.
Gross Morphology
 The tumour consists of
multiple growths of variable
size with exophytic growth
pattern.5/20/2016 14
Bowen’s Disease
 Bowen’s disease AKA
squamous cell carcinoma in
situ is a solitary, confined lesion
with ulceration located on the
shaft of the penis or the
scrotum.
 It is a premalignant lesions
Malignant tumours
Squamous Cell Carcinoma
 Overall incidence of penile cancer is less than
1% of all cancers in males in America.
 In some parts of Asia, Africa, and South
America, it ranges from 10% to 20%.
 More common in blacks than in whites (3-4
times more common than whites).
Squamous Cell Carcinoma………..
 Disease is rare in circumcised men.
 Predisposing factors include poor personal
hygiene and venereal disease
 Associated to high-risk HPV infection types
16, 18, 31, and 33.
 The greatest incidence of penile cancer occurs in
those between 45 and 60 years.
Gross Morphology
 The tumour is located, in
decreasing frequency, on
frenum, prepuce, glans and
coronal sulcus.
 The tumour may be
cauliflower-like and papillary,
or flat and ulcerating.
DISEASES OF THE TESTIS AND
EPIDIDYMIS
Introduction
 Diseases of testes and epididymis are common.
 In epididymis, the most frequent are
inflammatory diseases.
 In the testes, the major lesions are tumors.
Congenital Anomalies
Cryptorchidism
 This is a failure of the testicle to descended into
the scrotum.
 The testicle is arrested at some point along its
descent.
Etiology
 Mechanical factors e.g. short spermatic cord,
narrow inguinal canal, adhesions to the
peritoneum.
 Genetic factors e.g. trisomy 13,
maldevelopment of the scrotum.
 Hormonal factors e.g. deficient androgenic
secretions
Gross Morphology…………..
 Usually asymptomatic
 Cryptorchidism is unilateral
in 80% cases.
 The cryptorchid testicle is
small in size, firm and
fibrotic.
Complications
 Testicular atrophy
 Sterility-infertility
 Malignancy 30-50 times increased risk
Inflammatory conditions of the testis
Orchitis/ Epididymitis
 Orchitis is an inflammation of the testicle
secondary to infection.
 Commonly occurs with epididymitis.
 It may be acute or chronic.
Etiopathogenesis
 The most common pathogens is
 In boys younger than 14 years are E. coli and
mumps
 In men aged 14 - 35 years are Neisseria
gonorrhea and Chlamydia trachomatis.
 In men older than 35 years is E. coli and
Mycobacterium tuberculosis.
Etiopathogenesis …………
 The common routes of spread of infection are
 Via the vas deferens
 Via lymphatic and
 Hematogenous routes.
Signs and symptoms
 Gradual onset of scrotal
pain and swelling
 Usually located on 1 side
 Fever and chills (in 25% of
adults and 71% of children
with acute epididymitis)
 Urethral discharge preceding
the onset of acute
epididymitis (in some
cases).
Gross morphology
 In acute stage the testicle is firm, tense,
enlarged and congested.
 There may be multiple abscesses, especially in
gonorrheal infection.
Torsion of the spermatic cord
 It is the twisting of the spermatic cord leading
to cutting off the venous and the arterial blood
supply to the testicle.
 Common in boys and young men
Signs and symptoms
 Enlargement of the
testicle; edema involving
the entire scrotum
 Scrotal erythema
 Fever (uncommon
 Nausea or vomiting
 Pain duration of less than
24 hours
Morphologic features
 There may be coagulative
necrosis of the testis and
epididymis, or
 There may be hemorrhagic
infarction
 Twisting of the spermatic
cord
Other Conditions
Hydrocele
 Is an abnormal collection of serous fluid in the
tunica vaginalis.
 It may be congenital or acquired which can be
acute or chronic.
Pathophysiology
 Congenital: Embryologically, the processus
vaginalis is a diverticulum of the peritoneal
cavity.
