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GU / GYN & Renal > Overview: GU Pathology > Flashcards

Overview: GU Pathology Flashcards

1
Q

Bladder

Noninvasive Papillary Neoplasms

A
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2
Q

Bladder

  • Benign
  • Simple papillary architecture (fibrovascular cores)
  • Lined by cytologically normal urothelium (no atypia)

Histology

A

Papilloma

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3
Q

Bladder

Most common urinary tract tumor; 90% of all primary bladder tumors

A

UC

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4
Q

Bladder

  1. Industrial exposure to aniline dye
  2. Cigarette smoking
  3. Long-term treatment with cyclophosphamide
  4. Schistosomiasis
  5. Analgesic abuse
  6. Sex: M > F
  7. Age: >50 years

Risk Factors

A

UC

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5
Q

Bladder

  • More common: ~80%
  • Progresses to LGUC
  • Genetically stable
  • Recurrence rate: high
  • Low risk of progression: <1-5% (nonaggressive)
  • Genetic abnormalities:
    * CDKN2A deletion (encodes p16 protein)
    * FGFR3 alterations (activating point mutations; ~80%)

UC Pathogenesis

A

Hyperplasia pathway

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6
Q

Bladder

Most common urothelial tumor

A

LGUC

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7
Q

Bladder

  • Less common: ~20%
  • Leads to HGUC
  • Genetically unstable
  • Recurrence: high
  • High risk of progression
  • Genetic abnormalities
    * RAS mutation
    * p53 mutation (60%)

UC Pathogenesis

A

Dysplasia pathway

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8
Q

Bladder

  • Papillary architecture
  • Normal / increased epithelial thickness (layers)
  • Mild cytologic atypia & infrequent mitotic figures

Histology

A

LGUC

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9
Q

Bladder

  • Papillary architecture
  • Marked cytologic atypia & frequent mitotic figures
  • Necrosis common

Histology

A

HGUC

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10
Q

Bladder

  • Flat high-grade lesion (no mass)
  • Poorly cohesive cells often shed into urine & appear velvety on cytoscopy
  • 20-80% progress to invasion

Histology

A

Flat urothelial CIS

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11
Q

Bladder

Diffuse thin, finger-like, hyperchromatic cords forming tentacular pattern

Histology

A

Invasive UC

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12
Q

Bladder

Low-grade UC

Treatment

A
  • Tumor resection
  • Follow-up: biopsy / urine cytology
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13
Q

Bladder

High-grade non-invasive / superficially invasive UC

Treatment

A
  • Tumor resection
  • Biotherap: BCG, interferon
  • Chemotherapy
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14
Q

Bladder

High-grade with deep (muscle) invasion

Treatment

A
  • Cystectomy
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15
Q

Bladder

  • Most frequent in Middle East & along Nile Valley
  • Associated with chronic inflammatory processes:
    * Chronic bacterial infection
    * Schistosomiasis
  • Can be associated with renal calculi
A

Bladder SCC

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16
Q

Bladder

Squamous differentiation:
* Intraceullar keratin
* Keratin pearls
* Intercellular bridges

Histology

A

Bladder SCC

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17
Q

Bladder

  • Associated with intestinal metaplasia & bladder exstrophy
  • Combination of glands, mucinous pools & signet-ring cells

Histology

A

Bladder adenocarcinoma

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18
Q

Prostate

Site of origin for most BPH

A

Transitional zone

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19
Q

Prostate

Major site of prostatic cancer

A

Peripheral zone

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20
Q

Prostate

  • Proliferation of stromal & glandular elements leading to prostatic enlargement
  • Very common (50% of males at age 50; 80% at age 80)
  • Involves central gland –> urinary obstruction
A

BPH

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21
Q

Prostate

  • Irregular, nodular
  • Gland may be distorted
  • Weight may be >100 g (normal = 20-30g)

Gross Appearance

A

BPH

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22
Q

Prostate

  • Nodules may be pure glands, pure stroma, or mixture
  • Compresses adjacent tissue

Histology

A

BPH

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23
Q

Prostate

BPH

Treatment

A
  • Symptomatic Tx:
    • Decrease fluid intake before bed
    • Avoid alcohol & caffeine
  • Medical Tx:
    • Decrease muscle tone: a-Blockers
    • Shrink prostate: 5-a-Reductase inhibitors
  • Surgical Tx: transurethral resection of prostate (TURP)
    • First-line Tx w/ recurrent urinary retention
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24
Q

