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Renal Path MC > Renal 5 > Flashcards

Renal 5 Flashcards

1
Q

examples of interstitial disease

A

ischemic papillary necrosis, toxic and HS (drugs)

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2
Q

most common cause of intrinsic renal disease and ARF

A

ATN

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3
Q

two most common causes of ATN

A

acute toxic or ischemic damage (loss blood flow)

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4
Q

this combination depicts spectrum of symptoms present in ATN

A

loss tubular function and GFR

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5
Q

what occurs due to toxic or ischemic damage of tubules

A

acute necrosis of tubular epithelium with acute suppression renal function

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6
Q

what occurs intracellularly due to tubular ischemic injury

A

depletion ATP, accumulation Ca, activation proteases and phospholipases

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7
Q

morphology of ATN (regardless of etiology)

A

focal tubular epithelial necrosis/apoptosis, rupture BM, occlusion tubular lumens by casts

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8
Q

part of tubule most commonly injured by toxins

A

proximal segment

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9
Q

toxicity of carbon tetrachloride is characterized by this

A

neutral lipid accumulation

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10
Q

characterizes ethylene glycol poisoning of kidney

A

ballooning and hydropic or vacuolar degeneration w/ formation calcium oxalate crystals

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11
Q

what occurs in initiating phase of ATN

A

declining urine output, increasing BUN (36 hours)

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12
Q

what occurs in recovery phase of ATN

A

increase urine output (3 L/day), hypokalemia, gradual improvement concentrating ability

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13
Q

what occurs in maintenance phase of ATN (several days)

A

diminished renal output, salt and water overload, increased BUN, hyperkalemia, metabolic acidosis (ALL FROM DECREASED GFR)

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14
Q

possible causes of acute interstitial nephritis

A

HS to drugs or metabolic dysfunction, ARF

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15
Q

gentimycin potentially causes this kind of kidney damage

A

ATN

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16
Q

synthetic penicillins (methicillin, ampicillin) potentially cause this kind of kidney damage

A

acute interstitial nephritis

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17
Q

drugs that are known to cause acute interstitial nephritis

A

sulfonamides, synthetic penicillins, diuretics (thiazides), NSAIDS (phenylbutazone)

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18
Q

chronic analgesic abuse is associated with development of this

A

transitional papillary carcinoma of renal pelvis

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19
Q

this is associated with development of transitional papillary carcinoma of renal pelvis

A

chronic analgesic abuse

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20
Q

causes of papillary necrosis

A

analgesic nephropathy, diabetes, urinary tract obstruction, sickle cell (anemia or trait), renal TB

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21
Q

benign renal tumor with eosinophilic cells and LOTS of mitochondria

A

oncocytoma

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22
Q

clinical presentation of Wilm’s tumor (nephroblastoma)

A

large abdominal mass, hematuria/pain after trauma, intestinal obstruction, HTN (damage to blood flow)

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23
Q

what renal cell carcinoma tumors arise from

A

tubular epithelium

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24
Q

nephrotoxic agents that can cause ATN

A

gentamicin, radiographic contrast agents, heavy metals, carbon tetrachloride

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25
Q

common scenarios that lead to ATN

A

transfusion reaction, ethylene glycol or methanol poisoning, hemoglobinuria or myoglobinuria (crush injury, alcohol binges), shock

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26
Q

ischemic changes seen in tubular cell injury

A

cell swelling, blebbing, loss of polarity, necrosis/apoptosis

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27
Q

this signals feedback mechanism to constrict afferent arteriole (decreasing delivery of filtrate) in ATN pathogenesis

A

increased Na in distal tubules

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28
Q

this complicates tubular ischemia (other than change in glomerular flow rate)

A

reflex vasoconstriction and decreased GFR

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29
Q

this determines re-epithelializatoin and return of tubule function

A

integrity tubular BM

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30
Q

this makes up casts in ATN -> huge glycoprotein secreted in loop of Henle and distal tubules

A

Tamm-Horsfall protein

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31
Q

these all contribute to cast formation in ATN (eosinophilic hyaline or pigmented granular casts)

A

Tamm-Horsfall protein, hemoglobin, myoglobin, plasma proteins

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32
Q

where Tamm-Horsfall proteins are secreted

A

loop of Henle and distal tubules

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33
Q

morphology of regenerating epithelial cells

A

flattened, hyperchromatic nuclei, mitotic figures

34
Q

form of ATN that is usually related to non-oliguric presentation (50%)

A

toxic

35
Q

primary cause of interstitial disease; secondary?

A

infection, toxin, obstruction; vascular, cystic, glomerular disease progression

36
Q

this distinguishes interstitial nephritis from other renal disease

A

absence nephritic/nephrotic syndrome

37
Q

signs of secondary tubular function defect related to interstitial disease

A

impaired concentrating ability, salt wasting, metabolic acidosis, isolated defect tubular reabsorption/secretion

38
Q

possible cause of chronic interstitial nephritis; what is morphology?

A

slowly progressing toxic dysfunction (analgesic abuse); infiltration mononuclear cells, interstitial fibrosis, tubular atrophy

39
Q

symptoms of HS reaction in acute drug-induced interstitial nephritis -> 2-6 weeks after exposure

A

fever, eosinophilia, rash (25%), renal abnormalities (ARF, increasing serum Cr)

40
Q

associated condition with chronic analgesic abuse

A

chronic tubulointerstitial nephritis with renal papillary necrosis

41
Q

this analgesic has metabolites with direct toxic effects to the kidney; how does it cause damage?

