Genitourinary Pathology

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Genitourinary Pathology
2010-11-29 16:39:31

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  1. Where is the most common malformation of the penis?
    What is Hypospadias? Epispadias?
    • Distal Urethral Orifice.
    • Hypospadias: Abnormal opening of the urethra along the ventral aspect of the penis. 1/250 males, opening may be restricted, Inc. chance of UTI
    • Epispadias: Urethral opening on dorsal aspect of the penis. Inc. chance of UTI and Urinary Incontinence.
  2. How do Premalagnant Lesions appear clinically on the penis?
    White/Red plaques, thickenings, areas of redness. Histologically have some level of dysplasia.
  3. What is Carcinoma in-situ?
    Final stage of pre-cancerous lesion before it becomes a squamous cell. Neoplastic cells that have NOT invaded other tissues. (If it originated in the epithelium, it hasn't invaded CT or surrounding structures).
  4. What is Bowen Disease?
    is it specific to the penis?
    Clinical importance?
    • Bowen disease is a synonym for carcinoma in-situ (a premalagnant lesion) anywhere on the body.
    • It is NOT specific to the penis, can occur on other mucosal surfaces including the vulva and oral cavity.
    • Clinically important because it has the potential to progress into an invasive squamous cell carcinoma.
  5. What is Erythroplasia of Queyrat?
    Specific to the penis?
    • Erythroplasia of Queyrat: An erythematous patch on the glans penis. It is a premalignant lesion!
    • It is specific to the penis.
  6. What is Bowenoid Papulosis?
    Bowenoid Papulosis: When significant epithelial dysplasia is intermixed with histopathologic features of HPV infection. Clinically seen as multiple reddish brown papules on the glans penis. Premalignant lesion.
  7. Is Squamous cell carcinoma common on the penis?
    HPV involved?
    Affects of Circumcision?
    How do they present clinically?
    5 year survival rate?
    • Not common
    • HPV may be involved
    • Circumcision improves hygiene, decreases chance of infection and disease.
    • Crusted papule that usually develops a central ulceration or less frequently a papillary mass.
    • 25% metastasis
    • 5 year survival rate = 70%
    • Tx: Surgical excision.
  8. What are three disorders of the testis?
    • Cryptorchidism: (failure of testicular descent)
    • Orchitis: Inflammation of the testes
    • Neoplasms: Tumors.
  9. Cryptorchidism:
    What is it?
    Is it common? frequency?
    Association with cancer?
    • Incomplete descent of the testis from the abdomen to scrotum.
    • 1% of 1 year old males has it
    • Bilateral (some cases unilateral) cryptorchidism is associated with sterility!
    • 3x5 fold increased risk of testicular cancer.
    • Tx: Ochiopexy (proper placement/surgical placement of testis) reduces risk of sterility and cancer.
  10. What is Orchitis? Epididymitis? Which is more common?
    Associated with STDs?
    It can be a complication of another disease in adults?
    • Orchitis: Inflammation of the testes. Epididymitis: inflammation of the epididymis (more common).
    • Swelling and Tenderness
    • Complication from UTI
    • Often associated with STD
    • Orchitis complicates mumps in 20% of adults. Mumps-associated ochritis can result in sterility.
  11. What is the most common cause of painless testitcular enlargement?
    Testicular Tumor
  12. Testicular Tumors/Neoplasms:
    What type of cell do they arise from?
    What percent is malignant?
    Overall facts about frquency, peak incidence, ect.
    • 95% arise from Germ Cells. Almost ALL are MALIGNANT.
    • There is an increase in frequency of undescended testes. 5/100,000 males, peak incidence 20-34 years. 8,000 new cases annually in US <400 die.
  13. Testicular Tumors are divided into 2 groups... What are they?
    Seminomas germ cell tumors and Nonseminomatous germ cell tumors.
  14. Describe the Seminomas germ cell tumors of the testes?
    Most treatable and curable cancers. Up to a 95% cure rate. Most tumors remain confined to the testes for a long period or time. Doesn't spread or metstatsis for a long period of time, if it does it spreads through the lymphatics. Respond well to chemotherapy and are very radiosensitive.
  15. Non Seminomatous Germ Cell Tumors of the Testes
    Tend to spread earlier via lymphatics and blood vessels. Very small when starts spreading so hard to catch. Lungs, liver, and brain are frequent metastatic sites. Less radiosensitive, smaller, less differentiated, harder to cure/treat. Tumor markers: a-fetoprotein (AFP) and Human Chorionic gonadotropin (HCG). Prognosis improved with newer chemotherapy regimens.
  16. What are two Tumor markers for detecting Testicular Tumors?
    What type of Testicular Tumor does it generally detect?
    a-fetoprotein and human chorionic gonadotropin (HCG). These markers are rarely positive in seminomas but frequently beneficial in nonseminomatous tumors.
  17. What is Prostatitis?
    What is it often caused by?
    Two categories?
    Important Cause of what?
    • Prostatitis: Prostate inflammation, enlargment and tenderness.
    • Often caused by bacteria associated with UTIs (E. Coli).
    • Acute or chronic
    • Symptoms: dysuria, frequency of urination, low back pain, and pelivc pain, often clinically silent.
    • Important cause of recurrent UTI in men!
  18. Nodular Hyperlasia of the Prostate:
    What is it? How is it caused?
    • aka: BPH (Benign Prostate Hypertrophy). It's a hyperplastic enlargement of the prostate and often is associated with urinary symptoms.
    • Proliferation of stromal and glandular elements of the prostate lead to enlargements and may cause urinary obstruction.
    • Central portions/Inner periurethral zones of the prostate are involved most frequently, and compress the prostatic urethra, causing dysuria.
  19. Nodular Hyperplasia/BPH:
    Is it common?
    Clinical symptoms?
    What can happen with chronic obstruction?
    Do we know how this happens?
    • It is common. 20% of men affected at age 40, 90% at age 70.
    • Clinical symptoms include: hesitancy, urgency, nocturia, and poor urinary stream.
    • Chronic obstruction predisposes to recurrent urinary tract infection.
    • Etiology incompletely understood. It is thought that some hormonal stimulus (androgens) is invloved.
  20. What are treatments of Nodular Hyperplasia?
    Surgical managment (TURP): Trans urethral resection. Not invasive/open surgical procedure, enters through the urethra.