Prostate

  • Most common form of cancer in men (27%)
  • Only causes ~10% of cancer deaths in US
  • Most pts >60 yrs of age (incidence increases w/ age)
  • More common in African-Americans
  • More common in Western hemisphere

Epidemiology

A

Prostatic adenocarcinoma

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25
Q

Prostate

  1. Age
  2. Androgens
  3. Environmental factors:
    • Increase risk: high fat intake
    • Decrease risk: lycopenes, Vit A, Vit E, soy
  4. Genetic factors:
    • 1 first-degree relative = 2x risk
    • 2 first-degree relatives = 5x risk
    • Acquired somatic mutations:
      • 40-60% have TMPRSS2-ETS fusion genes
      • LOF mutations involving PTEN (TSG)

Risk Factors

A

Prostatic adenocarcinoma

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26
Q

Prostate

  • Urinary obstruction
  • Firm, irregular nodules / masses on digital rectal exam
  • Elevated PSA (>10 or greater)

Clinical Presentation

A

Prostatic adenocardinoma

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27
Q

Prostate

BPH vs. Prostate Cancer

Gross Appearance

A

Cancer: peripheraly located; ill-defined border; yellow discoloration
BPH: transitional zone / periurethral; nodular; whitish

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28
Q

Prostate

  • Abnormal architectural pattern
  • Single luminal cell layer (loss of basal cells)
  • Enlarged nuclei
  • Nuclear hypochromasia
  • Prominent nucleoili
  • Mitoses / apoptosis
  • Amphophilic cytoplasm
  • Blue mucinous secretions
  • Pink amorphous secretions
  • Crystalloids

Histology

A

Prostatic adenocarcinoma

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29
Q

Prostate

Often metastasizes to lumbar spine

A

Prostatic adenocarcinoma

Osteoblastic metastases

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30
Q

Prostate

Spread to lymph nodes (usually obturators) is eventually fatal

A

Prostatic adenocarcinoma

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31
Q

Prostate

PIN-4 immunostain

Histology

A

Basal cells are absent in invasive prostate cancer

If basal cells are present, prostatic cancer = in situ

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32
Q

Prostate

Basal cell markers

PIN-4 immunostain

A
  1. p63 = nuclear
  2. CK903 = cytoplasmic

If positive, non-invasive tumor

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33
Q

Prostate

Racemase (P504S, AMACR)

PIN-4 immunostain

A

Cytoplasmic marker overexpressed in prostate cancer (both in situ & invasive) but is absent in benign cells

If positive, prostate cancer (PIN or invasive); if negative, benign

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34
Q

Prostate

  • Basal cell markers = +
  • Racemase = -

PIN-4 immunostain results

A

Benign cells

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35
Q

Prostate

  • Basal cell markers = +
  • Racemase = +

PIN-4 immunostain results

A

Prostate cancer: PIN (in situ)

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36
Q

Prostate

  • Basal cell markers = -
  • Racemase = +

PIN-4 immunostain results

A

Prostate cancer: invasive

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37
Q

Prostate

  • Lobular arrangement
  • Tightly packed glands

Gleason’s Score

A

Gleason’s Score: 1

Lowest grade prostatic adenocarcinoma; very rare

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38
Q

Prostate

  • Loose lobular arrangement
  • Larger glands

Gleason’s Score

A

Gleason’s Score: 2

Very rare

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39
Q

Prostate

  • Small infiltrative individual glands
  • Well-formed glands

Gleason’s Score

A

Gleason’s Score: 3

Most common prostatic adenocarcinoma

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40
Q

Prostate

  • Fused or poorly formed glands
  • Cribriform pattern

Gleason’s Score

A

Gleason’s Score: 4

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41
Q

Prostate

  • Solid sheets with central necrosis
  • Individual cells

Gleason’s Score

A

Gleason’s Score: 5

Highest grade prostatic adenocardinoma

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42
Q

Grading Prostatic Adenocarcinomas

Total Gleason Score

A

X + Y = Total Gleason Score
* X = Dominant Score Pattern
* Y = 2nd Score Pattern

If there is no 2nd pattern, X + X = Total Score

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43
Q

Prostate

  • Prostatic duct retains myoepithelial layer
  • Ductal epithelium is atypical & hyperplastic with papillary projections into lumen

