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REGUB > 10. Male GU > Flashcards

10. Male GU Flashcards

1
Q

What is the normal anatomy of the prostate?

A
  • Small, round organ @ base of bladder, encircling urethra
  • Posterior part palpable by DRE
  • Consists of:
    1. Glands:
  • Luminal cells (inner)
  • Basal cells (outer): secrete alkaline (for sperm + seminal vescicle = semen)
  • make PSA, which liquifies semen
    2. Stroma
  • Glands and stroma maintained by androgens
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2
Q

What are 2 prostatic pathologies? Describe.

A
  1. Prostatitis
    - Mostly clinical relevance, not a specific query to a histopathologist (but prostage specific antigen –PSA - can increase and thus raise concern for cancer)

A) Acute bacterial prostatitis
- Secretions: WBCs, and culture +ve for bacteria
- Bacteria: Chlamydia trachomatis, Neisseria gnorrhoea
o Usually seen in UTI
o Mostly in adult men
o Systemic and local symptoms —> dysuria, fever, chills

B) Chronic Bacterial Prostatitis
- Chronic inflammation
- Secretions: WBCs, culture -ve
o As for acute, relapsing, lesser symptoms —> dysuria, lower back pain

  1. Benign Prostatic Hyperplasia
    - Hyperplasia of stroma and glands
    - Related to DHT (dihydrotestoterone)
    - Occurs in periurethral zone
    - PSA increases b/c increase in number of glands
    —> Testosterone converted to DHT by 5a reductive
    —> DHT acts on androgen receptors + epithelial cells = hyperplastic nodules
    - Very common disorder and a very frequent referral to a urologist
    - Aetiology: hormonal, age-related (60y), genetic predisposition
    - Symptoms (prostatism):
    o Obstructive (from prostate):
    —> Poor flow
    —> Hesitancy
    —> Feeling of incomplete bladder emptying
    —> Dribbling
    o Irritative (from bladder)
    —> Urgency
    —> Frequency incl. nocturia
  • Tx:
    1) a1 antagonist (Terazosin): relax smooth muscle and decrease BP
    2) 5a-reductase inhibitor: blocks conversion of testosterone to DHT
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3
Q

Describe prostate cancer?

What are the malignant prostate tumours?
Primary (2)
Secondary (2)

What are the risk factors?
(4)

What is the epidemiology?

What are the symptoms?
(3)

A 
PRIMARY 
1.	Adenocarcinoma: malignant proliferation to prostatic glands 
a . Microacinar variant
b.	Ductal variant
c.	Others
2.	Others (rare) 
a.	Squamous cell carcinoma
b.	Small cell carcinoma
c.	Sarcoma, lymphoma

SECONDARY

  1. Rare
  2. Usually direct examination of bladder or rectal cancer

RISK FACTORS

  1. Age (very rare < 40, rare <50)
  2. Ethnicity
  3. Genetic: family history, BRCA, Lynch
  4. Hormones, diet, obesity

EPIDEMIOLOGY

  • 5 year cancer specific survival in early detected cancers is >95%
  • US —> lifetime risk of being diagnosed with prostate cancer is 16% but the risk of dying from prostate cancer is 2.9%
  • Autopsy studies show that up to 50% of men over 60 have prostate cancer

SYMPTOMS (clinically silent)

  1. Most are incidental pick-ups
    a. PSA test
    b. Digital rectal examination
    c. Resection for BPH, pathologist finds cancer
  2. Local (late, may mimic BPH)
  3. Metastatic (bony)
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4
Q

What are the non-skin cancer incidences in men?
(3)

What are the 3 cancers that cause morality in men?

A

NON - SKIN INCIDENCES

  1. Prostate
  2. Colorectal
  3. Lung

MORTALITY

  1. Lung
  2. Colorectal
  3. Prostate
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5
Q

What is prostate specific antigen? (PSA)

A
  • Small glycoproteins secreted by prostatic epithelial cells to liquify semen in seminal vesicle ejaculate
  • Leaked into serum in very low quantities in normal men (usually <4 ng/mL)
  • Serum PSA increased in prostate cancer, but also increased for other reasons
  • Widely used as screening for prostate cancer
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6
Q

How is prostate cancer diagnosed?
(3)

What are the pathological features - micro and macro?