 It descends with the testes into the scrotum via
the inguinal canal around the 28th week with
gradual closure through infancy and childhood.
Pathophysiology……………….
 In congenital hydrocele (communicating
hydrocele), a processus vaginalis does not close
completely permitting the flow of peritoneal fluid
into the scrotum leading to accumulation of fluid
in the tunica vaginalis.
 Noted in children between 1 – 2 years.
 Acquired hydrocele are usually late-onset
(secondary) noted in men above 40 years.
 It may be due to local injury, infections, and
radiotherapy
Signs and symptoms…………..
Hematocele
 Is an accumulation of blood
in the tunica vaginalis.
 It is most often caused by
trauma, although
occasionally can be due to a
malignant tumor of the
testis.
TESTICULAR TUMOURS
Introduction
 Testicular tumours are the cause of about 1% of
all cancer deaths in men.
They have trimodal age distribution
 The first peak is 0 – 10 years
 Another pick during late adolescence and early
adulthood 20 – 40 years – Maximum
 The third peak after 60 years of age.
Introduction …………
 99% of all tumours are malignant.
 Most testicular cancers (95%) are of germ cells
and are all malignant.
Risk factors
 Undescended testicle
 Family history, HIV infection, Age
 Race and ethnicity – whites 4-5 times affected
than blacks and 3 times than Asians
Most common types of testicular
cancers
Seminoma
 Seminoma is a malignant tumor.
 It is analogous to dysgerminoma – ovary tumor.
 It is the most frequently occurring tumor,
accounting for 40%.
 Peak incidence is in the mid-30s age group.
Presenting features
 Painless enlargement of the
testicle.
 It is associated with increased
serum human chorionic
gonadotropin (hCG) hormone.
Gross morphology
 The testis is uniformly enlarged
 The surface is smooth
 On cut section is uniform grey
white appearance
Embryonal carcinoma
 Embryonal carcinoma is a second most common
testicular tumor, accounting for 20%–30%.
Clinical features
 Painful enlargement of the testicle.
 The serum hCG is often increased.
 The prognosis is much poor than for seminoma.
Signs and symptoms…………..
Teratomas
 It is a germ cell tumor
derived from two or more
embryonic layers.
 It is mostly malignant.
 It contains multiple tissue
types, such as cartilage,
ciliated epithelium, liver cells,
embryonic gut, striated
muscle or hair.
PROSTATE DISORDERS
Introduction
 The most 3 important categories of prostate
disorders are;
 Inflammatory lesions (prostatitis)
 Nodular hyperplasia and
 Carcinoma.
Prostatitis
 Prostatitis is inflammation of the prostate
gland.
 It may be acute or chronic.
 It is due to;
 Ascension of bacteria from the urethra
 Descent of bacteria from the upper urinary
tract or bladder
 Lymphatic system or haematogenous
spread of bacteria from a distant focus of
infection.
Causative micro-organism
 The common ones are those which cause UTIs
 Most frequently E. coli,
 Others are Klebsiella, Proteus, Pseudomonas,
Enterobacter, Gonococci, Chlamydia
trachomatis, Staphylococci and Streptococci.
Clinical findings
 Fever, low back pain, perineal pain, dysuria
 Pain on digital rectal examination
Gross morphology
 The prostate is enlarged, swollen and tense.
 Cut section shows multiple abscesses and
pockets of focal necrosis.
Benign prostate hyperplasia (BPH)
 AKA as benign prostate hypertrophy, is a
histologic diagnosis characterized by
proliferation of the cellular elements of the
prostate.
Etiology/ Risk factors
 Even though the exact cause is unknown, a
number of risk factors have been identified:
Demographic factors:
 Age: The prevalence of BPH increases with age
 Race The risk of acquiring BPH is 47% higher
among black men
Genetic factors:
 Family - There is a three-fold increase in the
risk of BPH in twins
Etiology/ Risk factors…………….
 Vitamin D3 — vitamin D receptor regulates
both epithelial and cell growth proliferation.
