Minarcik robbins 2013_ch21-lower_ut


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  • Two principles:
    1) The ENTIRE lower urinary tract reacts to inflammatory and neoplastic influences SIMILARLY, if not identically? Why? It is ALL the same type of mucosa, i.e., transitional. Or urothelial. Histologically, and embryologically, too.
    2) The lower urinary tract is a classical example of how a neoplastic influence acting on ONE part of the urothelium, is also acting on OTHERS!. E.g., cut out a cancer in one place, the etiologic agents are STILL acting on other transitional mucosal places.
  • GENERAL scheme of the ENTIRE lower urinary tract = 1) transitional epithelium + 2) smooth muscle!
    Why is “transitional” epithelium called “transitional”?
  • Understanding the origins of the lower urinary, female, and male tracts, means understanding the simple embryology.
    Mullerian tissue behaves similarly, Wolffian tissue behaves similarly, and metanephric tissue behaves similarly also! Most of the lower urinary tract is METANEPHRIC tissue.
    In MALES, there is considerable overlap between the Wolffian system and the –nephric system. In females there is none.
  • What are the three most likely places to have ureteral constriction just from the gross anatomy alone?
    1) UPJ
    2) Pelvic brim
    3) Bladder
  • Identify, mucosa, wall, detrusor muscle, prostate, prostatic urethra, seminal vesicles, perivesicle fat. Classically, the bladder submucosa is often called, interchangeably, the lamina propria because there is no clear cut differentiation between the two. Where would the membranous urethra be? Where would the “spongy” urethra be?
  • Ductus deferens may be grossly indistinguishable from the seminal vesicles, but are MEDIAL to them.
  • This is probably the most classical bladder you will ever see.
  • Classically the textbooks say urothelium ranges from, say, 4-8 layers thick normally from calyces to urethra, but this is highly variable, even with normal distension vs. relaxation. Can you COUNT the “layers” of transitional cells, This is important because it can help you determine sometimes if hyperplasia or neoplasia is present.
  • Typical real life bladder wall. What would be the difference between adventitia and serosa? Where are they?
  • How many layers? 4? 5? 6?
  • Once again, if we go back and try to classify diseases into DEG, INF, NEO, we find very few DEG diseases of the LUT, but many “anomalies”.
    In fact the urinary tract is the MOST LIKELY site for ANY congenital anomaly, having an anomaly rate classically quoted as being around 10% of all births, most of which are minor.
  • This is a real person with a GREAT CT reconscruction!
  • Please keep in mind the transitional mucosa/smooth muscle prototype.
  • Double ureters
  • UPJ obstruction, this is the KEY concept in all LUT obstruction, i.e., distention or dilatation proximal (upstream) to the obstruction.
    Doesn’t this seem to apply to just about all of the tubular structures in the body? YES And does inflammation go hand in hand with obstruction? YES
  • IVP UPJ obstruction. Can you see the renal pyramid’s tip (papilla)?
  • HYDROURETER, which side?
  • The ENTIRE lower urinary tract are generally infected by the same types of bacteria, generically lumped as enteric gram negatives, of which E. coli is always the most common on ANY study.
  • Ureteritis cystica is the ureteral counterpart ofd cystitis cystica, i.e., little mucosal cysts lined by COLUMNAR epiothelium, NOT transitional. Is this metaplasia? Sure it is!
  • You know the drill. Acute urothelial –itis = neutophils (POLYs), and chronic urothelial –itis = lymphs and macrophages (i.e., MONO-nucleated cells)
  • The disease means exactly what it is named!
    Why is it generally regarded as “auto-immune”?
  • As a general rule, ANY papillary tumor, lined by urothelium, is usually called carcinoma, no matter WHAT the cells like, in ANY part of the LUT
  • Why would you expect a URETERAL UROTHELIAL CA rather than a pelvic or bladder?
  • Fibroepithelial “polyp”. Why?
    Why would the distinction be made between polyp and papilloma?
  • Leiomyoma. Why?
    Is this smooth muscle?
    Could it be fibroblasts?
    How can you tell the difference?
    What is a cigar?
  • Transitional cell carcinoma, ureter, gross.
