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Urethra and male genital system


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Urethra and male genital system

  2. 2. ANATOMY OF URETHRA • In males – Urethra is 20 cm in length – three named regions – Prostatic urethra • Passes through the prostate gland – Membranous urethra • Through the urogenital diaphragm – Spongy (penile) urethra • Passes through the length of the penis
  4. 4. URETHRA  Epithelium of urethra  Transitional epithelium  At the proximal end (near the bladder) Stratified and pseudostratified columnar – mid urethra (in males)  Stratified squamous epithelium   At the distal end (near the urethral opening)
  5. 5. STRUCTURE OF URETHRA  Muscle layer  Submucosa layer  Mucosa 5
  6. 6. URETHRA  Inflammation (Urethritis) Causative agents: Gonococcal urethritis( N.gonococcus) Nongonococcal urethritisE.coli/ other enteric bacteria C.trachomatis Mycoplasma Urethritis is often accompanied by cystitis in women and prostatitis in men. Symptoms: local pain, fever, itching and frequency. Reiters syndrome: clinical triad of arthritis, conjunctivitis and urethritis. Morphology: changes are typical of inflammation.
  7. 7. TUMOR AND TUMOR-LIKE CONDITIONS  Urethral caruncle Present as a small, red ,painful mass about the external urethral meatus. It may be covered with intact mucosa but is extremely friable and bleeds to slightest trauma. Histologic examination- inflamed granulation tissue, polyp can be seen.  Benign epithelial tumors includes Squamous and urothelial papilloma Inverted urothelial papilloma Condylomas
  8. 8.  URETHRAL POLYP These include: Inflammatory polyp Caruncle Urothelial papilloma Nephrogenic adenomas and polyp Presentation: Dysuria and hematuria
  9. 9.  Histology Polyps are lined by prostatic-type epithelium , may be solitary or multiple. characterised by a papillary or filiform fibrovascular core covered by glandular epithelium. The luminal layer is columnar whereas the basal layer is cuboidal or flat. Polyps may also contain acini some with corpora amylacea.
  10. 10.  Majority of these polyps stain strongly for PSA and PSAP using IHC techniques.  Histogenesis of these benign polyps is unclear but possibilities include: Activation of embryonic nests Metaplasia Overgrowth of the urothelium by proliferating prostatic epithelium.   
  11. 11. CONGENITAL POSTERIOR URETHRAL POLYP / FIBROEPITHELIAL POLYPS  Seen in young boys who present with mild symptoms of bladder outlet obstruction and hematuria. Located in the area of verumontanum. Histologically, they are characterised by congested or edematous fibrovascular stroma lined by transitional epithelium.
  12. 12. CARCINOMA OF URETHRA  Male urethral cancer Prostatic and membranous urethra: tumors arising are usually transitional type and most commonly associated with bladder tumors. These do not express PSA or PSAP antigens and are not hormone sensitive. Bulbous and membranous urethra: tumors are mostly squamous type and rarely associated with vesical neoplasm.
  13. 13.  Female urethral cancer Usually epidermoid. Proximal two-thirds of female urethra: tumors arising are transitional cell type and associated often with vesical neoplasm's. Distal one-third of urethra: are usually squamous cell type.
  14. 14.  Adenocarcinomas of urethra These are rare tumors and arise from the periurethral glands or through metaplasia of the surface urothelium.
  15. 15. ANATOMY OF PENIS Consists of:  foreskin, glans, shaft, & root
  16. 16.  Penis - formed of three cylindrical masses of erectile tissue enclosed in separate fibrous coverings - held together by a covering of skin  Root at base of penis, divides into crura which are attached to the pelvic bones  Glans is at the tip of the penis and is the most sensitive part for most men - covered by prepuce or foreskin which may be removed by a surgical procedure called circumcision smegma - secretion that can accumulate under foreskin of penis  Corona (crown) - ridge between glans and foreskin  Frenulum - connects glans to shaft on underside of penis
  17. 17. Two "corpora cavernosa"  One "corpus spongiosum" which lies ventrally in the penis and houses the spongy urethra. Expands at the end of the penis into the "glans penis. 