 Cytochrome P45017 mediates sex steroid
hormone synthesis, which may influence BPH
risk
 5α-reductase enzyme converts testosterone
to dihydrotestosterone (DHT), which
promotes prostate cell proliferation.
Risk factors…………….
Behavioral factors:
 Obesity
 High intake of fats (animal fat) increases the
risk of BPH
Pathophysiology
 Prostatic enlargement depends on androgen
hormones [testosterone (most important) and
estrogen].
 In the prostate, 5-alpha-reductase
metabolizes the circulating testosterone into
DHT which works locally.
Pathophysiology…………….
 DHT binds to androgen receptors in the cell
nuclei to increase their mitotic activity (both
stroma and epithelial cells) leading to BPH.
 Balance between cellular proliferation and
apoptosis exists in patients with normal intra-
prostatic levels of androgen and estrogen.
 But DHT imbalance occurs with advancing age,
favoring prostatic epithelial and stromal cell
proliferation.
Signs and symptoms
 S/S are those related to the constriction and
obstruction of the flow of urine.
 Urine retention
 Urinary frequency
 Urinary urgency
 Hesitancy - Difficulty initiating the urinary
stream; interrupted, weak stream
Signs and symptoms………….
 Incomplete bladder emptying - The feeling
of persistent residual urine, regardless of the
frequency of urination.
 Straining - The need to strain or push to
initiate and maintain urination in order to more
fully evacuate the bladder
 Decreased force of stream - The subjective
loss of force of the urinary stream over time
Signs and symptoms………….
 Dribbling - The loss of small amounts of urine
due to a poor urinary stream.
Gross morphology
 The enlarged prostate is nodular, smooth
and firm and weighs 2-4 times than its
normal weight i.e. may weigh up to 40-80 gm.
 There is enlarged lateral lobes and median
lobe that obstructs the prostatic urethra.
Gross morphology…………..
Gross morphology…………..
 On cut section, (glandular
hyper) the tissue is yellow-
pink, soft, honey-combed,
and produces milky fluid
when squeezed.
Carcinoma of prostate
Introduction
 Cancer of the prostate is the second most
common form of cancer in males.
 It is a disease of men above the age of 50 years
and its prevalence increases with increasing age
 More than 50% of men aged 80 have
asymptomatic (latent) carcinoma of the
prostate.
Classifications
 Latent carcinoma: This is found
unexpectedly in the prostate during autopsy
studies in men dying of other causes.
 Incidence - 25-35%.
 Incidental carcinoma: About 15-20% of
prostatectomies done for BPH reveal incidental
carcinoma of the prostate.
Classifications………
 Occult carcinoma: the patient has no
symptoms of prostatic carcinoma but shows
evidence of metastases on clinical examination
and investigations.
 Clinical carcinoma: this type is detected by
rectal examination and other investigations and
confirmed by pathologic examination of biopsy
of the prostate.
Etiology
 The cause of prostatic cancer remains unknown.
 However, a few factors have been suspected.
 Endocrine factors; Androgens are considered
to be essential for the development and
maintenance of prostatic cancer.
 Racial and geographic influences; There are
some racial and geographic differences in the
incidence of prostate cancer.
Etiology…………….
 Environmental influences; These include high
dietary fat, and exposure to polycyclic aromatic
hydrocarbons.
 Heredity; It is observed in families and it is 2-
fold higher in first-degree relatives.
Etiology…………….
 Sexual factors: early sex and many sexual
partners.
 This correlation suggests a sexually
transmissible infections (STI) may cause some
prostate cancer cases e.g. HPV 16, 18 and HSV
2 – more studies are needed in this area.
Clinical features
 On rectal examination a hard and nodular
gland fixed to the surrounding tissues is felt.
 Urinary obstruction with dysuria and
increased frequency
 Hematuria
 In 10% of cases pain in the back due to
skeletal metastases.
Gross morphology
 The prostate may be enlarged, normal in size or
smaller than normal.
 The malignant prostate is firm and fibrous.