  • Transitional cell carcinoma, ureter, microscopic. Up until now all of the “Papillary” tumors we talked about were ADENOCARCINOMAS or SQUAMOUS. In the lower urinary tract however, all of the papillary tumors are TRANSITIONAL (UROTHELIAL) carcinomas, NOT adenocarcinomas.
  • Movin’ on down the LUT, let’s repeat the same way of thinking for the bladder, as we did for the ureter.
  • X-ray cystogram, bladder diverticulum.
    What proof do you have that this diverticulum communicates with the lumen of the bladder?
  • Diverticula, bladder, concept.
    Do they have to communicate with the main bladder lumen? Ans: No
  • Diverticula, bladder, real, these do not have to communicate with the main lumen..
  • EXTROPHY means EVERSION of an organ, but usually used in reference to the bladder, mostly males, 1/50,000 births.
  • Reflux has the same consequences as obstruction in that it is associated with chronic infection and proximal dilatation. Remember BACTERIA are normally in the bladder urine, the HIGHER this refluxes, the more likely it is to cause infection.
  • Bilateral vesicoureteral reflux. Which side is worse?
  • Hemmorhagic?
    Is hemorrhagic more likely to be acute or chronic?
  • More hemorrhagic?
    Would you expect neutrophils (POLYs) or lymphs and macrophages (MONOs) to infiltrate predominantly here?
  • “Follicular”?
  • Eosinophilic?
    Might you suspect an allergic or parasitic etiology, always, when you see eosinophils? Ans: YES
  • What is “URO-sepsis”?
  • Interstitial cystitis is still a mysterious disease with all kinds of “theories”. But remember, it is largely “interstitial” which means fibrosis of the muscular bladder wall itself, if common.
    Malacoplakia is also mysterious (soft yellow plaques filled with macrophages and calcium) but is associated with:
    Prolonged therapy with systemic corticosteroids
    Organ transplantation
    Diabetes mellitus
    Rheumatoid arthritis
  • Interstitial cystitis is still a mysterious disease with all kinds of “theories”. But remember, it is largely “interstitial” which means fibrosis of the muscular bladder wall itself, if common.
  • Why are they called “glomerulations”?
  • Malacoplakia is also mysterious (soft yellow plaques filled with macrophages and calcium) but is associated with:
    Prolonged therapy with systemic corticosteroids
    Organ transplantation
    Diabetes mellitus
    Rheumatoid arthritis
  • Where is the pigment?
    What is it?
    How would you prove what it is?
  • Brunn nests are clusters of urothelium which usually lie UNDER the surface mucosa. They can undergo glandular (i.e., columnar) metaplasia.
    SO, the transitional epithelium of the lower urinary tract can METAPLASE in two ways:
  • Is there anything here to suggest malignancy? Ans: NO
    Is cystitis cystica PRE-malignant? NO
    Do adenocarcinomas of the bladder usually arise in previously existing cystitis cystica (glandularis)? : YES
  • Columnar or transitional? Hard to say for sure, isn’t it?
  • Whereas squamous metaplasia of transitional mucosa can be nonspecific, it is almost universally found with shistosome infections of the bladder, i.e., bilharziasis.
    Squamous cell carcinoma of the bladder arises from squamous metaplasia and is VERY VERY common in Egypt, where bilharziasis is rampant.
  • The general rule is: ALL papillary tumors of the bladder are regarded as cancer or potentially cancer. You will ALMOST NEVER see a path report of a SQUAMOUS PAPILLOMA, especially in the USA.
  • Good rule of thumb: All papillary tumors of urothelium are carcinomas, not papillomas!
  • Ques: Why is this LOW grade?
    Ans: It looks like normal transitional mucosa.
  • How many “layers” of epithelial cells are here?
  • Ques: Why is this HIGH grade?
    Ans: It does NOT look like normal transitional mucosa, and its very pleomorphic and hyperchromatic.
    Can you see many mitoses? Ans: I’m having a hard time finding even one.
  • Can you tell this is HIGH or LOW grade just from the cystoscopists view?
    Ans: NO
    Can you tell if it is bleeding much?
    Ans: It is NOT bleeding much
    Can you tell if it is invading the wall?
    Ans: NO
    Does it look necrotic?
    Ans NO
  • NECROSIS, INVASION, HEMORRHAGE are present here. Find them.
  • “SKIP” areas. What are “skip” areas?
  • Urine cytology of normal patient and bladder cancer patient. Which is which?
