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Nephrology Fellowship Reviewer > OncoNephro > Flashcards

OncoNephro Flashcards

1
Q

2nd most common hematologic malignancy

A

multiple myeloma

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2
Q

unexplained kidney injury that occurs over less than 6 months with FLC concentration of > 1599 mg/L

A

cast nephropathy

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3
Q

excess light chains precipitate with tamm horsfall protein in the distal tubule

A

cast nephropathy

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4
Q

diagnostic for cast nephropathy

A

serum and urine immunofixation and serum flc analysis

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5
Q

Tx for cast nephropathy

A

volume resuscitation

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6
Q

proteinuria, renal insufficiency, nodular sclerosing glomerulopathy (mesangial and matrix expansion), crea > 4

A

light chain deposition disease

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7
Q

more uniform mesangial nodules, irregular thickening and double contours of GBM, linear staining of basement membranes with monotypic light chains

A

light chain deposition disease

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8
Q

pathogenic light chains unfold and deposit as insoluble fibrils within tissues

A

Amyloid light chain amyloidosis

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9
Q

AKI more common in allogenic vs autologous

A

allogenic

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10
Q

AKI typically develops in the first 3 weeks

A

myeloablative hct

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11
Q

aki distributed over the 1st 3 months

A

nonmyeloablative hct

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12
Q

pathogenesis of gvhd that lead to ckd

A

direct Tcell damage via cytokine induced inflammation or through CNI therapy

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13
Q

within first few days of hct, preservation of stem cells causing hemolysis

A

marrow infusion syndrome, hemoglobinuric AKI

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14
Q

tender hepatomegaly, fluid retention with ascites formation and jaundice; fibrous narrowing of small hepatic venules and sinusoids;

A

sinusoidal occlusion syndrome

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15
Q

hyperdynamic vital signs, oliguria, hyponatremia and low urinary sodium concentration, minimal proteinuria and muddy brown granular casts, fluid retention resistant to diuretics

A

sinusoidal occlusion syndrome

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16
Q

commonly associated with pretreatment with cyclophosphamide, busulfan, and/or TBI

A

sinusoidal occlusion syndrome

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17
Q

Endothelial damage leading to thickened glomerular and arteriolar vessels, the presence of fragmented red blood cells, thrombosis, and endothelial cell swelling

A

transplant associated thrombotic microangiopathy

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18
Q

(+) schistocytes on peripheral smear, elevated LDH ,doubling of crea, unexplained cns dysfunction, negative coombs, thrombocytopenia, anemia, decreased haptoglobulin

A

transplant associated thrombotic microangiopathy

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19
Q

Tx options of transplant associated microangiopathy

A

gvhd prophlaxis, tpe, rituximab, defibrotide

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20
Q

converts uric acid to water solluble allantoin decreasing uric acid levels and urinary acid excretion

A

rasburicase

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21
Q

gradual onset of nonoliguric AKI, direct tubular toxicity in a low Cl environment

A

cisplatin nephrotoxicity

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22
Q

decrease in gfr in clisplatin nephrotoxicity occurs when?

A

3-5 days after the exposure

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23
Q

promotion of better DNA repair and elimination of free radicals that can be used in cisplatin

A

amifostine

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24
Q

apoptosis of renal proximal tubular cells induced resulting in wasting of K, Mg, Ca and HCO3

A

cisplatin

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25
Q

alkylating drug that causes renal toxicity either directly or through a metabolite, chloroacetaldehyde, which directly damages tubular epithelial cells

A

ifosfamide

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26
Q

increased urinary B2 microglobulin

A

ifosfamide

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27
Q

hemorrhagic cystitis but not tubular injury

A

cyclophosphamide

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28
Q

increased ADH activity causing hyponatremia

A

cyclophosphamide

29
Q

prevention of cyclophosphamide nephrotoxicity

A

MESNA

30
Q

synthetic sulfhydryl compound that detoxifies metabolites in the urine preventing hemorrhagic cystitis