    Medical Management: Drugs.
  21. Carcinoma of the Prostate: What kind of carcinoma is it?
    Peak incidence?
    clinically latent?
    • Adenocarcinoma (glandular origin).
    • Extremely common cancer in men. Ranked second (lung is the first).
    • Peak incidence between ages 65-75.
    • May be clinically "latent" 50% men over age 80.
    • Metastasis to lymph nodes, blood stream and bone may be seen.
  22. Carcinoma of the Prostate:
    Most commonly arise on what parts of the prostate?
    How is it detected?
    Most commonly arise in the outer (peripheral) glands/zones of the posterior lobe of the prostate. (Therefore dysuria is not an early sign).

    Detectable via digital rectal examination: Very important for carcinoas of the prostate, useful method for detection of early prostatic cancers.
  23. Carcinoma of the Prostate:
    • Unknown.
    • Pathogenesis is thought to be caused by hormones, genes and environmental factors.
    • Evidence suggests that androgens contribute significantly to the development of this cancer.
  24. What is Prostate Specific Antigen? (PSA)
    • Useful marker in management of prostate cnacer, however, elevation above normal can be due to cancer or non-neoplastic conditions. Not very helpful alone, but with digital rectal exam, sonography, needle biopsy, it can be helpful.
    • PSA is also important in staging of the neoplasm.
  25. Carcinoma of the Prostate:
    Various combinations of surgery, radiation therapy and hormonal manipulation.

    Prognosis: Depends on anatomic extent of disease. 10 year surfavial rate of 10-40% for disseminated disease.
  26. Syphilis:
    What is it caused by specifically (organism)

