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Urogenital > Urogenital 2 > Flashcards

Urogenital 2 Flashcards

1
Q

What types of kidney tumours are there?

A

Malignant
1. Renal Cell Carcinoma
2. Urothelial Carcinoma
3. Nephroblastoma (Wilms Tumour) - children

Benign
1. Angiomyolipoma

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2
Q

Where does renal cell carcinoma arise from?

A

Tubular Epithelium

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3
Q

What 3 types of RCC are there?

A
  1. Clear Cell RCC
  2. Papillary RCC
  3. Chromophobe RCC
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4
Q

What is underlying pathology behind Clear Cell RCC

A
  1. Sporadic
  2. Von Hippel Lindau (VHL) syndrome (a/w chromosome 3p deletions and mutations of VHL gene)
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5
Q

What are the clinical features of RCC?

A
  1. Painless hematuria
  2. Mass in Flank
  3. Fever due to necrosis
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6
Q

What are the gross features of RCC (clear cell)

A

1, Solitary, unilateral with circumscribed appearance
2. Yellowish cut surfaces with foci of necrosis
3. Invasion of renal vein
4. Tendency to metastasize widely, albeit late

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7
Q

What are the microscopic features of RCC (clear type)

A
  1. Polygonal Cells with clear cytoplasm
  2. Delicate branching vasculature
  3. Invasion of renal vein and its branches may be seen
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8
Q

What types of urothelial carcinoma are there?

A

non-invasive papillary urothelial carcinoma OR invasive urothelial carcinoma

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9
Q

Which areas do urothelial carcinomas affect?

A

areas of kidney lined by urothelium (ie pelvi-calyceal system)

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10
Q

Can urothelial carcinoma be multifocal? where else?

A

yes. ureter and bladder

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11
Q

How does urothelial carcinoma present microscopically?

A

Grossly and microscopically identical to urothelial carcinoma of the bladder

Papillary structures: fibrovascular cores lined by malignant urothelium

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12
Q

What is Wilms Tumour associated with?

A

Congenital Malformations - WAGR syndrome, Denys-Drash Syndrome and Beckwith-Wiedemann Syndrome

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13
Q

When is Wilms Tumour most common?

A

2 and 5 years old

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14
Q

What are clinical features of Wilms Tumour?

A
  1. Large abdominal Mass
  2. Fever due to necrosis and hemorrhage
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15
Q

What is the treatment for Wilms Tumour?

A

Nephrectomy and Chemotherapy

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16
Q

What are the gross features of Wilms Tumour?

A

Well-circumscribed grayish white, soft mass

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17
Q

Where does Wilms Tumour begin and where does it spread to

A

Begins in renal cortex and replaces entire kidney

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18
Q

What are the microscopic features of Wilms Tumour?

A
  1. Sheets of Small Blue Cells (blastemal component)
  2. Abortive tubular and glomeruloid structures (epithelial component)
  3. Spindle-shaped cells (stromal components)
  4. Heterologous elements such as striated/smooth muscle and cartilage may be found
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19
Q

Where might Wilms Tumour metastasise to? Method of spread?

A

Lungs, liver, brain, lymph nodes

via hematogenous spread & lymphatic spread

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20
Q

What is angiolyolipoma?

A

Common mesenchymal tumour of the kidney

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21
Q

What does angiomyolipoma consist of?

A
  1. Adipose Cells
  2. Myoid Spindle Cells
  3. Blood Vessels
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22
Q

What family does angiomyolipoma belong to? What are other tumours in this family?

A

PEComas (tumours containing perivascular epitheloid cells)

Lymphangioleiomyomatosis
Clear cell ‘sugar’ tumours of the lung, pancreas, and uterus,
Cardiac rhabdomyomas

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23
Q

Where are angiomyolipomas commonly found?

A

Kidney, liver, retroperitoneum and lungs

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24
Q

What is underlying pathology for angiomyolipoma?

A

Sporadic, associated with tuberous sclerosis (80% of pt with TS will get angiomyolipomas)

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25
Q

When does angiomyolipoma occur?

A

All ages, usually resected in patients around 40 years and older

26
Q

How is angiomyolipoma usually diagnosed?

A

CT; via its fat content

27
Q

What is the risk of angiomyolipoma?

A

Benign tumour but can rupture and bleed with serious or fatal clinical outcomes

28
Q

What is the gross appearance of angiomyolipoma?

A
  1. Unencapsulated
  2. Variegated cut surface, with yellow (fatty) areas
29
Q

What are the microscopic appearances of angiomyolipomas?

A
  1. Mixture of myoid spindle and epitheloid cells, adipocytes and blood vessels, often thick walled
  2. Myoid cells show immunostaining for HMB-45
30
Q

What types of bladder tumours are there?

A

Malignant
1. Papillary Urothelial Carcinoma (non-invasive)
2. Invasive urothelial carcinoma
3. Squamous Cell Carcinoma
4. Adenocarcinoma

Benign
1. Papilloma
2. Inverted Papilloma
3. Nephrogenic Adenoma

31
Q

What are risk factors for bladder carcinoma?

A

Occupational
1. 2-napthylamine
2. 4-aminobiphenyl
3. Benzidene

Non-occupational
1. Cigarette Smoking
2. Schistosomiasis
3. Cyclophosphamide
4. Phenacetin

32
Q

What may invasive urothelial carcinoma arise from?

