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6. HDS GI Repro > Male GU Disorders > Flashcards

Male GU Disorders Flashcards

1
Q

Male Genital Disease

Introduction

A
  • Wide range of benign and malignant conditions
  • Effect 80-100% of men in their lifetime (if include BPH)
  • Dx predominantly by hx and PE
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2
Q

Penis

Anatomy

A
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3
Q

Male Genital Disease

History

A
  • Presenting complaints vary from asymptomatic mass to acute pain
  • ID prodromal sx
  • Localize pain, intensity and duration
  • Question both voiding and defecation patterns
  • Sexual function/libido issues
  • Hx of infections/STD’s
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4
Q

Male Genital

Exam

A
  • Perform both standing and supine
  • Wear gloves
  • Explain to pt the plan
  • Be sensitive to the intimacy of the exam
  • Examine penis, scrotum, scrotal contents, neurologic status, anal anatomy and prostate
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5
Q

Hypospadias

A

Abnormal opening of urethra on ventral surface of penis.

  • Relatively common, 1/300 live male births
  • No specific genetic deficiency
  • 70% have distal type
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6
Q

Epispadias

A

Abnormal opening of the urethra on dorsal surface of penis.

  • Can be associated w/ bladder exstrophy or undescended testis
  • Rare: 1/100,000 male births
  • Can cause partial urinary obstruction that can lead to UTI
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7
Q

Phimosis

A
  • Definition: The prepuce cannot be retracted over the glans of penis.
    • Most frequently the result of chronic infection w/ scarring due to poor hygiene
    • Less frequently presents as a congenital anomaly
  • Clinical findings: swelling, redness, pain
  • Inflammation is caused by smegma
    • Aggregation of desquamated epithelial cells, secretions and inflammatory debris that forms beneath the prepuce in uncircumcised males
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8
Q

Balanoposthitis

A

Inflammation of the foreskin and glans.

  • Can be due to a variety of organisms
  • Can result from poor local hygiene esp. if uncircumcised
  • Leads to inflammation & scarring
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9
Q

Systemic Dermatoses

Penile Manifestations

A

Inflammatory disorders affecting the penis:

  • Contact dermatitis
  • Fungal and parasitic infestation
  • Lichen planus
  • Psoriasis vulgaris
  • Fixed drug eruptions
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10
Q

Sexually Transmitted Diseases

A
  • Syphilis
  • Gonorrhea
  • Chancroid
  • Granuloma inguinale
  • Lymphogranuloma venereum
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11
Q

Balanitis Xerotica Obliterans

A
  • Atrophy of glans penis
    • Counterpart to vulvar lichen sclerosus in women
  • Present in 37% of penile carcinomas
  • May present as phimosis or stricture of distal urethra
    • See pale gray areas around the urethra
  • Histology:
    • Marked epithelial atrophy w/ absence of rete pegs
    • Band-like homogenous pale tissue in upper dermis
    • Lymphocytic infiltrate perivascular and periappendiceal
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12
Q

Condyloma Acuminatum (Genital Wart)

Pathogenesis

A
  • Results from infection w/ human papillomavirus (HPV)
    • Sexually transmitted disease
  • Virus appears to ⊗ terminal differentiation of squamous cells
  • Condylomas almost all pts w/ HPV 6 and/or 11
  • Can occur at various sites including the urethral meatus (frequently) penile urethra, penis, perineum, and anus
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13
Q

Condyloma Acuminatum (Genital Wart)

Histomorphology

A
  • Single or multiple
  • Papillary, sessile or pedunculated
  • Manifests as papillomatosis, acanthosis, focal parakeratosis, and hyperkeratosis of epithelium
  • Prominent branching of rete ridges
  • Koilocytosis of the superficial malpighian (prickle) layer
  • Koilocyte: cell w/ large, hyperchromatic, irregular nucleus surrounded by a clear halo
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14
Q

Bowen Disease

A
  • Carcinoma in Situ (CIS)
  • Associated w/ infection w/ high-risk HPV
  • Seen in men and women, usually > age 35
  • Gross:
    • Gray-white thickened opaque plaque on penile shaft or scrotum
    • Shiny or velvety red plaques on glans or prepuce
  • Micro:
    • Hyperproliferative epidermis w/ many mitoses
    • Dysplastic cells w/ large, hyperchromatic nuclei
  • Can become invasive Squamous Cell Carcinoma (SCC) in 10% of cases
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15
Q

Bowenoid Papulosis

A
  • Younger pts
  • Multiple (rather than solitary) reddish–brown papular lesions
  • Usually regresses spontaneously, does not become invasive
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16
Q

Squamous Cell Carcinoma (SCC)

Characteristics

A
  • Linked to high-risk HPV infection
  • Circumcision is protective
    • Reduces exposure to carcinogens that may be concentrated in smegma
    • ↓ likelihood of infection w/ oncogenic HPV
  • Macroscopic patterns:
    • Papillary: looks like a condyloma
      • Cauliflower-like fungating mass
    • Flat: thickened gray fissured plaque, then ulcerates
    • Verrucous: locally invasive but rare metastasis
  • Epidemiology:
    • Incidence: 0.7-0.9/10k men
    • 1% of CA in US males, less than 0.2% of CA deaths
  • Presentation:
    • Peaks at 50-70 y/o
    • Indurated, usu. ulcerated lesion
    • Most commonly on the glans, prepuce or coronal sulcus
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17
Q