 Cut section is homogeneous and contains
irregular yellowish areas.
Gross morphology ………….
Metastasis
 It may spread by the following routes:
 Direct spread; Direct extension of the tumour
occurs into the prostatic capsule and beyond.
 Lymphatic and Hematogenous routes.
 Sites of spread includes the pelvis and the
lumbar spine, lungs, kidneys, breast and
brain.
References
 Robbins, S.L, Kumar, V and Abbas, K (2010). Pathologic
Basis of Disease (8th Edition). W.B Saunders Company,
Philadelphia.
 Robbins SL and Kumar V (2007). Basic Pathology (8th
Edition).WB Saunders Co. London.
 Harsh Mohan, (2010). Textbook of Pathology (6th Edition).
Jaypee brothers medical publishers (p) ltd, India
 Riede and Werner, Color Atlas of Pathology © 2004 Thieme

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Pathology of the male reproductive system 2

  • 1. PATHOLOGY OF THE MALE REPRODUCTIVE SYSTEM BY CHAPIMA F. MSc. PTH - Clinical Pathology (UNZA), B.Sc. (UNZA)
  • 2. Introduction  Reproduction is the complex set of biological processes that result in the formation of a new organism.  Pathologies and diseases of the reproductive system are quite common and can not only lead to sickness but also to a loss in production and death.
  • 3. Introduction…………………….  In this lecture we will cover common Pathologies and diseases of the male reproductive system.  The male reproductive system comprises of the penis, testis and the prostate grand.
  • 4. Lecture outline  Diseases of the penis  Diseases of the testis and epididymis  Prostate Disorders
  • 5. DISEASES OF THE PENIS Congenital Anomalies Phimosis  Phimosis is a condition in which the prepuce is too small to allow normal retraction behind the glans penis.  It may be congenital or acquired.
  • 6. Phimosis…………..  Congenital phimosis is a developmental anomaly  Acquired phimosis may result from inflammation or trauma which results narrowing of the prepuce.
  • 7. Paraphimosis  Paraphimosis is an abnormally tight foreskin that is difficult or impossible to retract back over the glans penis.  This condition may be congenital or result from inflammation or trauma.
  • 8. Hypospadias  Hypospadiasis is a developmental defect of the urethra in which the urethral meatus fails to reach the end of the penis, but instead, opens on the ventral surface of the penis.
  • 9. Epispadias  Epispadias is a congenital anomaly in which the urethral meatus opens on the dorsal surface of the penis.  It is less common than hypospadias.
  • 10. Priapism  Priapism is a persistent painful erection.  Common in sickle cell disease and can be due to penile trauma.
  • 11. Peyronie's disease  Peyronie's disease; these are painful contractures of the penis leading to lateral curvature of the penis (in it’s erect status)  It makes sexual intercourse difficult.  Common in the middle aged men.  About 1% of men are affected.
  • 12. Etiology  Caused by scar tissue within the corpora cavernosa.  The cause of scar is unknown but research suggests that the condition could have been due to trauma such as bending or hitting to the penis which causes bleeding in the corpora cavernosa and subsequent scar tissue formation.
  • 13. Inflammatory disorders Balanitis  Balanitis is inflammation of the glans penis.  This condition is often associated with poor hygiene, allergies and STIs.  It is rare in circumcised individuals
  • 14. NEOPLASMS Benign tumours Condyloma Acuminatum  AKA anogenital warts are benign tumours caused by human papilloma virus especially types 6 and 11. Gross Morphology  The tumour consists of multiple growths of variable size with exophytic growth pattern.5/20/2016 14
  • 15. Bowen’s Disease  Bowen’s disease AKA squamous cell carcinoma in situ is a solitary, confined lesion with ulceration located on the shaft of the penis or the scrotum.  It is a premalignant lesions
  • 16. Malignant tumours Squamous Cell Carcinoma  Overall incidence of penile cancer is less than 1% of all cancers in males in America.  In some parts of Asia, Africa, and South America, it ranges from 10% to 20%.  More common in blacks than in whites (3-4 times more common than whites).