What are the histological features?
(3)

A

DX

  1. Blood test (PSA)
  2. Radiology
  3. Clinical Symptoms, DRE findings

PATHO

  • Prostate cancer is very subtle
    1. Macroscopic: multifocal, infiltrative, usually not seen
    2. Microscopic: minimal pleomorphism, mitotically inactive, often small foci

HISTO FEATURES (of prostatic adenocarcinoma)

  • No single defining feature
    1. Architecture: small crowded glands
    2. Nuclear features: nuclear enlargement and large nucleoli
    3. Immunohistochemistry: lack of basal myoepithelial cells
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7
Q

What is the prognosis - how is it staged?
(2)

What is prostatic biopsy?
(3)

How does a high risk prostate present?

A
  1. Clinical Staging: TMN: show small, invasive glands w/ prominent nucleoli
    - T1: incidentally detected cancer (T1a and T1b on TURP, T1c on need core)
    - T2: confined to prostate
    - T3: extraprostatic
    - T4: into adjacent organ
    - N0/N1: regional nodes
    - M0/N1: distant sites
  2. Biopsy Gleason Grade: based on architecture (glandular pattern) not nuclear atypia
    - Gleason score = predominant pattern + second pattern
    a. Gleason score could be 2-10 but in reality almost all diagnosed now are 6-10
    b. Grade groups
    i. Gleason score 6
    ii. Gleason score 3+4=7
    iii. Gleason score 4+3=7
    iv. Gleason score 8
    v. Gleason score 9-10

A) Patterns 1-2: rarely used now
B) Pattern 3: single, well formed glands
C) Pattern 4: poorly formed / fused glands
D) Pattern 5: no glands —> single cells, sheets, rows

PROSTATIC BX
1. Transrectal: extended sextant 12 cores
2. Template biopsy
3. Targeted biopsy
- Main limitation = lack of targeting
—> Negative biopsy +/- no prostate cancer
—> Cancer extent and grade in biopsy may not reflect actual cancer extent and grade in prostate (although it often does)

HIGH-RISK PROSTATE  
-	15% of diagnosed cancers
o	Clinical stage T3
o	Gleason score >8
o	PSA >10
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8
Q

What is the treatment of adenocarcinoma?

2

A
  1. Prostatectomy (local)
  2. Hormone suppression (advanced): decreases testosterone + DHT
    - Continuous GnRH analogue (Leuprolide)
    - Flutamide: competitive inhibitor of adrenal receptor
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9
Q

What are the testicular tumours?
(3)

What is the general clinical presentation
(1)

A
  1. Germ cell tumour, GCT (~90%)
    a. Seminoma
    b. ‘Non-seminoma’
  2. Sex cord / stromal tumours (<10%)
    a. Leydig cell tumour: the most common and most are benign —> produce androgen = causes precocious puberty and gynaecomastia
    b. Sertoli cell tumour: clinically silent
  3. Other rare tumours: lymphomas (B cell) and metastases (older men)

CP
1. Firm, painless testicular mass that can’t be transilluminated

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10
Q

Explain germ cell tumours (GCT). What is it divided into?
(2)

What are the risk factors?
(3)

What is the incidence?
(3)

A
  • Malignant tumours

CLASSIFICATION

  1. Seminoma
  2. Non seminoma

INCIDENCE
o Rare tumours, 175 cases/year in Ireland 2008-10
o Mean age is 30s to 40s
o Most common solid tumour in young men
- Survival very good b/c chemo and radiation tx
—> Chemo might make cancer differentiate into teratoma (increased AFP and B-hCG)

RISK FACTORS

  1. Racial: white > black
  2. Cryptorchidism
  3. Others (rare): Klinefelter syndrome
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11
Q

Explain seminomas.