A
  1. previously non-invasive papillary urothelial carcinoma
  2. urothelial carcinoma in situ (
33
Q

What is the risk of patients with urothelial carcinoma?

A

Synchronous and subsequent urothelial tumours anywhere in the urothelial tract, as well as recurrent tumours

34
Q

Please view and familiarise with the images and annotations for Urothelial Carcinoma

A

-

35
Q

What are the two pathologies for prostate?

A
  1. BPH
  2. Prostate Cancer
36
Q

What is the pathogenesis of BPH?

A
  1. In the prostate, type 2 5-alpha reductase in the stromal cells converts testosterone to dihydrotestosterone (DHT)
  2. DHT binds to androgen receptors in the epithelial and stromal cells, inducing production of growth factors that increase the growth/decrease the death of these cells
  3. Then there is hyperplasia of the epithelial and stromal cells which is usually nodular
  4. Prostatic smooth muscle tone (mediated by alpha1-adrenergic receptors) worsens the lower urinary tract obstruction
37
Q

Where does nodular hyperplasia occur?

A
  1. Occurs in transitional zone
38
Q

What clinical symptoms of BPH? Why?

A

Urinary hesistancy, urgency, nocturia, poor urinary stream

Because there is compression of prostatic urethra

39
Q

What are complications of nodular hyperplasia of prostate?

A
  1. Bladder hypertrophy
  2. Bladder distention with hypotonia
  3. Bladder Diverticulum
  4. Urinary Tract Infection (due to stasis or urine)
  5. Urolithiasis
  6. Hydronephrosis and hydroureter
  7. Chronic Kidney Disease
40
Q

When do people get prostatic carcinoma?

A

above 50 years old

41
Q

What tests are used to diagnose prostate cancer? what are their limitations?

A
  1. Serum Prostate Specific Antigen - does not correlate with presence/absence of prostatic carcinoma, unless significantly elevated; thus inherent false negative and false positive rates
  2. Prostate core biopsy - inherent false neg due to sampling
42
Q

What is the most common type of prostatic carcinoma? Less common one is?

A

Acinar Adenocarcinoma; Ductal adenocarcinoma

43
Q

What is risk of prostatic carcinoma?

A

Metastases (commonly to bone) is uniformly fatal

44
Q

Some histologic patterns of presentation of prostate carcinoma?

A
  1. Cribiform pattern
  2. Single cells in sheets with no holes
  3. Extraprostatic extension
45
Q

What is a benign tumour of the penis? Where does it occur? What is it associated with?

A

Condyloma acuminatum; Coronal sulcus, inner surface of prepuce; Human papilloma virus type 6 and 11

46
Q

What is penile squamous cell carcinoma associated with? What helps lower risk?

A

Associated with HPV 16 and 18; circumcision

47
Q

What is the clinical course of penile squamous cell carcinoma?

A
  • slowly growing
  • locally invasive
  • metastasis to inguinal or iliac lymph nodes (grim prognosis)
48
Q

What do testicular tumours arise from?

A

Germ cell neoplasia in situ

49
Q

What are predisposing factors to testicular tumours?

A
  1. Crytorchidism
  2. Genetic Factors
  3. Testicular Dysgenesis
50
Q

What are two types of testicular germ cell tumours and their prognosis?

A
  1. Seminomatous: Remain localised for a long time, radiosensitive, spread by lymphatic to para-aortic nodes
  2. Non Seminomatous germ cell tumour: radioresistant, metastasise earlier via hematogenous route
51
Q

What are clinical features (1) and tumour markers (2) indicative of testicular tumours?

A
  1. Painless Enlargment of testis
  2. Raised serum alpha-fetoprotein in some cases
  3. Raised serum human chorionic gonadotrophin (beta subunit)
52
Q

5 types of mixed tumours?

A
  1. Seminoma + any NSGCT
  2. Teratoma + Embryonal Carcinoma
  3. Seminoma + Embryonal Carcinoma
  4. Teratoma + Choriocarcinoma
  5. Others
53
Q

Is seminoma common? What age does it occur?

A

Yes most common germ cell tumour. Peals in third to 4th decade

54
Q

Histological features of seminoma?

A
  1. Homogenous
  2. Lymphocytes in septa
  3. Cells moderate amount of clear cytoplasm
  4. Sheets of cells separated by septa
55
Q

When do embryonal carcinomas occur?

A

20-30years old

56
Q

How do embryonal carcinomas spread?

A

Hematogenous spread

57
Q

What is the problem with treating embryonal carcinomas?

A

Radioresistant

58
Q

How do embryonal carcinomas present histologically?

A

Big bad cells
prominent nuclei
necrosis
glands or sheets

59
Q

What is a yolk sac tumour?

A

Neoplastic germ cells differentiating along extra-embryonic lines

60
Q

How does it occur in children and adults?

A

Children: Most common testicular tumour in infants
Adults: Occurs in combination with embryonal carcinoma or seminoma

61
Q

What is another example of a neoplastic germ cell tumour differentating along extra-embryonic lines?

A

Choriocarcinoma

62
Q

What do teratomas consist of?

A

variety of mature and/or immature tissue types, often from more than one germ layer

Urogenital (3 decks)

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