A

MESNA

31
Q

mechanisms of AKI in methotrexate

A

intrarenal obstruction, direct tubular toxicity, prerenal azotemia due to efferent arteriolar vasoconstriction

32
Q

medication that can be given to reduce systemic toxicity associated with MTX and AKI

A

leucovorin high dose

33
Q

associated with massive proteinuria

A

Interferon alfa

34
Q

systemic capillary leak syndrome

A

IL2

35
Q

prevention of IL2 induced AKI medication

A

low dose dopamine

36
Q

monoclonal Ab against vegf with assoc hypertension and proteinuria

A

bevacizumab

37
Q

monocloal Ab against egfr used in metastatic colon Ca, renal Mg wasting

A

cetuximab

38
Q

pathology in CNI causing AKI

A

direct afferent arteriolar vasoconstriction leading to decrease in the GF pressure and GFR

39
Q

arteriolar damage, interstitial fibrosis, tubular atrophy and glomerulosclerosis

A

CNI chronic nephrotoxicity

40
Q

reason for hyperK in CNI

A

tubular resistance to aldosterone

41
Q

Tx for hypercalcemia of malignancy

A

bisphosphonates

42
Q

most comon pathologic finding on renal biopsy in bisphosphonate toxicity

A

acute tubular necrosis

43
Q

highly protein bound, reducing risk of renal toxicity kind of bisphosphonate

A

ibandronate

44
Q

monoclonal antibody antiresorptive not cleared by kidney, preferred; may be used in breast/prostate Ca CKD stage 4

A

denosumab

45
Q

mean time to achieve normocalcemia with bisphosphonate

A

4 days

46
Q

inhibit osteoclastic bone resorption by decreasing tumor production of locally active cytokine

A

glucocorticoids

47
Q

pattern of injury in radiation induced AKI

A

tubular + glomerular

48
Q

Tx of radiation induced AKI

A

RAAS blockade

49
Q

most common malignancies to metastasize in the kidneys

A

lymphoma and leukemia

50
Q

criteria to support diagnosis of metastates to kdiney

A

renal enlargement without obstruction, absence of other causes of kidney disease, rapid improvement of kidney function and RT and chemotherapy

51
Q

reactive disorder that results from intense macrophage activation and cytokine release

A

cytotoxic nephropathy/

hemphagocytic syndrome

52
Q

Suspected in any patient with malignant lymphoma in whom unexplained multiple-organ dysfunction including AKI develops

A

cytotoxic nephropathy/

hemphagocytic syndrome

53
Q

definitive diagnosis fro hemophagocytic syndrome

A

bone marrow aspiration

54
Q

Tx for Hemophagocytic syndrome

A

IVIG, TPE, HCT; dexamehtasone and etoposide

55
Q

when to do TPE for TMA in patients with cancer?

A

TMA after bone marrow transplantation.

56
Q

classic drug that can cause thrombotic microangiopathy

A

mitomycin C

57
Q

Nonimmune hemolytic anemia, thrombocytopenia, varying degrees of encephalopathy, and renal failure due to platelet thrombi in the microcirculation of the kidneys

A

thrombotic microangiopathy

58
Q

better prognosis

A

papillary renal cell ca

59
Q

papillary and clear cell came from

A

proximal tubule

60
Q

Chromophone renal cell ca

A

collecting duct

61
Q

most common benign tumors

A

angiomyolipoma

oncocytoma

62
Q

cut off size T1

A

4-7

63
Q

T2

A

7-10

64
Q

T3

A

> 10

65
Q

when to do active surveillance

A

2 cm or smaller with high operative risk, monitor q3-6 months

66
Q

post tx surveillance

A

bet 3-12 months

yearly up to 3 (partial nephrec) and 5 (ablative therapy)

67
Q

initial immune therapy

A

interferon alfa and IL2

68
Q

targets vegf preventing angiogenesis

A

bevacizumab

69
Q

seattle criteria 2 of 3: jaundice, painful hepatomegaky, fluid retention or wt gain within 20’days of hsct

A

sinusoidal obstruction syndrome

Nephrology Fellowship Reviewer (29 decks)

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