A
  • Malignat tumour with large cells with clear cytoplasm + central nuclei —> forms homogenous mass with no hemorrhage / necrosis
  • 55% of cases
  • Age peak 40s
  • Excellent prognosis
  • Mets late
  • Adjuvant radiation (radiotherapy) = good
  • No specific tumour marker in blood but LDH often increased
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12
Q

Describe non-seminomas. What the types?

5

A
  • Age 30s
  • Mets early
  • Adjuvant chemotherapy
  • Some secrete “specific” tumour markers —> hCG, AFP, and LDH increased

TYPES

  1. Embryonal ca: malignant tumour of primitive cells that may produce glands
    - Forms hemorrhage mass w/ necrosis
    - Aggressive w/ haematogenous spread
  2. Teratoma: mature fetal tissue (increased AFP and b-HCG)
  3. Yolk Sac Tumour: endodermal sinus malignant tumour that resembles yolk Sac elements (MOST COMMON)
    - Histology: Schiller - Duval Bodies
    - Increased AFP
  4. Choricocarcinoma: malignant tumour of syctiotrophoblast and crytopblasts
    - Spreads via blood (haematogenous)
    - B-hCG increased = causes: hyperthyroidism, gyaecomastia
  5. Mixed cell carcinoma
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13
Q

How do you stage GCTs?
(1)

How does it spread?
(2)

A

TMN Staging

  1. T1: limited to testis
  2. T2: limited to testis but invades through tunica albuginea and/or shows vascular invasion
  3. T3: invades cord
  4. T4: invades scrotum

SPREAD

  1. Lymph nodes:
    a. Common / internal iliac nodes FIRST
    b. Then, upwards towards chest
    c. NOT inguinal nodes
  2. Haematogenous:
    a. Lungs, brain
    b. Most common in non- seminoma (choriocarcinoma)
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14
Q

What are some pathologies of the penis / scrotum?

2

A
  1. Congenital

2. Inflammatory

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15
Q

Describe the congenital pathologies of the testis / scrotum.

3

A
  1. Hypospadia
    - Abnormal opening of urethra b/c of failure of urethral folds to close
    - More common than epispadia
    - Occurs on the inferior surface
    - A/w bladder estrophy (exposed)
  2. Epispadia
    - Abnormal opening of urethra due to abnormal positioning of genital tubercle
    - Occurs on superior surface
    - A/w with bladder exstrophy (exposed)
  3. Phimosis
    a. Inability to retract foreskin from gland penis
    b. Normal for boys have ‘phimosis’
    d. Chronic inflammation
    i. Poor hygiene
    ii. Lichen sclerosis (‘balanitis xerotica obliterans’)
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16
Q

Describe the inflammatory pathologies of the testis / scrotum.
(2)

A
  1. Lymphogramulma Venerum
    - Due to STDs: Herpes Simplex, Syphillis, Gnorrhea, Chlamydia
    - Gnorrhea and chlamydia cause urethral inflammation and not external genital problems
  2. Condyloma Accuminatum
    - Genital Warts
    - Caused by: HPV 6+11
    - Increased risk of penile cancer
17
Q

What is penile cancer (SCC)?

What is the aetiology?
(3)

How is it staged?
(1)

A
  • Malignant proliferation of squamous cell penile of skin
  • Rare cancer here
  • Almost all are SSC
  • Usually seen in males > 55 y/o

AETIOLOGY

  1. Infection: a/w HPV and history of genital warts (HIV also increases risk)
  2. Hygiene: Phimosis, poor hygiene, lack of circumscion
  3. Lichen sclerosis (or BXO)

TNM STAGING

  1. pTis: carcinoma in situ
  2. pT1: invasion of subepithelial tissues
  3. pT2: invasion of corpus spongiosum* —> +/- invasion of urethra
  4. pT3: invasion of Corpus cavernosum* —> +/- invasion of urethra
  5. pT4: invasion of adjacent structures
  • Usually spreads to lymph nodes  inguinal nodes affected FIRST

REGUB (22 decks)

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