Histology

A

Prostatic intraepithelial neoplasia (PIN)

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44
Q

Prostate

Prognosis of prostatic adenocarcinoma

A

90% survival for 15 years

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45
Q

Testis

  • Failure of testis to complete normal descent into scrotum
  • Most commonly unilateral, slight predilection for right testis
  • May result in infertility or germ cell neoplasms
A

Cryptorchidism

Congenital Anomaly

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46
Q

Testis

Cryptorchidism

Treatment

A
  • Orchiopexy (surgical placement of undescended testis into scrotum)
    OR
  • Orchiectomy
47
Q

Testis

  • Occurs in children & young adults
  • Sudden onset of testicular pain after physical activity
  • Urological emergency
    • Surgical correction (detorsion & orchiopexy) required within 6 hours
    • Otherwise results in swelling, hemorrhagic infarct, and necrosis
A

Testicular Torsion

Vascular Pathology

48
Q

Testis

  • Incidence: 6/100,000 males
  • More common in Caucasians than African-Americans

Epidemiology

A

Testicular tumors

49
Q

Testis

  1. Cryptorchidism: 3-5x increased risk in undescended testis; increased risk in contralateral decended testis
  2. Family Hx: brothers have 8-10x increased risk
  3. Intersex syndromes: androgen insensitivity; gonadal dysgenesis

Risk Factors

A

Testicular tumors

50
Q

Testis

Types of testicular tumors

Histology

A
  1. Germ cell tumors (GCT): 95%
  2. Sex-cord stromal tumors: 5%
  3. Lymphoma
51
Q

Testis

Most common type of testicular tumor

A

GCT

>95% of cases

52
Q

Testis

Age: 25-45 yrs

Characteristics of Testicular Tumors

53
Q

Testis

Behavior: highly aggressive, but curable

Characteristics of Testicular Tumors

54
Q

Testis

Clinical: painless enlargement of testis

Characteristics of Testicular Tumors

55
Q

Testis

Genetic abnormalities: isochromosome 12p

Characteristics of Testicular Tumors

56
Q

Testis

Treatment: radiation and/or CTX

Characteristics of Testicular Tumors

A

GCT

80-90% can be successfullly treated

57
Q

Testis

Age: prepubertal

Characteristics of Testicular Tumors

A

Sex-cord stromal tumors

58
Q

Testis

Behavior: ~90% are benign

Characteristics of Testicular Tumors

A

Sex-cord stromal tumors

59
Q

Testis

Most common testicular neoplasm in men age > 60

A

Lymphoma

DLBCL type

60
Q

Testis

Most common tumors in men ages 15-40

61
Q

Testis

  • More common in white population
  • Most cases are preceded by intratubular neoplasia

Epidemiology

62
Q

Testis

  • Cryptorchidism: 3-5x increase
  • Testicular (gonadal) dysgenesis

Risk Factors

63
Q

Testis

Painless testicular mass / enlargement

Clinical Presentation

64
Q

Testis

Types of GCT

Histology

A
  1. Seminoma: 35-45%
  2. Non-seminomatous GCT
  3. Mixed GCT: 32-54%
65
Q

Testis

Prepubertal tumors

Histogenesis

A
  • GCT: endodermal sinus tumor; teratoma
  • Behavior: usually benign
66
Q

Testis

Postpubertal tumors

Histogenesis

A
  • 95% of all testicular tumors are GCT
  • All are malignant
67
Q

Histology: Testis

A
  • Functional units: seminiferous tubules
    • Site of spermatogenesis
    • Contains germ cells & supporting cells
      • Germ cells: spermatogonia, spermatocytes, spermatids, spermatozoa
      • Supporting cells: Sertoli cells
  • Stroma between tubules provides support
    • Supporting cells: Leydig cells
68
Q

Testis

GCT composed of mature fetal tissue dervied from 2-3 embryonic layers

GCT Subtypes

A

Teratoma

Somatic cell lineage

69
Q

Testis

GCT composed of immature, primitive fetal tissue

A

Embryonal carcinoma

70
Q

Testis

GCT that resembles undifferentiated spermatogonia

GCT Subtypes

71
Q

Testis

GCT that mimics yolk sac elements

GCT subtypes

A

Endodermal sinus tumor

Extraembryonic cell lineage

72
Q

Testis

GCT composed of cytotrophoblasts & syncytiotrophoblasts that mimics placental tissue