  • 17. Squamous Cell Carcinoma………..  Disease is rare in circumcised men.  Predisposing factors include poor personal hygiene and venereal disease  Associated to high-risk HPV infection types 16, 18, 31, and 33.  The greatest incidence of penile cancer occurs in those between 45 and 60 years.
  • 18. Gross Morphology  The tumour is located, in decreasing frequency, on frenum, prepuce, glans and coronal sulcus.  The tumour may be cauliflower-like and papillary, or flat and ulcerating.
  • 19. DISEASES OF THE TESTIS AND EPIDIDYMIS Introduction  Diseases of testes and epididymis are common.  In epididymis, the most frequent are inflammatory diseases.  In the testes, the major lesions are tumors.
  • 20. Congenital Anomalies Cryptorchidism  This is a failure of the testicle to descended into the scrotum.  The testicle is arrested at some point along its descent.
  • 21. Etiology  Mechanical factors e.g. short spermatic cord, narrow inguinal canal, adhesions to the peritoneum.  Genetic factors e.g. trisomy 13, maldevelopment of the scrotum.  Hormonal factors e.g. deficient androgenic secretions
  • 22. Gross Morphology…………..  Usually asymptomatic  Cryptorchidism is unilateral in 80% cases.  The cryptorchid testicle is small in size, firm and fibrotic.
  • 23. Complications  Testicular atrophy  Sterility-infertility  Malignancy 30-50 times increased risk
  • 24. Inflammatory conditions of the testis Orchitis/ Epididymitis  Orchitis is an inflammation of the testicle secondary to infection.  Commonly occurs with epididymitis.  It may be acute or chronic.
  • 25. Etiopathogenesis  The most common pathogens is  In boys younger than 14 years are E. coli and mumps  In men aged 14 - 35 years are Neisseria gonorrhea and Chlamydia trachomatis.  In men older than 35 years is E. coli and Mycobacterium tuberculosis.
  • 26. Etiopathogenesis …………  The common routes of spread of infection are  Via the vas deferens  Via lymphatic and  Hematogenous routes.
  • 27. Signs and symptoms  Gradual onset of scrotal pain and swelling  Usually located on 1 side  Fever and chills (in 25% of adults and 71% of children with acute epididymitis)  Urethral discharge preceding the onset of acute epididymitis (in some cases).
  • 28. Gross morphology  In acute stage the testicle is firm, tense, enlarged and congested.  There may be multiple abscesses, especially in gonorrheal infection.
  • 29. Torsion of the spermatic cord  It is the twisting of the spermatic cord leading to cutting off the venous and the arterial blood supply to the testicle.  Common in boys and young men
  • 30. Signs and symptoms  Enlargement of the testicle; edema involving the entire scrotum  Scrotal erythema  Fever (uncommon  Nausea or vomiting  Pain duration of less than 24 hours
  • 31. Morphologic features  There may be coagulative necrosis of the testis and epididymis, or  There may be hemorrhagic infarction  Twisting of the spermatic cord
  • 32. Other Conditions Hydrocele  Is an abnormal collection of serous fluid in the tunica vaginalis.  It may be congenital or acquired which can be acute or chronic.
  • 33. Pathophysiology  Congenital: Embryologically, the processus vaginalis is a diverticulum of the peritoneal cavity.  It descends with the testes into the scrotum via the inguinal canal around the 28th week with gradual closure through infancy and childhood.
  • 34. Pathophysiology……………….  In congenital hydrocele (communicating hydrocele), a processus vaginalis does not close completely permitting the flow of peritoneal fluid into the scrotum leading to accumulation of fluid in the tunica vaginalis.  Noted in children between 1 – 2 years.  Acquired hydrocele are usually late-onset (secondary) noted in men above 40 years.  It may be due to local injury, infections, and radiotherapy
  • 36. Hematocele  Is an accumulation of blood in the tunica vaginalis.  It is most often caused by trauma, although occasionally can be due to a malignant tumor of the testis.