Squamous Cell Carcinoma (SCC)

Clinical Management

A
  • Treatment:
    • Partial or total penectomy w/ inguinal node dissection
  • Prognosis:
    • 65% survival at 5 yrs when confined to penis
    • 25% when LN involved
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18
Q

Testicle

Microanatomy

A
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19
Q

Cryptorchidism

A
  • Undescended testis
    • Seen in 1% of 1 y/o boys
    • 75% unilateral, 25% bilateral
  • Two phases of testicular descent:
    • Transabdominal
      • Controlled by Muellerian-inhibiting substance
      • Arrest here is rare
      • 5-10% of cases
    • Inguinoscrotal
      • Androgen-dependent
      • Testis can be located anywhere along path of descent
  • Normally, descent into the scrotum takes place by ~ 7th month of gestation
  • Should not dx cryptorchidism until after age 1 ⇒ may spontaneously descend up to that time
  • Cause is unknown
  • Associated w/: Trisomy 13, Beckwith’s syndrome, Prader-Willi and Fanconi’s syndrome
  • Consequences:
    • 7-11x ↑ risk for development of germ cell neoplasms
      • Risk persists even if corrected (orchiopexy) before age 2
      • ↑ risk is also in unaffected testis thus
      • Intrinsic defect in testicular development
    • Infertility can also result
  • Histology:
    • Undescended testis is small
    • ↓ tubular diameter
    • ↓ number of germ cells
  • Treatment: Orchiopexy, the earlier the better
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20
Q

Hypospermatogenesis

A
  • ↓ number of spermatogonia, spermatocytes, spermatids and spermatozoa
  • Non-specific etiologies
  • May be reversible
  • Maturation arrest: Near total lack of mature forms
    • @ Spermatocyte stage
      • Ass. w/ chromosomal and genetic abnormalities
    • @ Spermatogonial stage
      • Ass. w/ radiation & chemotherapy
  • Germ Cell Aplasia (Sertoli cell-only syndrome)
    • No germ cells
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21
Q

Gonadal Atrophy

A
  • Gonad size is reduced due to shrinkage of seminiferous tubules
  • Shrinkage is due to loss of spermatogenic activity
  • Ass. w/ thickening of the peritubular tissue
  • Causes: Atherosclerosis, end stage inflammatory orchitis, cryptorchidism, hypopituitarism, malnutrition, irradiation, anti-androgen therapy, Klinefelter syndrome, alcohol abuse & cirrhosis, Vit E def, DM, AIDS
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22
Q

Hydrocele

A

Accumulation of fluid in the sac between visceral and parietal tunics vaginalis

Types:

  • Congenital w/ communication to the abdominal cavity
  • Infantile w/ no communication
  • Acquired as a result of trauma, cardiac failure or renal disease
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23
Q

Granulomatous Orchitis

(Autoimmune)

A
  • Unknown etiology, may be due to trauma, autoimmunity to lipid fraction of sperm
  • Causes unilateral painless testicular enlargement w/ oligospermia
  • Histology: non-caseating granulomas around seminiferous tubules
  • Differential dx includes TB, syphilis, brucellosis, leprosy, sarcoidosis, and infection w/ fungi, rickettsia or parasites
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24
Q

Gonorrhea

Histology

A

Epididymis shows acute inflammation

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25
Q

Mumps

GU Effects

A
  • Testicular involvement is more frequent in adults (20-30%) than in children
  • Unilateral orchitis usually follows parotiditis
  • Histology: edema and infiltration of lymphocytes, plasma cells and MΦ
  • Process is patchy w/in the testis and usually does not result in infertility
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26
Q

Varicocele

A
  • Most common cause of male infertility (37%)
  • Congenital absence or insufficiency of valves in internal spermatic vein leads to reflux
  • Causes varix-like distention in the pampiniform plexus
  • More frequent in the left side
    • Left spermatic vein → left renal vein
      • 8-10 cm longer than right
      • Courses b/t superior mesenteric artery and aorta
    • Right spermatic vein → inferior vena cava
  • Treatment: surgical excision
  • Recovery of spermatogenesis in up to 80% of pts
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27
Q

Testicular Torsion

A
  • Types:
    • Infantile (8%)
    • Adults (92%)
      • Bell-clapper abnormality
        • Tunica vaginalis reflected from spermatic cord vs anterior portion of testis
        • Results in lack of connections to scrotal wall
        • 10% men
  • Torsion may occur w/ trauma or exertion, but can also happen during sleep
  • Clinical:
    • Sudden severe testicular pain, followed by scrotal tenderness
    • ± Swelling, leukocytosis, nausea, fever
    • Urologic emergency
  • Histology:
    • First 6 hours: congestion, edema, and hemorrhage but the germinal cells appear viable
    • After 6 hours: hemorrhagic infarction
  • Dx: Need to obtain Doppler US if torsion suspected to evaluate blood flow
  • Treatment:
    • Surgical correction w/in 4-6 hrs might salvage the testis
    • Bell-clapper abnl is b/l ⇒ requires contralateral orchiopexy
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28
Q

Erectile Dysfunction (ED)

Overview

A

The consistent inability to achieve and/or maintain an erection or erection satisfactory for intercourse.