    Whites:Black people infected?
    • a spirochete: Treponema Pallidum
    • Black people are infected 30x more than white people
  27. What are the two types of antibodies produced by Syphilis?
    • Nonspecific antibody: Syphilitic reagin
    • Specific antibody: Treponemal antibody.
  28. 3 Stages of Syphilis:
    Describe the Primary stage:
    • Primary: painless ulcer (chancre) develops at site of inoculation 9-90 days after initial infection. (external genitalia most often, oral sites possible).
    • Systemic dissemination of organism continues while host mounts immune response (production of antibodies).
    • Resolves spontaneously in 4-6 weeks
    • If untreated, 25% of patients develop secondary syphilis approximately 2 months after resolution of the chancre
  29. 3 Stages of Syphilis:
    Describe Secondary Syphilis:
    • Approximately 2 months following resolution of the chancre.
    • Generalized lymphadenopathy and mucocutaneous lesion.
    • Maculopapular rash affecting skin (palms and soles); condyloma lata and mucous patches may affect mucosa (genital and oral).
    • Resolves spontaneously over several weeks, at which point patient enters the latent phase.
    • If untreated, close to 1/3 of patients develop tertiary syphilis over a period of 5-20 years.
  30. 3 Stages of Syphilis:
    Describe Tertiary Syphilis:
    What are the tree categories of 3* syphilis.
    • Develops after latent period of 5+ years
    • 1. Cardiovascular syphilis (80%): proximal aortitis, aortic insufficiency, and aneurysms.
    • 2. Neurosyphilis (10%): Involvement of the brain, meninges and spinal cord.
    • 3. Benign Tertiary Syphilis: Focal granulomatous lesions called gummas develop in bone, skin and mucous membranes of the upper airway and mouth.
  31. In what stages is Syphilis most contagious?
    1st and 2nd stage, not as contagious in 3rd stage.
  32. Congenital Syphilis:
    What is it?
    3 patterns, what are they?
    • Maternal transmission of syphilis across the placenta.
    • 3 patterns:
    • 1. Stillbirth.
    • 2. Infantile syphilis: live-born infants with clinical manifestations at birth or with in first few months of life.
    • 3. Late congenital syphilis (uncreated, >2years duration) Causes Hutchinson's Triad.
  33. Congenital Syphilis:
    In late congenital syphilis what "triad" of sympoms will you see.
    • Hutchinson's triad: (If congenital syphilis goes untreated for over two years these symptoms occur)
    • 1. Hutchinson's Teeth
    • 2. Interstitial Keratitis.
    • 3. CN VIII deafness.
  34. Diagnosis of Syphilis:
    What are some screening tests?
    What are some specific tests for syphilis?
    • Screening tests: RPR (rapid plasma reagin) and VDRL (Venereal Disease Research Laboratory). Often negative in early stages of disease. 15% false-positive test.
    • Specific Tests: FTA (Fluorescent Treponemal Antibody). Positive later in disease course. Remain positive indefinitely, even after successful treatment. Treatment: Antibiotics (penicillin)
  35. At what point in time can you successfully treat congenital syphilis?
    What is the treatment for syphilis?
    • Treatment within the first four months of therapy will prevent clinical complications.
    • Tx for syphilis: penicillin, with tetracycline utilized in patients allergic to the primary choice.
  36. Gonorrhea:
    What (organism) is this caused by?
    Diplococcus evokes what type of reaction resulting in what?
    • Neisseria Gonorrhoeae, a gram negative diplococcus.
    • This infection is second only to chlamydia as the most common reportable communicable disease in the U.S.
    • Diplococcus evokes a neutrophilic inflammatory reaction which produces copious amounts of pus.
  37. Gonorrhea:
    Asymptomatic males? females?
    untreated can lead to what?
    treat with?
    • Common STD 650,000 cases annually in US
    • 40% asymptomatic males, 80% asymptomatic females
    • untreated can lead to sterility.
    • Treated with penicillin.
  38. How do you diagnose Gonorrhea?
    Culture of the organism from discharges has been the primary diagnostic test.
  39. What is the most common STD?
    Nongonococal urethritis and cervicitis.
  40. Nongonococcal Urethritis and Cervicitis:
    Majority are caused by?
    Clinically similar to gonorrhea? How is it recognized?
    • Chlamydia Trachomatis!
    • Clinically similar to gonorrhea in both men and women, it is usually recognized by PERSISTENT disease following antibiotic treatment for suspected gonorrhea.
    • Tx: Ceftriaxone and doxycycline (effective against gonorrhea and chlamydia).
  41. Genital Herpes Simplex:
    How many people does it affect in the US?
    Caused by? (viruses?)
    Transmitted how?
    Neonatal herpes?
    • Affects about 50 million people in the US.
    • Caused by HSV-2 (sometimes HSV-1)
    • Transmission by direct contact.
  42. Neonatal herpes: occurs in children born to mothers with genital herpes; mortality is high (60%).
  43. Most cases of herpes are caused by what HSV type?
    Genital Herpes Simplex:
    Initial Primary infection:
    Recurrent lesions:
    Neonatal herpes.
    • HSV II
    • Initial (primary) infection: may be asymptomatic or causes painful mucocutaneous eruptions with lymphadenopathy and malaise; heal 3-6 weeks.
    • Recurrent lesions are small painful vesicles that quickly ulcerate; heal in 7-10 days.
    • HSV is actively shed during peiords of clinical lesions.
  44. Human Papillomavirus Infection
    Most common types/form?
    Describe apperance?
    Occur in what regions?
    • Responsible for a number of proliferative lesion on the genital mucosa (benign and malignant).
    • Most common, condyloma acuminatum (aka-venereal warts) caused by HPV 6 and 11.
    • Benign paillary nodules that frequently appear in clusters.
    • Occur in anogenital region and oral mucosa (not uncommon to develop synchronous lesions).
  45. What are high Risk forms of HPV?
    HPV types 16 and 18 are the high risk types. They can form cancer.