Note: the following material is for personal use only see below for

Bacterial prostatitis

1. 
   ascending urethral infection
   
2. 
   reflux of infected urine into prostatic ducts entering into the posterior urethra
   
3. 
   invasion of colonic bacteria through direct extension or lymphatic spread
   
4. 
   hematogenous seeding
   

Organisms: E. coli, GNR, Pseudomonas, Proteus, Klebsiella, S. aureus, coagulase-negative Staphyloccocus

fever, chills, dysuria / UTI organisms / do not express prostatic secretions (risk of

bacteremia) / urine culture usu. positive / fast response to IV antibiotics (treat 4 weeks)
Chronic bacterial prostatitis

WBC’s in secretions / diagnosed by quantitative bacterial localization cultures (3 cultures,

1^st 10 ml, 2^nd 10 ml, post-DRE 10ml, which it the EPS sample) / may require 1-2 months

abx / TURPS in refractory cases, but relapse is common if infection not completely cleared

chlamydia (current thinking actually is that chlamydia does not play much role in

prostatitis), ?ureaplasma / fungal, anaerobes, RPR, viral / can get chemical prostatitis from

urethral spasm and reflux / alpha-adrenergic blockers can sometimes help with voiding

foreign body reaction to extravasated secretions / hard nodule / may resemble carcinoma

systemic Tb / may follow BCG immunotherapy for bladder Ca (PSA will return to normal)

occurs 10 yrs earlier in blacks

Symptoms: urinary retention, control / urinary tract infection, prostatitis

Complications: may lead to bladder SMC hypertrophy, diverticulum

Pathology: transition zone and periurethral glands / 2 cell layers is a good sign

Treatment:

• 
  Medical: a-1 blockers reduce smooth muscle contraction (more immediate benefit with smaller
  

hypertrophy and male pattern hair loss)

• 
  Surgical (no longer 1^st line): TURP (prostatectomy) / ? laser and cryoablation
  

Prostate Cancer

prostate cancer; 16% of cases have elevated PSA as only symptom) / usu. posterior peripheral zone, prominent nucleoli

• 
  Blacks – early, high grade
  
• 
  White – middle onset, variable aggresivity
  
• 
  Asian – later onset, less aggressive (more dietary)
  

• 
  PSA > 3 ng/ml over age 40 (repeat test x 1) / 4.0 to 10.0  marginal level (25% chance of malignancy), but must chart over time, because 2 is moving up the curve already / 26-68% newly diagnosed have proven extra-prostate mets / free PSA can help for marginal total PSA (high free fraction is good because it could mean the high total was misleading due to nature of assay)
  
• 
  Bone scan: osteoblastic activity well seen (unlike myeloma and sometimes thyroid, renal mets which are osteolytic and do not take up tracer)
  
• 
  MRI if trying to assess resectability
  

sum of 1^st and 2^nd most predominant architectural pattern / 2-10 (over 5-6, aggressive)

Stage B (palpable) note: A2 may have worse prognosis than B1

Stage C (extra-prostatic) most patients present with stage C or D

Stage D (distant mets)

yearly DRE and PSA screening > 50 yrs (blacks > 40 yrs) / if value increased > 20% in 1 yr (considered positive PSA test  consider biopsy)

• 
  radical retropubic prostatectomy (may be curative in early stage; impotence, incontinence may result, but sometimes function returns over 4-6 months)
  
• 
  radiation therapy another option / PSA levels slowly decline after (side effects occur late)
  
• 
  LHRH (GnRH) agonist (goserelin, buserelin leuprolide)  most efficacious (1^st line)
  
• 
  antiandrogen (flutamide)  not quite as efficacious, does not cause impotence
  
• 
  combination LHRH + anti-androgen  more side effects (impotence), only very slight
  

• 
  orchiectomy  works but most men don’t want this
  
• 
  adrenalectomy  ?
  