  • Very common condition with many men
  • Undiagnosed for many reasons
  • Multifactorial etiology: vascular, neurologic, DM, trauma, surgery, meds, psychological, HTN, HLD
  • ED prevalence ↑ with age
  • Hx is essential for diagnosing ED accurately
  • Must differentiate from premature ejaculation and situational issues
  • Work up includes PE, measurement of serum testosterone levels
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29
Q

Erectile Dysfunction (ED)

Associated Meds

A

Drugs Associated with ED include:

  • Estrogens, Antiandrogens
  • Antihypertensives: Clonidine, methyldopa, HCTZ, β-blockers, Spironolactone, Diuretics
  • Psychotropics: MAOi, TCAs, antidepressants, phenothiazine, benzodiazepines, SSRIs
  • CNS depressants: sedatives, narcotics, alcohol
  • Alcohol, Marijuana, Narcotics, Cigarettes, Cocaine
  • H2 blockers, anticholinergics, Atropine, lipid-lowering agents, NSAIDs
  • Cytotoxic drugs, Ketoconazole
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30
Q

Erectile Process

A
  • Muscles of the arteries and sinusoids relax
  • Erectile tissue fills w/ blood at arterial pressure
  • Compression of the plexus of subtunical arteries ⇒ ↓ venous outflow
  • Detumescence occurs through the reversal of this process
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31
Q

Erection Control

A
  • Erection
    • Extrinsic factors via supraspinal pathways + neurotransmission ⇒ ∆ cavernosal artery tone
    • Central neural input is an absolute requirement
      • NANC (nonadrenergic noncholinergic) system
        • Key neural pathway
        • Releases nitric oxide (NO)
        • Within cavernosal smooth muscle cells:
          NO ⇒ ⊕ guanylate cyclase ⇒ ↑ cGMP ⇒ ↓ intracellular Ca2+ ⇒ relaxation ⇒ engorgement
  • Detumescence
    • Cyclic GMP broken down 1° by phosphodiesterase-5
      • Partly accounts for detumescence
    • Norepi released from SNS nerves plays a larger role
      • cAMP & cGMP involved in smooth muscle relaxation
      • Work via kinases ⇒ ℗ of proteins that leads to:
        • Opening of K+ channels ⇒ hyperpolarization
        • Sequestration of intracellular Ca2+ by ER
        • ⊗ Voltage-dependent Ca2+ channels ⇒ ⊗ Ca2+ influx
        • Activation of myosin phosphatase
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32
Q

Erectile Dysfunction (ED)

Therapeutic Options

A
  • First try lifestyle changes or if possible, termination of drugs which may cause ED
  • 5-Phosphodiesterase Inhibitors ⇒ mainstay of therapy
    • Therapeutic effect is via nitric oxide pathway resulting in smooth muscle relaxation and vasodilation
    • Effective in 60% of men
  • Testosterone (T) replacement therapy
    • Topical gels or injections
      • Gels better: more convenient & provides steady-state T levels
    • T can stimulate existing prostate CA & exacerbate BPH
      • No evidence that T replacement causes cancer or BPH
  • Penile injection therapy with vasoactive agents
  • Vacuum device
  • Penile prosthesis
  • Sexual counseling for psychogenic ED
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33
Q

Injectable

ED Drugs

A
  • Injected into base of the penis
    • There are minimal pain fibers in the penis
  • Takes 5-10 min to work
  • Response rate is excellent
    • Drugs can be effective if PO meds fail
  • Most common AE is pain @ injection site
  • Fibrotic episodes are rare
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34
Q

PGE1

[Alprostadil]

A

Vasodilator

  • 1st drug approved for ED as an injection
  • Intraurethral form available
  • Less effective and may cause burning and itching
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35
Q

Trimix

A

Contains phentolamine, papaverine, and prostaglandin E1

  • Phentolamine ⇒ ⊗ α-adrenergic receptors which can cause constriction
  • Papaverine ⇒ vasorelaxation either directly or via ⊗ of phosphodiesterase
  • PGE1 ⇒ ↑ cAMP
  • Combo allows pharmacologic synergy
  • Each agent used @ lower concentration ⇒ ↓ penile fibrosis
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36
Q

Phosphodiesterase-5 Inhibitors

A
  • > 50 phosphodiesterase enzymes in the body
  • 5 PDE enzymes in penile tissues
    • Most prominent form is PDE-5, found in the corpus cavernosum
  • AEs of PDE-5 inhibitors attributed to ⊗ of enzyme in other tissues
  • Mechanism of action:
    • ⊗ PDE-5 ⇒ potentiates relaxant effects necessary for erection initiated by NO release from autonomic nerves of PNS and vascular endothelium
    • ⊗ PDE-5 ⇒ prevents degradation of cGMP ⇒ potentiates relaxation of corporeal arterial and sinusoidal smooth muscle
  • Contraindications:
    • Recent hx of CVA, MI, low BP, unstable angina, severe cardiac failure, severe liver impairment and/or ESRD
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37
Q