  • 37. TESTICULAR TUMOURS Introduction  Testicular tumours are the cause of about 1% of all cancer deaths in men. They have trimodal age distribution  The first peak is 0 – 10 years  Another pick during late adolescence and early adulthood 20 – 40 years – Maximum  The third peak after 60 years of age.
  • 38. Introduction …………  99% of all tumours are malignant.  Most testicular cancers (95%) are of germ cells and are all malignant. Risk factors  Undescended testicle  Family history, HIV infection, Age  Race and ethnicity – whites 4-5 times affected than blacks and 3 times than Asians
  • 39. Most common types of testicular cancers Seminoma  Seminoma is a malignant tumor.  It is analogous to dysgerminoma – ovary tumor.  It is the most frequently occurring tumor, accounting for 40%.  Peak incidence is in the mid-30s age group.
  • 40. Presenting features  Painless enlargement of the testicle.  It is associated with increased serum human chorionic gonadotropin (hCG) hormone. Gross morphology  The testis is uniformly enlarged  The surface is smooth  On cut section is uniform grey white appearance
  • 41. Embryonal carcinoma  Embryonal carcinoma is a second most common testicular tumor, accounting for 20%–30%. Clinical features  Painful enlargement of the testicle.  The serum hCG is often increased.  The prognosis is much poor than for seminoma.
  • 43. Teratomas  It is a germ cell tumor derived from two or more embryonic layers.  It is mostly malignant.  It contains multiple tissue types, such as cartilage, ciliated epithelium, liver cells, embryonic gut, striated muscle or hair.
  • 44. PROSTATE DISORDERS Introduction  The most 3 important categories of prostate disorders are;  Inflammatory lesions (prostatitis)  Nodular hyperplasia and  Carcinoma.
  • 45. Prostatitis  Prostatitis is inflammation of the prostate gland.  It may be acute or chronic.  It is due to;  Ascension of bacteria from the urethra  Descent of bacteria from the upper urinary tract or bladder  Lymphatic system or haematogenous spread of bacteria from a distant focus of infection.
  • 46. Causative micro-organism  The common ones are those which cause UTIs  Most frequently E. coli,  Others are Klebsiella, Proteus, Pseudomonas, Enterobacter, Gonococci, Chlamydia trachomatis, Staphylococci and Streptococci.
  • 47. Clinical findings  Fever, low back pain, perineal pain, dysuria  Pain on digital rectal examination Gross morphology  The prostate is enlarged, swollen and tense.  Cut section shows multiple abscesses and pockets of focal necrosis.
  • 48. Benign prostate hyperplasia (BPH)  AKA as benign prostate hypertrophy, is a histologic diagnosis characterized by proliferation of the cellular elements of the prostate.
  • 49. Etiology/ Risk factors  Even though the exact cause is unknown, a number of risk factors have been identified: Demographic factors:  Age: The prevalence of BPH increases with age  Race The risk of acquiring BPH is 47% higher among black men Genetic factors:  Family - There is a three-fold increase in the risk of BPH in twins
  • 50. Etiology/ Risk factors…………….  Vitamin D3 — vitamin D receptor regulates both epithelial and cell growth proliferation.  Cytochrome P45017 mediates sex steroid hormone synthesis, which may influence BPH risk  5α-reductase enzyme converts testosterone to dihydrotestosterone (DHT), which promotes prostate cell proliferation.
  • 51. Risk factors……………. Behavioral factors:  Obesity  High intake of fats (animal fat) increases the risk of BPH
  • 52. Pathophysiology  Prostatic enlargement depends on androgen hormones [testosterone (most important) and estrogen].  In the prostate, 5-alpha-reductase metabolizes the circulating testosterone into DHT which works locally.
  • 53. Pathophysiology…………….  DHT binds to androgen receptors in the cell nuclei to increase their mitotic activity (both stroma and epithelial cells) leading to BPH.  Balance between cellular proliferation and apoptosis exists in patients with normal intra- prostatic levels of androgen and estrogen.  But DHT imbalance occurs with advancing age, favoring prostatic epithelial and stromal cell proliferation.