  18. 18.  Congenital Anomalies 1. Epispadias & Hypospadias =Malformations of the urethral groove: • • • Epispadias - opening on the Dorsal surface of penis Hypospadias - More common(1 in male 300 births)- opening on ventral surface of penis Complications: Urinary obstruction ↑ risk of ascending UTI, can’t ejaculate properly infertility.
  19. 19. 1. HYPOSPADIAS & EPISPADIAS HYPOSPADIAS opening in the ventral surface of penis More common EPISPADIAS opening in the DORSAL surface of penis ↑ risk of infection can’t ejaculate properly
  20. 20.  2. Phimosis =Abnormally narrow prepuce – prevents normal retraction; Results in Urinary obstruction, ↑ risk of recurrent infections, ↑ risk of cancer.  3. Paraphimosis = forcible retraction of the prepuce in cases of Phimosis, extremely painful, severe congestion of the Glans, acute urinary obstruction
  22. 22. • Inflammations • 1. Balanitis : Inflammation of the Glans, Commonly caused by Phimosis. • 2. Balanoposthitis : Infection of the Glans and prepuce. • Both caused by-pyogenic bacteria including gonococcus, anaerobic bacteria – Fungi – Candida (seen in diabetics) – Mycoplasma, Chlamydia, gardnerella Most often consequence of poor local hygiene in uncircumcised males & underlying systemic disorder such as Diabetes.
  23. 23. 3. Specific STD’s • • • • • • • Syphilis Gonorrhea Chanchroid Granuloma inguinale Lymphogranuloma venereum Herpes (HSV-2) HPV
  24. 24. PENILE FIBROMATOSIS (PEYRONIE'S DISEASE) Mostly affects men between ages 40-60.  A history of penile trauma and urethritis is present in some instances, suggesting a sclerosing inflammatory process in the genesis of the lesion.  It presents as an indurated plaque or indentation in the corpora cavernosa.  30% of cases are associated with erectile dysfunction. 
  25. 25. TUMORS OF PENIS • Benign tumors • Condyloma Accuminatum (genital warts) = Benign, HPV (types 6 & 11) Gross: Occurs as a papillary excrescence at coronal sulcus or inner surface of the prepuce.
  26. 26. Histologically: Papillae covered by Hyperplastic  Hyperkeratotic ( acanthosis)  Stratified squamous epithelium of orderly maturation sequence  Koilocytosis (vacuolation) of scattered superficial cell. 
  27. 27. CONDYLOMA ACCUMINATUM koilocytosis
  28. 28. MALIGNANT • Carcinoma in Situ( CIS)- includes: - Bowen diseaseSeen in both men and women over the age of 35 years. Strongly associated with HPV especially type 16. In men it involves the skin of the shaft of the penis an scrotum. Gross- solitary thickened gray white opaque lesion. Erthroplasia of Queyrat- clinical variant of bowen disease presenting as a shiny red velvety plaque. shiny red plaque •
  29. 29. Histology Epidermis shows proliferation with numerous mitosis , markedly dysplastic cells with large hyperchromatic nuclei and lack of orderly maturation. However, the dermal-epidermal border is sharply delineated by an intact basement membrane.
  30. 30.  Bowenoid papulosis Occurs in sexually active adults Presence of multiple reddish brown papular lesions. Histologically similar to bowen disease and is also related to HPV 16 But virtually never develops into invasive carcinoma.
  31. 31. Feature Bowen’s Disease (Carcinoma in situ ) Bowenoid Papulosis Age >30 yrs <30 yrs lesions Solitary, Gray- white Multiple, reddish brown Behavior ↑risk of invasive carcinoma (10% cases) Never Visceral malignancies ↑risk of visceral malignancies No Histology Carcinoma in situ (HPV-16) Same as Bowen’s (HPV-16)
  33. 33. MALIGNANT CANCER OF PENIS • • • • • • Invasive carcinoma Age- 40 to 70yrs Almost exclusively seen in non-circumcised males (Possible carcinogens in smegma); Cause : HPV types 16 & 18; Cigarette smoking elevates the risk. Circumcision confers protection.