Sildenafil

[Viagra]

A

Phosphodiesterase-5 Inhibitor

  • Pharmacodynamics:
  • Onset of action usu. hour after PO ingestion
  • High fat meals ↓ rate of absorption
  • Recommended that drug be taken 1 hour before sexual intercourse and not w/ heavy meals
  • T½ 4-6 hrs
  • Duration of effect 4-5 hrs
  • Pharmacokinetics:
  • Degraded in liver by cytochrome P-450 3A4 and 2C9
  • Pts w/ hepatic dysfunction, > 65 y/o, or taking cytochrome P-450 inhibitors will have ↑ levels
  • Ex. of drugs that inhibit the same P-450 system: grapefruit juice, cimetidine, erythromycin
  • Ritonavir inhibits both P-450s
  • Efficacy:
  • 70% of pts will get an erection even w/ comorbidities such as CAD/PVD
  • ↓ Response in diabetics
  • Some pts may switch to injectables b/c rigidity of erection is greater
  • Oral form is more convenient
  • Adverse effects:
  • Headache (16%), flushing (10%), dyspepsia (6%), nasal congestion (4%), altered vision (3%), and diarrhea
  • Visual disturbance: subtle change in color perception (blue aura)
  • Priapism
  • Only occurred if sildenafil used in combo w/ other therapies for ED
  • Interactions and contraindications:
    • Can potentiate effect of NO donors ⇒ life-threatening hypotension
    • Caution in pts taking α-blockers
    • Caution in pts w/ coronary related problems
    • ? Ass. w/ Nonarteritic anterior ischemia optic neuropathy (NAION)
38
Q

Vardenafil

[Levitra]

A

Phosphodiesterase-5 Inhibitor

All aspects are similar to sildenafil

39
Q

Tadalafil

[Cialis]

A

Phosphodiesterase-5 Inhibitors

  • Pharmacokinetics and pharmacodynamics:
    • T½ 18 hrs (longer than Sildenafil and Vardenafil)
    • Duration of effect 36 hrs
    • Onset of action maybe slightly longer
    • Plasma concentration unaffected by food
    • Similar effects in regard to cytochrome P-450
  • Efficacy:
    • Similar efficacy but longer duration of action
    • Pts may prefer Tadalafil over Sildenafil
  • Adverse effects:
    • Similar to the other two
    • Drug has greatest selectivity of PDE5 vs PDE3A
      • Potentially less cardiac effects
    • Greater selectivity for PDE5 vs PDE6 (found in the retina)
      • Potentially less visual effects
40
Q

PDE-5 Inhibitor

Treatment Failure

A
  • Pts failing one inhibitor may respond to another in the class
  • Tx should not be considered a failure unless they have not responded to the maximum dose
  • Some pts may respond to continuous dosing
  • Some pts may require androgen replacement therapy
41
Q

Apomorphine

A
  • Centrally acting agent
  • Dopamine D1/D2 agonist
  • Works at the level of the hypothalamus
  • Sublingual formulation works within 20 min
  • Efficacy: ~ 50% as effective as PDE inhibitors
  • Adverse effects: nausea, headache, yawning, and dizziness
42
Q

Testicular Tumors

Overview

A

Less than 1% of all tumors in men

Types:

  • Germ cell neoplasms (94%)
    • Intratubular germ cell neoplasia (CIS)
      • Seminomatous Tumors
        • Seminoma
        • Spermatocytic seminoma
    • Non-Seminomatous Germ Cell Tumors (NSGCT)
      • Embryonal carcinoma
      • Yolk sac tumor (endodermal sinus tumor)
      • Teratoma
        • Mature
        • Immature
      • Choriocarcinoma
  • Gonadal stromal (sex-cord) neoplasms (5%)
    • Leydig cell tumor
    • Sertoli cell tumor
    • Granulosa cell tumor
    • Mixed/undifferentiated sex cord tumors
      • Gonadoblastoma
      • Germ cell-stromal-sex cord tumor
  • Lymphomas (1%)
43
Q

Germ Cell Neoplasms

Characteristics

A
  • Prevalence:
    • Most common tumor in men age 15-34
    • Causes 10% of cancer deaths
  • Incidence:
    • 6/100k males in the US per yr
    • White to black ratio of 5:1
  • Risk factors:
    • Cryptorchidism, dysgenetic gonads
    • Hx of germ cell tumor on contralateral side
    • Vasectomy does not ↑ risk
44
Q

Germ Cell Tumors

Genetic Factors

A
  • Strong familial predisposition
    • Fathers and sons of pts have 4x risk
    • Brothers of pts have 8-10 x risk
  • Several genetic loci linked to this risk
    • Gene encoding ligand for receptor tyrosine kinase KIT and BAK
      • Inducer of apoptotic cell death
    • Cytogenetic changes in chromosome 12 and 1 are seen
      • Esp. isochromosome of short arm 12i (12p) ⇒ pathognomonic for germ cell tumor
45
Q