A

phenacetin; oxidative damage

42
Q

this potentiates phenacetin oxidative injury on kidney

A

prostaglandin inhibitors (causes ischemia)

43
Q

what occurs first in chronic analgesic abuse: papillary necrosis or tubulointerstitial nephritis?

A

papillary necrosis

44
Q

morphology of acute HS interstitial nephritis

A

edema, interstitial monocyte/lymphocyte infiltrate (some PMN and eosinophil also)

45
Q

these drugs cause interstitial granuloma formation

A

methicillin, thiazides

46
Q

chronic morphological changes in interstitial nephritis

A

tubular atrophy, interstitial fibrosis, inflammation, surface depression, papillary necrosis/calcification/fragmentation, coagulative necrosis

47
Q

signs/symptoms of analgesic nephropathy

A

inability concentrate urine, metabolic acidosis, stone formation, HA, anemia, GI symptoms, HTN

48
Q

consequences of papillary necrosis

A

urinary obstruction, infection, stone formation

49
Q

various mechanisms of NSAID nephropathy

A

lack vasodilation causing ARF, acute HS reaction, acute interstitial nephritis and lipoid nephrosis, membranous GN w/ nephrotic syndrome

50
Q

consequence of hypercalcemia and nephrocalcinosis -> deposition of calcium leading to chronic tubulointerstitial disease

A

tubular atrophy, interstitial fibrosis and inflammation

51
Q

mechanisms of interstitial fibrosis

A

CRF, transplant, angiotensin II (chronic activation RAS), TGF-b induction thru NFK-b

52
Q

direct complications of MM tumor leading to renal disease

A

hypercalcemia, hyperuricemia, obstruction ureters

53
Q

forms of MM related kidney disease

A

light-chain GN, tubular obstruction and cast nephropathy (deposition, combine with Tamm-Horsfall to make casts)

54
Q

morphology of MM kidney disease

A

Bence Jones tubular casts, adjacent interstitial inflammation, amyloid deposits, granulomatous inflammatory rxn

55
Q

MM related ARF may be precipitated by these factors

A

dehydration, hypercalcemia, infection, nephrotoxic antibiotics

56
Q

characteristic of amyloidosis

A

Congo red positive fibrillary deposits in mesangium and sub endothelium, obliteration glomerulus, blood vessel walls, kidney interstitium

57
Q

where are benign renal papillary adenomas found? what are they derived from?

A

cortex; tubular epithelium

58
Q

renal papillary adenoma does not differ from this malignant cancer -> only distinguishing feature is size

A

low-grade papillary renal cell carcinoma

59
Q

benign renal tumor in children

A

cystic nephroma

60
Q

most common primary renal tumor of childhood (ages 2-5)

A

Wilm’s tumor (nephroblastoma)

61
Q

inheritable syndromes of wilm’s tumor associated with this

A

specific aberrations multiple loci chromosome 11 (WT1 -> tumor supressor gene)

62
Q

premalignant condition associated with wilm’s tumor -> multi centric or diffuse foci immature nephrogenic elements

A

nephroblastomatosis

63
Q

found in nephroblastomatosis (premalignant) -> second genetic insult results in malignant tumor formation

A

immature nephrogenic elements

64
Q

diagnostic morphology of Wilm’s tumor

A

recapitulation different stages nephrogenesis, metanephric blastemic and immature stromal/epithelial elements

65
Q

this may represent precursor lesions to Wilm’s tumor

A

neprogenic tests

66
Q

associated clinical syndrome of Wilms tumor -> WAGR

A

wilms tumor, aniridia, GU anomalies, mental retardation

67
Q

associated clinical syndrome of Wilms tumor -> Denys-Drash syndrome (DDS)

A

wilms tumor, intersexual disorders, glomeruopathy

68
Q

associated clinical syndrome of Wilms tumor -> Beckwith-Wiedemann syndrome (BWS)

A

wilms tumor, overgrowth (gigantism), visceromegaly, macroglossia

69
Q

renal cell carcinoma cells resemble these

A

clear cells of adrenal cortex

70
Q

risk factors for renal cell carcinoma

A

tobacco, obesity, HTN, unopposed estrogen tx, asbestos/petroleum exposure, CRF, dialysis (acquired cystic disease)

71
Q

genetic abnormality associated with clear cell carcinoma (most common renal cell carcinoma)

A

unbalanced translocation chromosome 3 -> loss of VHL gene

72
Q

what gives rise to chromophobe renal carcinoma (excellent prognosis)

A

intercalated cells collecting ducts

73
Q

autosomal dominant cause of renal cell carcinoma -> characterized by renal cysts and bilateral renal cancer, hemangioblastomas of cerebellum and retina

A

Von Hippel-Lindau syndrome

74
Q

genetic abnormalities in hereditary papillary carcinomas

A

trisomies 7, 16, 17, loss of y in male, mutation c-met protooncogen

75
Q

morphology of renal cell carcinoma

A

upper pole (more commonly), solitary or unilateral lesion, bright yellow/gray-white, large necrotic area

76
Q

where does renal cell carcinoma tend to fungate?

A

ureter and renal vein (thru IVC to right side of heart)

77
Q

morphology of papillary tumors

A

multifocal or bilateral, hemorrhagic and cystic

78
Q

can stain for these components in clear cell carcinoma

A

glycogen and lipids

79
Q

morphology of clear cell carcinoma

A

rounded or polygonal, delicate branching vasculature, cystic or solid, glycogen and lipids

80
Q

morphology of papillary carcinoma

A

papillary formations, cuboidal or low columnar cells, psamomma bodies

Renal Path MC (5 decks)

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