  • An alternative route would be: PAPILLOMA CARCINOMA
  • Isn’t this totally explanatory of the biologic behavior? Ans: YES
  • What is the EXACT definition of cystocele (Wiki it please)
    A cystocele  is a medical condition that occurs when the tough fibrous wall between a woman's bladder and her vagina (the pubocervical fascia) is torn by childbirth, allowing the bladder to herniate into the vagina.
    What is a rectocele?
    A rectocele results from a tear in the rectovaginal septum (which is normally a tough, fibrous, sheet-like divider between the rectum and vagina). Rectal tissue bulges through this tear and into the vagina as a hernia. There are two main causes of this tear: childbirth, and hysterectomy.
  • Urethral caruncles, which often originate from the posterior lip of the urethra, may be described as fleshy outgrowths of distal urethral mucosa. They are usually small but can grow to 1-2 cm in diameter. They are caused by distal urethral prolapse and related to estrogen withdrawal.
  • Caspar Friedrich Wolf
  • Excellent conceptual diagram to review gross anatomy.
    Recall the journey of Herm the sperm from the seminiferous tubule to the urethral meatus.
  • Remember the order of sperm transfer from seminiferous tubules to urethra.
  • Excellent conceptual diagram to review gross anatomy.
  • Main players of seminiferous tubules.
  • Straight tubules are 100% sertoli cells.
  • Testicular epididymeal junction
  • Cilia vs. stereocilia
  • Vas deferens. Is the inner smooth muscle layer circular or longitudinal?
  • Seminal vesicles, look for significant atypia. Almost every pathologist I know, including myself, has mistaken the NORMAL ATYPIA seen in the seminal vesicles for prostate cancer!
  • Paired ejaculatory duct leading from the seminal vesicles to the prostatic urethra. Nothing exciting here.
  • Q: What is the utricle analogous to in the female? A: Uterus and Vagina
  • Don’t forget the Cowper’s (bulbourethral) glands.
  • EXTREMELY slippery secretion, but very low volume, from the glands of Littré.
  • Urethral deviations and prepuce contractions.
  • Hypospadias
  • Epispadias
  • Phimosis
  • Smegma (Greek smēgma, "soap"), sometimes described as a "cheesy substance", is a combination of exfoliated (shed) epithelial cells, transudated skin oils, and moisture. It occurs in both female and male mammalian genitalia. If the penis was a toe, smegma would be called toe jam.
  • Condyloma accuminata, EXACTLY the same appearance and etiology as on the female external genitalia.
  • Condyloma accuminata, EXACTLY the same appearance and etiology as on the female external genitalia.
  • Koilocytosis is perinuclear vacuolization, quite classical for HPV, this can be seen on cytology, as well as histology.
  • Common nomenclature
  • Bowen’s Disease of the penis also goes by the name Erythroplasia of Queyrat.
    BOWEN’S diseases can be thought of as squamous cell carcinoma-in-situ of not only the skin of the penis, but skin ANYWHERE!
  • Note the surface cells are not much different from the base cells, this is defined as a “loss of maturation” pattern, and is quite typical of squamous CIS everywhere.
  • Infiltrating SCC, penis.
  • Infiltrating SCC, penis.
    At this point EVERYBODY should immediately recognize this as:
    Where are the intercellular bridges?
  • Do you think these are all logical? Of course you do!
  • Testicular atrophy, classical pattern, showing ghosting or fibrosis of tubules, NO spermatogenesis, INCREASED interstitial cells of Leydig. Are the Leydig cell hyperplastic because of the atrophy and endocrine feedback mechanisms? Ans: YES
  • Often, Inflammations in the testicle ALSO involve the epididymis, and vice versa. Commonly urinary tract gram negatives infect BOTH.
  • Infarcted, purple, testicle and epididymis due to “torsion”. Inflammatory vs. ischemic? Ans: Ultimately, ISCHEMIC
  • Most testicular tumors are malignant germ cell tumors.
    Most germ cell tumors of the testes are MALIGNANT.
    Most ovarian tumors are benign NON-germ cell tumors (cystic).
    Most germ cell tumors of the ovary are BENIGN (dermoid cysts)
  • The larger cells are GERM cells and they often DO look like spermatocytes, from normal histology.
    The smaller cells look like typical lymphocytes bacause they ARE typical lymphocytes.