Germ Cell Tumor (GCT)

Types

A
  • Seminomatous
    • Cells resemble primordial germ cells
  • Non-Seminomatous
    • Undifferentiated cells
    • Can resemble cells along embryonal stem cell line, yolk sac line, choriocarcinoma, or teratoma
46
Q

Intratubular Germ Cell Neoplasia (ITGCN)

A

CIS = Intratubular Germ Cell Neoplasia

  • Precursor lesion for most germ cell carcinomas
    • Seminoma, embryonal carcinoma, teratocarcinoma, mixed germ cell tumors
  • Not present in: yolk sac tumors, benign teratomas, spermatocytic seminomas
  • ITGCN appears to arise in utero
  • Stays dormant until puberty
  • Then can progress to seminoma or non-seminoma GCT
47
Q

Seminoma

Characteristics

A
  • Most common type of germ cell tumor
    • Corresponds to dysgerminoma in the ovary
  • Clinical presentation:
    • 3rd to 4th decade, rare in children in its pure form
    • Painless enlargement
  • Behavior and prognosis:
    • Tend to grow locally
    • < 10% of stage I tumors (confined to the testis) have LN metastases at presentation
    • If only surgical treatment: 16% relapse
      • Can spread to retroperitoneal LNs
    • Tumor is exquisitely radiosensitive w/ cure rates of 95% for stage I patients
48
Q

Seminoma

Morphology

A
  • Gross findings:
    • Gray/white cut surface
    • Hemorrhage and necrosis only seen in large tumors
  • Histology:
    • Typical (85-90%)
      • Uniform sheets of large uniform cells interspersed w/ prominent lymphocytic infiltrate
      • Cells are PAS-positive, contain glycogen
    • Anaplastic (10%)
49
Q

Spermatocytic Seminoma

Characteristics

A
  • Epidemiology:
    • Accounts for 1-2% of all testicular neoplasms
    • 5% of all seminomas
    • Occurs exclusively in older men
  • Behavior and Prognosis:
    • Slow growing
    • Treated w/ surgical excision
    • Very rarely produces metastases
50
Q

Spermatocytic Seminoma

Morphology

A
  • Gross:
    • Tend to be larger than seminomas
    • Well-circumscribed, bulging
    • No necrosis or hemorrhage
  • Histology:
    • Tumor cells are arranged in solid sheets separated by fine septa
    • No lymphocytic infiltrate (differs from seminoma)
    • Cells do not contain glycogen (PAS ⊖)
    • Atypical mitosis can be seen
51
Q

Non-Seminomatous Germ Cell Tumor (NSGCT)

Subtypes

A
  • Embryonal carcinoma
  • Teratocarcinoma
  • Mixed germ cell tumors
    • Composed of seminoma and immature teratoma
52
Q

Embryonal Carcinoma

Characteristics

A
  • Demographics:
    • Rare in its pure form
    • Seen more often as a component of a:
      • Teratoma
        • See embryonal CA + somatic tissues and extraembryonic tissues like yolk sac or trophoblastic epithelium
      • Mixed germ cell tumor
  • Clinical presentation:
    • 25-35 y/o
    • Scrotal mass and some discomfort
    • 10% w/ metastases @ presentation
      • Can be hard to find 1° tumor in these pts
    • 70% w/ extended beyond testis @ presentation
  • Behavior and Prognosis:
    • Highly aggressive tumors
    • Tx is surgical resection followed by chemotherapy followed by resection of residual tumor metastases
    • Prognosis varies w/ stage of the tumor but is good overall
53
Q

Embryonal Carcinoma

Morphology

A
  • Gross:
    • Large, irregular hemorrhagic, necrotic mass
    • Local extension to spermatic cord is frequent
  • Histology:
    • Varies depending on components
    • Solid sheets, trabeculae, abortive glands, papillary and cleft-like spaces
    • No lymphoplasmacytic infiltrate
    • Large cells w/ high N/C ratios, scanty cytoplasm
    • Mitosis is abundant
    • Cells can contain AFP and HCG
54
Q

Yolk Sac Tumor (Endodermal Sinus Tumor)

Characteristics

A
  • Demographics:
    • Pure form seen only in infants
    • Accounts for 2% of all testicular germ cell tumors
    • #1 testicular tumor in infants and children
  • Behavior and Prognosis:
    • 16% w/ metastases @ diagnosis
    • Prognosis is excellent
55
Q

Yolk Sac Tumor (Endodermal Sinus Tumor)

Morphology

A
  • Gross:
    • Tumors tend to be large
      • Compresses surrounding testis
      • Extend to epididymis
    • Yellow or pale gray
    • Can be solid or microcystic
    • Hemorrhage is frequent
  • Histology:
    • Lace-like (reticular) network of cuboidal “hobnailed” cells
    • Various histologic patterns including: microcystic, papillary, glandular, solid, and enteric glandular
    • Schiller-Duval bodies: papillary structures resembling glomeruli (20% of cases)
    • Intra and extracellular hyaline globules (AFP or AAT) (85% of cases)
      • AFP = Alpha-fetoprotein
      • AAT = Alpha1-antitrypsin
56
Q

