Renal Tumors Flashcards

1
Q
  1. Describe the epidemiology of renal tumors, which are the most common?
A
Renal cell carcinoma:
clear cell 85%
papillary type 1 10%
chromophobe 2%
(other rare: papillary type 2, collecting duct, renal medullary-Sickle, uncategorized)
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2
Q
  1. Describe the epidemiology of renal tumors, what are risk factors for getting RCC?
A

more common in males, 60+, the obese (hormonal and metabolic changes), smoking (chronic inflammation/HTN), African Americans, chronic HTN (inflammation)

(ESRD and Familial RCC)

incidence has been increasing since the 70s with 68,000 cases in 2013

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3
Q
  1. Describe the detection of renal tumors.
A

incidental finding on imaging for another indication

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4
Q

Discuss the classifications of TNM Staging kidney cancer.

A

T1A <4cm, T1b 4-7cm, T2 7+cm (limited to the kidney)

T3a extension T3b extension to VC, T3c VC above the diaphragm, T4 invades the fascia

N & M nodes and metastatic spread

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5
Q
  1. Describe the appropriate radiographic and pathologic evaluation of renal masses.
A

confirmatory imaging is an enhancing mass of CT (with contrast), non enhancing renal masses <4 are debatable

some patients with cysts that are complex and enhanced have malignant changes- Category I and II have no enhancement, III and IV do, IIF can go either way

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6
Q
  1. Give examples of clinical syndromes associated with renal cell carcinoma.
A

“classic triad” hematuria, flank pain, palpable mass

abrupt development of varicocele in men (backed up testicular veins),
spontaneous bleeding around kidney

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7
Q
  1. Give examples of (paraneoplastic) clinical syndromes associated with renal cell carcinoma.
A

excess or lacking of normal products: Vit D, renin, EPO and various prostaglandins

abnormal products: PTH-like hormones, lupus-type anticoagulant, hCG, insulin, cytokines and inflammatory mediators

these lead to: elevated sed rate, HTN, cachexia and weight loss, anemia/polycythemia, hypercalcemia (bad)

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8
Q

What is Stauffer Syndrome?

A

non-metastatic hepatic dysfunction due to renal carcinoma: elevated alk. phos, prothrombin time, serum bilirubin, transaminase or hypoalbuminemia (IL-6 and other cytokines implicated

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9
Q
  1. Describe the pathology of clear cell renal cell carcinoma.
A

(most common type) originates in the cells of the PCT

grossly is bright yellow, microscopic appearance of chicken wire

Von Hippel-Lindau genes at 3P in some cases, most are sporadic mutation

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10
Q

Describe the characteristics of Von Hippel Lindau disease.

A

(autosomal dominant) hemangioblastomas (spine and cerebellum), pheochromocytomas, angioatosis (retinal), ccRCC, renal cysts, other cysts

results form a mutation of VHL the prevents hypoxia inducible factor (HIF) inactivation which can then drive VEGF and PDGF production and cancer

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11
Q

Describe Birt, Hogg and Dube Syndrome.

A

mutation in foliculin gene (AD), a tumor suppressor gene found in the skin, distal nephron and type 1 pneumocytes

associated with renal cancer (chromophobe RCC), pneumothorax, and skin findings (fibrofolliculomas, trichodiscomas, achrochordons)

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12
Q
  1. Discuss appropriate therapies, both surgical and medical, for small and large renal masses, with or without metastasis.
A

cytoreductive nephrectomy with immunotherapy +3mo survival

metastectomy is very effective when feasible

new neo-adjuvant therapy is being evaluated

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13
Q
  1. Discuss appropriate therapies, focusing on small molecule interactions.
A

mutant VHL does not inhibit HIF so medical interventions can inhibit other factors that encourage HIF ie. mTOR inhibitors: everolimus or temserolimus

PDGF and VEGF inhibitors can decrease the products of HIF: bevacizumab (anti VEGF), sorefenib and sunitinib are kinase inhibitors

these lead to longer lives, not necessarily cures

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14
Q
  1. Discuss appropriate therapies, describing the latest improvements in surgical interventions.
A

RCC is a surgical disease, can remove the whole kidney but reducing morbidity by taking only parts (arthroscopically or robotic assist)

other approaches for older more high risk patients is a percutaneous approach that destroys part of the kidney via cytogenesis or ablation

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