    Ususlly, there are good numbers of BOTH kinds of cells.
    The GROSS appearance of a seminoma is usually the same gross appearance of a lymphoma. Why? Ans: Lymphs, very little fibrous tissue.
  • These cells are usually described as “primitive”, but usually show kind of a GLAMNDULAR pattern, which is why in the old days they were ofem call adenocarcinomas, but remember they are GERM cells, NOT glandular epithelial cells.
  • If you remember your placenta histology you might say this looks like a placental villus, with TROPHOBLAST.
    From a histology viewpoint alone, could this be from a female placenta or an ovary? Ans: YES
  • Most common testicular tumor in male CHILDREN
  • Most testicular teratomas are malignant.
    Most ovarian teratomas are benign (e.g., dermoid cyst)
    Why did I underline the first bullet? Because it is the MOST common thing found in ANY teratoma.
  • Wheras, most germ cell tumors are regarded as benign, most sex cord (NON germ cell) tumors are regarded as benign.
    Leydig cells make testosterone so you might guess that a Leydig cell tumor migh have a clinical syndrome of hypertestosteronism, or sometimes even feminizing features.
    Sertoli cells make a variety of hormonal and non-hormonal compounds which “nurse” the spermatocytes, hence the name “nurse” cells.
  • Testicular tumors do NOT metastasize to inguinal nodes but peri-aortic nodes. Why? Ans: Because that’s where they came from embryologically, so the RETROPERITONEUM is usually the first place to detect a metastatic testicular tumor.
  • CZ is nearest the urethra, PZ is nearest the capsule. TZ is between the two.
  • Acute prostatitis. Why? Ans: Neutrophils
  • Chronic prostatitis. Why? Lymphocytes
  • Granulomatous prostatitis.
    “TB or Not TB, that is the question”
  • Glandular hyperplasia, note ABSENCE of nucleoli.
    Also note nuclei are where they should be, i.e., basal.
    Also note glands are NOT back to back, but each one is separated by thin fibrous tissue.
    The above THREE conditions favor a BENIGN process.
  • PIN (Prostatic Intraepithelial Neoplasia) is the grey zone between BENIGN and MALIGNANT prostate glands.
    The can be LOW grade PIN, or HIGH grade PIN.
    Notice the secondary INFOLDING of epithelial “papillae” within the lumen.
  • NUCLEOLI separate benign from malignant prostate glands!!! Of course there are other differentiating features, but this is the MOST RELIABLE one. The presence of NUCLEOLI in most of these cells almost nails the diagnosis of malignancy.
  • Even if, theoretically, the prostate gland cells looked 100% benign, if they surround nerve spaces, they are malignant. Why?
  • TIP: Numerous bone metastases in males usually carcinoma of the prostate until proven otherwise.
  • Know this correct order of biologic behavior.
  • A Gleason’s final SCORE is the SUM of the predominant pattern (1-5) and the secondary pattern (1-5).
    So a Gleason GRADE ranges from 1-5, and a Gleason SCORE ranges from 2-10.
    Dr Gleason is certainly laughing at us today because he designed this numbering system just as a convenience, but so many people stake their LIFE on it, and it is SO subjective to boot!
  • Please don’t memorize this, but just think of the BIOLOGIC BEHAVIOR instead, and the anatomy!
  • Remember, the “S” stands for SPECIFIC for prostate, NOT SPECIFIC for cancer! Ask any urologist when has he seen the HIGHEST PSA ever, and he’ll probably tell you he saw it with massive hyperplasia!
  • Minarcik robbins 2013_ch21-lower_ut

    5. 5. LOWER Urinary Tract •Ureters •Bladder •Urethra (Anomalies, Infl., Neopl.) (Anomalies, Infl., Neopl.) (Anomalies, Infl., Neopl.)