Testicular Teratoma

Characteristics

A
  • General Info and demographics:
    • Germ cell neoplasm
      • Differentiates along multiple lines
      • Produces a variety of histological patterns
    • Pure benign teratomas in testis rare
      • 3% of germ cell tumors
      • Occur almost always before puberty
    • In contrast, ovarian benign (mature) teratoma is the most frequent germ cell tumor
      • Always occurs after puberty
  • Behavior:
    • Males: even undifferentiated tumors won’t metastasize
    • Females: Immature mesenchymal components associated w/ aggressive behavior
  • Clinical features:
    • Most occur before age 4
    • Can be present in the undescended testis
    • ↑ Levels of hCG and esp. AFP ⇒ look for NSGCT
  • Behavior and Prognosis:
    • Children: behave as benign tumors
    • Adults: treat as a malignant tumor
57
Q

Testicular Teratoma

Morphology

A
  • Gross:
    • Well-demarcated
    • Can have solid and cystic components w/ other materials like bone, cartilage, sebum, etc.
  • Histology:
    • Cysts lined by a variety of epithelia
    • Can see skin and adnexal differentiation, immature and mature neural tissue, respiratory and intestinal tract differentiation
58
Q

Sex Cord (Gonadal) Stroma Tumors

Overview

A
  • Account for 4-6% of all testicular neoplasms
  • Can be pure forms of Leydig, Sertoli or granulosa cells or mixed forms
  • Do not have the same predisposing conditions as germ cell tumors
59
Q

Leydig Cell Tumor

Characteristics

A
  • Constitute 1-3% of all testicular neoplasms
  • Clinical findings:
    • Testicular mass
    • Can produce ↑ androgens and estrogens ⇒ ± precocious puberty and gynecomastia
  • Behavior and Prognosis
    • Leydig cell tumors occurring in children are benign
    • ~10% of this tumor in adults are malignant
60
Q

Leydig Cell Tumor

Morphology

A
  • Gross:
    • Homogenous well-demarcated brown to light yellow mass
    • Measures between 3-5cm
    • Extension to cord and rete is infrequent (15%)
  • Histology:
    • Architecture of solid sheets, nests, or trabeculae surrounded by stroma
    • Polygonal cells w/ granular acidophilic, or vacuolated cytoplasm
    • Reinke crystals in 25-40% of cases
    • Lipofuscin is seen in most
61
Q

Sertoli Cell Tumor

Characteristics

A
  • Epidemiology:
    • < 1 % of all testicular tumors
    • Can be associated
      • Undescended testis
      • Testicular feminization
      • Peutz-Jeghers syndrome
  • Clinical effects:
    • Can induce endocrinologic changes like Leydig cell tumors
  • Behavior and prognosis:
    • Grow locally
    • Metastases are rare (<10%)
62
Q

Sertoli Cell Tumor

Morphology

A
  • Gross:
    • Small pale yellow or gray w/ areas of hemorrhage and necrosis
  • Histology:
    • Tubular arrangement w/ no lamina but surrounded by a BM
    • Two histological variants:
      • Tubules w/ eosinophilic masses (sex cord tumor w/ annular structures)
      • Large cell calcifying sertoli cell tumor
63
Q

Prostate Zones

A
  • Peripheral zone
    • Located at posterior and lateral aspect of gland
    • Constitutes 75% of the gland
    • Site of ≈ 70% of prostatic adenocarcinoma
  • Central zone
    • Cone shaped structure
    • Surrounds the ejaculatory ducts
    • Apex at the verumontanum, base at area between the SV and the bladder
    • Constitutes 20% of the gland
  • Transitional zone
    • Anteriorly located
    • Surrounds the urethra
    • Comprises 5% of the normal gland
    • Can markedly expand by a combination of glandular and stromal hyperplasia ⇒ Benign Prostatic Hypertrophy (BPH)
    • May cause obstruction of urinary flow by blocking urethral outflow tract
64
Q

Prostate

Microscopic Anatomy

A
  • Epithelial-Stromal units
    • Glands + adjacent connective tissue
  • Seen in all zones but not in:
    • Ejaculatory ducts
    • Vermontanum
65
Q

Prostatic Gland

Cell Types

A
  • Secretory cell
    • Lines the lumen
  • Basal Cell (Stem Cell)
    • Between BM and secretory cell
    • Intermediate cells
    • Possible stem cells
    • Not yet fully defined
66
Q

Prostate Specific Antigen (PSA)

A
  • Serine protease (gene at 19q13)
  • Function: liquefies the seminal coagulum, dissolves cervical mucous cap
  • Almost exclusively by prostate gland
    • Produced by normal, hyperplastic and most neoplastic glands
  • Used as serologic assay to follow prostatic CA
    • Normal value < 4.0 ng
    • Some experts believe in age adjustment of PSA values
    • Sensitivity 30-50%, specificity 50-80% ⇒ not an ideal screening test
  • Can be elevated from non-cancerous conditions: BPH, prostatitis, trauma, ejaculation, hormonal medications
  • Must be combined w/ DRE for best screening
  • Prostate biopsy next step to make dx
67
Q