• 
  DES (estrogen)  efficacious but increased MI, thrombosis
  
• 
  chemotherapy  no increased survival has been shown (this may have changed since ‘06)
  

¼ bilateral / contralateral, descended testis may show changes / XXY / seen by age 2

low germ cell development / hyalinization of seminiferous tubule BM / interstitial fibrosis

Treatment: scrotal placement < 2 yrs (sterility may ensue if not corrected before age 5) / resection to prevent CA
Leydig cell hyperplasia

Symptoms: inguinal hernias / orchiopexy may prevent infertility, but not neoplasm risk

hydrocoele (incomplete closure of tunica vaginalis)

hematocoele

chylocoele

varicoele (18% normal males on L or bilateral pampiniphorm plexus issue)

spermatocoele (semen fills duct)

under 35 C. trachomatis, N. gonorrhea

over 35 E. Coli, Pseudomonas
granulomatous orchitis

rare, unilateral enlargement / acute, fever, tender / autoimmune / plasma cells (occasional neutrophil) surrounded by rim of lymphocytes, fibroblasts

20% result in orchitis (may be bilateral) / usu. > 10 yrs old / 70% unilateral / usu. 1wk after

parotitis / mononuclear infiltrate - interstitial, patchy / usually does not cause sterility
tuberculosis

epididymis first, then testis / TB = testicular artery?

testis first, then epididymis / sterility occurs secondary to obliterative endarteritis

• 
  post-chemotherapy leukemia relative risk at 5 yrs (15-25%), which equals absolute risk of 0.5%
  
• 
  treatment-related solid tumors are radiation-related occurring in bladder, pancreas, stomach with latency of ~10 yrs
  

- peak incidence 15 - 34 yrs / preceded by intratubal germ cell neoplasia

• 
  seminomas vs. non-seminomatous GCTs
  
• 
  remain localized
  
• 
  mets via lymphatics first (?then hematogenous to lung)
  
• 
  relatively radiosensitive
  
• 
  usu. have normal tumor markers (hCG and/or aFP elevated in 75% NSGCTs)
  

• 
  typical treatment regimen might include cisplatin, etoposide, bleomycin or VBP (vincristine, bleomycin, cisplatinum)
  
• 
  decision whether or not to do RPLND (retroperitoneal lymph node dissection to look for mets); depends on stage and other factors [NEJM]
  
• 
  high hCG, aFP or LDH > 10x normal confers worse prognosis (still can have 50% cure rate) / half-life of aFP is 6 days, β-HCG is 1 day (both markers should be followed with treatment as levels may decrease differently because of production by different populations of tumor cells)
  
• 
  relapse for stage I 20-30% (usu. < 2 yrs, rare after 5 yrs) but still 98% eventually cured
  

20s / aggressive / variable pattern (alveolar, tubular, glandular) / nodules separated

by slits / most common testicular tumor in infants and children

intra/extracellular globules with aFP and a1-AT (Schiller-Duval bodies)

cyto/syncitiotrophoblastic cells / very aggressive (lymphatic spread) / produce hCG

Rx: MTX
Teratomas (see other) (3-5%)
Mixed NSGCT (35%)

1st - teratoma, embryonal carcinoma, yolk sac tumor w/ hCG syncitiotrophoblast

2nd - “teratocarcinoma” is a teratoma and embryonal carcinoma

3rd - seminoma, embryonal carcinoma

usually benign, may elaborate steroids

/ 10% invade / contain lipochrome pigment, lipid droplets, Reinke crystalloids (needle-like)

recapitulate seminiferous tubules / may secrete hormones (ABP) / 10% invasive

most common in > 60yrs / diffuse large cell lymphoma

90% transitional cell / squamous, adenocarcinoma

Risk factors: males 3x > females / smoking ↑ 2-4x / chronic cyclophosphamide, external beam radiation, aniline dyes, schistosomiasis

Presentation: hematuria, UTI

Diagnosis: urine cytology, cystoscopy

Treatment: resection and chemotherapy (even for local disease!) / BCG vaccine used as intravesicle treatment