    6. 6. URETERS • Anomalies (congenital) • Inflammation/Obstruction (i.e., ureteritis) – Acute, Chronic • Neoplasms – Benign vs. Malignant – Epithelial vs. “stromal” (i.e., mesoderm derived)
    7. 7. CONGENITAL Ureter Anomalies • DOUBLE Ureters • UPJ (Uretero-Pelvic Junction) Obstruction • Diverticula • Hydroureter
    8. 8. INFLAMMATION • The USUAL reasons • The USUAL patterns, i.e. ? • Linked to OBSTRUCTION • GLANDULARIS/CYSTICA • FOLLICULARIS
    10. 10. Sclerosing Retroperitoneal Fibrosis • 70% Idiopathic • 30% Drugs (ergot derivatives, beta blockers) or known retroperitoneal inflammatory conditions, e.g., Vasculitis, Diverticulitis, Crohn’s Disease
    11. 11. TUMORS • Benign – Fibroepithelial Polyp – Leiomyoma • Malignant – Transitional Cell Carcinoma, aka, TCC – Also called UROTHELIAL Carcinoma
    12. 12. Which Ureter? Which Part?
    13. 13. LOWER Urinary Tract •Ureters •Bladder •Urethra (Anomalies, Infl., Neopl.) (Anomalies, Infl., Neopl.) (Anomalies, Infl., Neopl.)
    14. 14. ANOMALIES • Diverticul-a (plural of –um) • Exstrophy • Vesico-Ureteral Reflux • Persistent Urachus • Fistulas: Vagina, Rectum, Uterus
    15. 15. EXSTROPHY Developmental Anomaly Very Good Surgical Correction Rate
    16. 16. Vesico-Ureteral Reflux • Most Common Anomaly • Very serious in its role in chronic pyelonephritis and hydronephrosis
    17. 17. ADJECTIVES for CYSTITIS • • • • • • • Acute Chronic Hemorrhagic Suppurative Follicular Eosinophilic Interstitial
    18. 18. CAUSES for CYSTITIS • E. coli • • • • • • • Proteus, Klebsiella, Enterobacter Shistosomes (Egypt) Chlamydia Mycoplasma Viruses, e.g., adenoviruses ChemoRX RadiationRX
    19. 19. SYMPTOMS for CYSTITIS • Frequency • • • • • Urgency Hematuria Abdominal Pain Dysuria Systemic Sepsis, i.e., fever, leukocytosis (urosepsis?)
    20. 20. Special Types of CYSTITIS • “Interstitial” cystitis, aka, Hunner Ulcer • Malacoplakia
    21. 21. “Interstitial” Cystitis • Women>> Men • Bladder Wall Fibrosis • Aka, “Hunner” ulcer
    22. 22. Malacoplakia • YELLOW Mucosal “Plaques” • Why Yellow? • Chronic bacterial infection • Michaelis-Gutmann bodies contain Fe and Ca in macrophages
    23. 23. METAPLASIA • Glandular(is) (Cystica), from Von Brunn nests • Squamous metaplasia
    24. 24. TUMORS • 95% Epithelial (urothelial), 5% mesenchymal, i.e., mesodermally derived (mostly smooth muscle) • Benign or Malignant • Primarily urothelial or transitional, but a few squamous, from antecedent squamous metaplasia, and a few adenocarcinomas, from antecedent glandular metaplasia
    25. 25. TCC TUMORS • MULTIPLE, MULTIPLE, MULTIPLE, i.e., “soil” theory • Papillomas vs. Carcinomas • Grading, I, II, III, or wellpoor • Staging, TNM, based on biologic behavior, really based on normal anatomy
    26. 26. TCC TUMORS • Causes/Risk Factors – Arylamines (aniline dyes) –Cigarettes –Shistosomiasis – Longstanding analgesics, same as analgesic nephropathy drugs, most common NSAIDS – ChemoRX, esp. cyclophosphamides – Radiation RX
    27. 27. Papillomas vs. Carcinomas • Very few pathologists will have enough guts to diagnose a transitional papilloma. Why? • PUNLMP, Papillary Urothelial Neoplasm of Low Malignant Potential – LOW grade PUC (TCC) – HIGH grade PUC (TCC)
    28. 28. LOW Grade
    29. 29. HIGH Grade
    31. 31. TNM example: • Ta----noninvasive, papillary • Tis---Carcinoma in situ, flat • T1----Lamina Propria • • • • T2----Muscularis propria T3a---Microscopic beyond the wall T3b---Grossly beyond the bladder wall T4----Invades adjacent structures
    32. 32. Bladder Neck OBSTRUCTION • Cystocele, MOST common cause in women • Prostate, MOST common cause in MEN • Congenital • Inflammation • Tumors • Foreign Bodies, Calculi • Neurogenic
    33. 33. LOWER Urinary Tract •Ureters •Bladder •Urethra (Anomalies, Infl., Neopl.) (Anomalies, Infl., Neopl.) (Anomalies, Infl., Neopl.)
