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Renal > PATH: Renal Neoplasia > Flashcards

PATH: Renal Neoplasia Flashcards

1
Q

What is an oncocytoma?

A

uncommon benign epitheilal neoplasm arising from the intercalated cells of the CD

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2
Q

What genetic changes are seen in oncocytomas?

A

Loss of chromosomes 1, 14, or Y

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3
Q

What is the gross pathology of an oncocytoma?

A

Round, Stellate scar visible with imaging, mahogany brown color (tan)

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4
Q

What is the microscopic pathology of an oncocytoma?

A

abundant cytoplasm with little red bacteria-size dots (that are lots of mitochondria that are there for no reason)

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5
Q

Where are you most likely to find a RCC in the kidney?

A

cortex

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6
Q

From what cells do RCCs arise?

A

renal tubular epithelium

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7
Q

Who gets RCC?

A

Men, around age 64, smokers, HTN, obese, who have occupational exposure to cadmium or have PCKD

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8
Q

How do RCCs like to spread?

A

through the renal capsule into the perinephric fat and veins (spreading hematogenously)

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9
Q

Where are RCCs most likely to metastasize?

A

Lung and bone!

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10
Q

What is the most common type of RCC?

A

Clear Cell carcinoma (65-70%)

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11
Q

What mutation is found in CCC?

A

AD mutation in von Hippel-Lindau tumor suppressor gene (NEEDS SECOND HIT)

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12
Q

What chromosome is the von Hippel-Lindau gene located on?

A

chromosome 3

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13
Q

What is the function of the von Hippel-Lindau tumor suppressor gene?

A

Degrades HIF so that you have less VEGF (if this is mutated, it causes excess VEGF)

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14
Q

What is the gross pathology of CCC?

A

Solitary
large diameter (well defined) tumors
Yellow color (due to lots of fat)
Tumoral blood vessels prone to rupture (hemorrhage is common)

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15
Q

What is the microscopic pathology of CCC?

A
  • Clear cells with vacuolated lipid-laden cytoplasm OR with granular pink cytoplasm and small/round nuclei
  • Lots of small blood vessels present
  • “Abortive tubules” may be present
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16
Q

What are the s/s of RCC?

A

Hematuria, dull flank pain, polycythemia (rare for malignancy!)

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17
Q

What is the prognosis for RCC?

A

usually remains silent and only is discovered after it metastasizes and causes symptoms

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18
Q

What is the main factor to gauge the prognosis of RCC?

A

Stage (extent)

Grade (how bad does the nucleus look- clear is lower grade; pink is higher grade)

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19
Q

What is the 2nd most common RCC?

A

Papillary RCC

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20
Q

What mutation is seen with papillary RCC?

A

activating mutations in the MET proto-oncogene

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21
Q

What chromosome is the MET proto-oncogene located on?

A

chromosome 7

22
Q

What is the function of MET proto-oncogene?

A

TK receptor for hepatocyte growth factor that spurs abnormal growth of PT epithelial cells

23
Q

What does the gross pathology of papillary RCC look like?

A

Mutlifocal and Bilateral
Less yellow (less lipid content)
Necrosis, hemorrhage, cystic degeneration

24
Q

What does the microscopic pathology of papillary RCC look like?

A
  • Short, nipple-like projections of tumor cells on fibrovascuar stalk
  • Cells commonly will have pink cytoplasm
25
Q

Dialysis will increase the likelihood of what types of RCC?

A

CCC- 60%

PRCC- 40%

26
Q

What is the third most common form of RCC?

A

Chromophobe RCC

27
Q

What is the cause of chromophobe RCC?

A

Hypoploidy (loss of entire chromosomes)

28
Q

Chromophobe RCC comes from what part of the nephron?

A

intercalated cells of the CD

29
Q

What is the gross pathology of chromophobe RCC?

A

-Tan-brown in color

30
Q

What is the microscopic pathology of chromophobe RCC?

A
  • Large, pale cells with prominent cell membranes
  • Nuclei are surrounded by halos of clear cytoplasm
  • Tumor cells stain more darkly
  • (+) for Hale’s Colloidal iron stain
31
Q

Which form of RCC has the best prognosis?

A

Chromophobe RCC has the best prognosis

32
Q

Other than the renal tubular epithelium, where do other renal primary tumors originate? Why?

A

urothelium of the renal pelvis (transitional cells). Associated with stones!

33
Q

What are “transitional cells”?

A

urothelial cells that look like a transition between a squamous cell and a mucous secreting cell

34
Q

What is another name for Wilm’s tumor?

A

nephroblastoma

35
Q

What is Wilm’s tumor?

A

uncommon renal neoplasm of young children (ages 2-5)

36
Q

What is the pathogenesis of Wilm’s tumor?

A

May arise sporadically or be familial (AD)–tumors derive from mesoderm (blastema cells)

37
Q

What is the gross pathology of Wilm’s tumor?

A
  • Large, solitary, well-circumscribed mass

- Tan-gray, soft, homogenous tumor with occasional foci of hemorrhage, cystic degeneration , and necrosis

38
Q

What is the triphasic combination seen in Wilm’s tumor?

A

1) Blastema cells (small, round, blue)
2) Epithelial cells (forming abortive tubules and glomeruli)
3) Stromal cells (look like fibroblasts)

39
Q

What are anaplastic cells? Why are they important?

A

Large, hyperchromatic, pleomorphic nuclei with abnormal mitoses–give a negative prognosis

40
Q

What are nephrogenic rests?

A

putative precursor lesions present int he parenchyma adjacent to the tumor (increase risk for WT in contralateral kidney)

41
Q

What are the S/S of Wilm’s tumor?

A

Abdominal Mass (pain)
Fever
Hematuria

42
Q

What is the treatment of Wilm’s tumor?

A

nephrectomy and chemotherapy (good prognosis unless anaplasia)

43
Q

What are the 3 syndromes of congenital malformations associated with Wilm’s tumor?

A

1) WAGR Syndrome
2) Denys-Drash Syndrome
30 Beckwith-Wiedemann Syndrome

44
Q

What is WAGR syndrome?

A

Wilms Tumor
Anirida (absence of iris)
Genital Abnormalities
Retardation

45
Q

What causes WAGR syndrome?

A

WT1 gene deletions (responsible for normal renal and gonadal development)

46
Q

What chromosome is WT1 on?

A

chromosome 11

47
Q

What is Denys-Drash Syndrome?

A

Gonadal Dysgenesis + Renal Abnormalities

48
Q

What causes Dens-Drash syndrome?

A

dominant negative inactivating mutations of WT1

49
Q

What is Beckwith-Wiedemann Syndrome?

A

Enlargement of individual organs (especially on one half of the body) with enlargement of adrenal cortical cells

50
Q

What causes Beckwith-Wiedemann Syndrome?

A

Abnormal genomic imprinting of WT2 that normally silences the maternal allele controlling the expression of insulin-like growth factor 2.–> now both paternal (normal) and maternal (not normal) alleles of IGF-2 are expressed (overexpression!!)

Renal (12 decks)

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