Acute Prostatitis

Characteristics

A
  • Acute inflammation of prostate
  • Cause: bacterial infection via urine or urothelium
    • GNRs, most frequently E. coli
    • ↑ Incidence in immunosuppressed
  • Systemic sx of infection, usu. sudden onset
    • Fever, chills, low back + perineal pain, urgency, dysuria
  • Rectal exam: swollen, tense gland
68
Q

Acute Prostatitis

Morphology

A
  • Histology
    • Acute inflammation in stroma
    • Gland destruction
    • Micro-abscesses
  • TURP Findings
    • Acute inflammation ≠ Symptomatic acute prostatitis
  • Biopsy
    • May be a cause of ↑ PSA
69
Q

Chronic Prostatitis

A
  • Bacterial
    • H/O UTI, ⊕ culture
    • Proteus, Klebsiella, Enterobacter and Pseudomonas
  • Non-bacterial
    • No UTI, ⊖ culture
    • Affected population: adult men, any age
  • Signs and sx: recurrent dysuria and nocturia, RBC & WBC in prostatic secretions, persistent pelvic pain
    • Not a cause of ↑ PSA
70
Q

Nodular Hyperplasia

“Benign Prostatic Hyperplasia (BPH)”

A
  • Growth in the transitional zone of the prostate
  • Probably a normal aging process
  • Affects nearly all men if you examine (DRE) the prostate
  • 50% men > 50 y/o
  • Almost 100% by ≥90 yrs of age
  • Associated w/ concomitant glandular atrophy
71
Q

Clinical Prostatism

A
  • Difficulty in initiating and termination or urination
    • ↓ Force and caliber of stream
  • Seen in only 10-25% of the population
  • Usually seen by 60-70 y/o
  • In 1990, there were over 400k TURPs for BPH
  • Now a very rare procedure
72
Q

BPH

Factors

A
  • Cause unknown
  • Required factors:
    • Testosterone source (testis)
      • Men castrated before puberty do not show BPH
      • Regression of BPH w/ androgen ablation Rx
    • Advancing age
      • Altered serum estrogen:testosterone ratio
      • Normal E:T ratio ↓ w/ age as testosterone level drops
      • When given w/ androgens, estrogen inhibits cell death
73
Q

BPH

Morphology

A
  • Variable histology
    • Glandular and stromal hyperplasia
    • Atrophy
    • Lymphocytic infiltrate
  • Largest nodules ⇒ periurethral
74
Q

BPH vs Prostate CA

Location

75
Q

Prostatic Intraepithelial Neoplasia (PIN)

A
  • Precursor lesion for adenocarcinoma (CA)
    • Peripheral zone lesion
    • Present in almost all prostates w/ CA
  • Two-tiered grading system
    • Low grade PIN
      • Stratification of secretory cells, minimal atypia, small nucleoli, retained basal cell layer
      • Management: unchanged
    • High grade PIN
      • Marked stratification of secretory cells
      • Marked atypia
      • Prominent nucleoli
      • Discontinuous basal cell layer
      • Management: re-biopsy
      • CA found in 30-50%
76
Q

Prostatic Adenocarcinoma

Epidemiology

A
  • Most common cancer in men, 2nd leading cause of cancer death in men
    • ~200k men are diagnosed each yr, 28k die
  • Variable risk in US: African American > Whites > Asians, Hispanics, Native Americans
  • Most cancers present as prostatism (like BPH)
  • Marked age-related ↑ in incidence
    • 40x ↑ from 50 to 85 y/o
  • Death rate has been declining
    • Reason for decline uncertain
    • Potential reasons include:
      • Early detection programs w/ DRE and PSA
      • Tx of localized disease
      • Environmental reasons: diet, supplements, exercise
77
Q

Prostate Cancer

Diagnosis

A
  • Most common presentation is elevated PSA only / asymptomatic
  • Sx usually occur only w/ advanced disease
    • Clinical prostatism
  • 20% of men w/ prostate CA have normal PSA and abnormal digital rectal examination (DRE)
  • Both PSA and DRE needed to screen properly
  • Biopsy makes definitive dx
  • Biopsy is performed in combo w/ transrectal US
78
Q

PSA and Prostate CA

A
  • Neoplastic cells secrete ~3x > vs normal cells
  • Normal PSA 2.5-6.5 ng/ml
    • Age dependent
    • 4 ng/ml considered ULN
    • PSA < 4 ng/ml seen in ~20% of prostate CA
      • If PSA < 4.0, ~20% have CA
      • If PSA > 20, ~100% have CA
  • Causes of ↑ PSA:
    • Benign: BPH, infarcts, acute prostatitis
    • Malignant: Adenocarcinoma
  • Recommended PSA as a marker to follow recurrence after tx
79
Q