  • 54. Signs and symptoms  S/S are those related to the constriction and obstruction of the flow of urine.  Urine retention  Urinary frequency  Urinary urgency  Hesitancy - Difficulty initiating the urinary stream; interrupted, weak stream
  • 55. Signs and symptoms………….  Incomplete bladder emptying - The feeling of persistent residual urine, regardless of the frequency of urination.  Straining - The need to strain or push to initiate and maintain urination in order to more fully evacuate the bladder  Decreased force of stream - The subjective loss of force of the urinary stream over time
  • 56. Signs and symptoms………….  Dribbling - The loss of small amounts of urine due to a poor urinary stream. Gross morphology  The enlarged prostate is nodular, smooth and firm and weighs 2-4 times than its normal weight i.e. may weigh up to 40-80 gm.  There is enlarged lateral lobes and median lobe that obstructs the prostatic urethra.
  • 58. Gross morphology…………..  On cut section, (glandular hyper) the tissue is yellow- pink, soft, honey-combed, and produces milky fluid when squeezed.
  • 59. Carcinoma of prostate Introduction  Cancer of the prostate is the second most common form of cancer in males.  It is a disease of men above the age of 50 years and its prevalence increases with increasing age  More than 50% of men aged 80 have asymptomatic (latent) carcinoma of the prostate.
  • 60. Classifications  Latent carcinoma: This is found unexpectedly in the prostate during autopsy studies in men dying of other causes.  Incidence - 25-35%.  Incidental carcinoma: About 15-20% of prostatectomies done for BPH reveal incidental carcinoma of the prostate.
  • 61. Classifications………  Occult carcinoma: the patient has no symptoms of prostatic carcinoma but shows evidence of metastases on clinical examination and investigations.  Clinical carcinoma: this type is detected by rectal examination and other investigations and confirmed by pathologic examination of biopsy of the prostate.
  • 62. Etiology  The cause of prostatic cancer remains unknown.  However, a few factors have been suspected.  Endocrine factors; Androgens are considered to be essential for the development and maintenance of prostatic cancer.  Racial and geographic influences; There are some racial and geographic differences in the incidence of prostate cancer.
  • 63. Etiology…………….  Environmental influences; These include high dietary fat, and exposure to polycyclic aromatic hydrocarbons.  Heredity; It is observed in families and it is 2- fold higher in first-degree relatives.
  • 64. Etiology…………….  Sexual factors: early sex and many sexual partners.  This correlation suggests a sexually transmissible infections (STI) may cause some prostate cancer cases e.g. HPV 16, 18 and HSV 2 – more studies are needed in this area.
  • 65. Clinical features  On rectal examination a hard and nodular gland fixed to the surrounding tissues is felt.  Urinary obstruction with dysuria and increased frequency  Hematuria  In 10% of cases pain in the back due to skeletal metastases.
  • 66. Gross morphology  The prostate may be enlarged, normal in size or smaller than normal.  The malignant prostate is firm and fibrous.  Cut section is homogeneous and contains irregular yellowish areas.
  • 68. Metastasis  It may spread by the following routes:  Direct spread; Direct extension of the tumour occurs into the prostatic capsule and beyond.  Lymphatic and Hematogenous routes.  Sites of spread includes the pelvis and the lumbar spine, lungs, kidneys, breast and brain.
  • 69. References  Robbins, S.L, Kumar, V and Abbas, K (2010). Pathologic Basis of Disease (8th Edition). W.B Saunders Company, Philadelphia.  Robbins SL and Kumar V (2007). Basic Pathology (8th Edition).WB Saunders Co. London.  Harsh Mohan, (2010). Textbook of Pathology (6th Edition). Jaypee brothers medical publishers (p) ltd, India  Riede and Werner, Color Atlas of Pathology © 2004 Thieme