GCT Subtypes

A

Choriocarcinoma

Extraembryonic cell lineage

73
Q

Testis

  • 1/3 - 1/2 of all testicular GCT
  • Most common between ages 15-40
  • Hx of cryptorchidism in 10% of cases

Epidemiology

74
Q

Testis

Clinical: painless testicular swelling
Gross: bulky homogenous grey-white lobulated mass
* Hemorrhage & necrosis: rare
* Usually limited by tunica albuginea

Presentation

75
Q

Testis

Seminoma

Approach to Therapy

A

Radiotherapy: high cure rate

76
Q

Testis

Subtypes of seminomas

Histology

A
  1. Classic type
  2. Spermatocytic type
77
Q

Testis

  • Cytology
    • Large round cell
      • Distinct membranes
      • Clear or light cytoplasm
    • Large central nucleus
      • Prominent nucleoli
  • Architecture
    • Nests or individual tumor cells divided by fibrous bands
    • Abundant lymphocytes
    • Possible granulomas
    • Equivalent to dysgerminoma in women

Histology

A

Seminoma, classic type

78
Q

Testis

Seminoma, classic type

Approach to Diagnosis

A

IHC
* Germ cell markers: OCT 3/4, CD117
* CD30-
* AFP-
* B-hCG+ (15% of cases)

79
Q

Testis

  • Patients age > 50
  • Benign, indolent behavior
  • Size: 2-20 cm (avg. of 7 cm)
  • Gross: large tumor of myxoid appearance
  • Exclusive in testicle, usually bilateral

Presentation

A

Seminoma, spermatocytic type

80
Q

Testis

  • 3 cell types: small, intermediate, large
  • Numerous mitotic fifures
  • No lymphocytes, granulomas, or ITGCN

Histology

A

Seminoma, spermatocytic type

81
Q

Testis

Seminoma, spermatocytic type

Potential Complications

A

Sarcomatous transformation: worse prognosis
* Rhabdomyosarcoma
* Undifferentiated

82
Q

Testis

Seminoma, spermatocytic type

Approach to Therapy

A

Surgical treatment only

83
Q

Testes

Peak occurence in ages 20-30s

Epidemiology

A

Embryonal carcinoma

84
Q

Testis

  • Aggressive with early hematogenous spread
    • Often metastatic at time of diagnosis
  • Most often seen as component of mixed GCT
  • Gross: fleshy grey-tan tumor often with prominent necrosis & hemorrhage
    • Often penetrates tunica albuginea

Presentation

A

Embryonal carcinoma

85
Q

Testis

  • Solid, glandular & papillary growth
  • Anaplastic cells
  • Necrosis

Histology

A

Embryonal carcinoma

86
Q

Testis

Embryonal carcinoma

Approach to Diagnosis

A

IHC
* B-hCG+ (60% of cases)
* CD30+
* Cytokeratin+

87
Q

Testis

Occurs at any age
* Children: pure form; 2nd most common testicular tumor in children
* Adult: common component of mixed GCT

Epidemiology

88
Q

Testis

  • Behavior depends on age
    • Child: benign
    • Adult: malignant; chemoresistant
  • Gross: heterogenous collection of differerentiated cells or organoid structures
    • Solid, cystic, or cartilaginous masses

Presentation

89
Q

Testis

  • Derivates from more than one germ layer
  • Elements may be mature or immature
    • Mature: resembling adult tissues
    • Immature: sharing histologic features with fetal / embryonal tissues
  • Fibrous or myxoid stroma

Histology

90
Q

Testis

Germ Layer Derivatives

Histology

A
  • Endoderm
    • Epithelium lining body tubes (e.g., GI tract)
    • Parenchyma: endocrine glands, liver
  • Mesoderm
    • Supporting tissues: muscles, cartilage, bone
    • Vascular system
  • Ectoderm
    • Nervous tissue
    • Skin
91
Q

Testis

  • Children: pure form
    • Most common testicular tumor in children
    • Very good prognosis
  • Adults: component of mixed GCT
    • Most often associated with embryonal carcinoma