    34. 34. URETHRA • Inflammations: – Gonococcus – Chlamydia – Mycoplasma – Reiter’s Syndrome (men) – “Caruncle” (women) • Neoplasms: – Transitional – Squamous – Glandular
    35. 35. Chapter 21 Male Genital Tract Diseases
    36. 36. Male Genital Tract • • • • • • • • • (long version) Seminiferous tubules  Straight Tubules  Rete Testis (mediast.)  Efferent Ductules  Epididymis  Vas deferens  Seminal Vesicles  Ejaculatory Ducts  Urethra: ProstaticSpongy
    37. 37. Efferent Ductules and Epididymis
    38. 38. LITTRÉ
    39. 39. Male Genital Tract (short version) • Penis: Congenital, Inflammation, Tumors • Testis/Epididymis: Congenital, Regressive, Inflammation, Vascular diseases, Tumors • Prostate: Inflammation, Benign Enlargement, Malignancy
    40. 40. Penis: Congenital • Hypospadias • Epispadias • Phimosis
    41. 41. Penis: Inflammation “Balanoposthitis” • • • • Candida Anerobes Gardnerella Pyogenic • Role of “smegma”
    42. 42. Penis: Neoplasia • Benign : Condyloma Acuminata (caused by HPV), aka venereal or genital “warts” • Malignant: Squamous cell carcinoma
    43. 43. Koilocytosis
    44. 44. Penis: Malignancy • In-situ = Bowen’s Disease • Invasive = Infiltrating or invasive SQUAMOUS Cell Carcinoma
    45. 45. BOWEN’s Disease = SQUAMOUS cell carcinomain-situ of the skin of the penis
    46. 46. Male Genital Tract (short version) • Penis: Congenital, Inflammation, Tumors • Testis/Epididymis: Congenital, Regressive, Inflammation, Vascular diseases, Tumors • Prostate: Inflammation, Benign Enlargement, Malignancy
    47. 47. Male Genital Tract (short version) •Testis/Epididymis: –Congenital –Regressive (Atrophy) –Inflammation –Vascular diseases –Tumors
    48. 48. Male Genital Tract (short version) • Testis/Epididymis: – Congenital: Cryptorchidism 1% – Regressive: Atrophy – Inflammation: Mumps, GC, Chlamydia, E. Coli, Pseudomonas, TB – Vascular diseases: Torsion – Tumors: Benign/Malig, Germ Cell/non-Germ Cell
    49. 49. Cryptorchidism • 1% of all births • 25% bilateral • Associated with significantly increased incidence of germ cell tumors
    50. 50. Male Genital Tract (short version) • Testis/Epididymis: – Congenital: Cryptorchidism 1% – Regressive: Atrophy – Inflammation: Mumps, GC, Chlamydia, E. Coli, Pseudomonas, TB – Vascular diseases: Torsion – Tumors: Benign/Malig, Germ Cell/non-Germ Cell
    51. 51. Testicular Atrophy • atherosclerotic narrowing of the blood supply in old age • the end stage of an inflammatory orchitis, whatever the etiologic agent • Cryptorchidism (undescended testes are sterile) • hypopituitarism • generalized malnutrition or cachexia • irradiation • prolonged administration of female sex hormones, as in treatment of patients with carcinoma of the prostate; and cirrhosis
    52. 52. Male Genital Tract (short version) • Testis/Epididymis: – Congenital: Cryptorchidism 1% – Regressive: Atrophy – Inflammation: Mumps, GC, Chlamydia, E. Coli, Pseudomonas, TB – Vascular diseases: Torsion – Tumors: Benign/Malig, Germ Cell/non-Germ Cell
    53. 53. Male Genital Tract (short version) • Testis/Epididymis: – Congenital: Cryptorchidism 1% – Regressive: Atrophy – Inflammation: Mumps, TB, GC, Chlamydia, E. Coli, Pseudomonas – Vascular diseases: Torsion – Tumors: Benign/Malig, Germ Cell/non-Germ Cell
    54. 54. Male Genital Tract (short version) • Testis/Epididymis: – Congenital: Cryptorchidism 1% – Regressive: Atrophy – Inflammation: Mumps, GC, Chlamydia, E. Coli, Pseudomonas, TB – Vascular diseases: Torsion – Tumors: Benign/Malig, Germ Cell/non-Germ Cell
    55. 55. Testicular TUMORS • GERM CELL (malig.) • NON-GERM (benign) – SEMINOMA • CELL, i.e., “sex cord” – – – – EMBRYONAL CHORIOCARCINOMA YOLK SAC TERATOMA –MIXED!!!!!, 60% – LEYDIG – SERTOLI
    56. 56. Seminoma (look for germ cells and lymphs)
    57. 57. Embryonal Carcinoma, Formerly called “adeno”carcinoma, so look for “glands” and AFP!!!)