  34. 34.  Clinical features Slow growing locally invasive lesion, usually non-painful unless there is secondary ulceration and infection. Progressive growth Spreads to inguinal & iliac lymph nodes, Later by blood. Prognosis: Overall 5-year survival rate is <50% (with positive nodes<30%).
  35. 35.  1. 2. . Morphology Usually begins on the glans or inner surface of prepuce near the coronal sulcus. Two macroscopic patterns : Papillary lesion- simulate condyloma acuminata , produces a cauliflower-like fungating. Flat lesions- areas of epithelial thickening along with graying and fissuring of the mucosal surface
  36. 36.  Histology- Both types are squamous cell carcinomas with varying degrees of differentiation. Majority of the usual SCC show infiltrating keratinization with moderate degrees of differentiation.  Verrucous carcinoma- exophytic well differentiated variant of SCC that has low malignant potential.
  37. 37.  Other less common subtypes of penile SCC includes Basaloid Warty( condylomatus) Papillary Sarcomatoid Pseudohyperplastic Pseudoglandular( adenoid) Adenosquamous variants
  39. 39. ANATOMY OF THE TESTIS     Testis are paired oval structures about 4 cm in the longest (vertical) diameter lying in the scrotal sac Epididymis , mass formed by tortuous tubules lies on its posterior border- It has a Head , Body and Tail Tunica vaginalis – outermost layer ,closed sac covering testis and epididymis , has visceral and parietal layers Tunica albuginea- deep to tunica vaginalis formed by a dense fibrous membrane
  40. 40. Substance of the testis divided into lobules containing highly convoluted seminiferous tubules involved in spermatozoa production  Each testis has about 200 lobules, one to three seminiferous tubules in each lobule  Tubules enter the fibrous tissue in posterior part of testis to form a network called rete testis  Tunica vasculosa lies deep to tunica albuginea, layer of vascular tissue 
  41. 41. • • Congenital anomalies Cryptorchidism : Failure of descent of testis from the abdominal cavity through the inguinal canal. Causes: Most common  idiopathic • epidemiology   about1% of males right > left, 25% bilateral Pathogenesis  Hormonal abnormalities  Testicular abnormalities  Mechanical problems
  42. 42.  CLINICAL COURSE When unilateral, may see atrophy in contralateral testis.  sterility  concomitant inguinal hernia  increased risk of testicular malignancy  Orchiopexy ( Placement in the scrotal sac) May help prevent atrophy  May not decrease risk of malignancy. 
  43. 43.  Morphology – – – – – – Atrophic changes by 2 yrs of age; Arrest in the development of germ cells Hyalinization and thickening of seminiferous tubules & interstitial fibrosis Sparing Leydig cells which become prominent With progressive tubular atrophy the testis becomes small and firm in consistency. Similar changes - contralateral descended testis
  44. 44. TESTICULAR ATROPHY Atrophy is a regressive change affecting scrotal testis It is the end stage of an inflammatory orchitis Possible causative factors: Atherosclerotic narrowing of the blood supply in old age  cryptorchidism  hypopituitarism  generalized malnutrition or cachexia  irradiation  prolonged administration of female sex hormones, as in treatment of patients with carcinoma of the prostate  Cirrhosis klinefelters syndrome.
  45. 45. Associated with decreased fertility, hypospermatogenesis, maturation arrest and sometimes vas deferens obstruction. Histology: Hyalinization of seminiferous tubules & interstitial fibrosis Sparing of Leydig cells.