PSA

Refined Measurements

A
  • PSA density (index):
    • Serum PSA value / gland volume (measured by transrectal US)
      • V = 0.52 x HxLxW
  • PSA velocity
    • ∆ Serum PSA over time
  • Free PSA
    • Majority of PSA is bound to serum proteins:
      • Alpha-1 anti-chymotrypsin and alpha-2 macroglobulin
80
Q

Prostate Cancer

Screening Controversy

A
  • Unclear if prostate cancer screening ↓ mortality
  • Over dx ⇒ significant morbidity (ED, incontinence) w/ questionable benefit to survival
  • Several different screening recommendations exist (AUA, ACS, ACP)
  • Pros and cons should be discussed w/ the individual pt
  • PSA should not be included as a routine blood test
  • Consider patient’s age, medical conditions, life expectancy
81
Q

Prostate Adenocarcinoma

Morphology

82
Q

Prostate Adenocarcinoma

Grading and Staging

A
  • Grading system is Gleason Score based on pathologic patterns on histology
    • Architecture of glands
  • TMN staging system
    • Most common stage is T1C
      • Elevated PSA is only presenting feature
    • Imaging studies not very useful in low stage disease
83
Q

Prostate Adenocarcinoma

Gleason’s Grading System

A

Gleason’s Grading System

  • Based on architecture of glands
  • 5-tiered system (patterns 1-5)
    • Most predominant pattern added to 2nd most common pattern to assign a score
  • Score range 2-10
    • Gleason pattern 1: Lobular masses, uniform small glands, no invasion outside the “lobule”
    • Gleason pattern 2: Lobular masses, irregular glands, minimal invasion
    • Gleason pattern 3: Irregular glands, infiltrative, cribriform and papillary patterns
    • Gleason pattern 4: Fusion of glands, sheets, infiltrative, some w/ clear cytoplasm
    • Gleason pattern 5: Sheets of anaplastic cells infiltrative, comedonecrosis

3-tiered classification based on Gleason score used for management:

  • Low grade cancer: Gleason scores 2-6
  • Intermediate grade cancer: Gleason score 7
  • High grade cancer: Gleason score 8-10
84
Q

Prostate Adenocarcinoma

Staging

A

TMN staging system

Most common stage is T1C

85
Q

Prostate Adenocarcinoma

Clinical Course & Prognosis

A
  • Slow doubling time compared w/ other tumors
  • Course determined by:
    • Stage of disease
    • Life expectancy
  • For stage A1:
    • Non-palpable carcinoma by rectal examination
    • Usu. incidentally found by TURP
    • ~16% will progress within the next 10 yrs if left alone
  • In stage A2:
    • Higher Gleason score and extensive disease
    • Still nonpalpable and discovered by TURP
    • ~50% will progress during the next 5 yrs if left untreated
  • In stage B:
    • Carcinoma palpated during DRE but confined to the prostate
    • Most of these will progress and should be treated
  • 85-90% 10-yr survival if tx given for early stage localized cancer
  • Surveillance still an option for some men
  • Survival 18-24 months in men w/ metastatic cancer
86
Q

Prostate Cancer

Treatment Options

A

Localized cancer with normal life expectancy:

  • Surgery
    • Radical retropubic prostatectomy
    • Radical perineal prostatectomy
    • Laparoscopic/Robotic assisted prostatectomy
    • Surgery not proven superior w/ localized disease
  • Radiation therapy
    • Pt is not a good surgical candidate
    • Doesn’t want surgery
    • Surgery & radiation w/ similar 10-15 yr cure rates
  • Hormonal therapy alone
  • Cryotherapy
  • Active surveillance/observation
87
Q

Prostate Cryosurgery

A
  • Transrectal US guided
  • Transperineal placement of 6-8 CRYOprobes
  • Transperineal placement of 4-6 TEMP probes
  • Warming device to preserve urethra
88
Q

Prostate Cancer

Forms of Radiation Therapy

A
  • Types of radiation:
    • External beam radiation (XRT)
    • Brachytherapy (seeds)
    • High dose radiotherapy (HDR)
  • Combination therapy:
    • XRT + Hormonal Tx
    • Brachy + XRT ± Hormonal Tx
    • HDR + XRT ± Hormonal Tx
89
Q

Prostate Cancer

Hormonal Antiandrogen Therapy

A
  • Palliation, for those w/ extension of CA beyond the prostate
  • Based on prostate CA being androgen (testosterone) sensitive
    • ↓ Serum testosterone ⇒ shrinkage of CA via apoptosis
  • Usually not curative but adds to effectiveness of Radiation Tx in certain pts
  • Used as 1° treatment in metastatic disease
  • Androgen ablation therapy
    • Orchiectomy
    • Luteinizing hormone releasing hormone (LHRH)
90
Q

Prostate Cancer

Treatment Toxicity

A

Surgical/radiation risks include urinary incontinence, erectile dysfunction and rectal/bowel complications

Hormonal therapy (male menopause) can cause cognitive decline, osteoporosis, vasomotor sx, loss of libido and erections

91
Q

Metastatic Prostate Carcinoma

A

Can use PSA immunohistochemical stain to determine that origin of metastatic tumor is from prostate.

Metastasis to bone is characteristic.

6. HDS GI Repro (30 decks)

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