    58. 58. CHORIOCARCINOMA look for “trophoblast”, and HCG!!
    59. 59. YOLK SAC TUMOR, aka “endodermal sinus tumor” Schiller-Duvall Body
    60. 60. TERATOMA MALIGNANT TERATOMA TERATOCARCINOMA clusters of squamous epithelium, hair, skin glands neural tissue retina muscle bundles islands of cartilage structures reminiscent of thyroid gland bronchial or bronchiolar epithelium bits of intestinal wall or brain substance
    61. 61. SEX Cord Tumors •Leydig, tumor cells look like Leydig cells •Sertoli , tumor cells look like sertoli cells
    62. 62. STAGING I • Stage : Tumor confined to the testis, epididymis, or spermatic cord II • Stage : Distant spread confined to retroperitoneal nodes below the diaphragm III • Stage : Metastases outside the retroperitoneal nodes or above the diaphragm
    66. 66. PROSTATITIS • ACUTE, usually same as Urinary Tract Pathogens • CHRONIC, usually A-bacterial, but also often recurrent or persistent from acute • GRANULOMATOUS, TB or nonTB, that is the question!
    67. 67. “BENIGN” Enlargement • BPH • • • • • (H= Hypertrophy) BPH (H= Hyperplasia) Glandular and Stromal Hyperplasia “Nodular” Hyperplasia Associated with old age Associated with urinary obstruction, frequency, bladder hypertrophy and bladder trabeculations • By itself, it is NOT premalignant, however….
    68. 68. P.I.N
    71. 71. BIOLOGIC BEHAVIOR • NORMAL PROSTATE  • HYPERPLASIA  • P.I.N. (Prostatic Intraepithelial Neoplasia), is like “dysplasia leading to adenocarcinoma-in situ  • INFILTRATION of “stroma”  • CAPSULE  • LYMPH NODES  • DISTANT, especially BONE 
    72. 72. GRADING • GLEASON SCORE = Predominant + pattern (1-5) Secondary pattern (1-5) • Best Score = 2, Worst Score = 10
    73. 73. STAGING TNM
    74. 74. T1 CLINICALLY INAPPARENT LESION (BY PALPATION/IMAGING STUDIES) T1a Involvement of ≤5% of resected tissue T1b Involvement of >5% of resected tissue T1c Carcinoma present on needle biopsy (following elevated PSA) T2 PALPABLE OR VISIBLE CANCER CONFINED TO PROSTATE T2a Involvement of ≤5% of one lobe T2b Involvement of >5% of one lobe, but unilateral T2c Involvement of both lobes T3 LOCAL EXTRAPROSTATIC EXTENSION T3a Extracapsular extension T3b Seminal vesical invasion T4 INVASION OF CONTIGUOUS ORGANS AND/OR SUPPORTING STRUCTURES INCLUDING BLADDER NECK, RECTUM, EXTERNAL SPHINCTER, LEVATOR MUSCLES, OR PELVIC FLOOR N0 NO REGIONAL NODAL METASTASES N1 METASTASIS IN REGIONAL LYMPH NODES M0 M1 M1a M1b M1c NO DISTANT METASTASES DISTANT METASTASES PRESENT Metastases to distant lymph nodes Bone metastases Other distant sites
    75. 75. TID-BITS • Prostate is #1 most common malignancy in men but NOT #1 killer. WHY? • 80% over 80 • Every elderly male presenting with widespread bone metastases is carcinoma of the prostate until proven otherwise • PSA (Prostate Specific Antigen) has been controversial as a screening test but is GREAT for follow up of a known prostate cancer