Epidemiology

A

Endodermal sinus tumor

92
Q

Testis

Endodermal sinus tumor

Approach to Diagnosis

A
  • Serum marker: AFP+
  • Histology:
    • Schiller-Duval bodies (35-50% of cases)
    • Eosinophilic hyalin globules (AFP)

Schiller-Duval bodies = pathognomonic

93
Q

Testis

  • Various growth patterns:
    • Reticular (lacelike network)
    • Microcysts, sheets, tubulo-papillary, etc.
  • Histological hallmark: Schiller-Duval bodies
    • Glomeruloid-like structure
    • Central blood vessel surrounded by loose primitive stroma w/ outer mantle of cuboidal-to-columnar neoplastic cells lined by flattened tumor cells

Histology

`

A

Endodermal sinus tumor

94
Q

Testis

  • Peak occurence in 30s
  • Rare (<1%); more commonly mixed

Epidemiology

A

Choriocarcinoma

95
Q

Testis

  • Aggressive tumor; lungs & liver usually involved
  • Gross: small (<5 cm) palpable masses w/ strikingly hemorrhagic appearance
    • Often no testicular enlargement
    • Often presents w/ hematogenous mets

Presentation

A

Choriocarcinoma

Strikingly hemorrhagic appearanc is characteristic

96
Q

Testis

Mass composed of cytotrophoblasts & syncytiotrophoblasts

Histology

A

Choriocarcinoma

97
Q

Testis

  • Small polygonal cell
  • Single nucleus
  • Clear / pale cytoplasm
  • Distinct membranes

Histology

A

Cytotrophoblasts

98
Q

Testis

  • Large multinucleated cell
  • Abundant eosinophilic cytoplasm
  • B-hCG+

Histology

A

Syncytiotrophoblasts

99
Q

Testis

Choriocarcinoma

Approach to Diagnosis

A
  • Clinically: characteristic hemorrhagic appearance
  • Serum marker: B-hCG
    • Produced by syncytiotrophoblasts
100
Q

Testis

Mixed GCT

A
  • Mixed: 2 or more GCT subtypes in same testis
  • Peak occurence between ages 15-30
  • Frequent components:
    • Embryonal carcinoma
    • Teratoma
    • Endodermal sinus tumor
  • 90% of cases: elevated B-hCG & AFP
101
Q

Testis

Benign, non-germ cell tumors derived from testicular interstitium

Pathology

A

Sex cord-stromal tumors

102
Q

Testis

Types of sex cord-stromal tumors

Histology

A
  1. Leydig cell tumor
  2. Sertoli cell tumor
103
Q

Testis

Testicular mass asssociated with hormonal symptoms:
* Precocious puberty
* Gynecomastia

Clinical Presentation

A

Leydig cell tumor

Testosterone is major hormone produced by Leydig cells

104
Q

Testis

  • Patients between ages 20-60
  • Testicular mass a/w hormonal symptoms:
    • Precocious puberty
    • Gynecomastia

Clinical Presentation

A

Leydig cell tumor

Testosterone is major hormone produced by Leydig cells

105
Q

Testis

  • Homogenous, solid, well-demarcated, circumscribed nodule
  • Yellow or brown color

Gross Appearance

A

Leydig cell tumor

106
Q

Testis

  • Diffuse, nodular growth pattern
  • Uniform polygonal cells with granular, eosinophilic cytoplasm
  • Histological hallmark: Reinke crystals (rare)
A

Leydig cell tumor

107
Q

Testis

  • Testicular mass / small firm nodules
  • Clinically silent

Clinical Presentation

A

Sertoli cell tumor

108
Q

Testis

Neoplastic cells arranged in trabeculae / tubules

Histology

A

Sertoli cell tumor

109
Q

Testis

Confined to testis, epididymis, or spermatic cord

Testicular Tumor: Staging

110
Q

Testis

Spread confined to retroperitoneal nodes below diaphragm

Testicular Tumor: Staging

111
Q

Testis

Spread outside of retroperitoneal nodes or above diaphragm

Testicular Tumor: Staging

112
Q

Testis

Testicular Tumors

Approach to Treatment

A

Radical orchiectomy and/or CTX

113
Q

Testis

Testicular Tumor

Prognosis

A
  • Seminoma: >95% of patients with localized disease (stage I) or spread to nodes below diaphragm (stage II) can be cured
  • Non-seminomatous: 90% can enter remission with aggressive treatment

GU / GYN & Renal (23 decks)

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