  46. 46. TESTICULAR ATROPHY Normal Normal Atrophy •Focal atrophy  infection (mumps) •↑ in space Atrophy hyalinized
  48. 48. VASCULAR DISORDERS  • TORSION Twisting of the spermatic cord which typically cuts off the venous drainage of the testis. There is intense vascular engorgement which may lead to hemorrhagic infarction Bilateral anatomic defect where the testis has increased mobility giving rise to “bell-clapper” abnormality
  49. 49. Neonatal torsion: occurs either in utero or just after birth.  Adult torsion: typically seen in adolescence.  C/f- sudden onset tesicular pain, often without any inciting injury. Testis should be surgically explored and manually untwisted within 6 hours to maintain its viability. Contralateral un-affected one should surgically fixed   ( Orchiopexy )
  50. 50.  Morphology Depends on the duration of the process. Intense congestion Extravasation of blood into the interstitial tissue Haemorrhagic testicular infarction Late stages: marked enlargement of testis sac of soft, necrotic, hemorrhagic tissue
  52. 52. INFLAMMATION • • • 1. Nonspecific Epididymitis & Orchitis Infection reaches the epididymis and testis from the urinary tract through either the vas deferens or via lymphatics of spermatic cord. causative agents: – – – children- Gram negative rods 15-35 year old (sexually active males)-Chlamydia & Neisseria Older men- E. coli & Pseudomonas;
  53. 53. • Histology: – Early stage: Acute suppurative inflammation characterised by congestion, edema and infiltration by neutrophils, macrophages and lymphocytes. – Later stages: Fibrosis & hyalinization  sterility Leydig cells - not affected (normal sexual activity) –
  54. 54. • 2. Granulomatous OrchitisAlso called “Autoimmune Orchitis” – Presents in middle age – Sudden onset of tender testicular mass; fever may be seen if painless and of insidious onset, may mimic testicular tumor –  Histology: Granulomas within seminiferous tubules
  55. 55. SPECIFIC INFLAMMATIONS  1. Gonorrheal Epididymo -OrchitisRetrograde infection from the posterior urethra to prostate, seminal vesicles and then to epididymis causing suppurative Epididymitis. may lead to development of frank abcesses and finally destruction of epididymis. In untreated cases, spread to testis (suppurative Orchitis)
  56. 56. 2. Mumps Orchitis1 week after onset of parotitis; seen in postpubertal males testicular involvement is rare in school aged children Orchitis is unilateral in 70% of cases. Histology: Interstitial inflammation with mononuclear cellular infiltrate Recovery is complete
  57. 57. 3. Tuberculous Epididymo - OrchitisPrimarily Epididymitis, with secondary spread to the testis. – – – Histology: Caseating granulomas. sinuses on the dorsal surface of the scrotum
  58. 58. 4. Syphilitic OrchitisStarts in the testis rarely spreading to epididymis Histology: production of Gummas or Diffuse interstitial inflammation with lympho plasmacytic infiltrate and obliterative endarteritis with perivasular cuffing of lymphocytes and plasma cells.
  59. 59. SPERMATIC CORD AND PARATESTICULAR TUMORS  Lipoma of spermatic cord common lesion affecting the proximal spermatic cord usually diagnosed at the time of inguinal hernial repair not a true neoplasm, rather represents retroperitoneal adipose tissue that has been pulled into the inguinal canal along with hernial sac
  60. 60.  Adenomatoid tumor most common benign paratesticular tumor involves the epididymis and also spermatic cord presents as painless , firm, intrascrotal mass typically , head of epididymis is affected Gross : Well circumscribed , firm, white to tan nodule , usually less than 2 cm.
  61. 61.  Microscopy characteristic solid to cystic tubules and cords of vacuolated cells cells lining the tubules are flattened to cuboidal with a prominent intervening fibrous stroma. the cellular vacuoles may yield a signet ringlike appearance cytoplasm is typically abundant and eosinophilic with vesicular nuclei. IHC shows positivity for CK, EMA and Calretinin
  62. 62.  Malignant paratesticular tumors in children: Rhabdomyosarcoma in adults: liposarcomas located at the distal end of spermatic cord.
  63. 63.  References : Robin – pathologic basis of disease. Sternberg. Urinary MG WHO. Internet.